[
{
"id": "Q1",
"orig": 1,
"title": "Tall thin patient with MVP",
"lesions": [
"MVP",
"AORTA",
"AR"
],
"lens": "vignette",
"items": [
{
"id": "Q1.1",
"q": "A 29-year-old woman, 185 cm tall and weighing 54 kg, is referred for atypical chest pain. Blood pressure is 114/52 mmHg. Echo shows bileaflet mitral valve prolapse. What underlying condition should you suspect?",
"a": "The combination of a tall, slender build, mitral valve prolapse, and a wide pulse pressure points toward Marfan syndrome, a heritable connective tissue disorder caused by fibrillin-1 defects. Weak elastic tissue lets the mitral leaflets become redundant and myxomatous, which is why prolapse is so common in these patients. The wide pulse pressure is a clue that the aortic root may already be dilated with some aortic regurgitation running off the diastolic pressure."
},
{
"id": "Q1.2",
"q": "When Marfan syndrome is suspected on echo, which other structures need careful assessment and why?",
"a": "Focus on the aortic root and ascending aorta. Measure the sinuses of Valsalva, sinotubular junction, and ascending aorta at end-diastole, leading edge to leading edge, because progressive root dilation is the life-threatening feature and it drives aortic regurgitation by stretching the annulus so the cusps no longer coapt. Also screen for dissection flaps, since a dilated Marfan aorta is prone to tearing. Quantify any AR and MR, and note the degree of MVP, because these findings determine follow-up interval and surgical timing."
}
],
"numbers": [],
"delta": null,
"pearl": "Tall, thin, wide pulse pressure plus MVP: look up, not down; the aortic root is the real question.",
"lookalike": {
"vs": "isolated myxomatous MVP",
"discriminator": "A normal-caliber aortic root and normal body habitus favor primary MVP; root dilation or ectopia lentis favors Marfan."
},
"related": [
"Q9",
"Q365"
],
"reviewed": "2026-08-26"
},
{
"id": "Q2",
"orig": 2,
"title": "New murmur with febrile illness",
"lesions": [
"ENDOCARDITIS",
"MR",
"TEE"
],
"lens": "vignette",
"items": [
{
"id": "Q2.1",
"q": "A 44-year-old man with no prior heart disease has had a week of fevers, chills, and malaise. His physician hears a systolic murmur that was never documented before. Echo shows a thickened, irregular anterior mitral leaflet with mild mitral regurgitation. What is the most likely explanation?",
"a": "Infective endocarditis of the mitral valve is the leading concern. Bacteria seeded into the bloodstream adhere to the atrial surface of the leaflet and build a vegetation of platelets, fibrin, and organisms, which on echo looks like a mobile or shaggy thickening that moves with the leaflet. As the infection destroys leaflet tissue, the valve leaks, producing the new regurgitant murmur. A new murmur plus fever in a young adult should be treated as endocarditis until proven otherwise."
},
{
"id": "Q2.2",
"q": "Which further tests help confirm suspected mitral endocarditis?",
"a": "Serial blood cultures, ideally three sets drawn before antibiotics, identify the organism and form the microbiologic half of the modified Duke criteria. Transesophageal echo supplies the imaging half: its higher frequency and closer proximity to the mitral valve pick up small vegetations, leaflet perforation, chordal rupture, and perivalvular abscess that transthoracic imaging can miss. TEE also grades the regurgitation more accurately, which matters when deciding whether surgery is needed."
}
],
"numbers": [],
"delta": null,
"pearl": "Fever plus a brand-new murmur equals endocarditis until cultures and TEE say otherwise.",
"lookalike": {
"vs": "myxomatous leaflet thickening",
"discriminator": "Myxomatous thickening is diffuse and smooth; a vegetation is focal, irregular, oscillates independently, and sits on the upstream (atrial) side of the leaflet."
},
"related": [
"Q8",
"Q319",
"Q321"
],
"reviewed": "2026-08-26"
},
{
"id": "Q3",
"orig": 3,
"title": "Pericardial knock and ascites",
"lesions": [
"CONSTRICTION",
"EFFUSION"
],
"lens": "physical-exam",
"items": [
{
"id": "Q3.1",
"q": "A 61-year-old woman has three months of worsening exertional breathlessness. Examination shows distended neck veins, ascites, and an early diastolic sound that the cardiologist calls a pericardial knock. What diagnosis best explains this picture?",
"a": "Constrictive pericarditis. A thickened, non-compliant pericardium lets the ventricles fill rapidly in early diastole but then stops filling abruptly when the heart reaches the fixed pericardial volume. That sudden halt produces the high-pitched early diastolic knock, which is essentially an exaggerated, early S3. Because filling is limited, systemic venous pressure rises, causing jugular distension, hepatic congestion, and ascites, while the fixed stroke volume causes exertional dyspnea. On echo, look for a septal bounce with respiratory shift, preserved or elevated medial e' (annulus reversus), and expiratory diastolic flow reversal in the hepatic veins."
}
],
"numbers": [
{
"label": "Medial e' supporting constriction",
"value": "> 7 (> 8 favors)",
"unit": "cm/s"
},
{
"label": "Hepatic vein expiratory diastolic reversal ratio",
"value": "≥ 0.79",
"unit": "ratio"
}
],
"delta": {
"was": "2011 card and the Mayo criteria (ASE 2013) set the constriction medial e' cut-off at ≥ 9 cm/s.",
"now": "ASE 2025 lowers the constriction medial e' cut-off to > 7 cm/s, with > 8 cm/s strongly favoring constriction; it pairs with respirophasic septal shift for about 80% sensitivity and 96% specificity.",
"source": "ASE 2025 diastolic function guideline"
},
"pearl": "Knock plus ascites plus preserved e' means the pericardium, not the myocardium, is the problem.",
"lookalike": {
"vs": "restrictive cardiomyopathy",
"discriminator": "Constriction keeps medial e' high (> 7 cm/s, > 8 favors constriction) and shows respirophasic septal shift; restriction has low e', high E/e', and no respiratory variation."
},
"related": [
"Q7",
"Q28",
"Q254"
],
"reviewed": "2026-08-26"
},
{
"id": "Q4",
"orig": 4,
"title": "Pulmonic valve notch and RV enlargement",
"lesions": [
"PH",
"ASD",
"CONTRAST"
],
"lens": "m-mode",
"items": [
{
"id": "Q4.1",
"q": "A 35-year-old woman with fatigue has cardiomegaly on chest film. Echo shows right atrial and right ventricular enlargement, a flattened interventricular septum, and pulmonic valve M-mode with mid-systolic closure and loss of the A wave. What do these findings indicate, and what should you do next?",
"a": "These are the classic signs of pulmonary hypertension. When pulmonary artery pressure is high, the RV ejects against a stiff, high-impedance bed, so flow decelerates abruptly in mid-systole and the pulmonic leaflets partially close, producing the notch (flying W). Elevated PA diastolic pressure also prevents atrial contraction from moving the leaflets, so the A dip disappears. The pressure-loaded RV dilates and pushes the septum flat in systole. Confirm with a TR jet estimate of RVSP, then inject agitated saline to look for an atrial-level shunt, because a long-standing ASD is a treatable cause of pulmonary hypertension in a young adult and would show bubbles crossing into the left atrium within a few beats."
}
],
"numbers": [
{
"label": "TR Vmax suggesting high PH probability",
"value": "> 3.4",
"unit": "m/s"
},
{
"label": "PA acceleration time suggesting PH",
"value": "< 105",
"unit": "ms"
},
{
"label": "mPAP defining PH (ESC/ERS 2022)",
"value": "> 20",
"unit": "mmHg"
}
],
"delta": null,
"pearl": "Mid-systolic pulmonic notch plus absent A wave equals high PA pressure; then ask why, and a bubble study is the first why.",
"lookalike": {
"vs": "RV volume overload from ASD without PH",
"discriminator": "Pure volume overload flattens the septum in diastole, whereas pressure overload flattens it in systole; the pulmonic notch appears only with elevated PA pressure."
},
"related": [
"Q10",
"Q26",
"Q28",
"Q269"
],
"reviewed": "2026-08-26"
},
{
"id": "Q5",
"orig": 5,
"title": "Young athlete with massive LVH",
"lesions": [
"HCM"
],
"lens": "vignette",
"items": [
{
"id": "Q5.1",
"q": "A 24-year-old man reports chest pain after exercise. Echo shows concentric hypertrophy with a 25 mm wall, a small LV cavity, no systolic anterior motion of the mitral valve, and no pericardial effusion. What is the most likely diagnosis?",
"a": "Hypertrophic cardiomyopathy. A wall thickness of 25 mm in a young person with no hypertension or aortic stenosis to explain it is far beyond physiologic athlete's heart, which rarely exceeds about 15 mm and comes with a normal or enlarged cavity. HCM is a sarcomere-gene disease in which myocyte disarray thickens the wall and shrinks the cavity, so diastolic filling is impaired and the hypertrophied muscle outstrips its blood supply, causing exertional chest pain. The absence of SAM simply means there is no resting outflow obstruction; it does not exclude HCM."
},
{
"id": "Q5.2",
"q": "No resting outflow gradient is found in a patient with HCM. What noninvasive tests can reveal latent obstruction?",
"a": "Provoke the gradient while recording the LVOT with continuous-wave Doppler. Valsalva strain and standing reduce preload, and amyl nitrite inhalation reduces afterload; each shrinks the LV cavity and pulls the mitral leaflet into the outflow tract by Venturi and drag forces, unmasking a dynamic gradient. Exercise stress echo is the preferred provocation in current practice because it reproduces the symptoms and a gradient of 50 mmHg or more identifies patients who benefit from septal reduction. The dynamic gradient has a late-peaking, dagger-shaped CW signal, unlike the symmetric signal of fixed aortic stenosis."
}
],
"numbers": [
{
"label": "Wall thickness in this vignette",
"value": "25",
"unit": "mm"
},
{
"label": "Provoked LVOT gradient considered significant",
"value": "≥ 50",
"unit": "mmHg"
}
],
"delta": null,
"pearl": "Dagger-shaped late-peaking CW envelope equals dynamic obstruction; symmetric envelope equals fixed valve stenosis.",
"lookalike": {
"vs": "athlete's heart",
"discriminator": "Athlete's heart has a large cavity, wall thickness usually under 15 mm, normal diastolic function, and regresses with deconditioning."
},
"related": [
"Q27",
"Q30",
"Q7",
"Q248",
"Q373"
],
"reviewed": "2026-08-26"
},
{
"id": "Q6",
"orig": 6,
"title": "EPSS and B-notch on M-mode",
"lesions": [
"DCM"
],
"lens": "m-mode",
"items": [
{
"id": "Q6.1",
"q": "A 41-year-old man with two months of severe exertional dyspnea has M-mode showing a dilated left ventricle, a wide E-point septal separation, a B-notch on the mitral valve trace, and globally reduced wall excursion. What do these findings suggest?",
"a": "Dilated cardiomyopathy. The E-point septal separation widens because a weak ventricle ejects a small stroke volume, so the mitral inflow that follows is also small and the anterior leaflet fails to reach the septum; an EPSS above about 7 mm tracks with a reduced ejection fraction. The B-notch, a shoulder on the A-C closure line, appears when the LV end-diastolic pressure is high and the leaflets drift toward closure before the ventricle contracts. Add a dilated cavity with poor excursion of both septum and posterior wall, and the M-mode alone tells you the ventricle is large, weak, and stiff, which is the DCM triad."
}
],
"numbers": [
{
"label": "Abnormal EPSS",
"value": "> 7",
"unit": "mm"
}
],
"delta": null,
"pearl": "Big EPSS means low EF; B-notch means high LVEDP; both together say dilated cardiomyopathy.",
"lookalike": {
"vs": "ischemic cardiomyopathy",
"discriminator": "Ischemic disease produces regional wall-motion abnormalities matching coronary territories, whereas idiopathic DCM is globally hypokinetic."
},
"related": [
"Q18",
"Q24",
"Q252"
],
"reviewed": "2026-08-26"
},
{
"id": "Q7",
"orig": 7,
"title": "Bright thick myocardium with small effusion",
"lesions": [
"RCM",
"EFFUSION"
],
"lens": "vignette",
"items": [
{
"id": "Q7.1",
"q": "A 63-year-old woman with cardiomegaly on chest film and worsening exertional dyspnea has an echo showing thick LV walls with a speckled, glittering myocardium, left atrial enlargement, and a small pericardial effusion. What diagnosis does this pattern suggest?",
"a": "An infiltrative restrictive cardiomyopathy, most often cardiac amyloidosis. Amyloid protein deposits between myocytes thicken the walls without true myocyte hypertrophy, which is why the ECG voltage is low despite an echo that looks like LVH, and the deposits scatter ultrasound to give the granular sparkle. The infiltrated ventricle is stiff, so filling pressures climb, the atria dilate, and a small effusion is common. Look for a restrictive filling pattern, markedly reduced global longitudinal strain with apical sparing, and thickened valves and atrial septum to strengthen the diagnosis."
}
],
"numbers": [],
"delta": null,
"pearl": "Thick walls on echo plus low voltage on ECG equals infiltration, not hypertrophy.",
"lookalike": {
"vs": "hypertensive LVH or HCM",
"discriminator": "Infiltrative disease has low ECG voltage, biatrial enlargement, thick valves and atrial septum, and apical-sparing strain; HCM and hypertensive LVH have high ECG voltage."
},
"related": [
"Q3",
"Q5",
"Q248",
"Q256",
"Q378"
],
"reviewed": "2026-08-26"
},
{
"id": "Q8",
"orig": 8,
"title": "Causes of a diastolic rumble",
"lesions": [
"MS",
"MASS",
"AR"
],
"lens": "physical-exam",
"items": [
{
"id": "Q8.1",
"q": "A 59-year-old woman with shortness of breath has a low-pitched, rumbling diastolic murmur. She denies any history of rheumatic fever. Name three cardiac lesions that could produce this murmur.",
"a": "First, rheumatic mitral stenosis (or, less commonly, tricuspid stenosis): a rumble comes from turbulent low-velocity flow across a narrowed atrioventricular valve, and many adults with rheumatic disease never recall the childhood illness. Second, a left atrial myxoma, which can prolapse into the mitral orifice in diastole and obstruct inflow, mimicking mitral stenosis both on auscultation and in symptoms; the tumor may also produce a diastolic plop. Third, significant aortic regurgitation with an Austin Flint murmur: the regurgitant jet strikes the anterior mitral leaflet and pushes it toward closure, creating functional mitral inflow obstruction and a rumble even though the mitral valve itself is normal. Echo separates these easily by showing leaflet doming and a reduced orifice in MS, a mobile atrial mass in myxoma, and a wide AR jet with a structurally normal mitral valve in Austin Flint."
}
],
"numbers": [
{
"label": "Severe MS valve area",
"value": "≤ 1.5",
"unit": "cm²"
},
{
"label": "Normal mitral valve area",
"value": "4–6",
"unit": "cm²"
}
],
"delta": null,
"pearl": "Diastolic rumble: stenosis, tumor, or Austin Flint; echo settles it in one apical view.",
"lookalike": {
"vs": "mitral stenosis vs Austin Flint",
"discriminator": "Austin Flint has a structurally normal mitral valve with a normal pressure half-time and a large AR jet; rheumatic MS has thickened, doming leaflets with commissural fusion."
},
"related": [
"Q2",
"Q29",
"Q25"
],
"reviewed": "2026-08-26"
},
{
"id": "Q9",
"orig": 9,
"title": "Tearing chest pain in a hypertensive",
"lesions": [
"AORTA",
"TEE"
],
"lens": "vignette",
"items": [
{
"id": "Q9.1",
"q": "A 34-year-old man with poorly controlled hypertension arrives with sudden, severe chest pain that he describes as tearing and that radiates to his back. What diagnosis must be considered first?",
"a": "Acute aortic dissection. Chronic hypertension stresses the aortic media, and once the intima tears, pulsatile blood strips the layers apart to create a false lumen; the propagation of that tear is what patients feel as ripping or tearing pain that migrates. Although myocardial infarction is on the differential, the character of the pain, the young age, and the hypertensive history all favor dissection, and giving anticoagulants for a presumed MI to a dissection patient can be fatal. Classify any dissection by whether the ascending aorta is involved: Stanford A (ascending involved, surgical) or Stanford B (descending only, usually medical)."
},
{
"id": "Q9.2",
"q": "Which noninvasive imaging test best confirms or excludes aortic dissection in this setting?",
"a": "Transesophageal echo and CT angiography are both first-line, with sensitivity near 98 percent. TEE can be done at the bedside in an unstable patient without contrast and shows the intimal flap, true and false lumen, entry tear, aortic regurgitation, and pericardial effusion in one study; its blind spot is the distal ascending aorta and proximal arch where the trachea intervenes. CT is faster to obtain in most emergency departments and images the entire aorta and branches. Transthoracic echo is a useful first look for a root flap, AR, or tamponade, but a normal TTE does not exclude dissection."
}
],
"numbers": [
{
"label": "TEE sensitivity for dissection",
"value": "~ 98",
"unit": "%"
}
],
"delta": null,
"pearl": "Tearing pain plus hypertension: image the aorta before anyone anticoagulates for MI.",
"lookalike": {
"vs": "acute MI",
"discriminator": "Dissection pain is maximal at onset and migrates; a pulse deficit, new AR murmur, or widened mediastinum favors dissection over MI."
},
"related": [
"Q1",
"Q283"
],
"reviewed": "2026-08-26"
},
{
"id": "Q10",
"orig": 10,
"title": "Apically displaced tricuspid valve",
"lesions": [
"EBSTEIN",
"ASD",
"CONTRAST"
],
"lens": "vignette",
"items": [
{
"id": "Q10.1",
"q": "A 19-year-old man with palpitations has cardiomegaly on chest film. Echo shows right atrial and right ventricular enlargement, and the septal tricuspid leaflet inserts far toward the apex. What is the most likely diagnosis?",
"a": "Ebstein anomaly. The septal and posterior tricuspid leaflets fail to delaminate from the RV wall during development, so their hinge points sit deep in the ventricle. The diagnostic threshold is apical displacement of the septal leaflet at least 8 mm/m² (roughly 20 mm in an adult) relative to the mitral annulus in the apical four-chamber view. The inflow portion of the RV above the displaced valve becomes atrialized, the true RA plus the atrialized RV form a huge right-sided chamber, and the malformed valve leaks, which explains the cardiomegaly. Palpitations are common because accessory pathways (WPW) accompany the anomaly in a sizable minority."
},
{
"id": "Q10.2",
"q": "What additional study should be performed during the echo in a patient with Ebstein anomaly, and why?",
"a": "An agitated saline contrast study to look for an interatrial communication. A secundum ASD or patent foramen ovale accompanies Ebstein anomaly in most patients, and the elevated right atrial pressure from severe tricuspid regurgitation drives right-to-left shunting, which produces cyanosis and a risk of paradoxical embolism. Bubbles appearing in the left atrium within a few beats of reaching the right atrium confirm the shunt; a Valsalva release during the injection increases the sensitivity."
}
],
"numbers": [
{
"label": "Septal leaflet apical displacement (indexed)",
"value": "≥ 8",
"unit": "mm/m²"
},
{
"label": "Septal leaflet apical displacement (adult)",
"value": "≥ 20",
"unit": "mm"
}
],
"delta": null,
"pearl": "Tricuspid hinge more than 20 mm below the mitral hinge in an adult equals Ebstein; then bubble it.",
"lookalike": {
"vs": "tricuspid valve dysplasia",
"discriminator": "Dysplasia thickens the leaflets but keeps the hinge points at the annulus; Ebstein moves the septal hinge apically beyond the threshold."
},
"related": [
"Q4",
"Q26",
"Q311",
"Q312",
"Q313",
"Q315",
"Q317"
],
"reviewed": "2026-08-26"
},
{
"id": "Q11",
"orig": 11,
"title": "LV segments in the short axis",
"lesions": [
"ANATOMY",
"VIEWS"
],
"lens": "anatomy",
"items": [
{
"id": "Q11.1",
"q": "In the parasternal short-axis view at the mitral valve level and again at the papillary muscle level, into how many segments is the left ventricle divided?",
"a": "Six segments at each level. The ASE 17-segment model slices the ventricle into basal (mitral valve level), mid (papillary muscle level), and apical rings; the basal and mid rings each contain six segments, the apical ring contains four, and the apical cap is the seventeenth. The mitral and papillary short-axis views therefore each display six wedge-shaped segments of 60 degrees, which lets you assign wall motion abnormalities to a coronary territory."
},
{
"id": "Q11.2",
"q": "Name the six left ventricular segments seen in the basal and mid parasternal short-axis views, and describe how they are oriented on screen.",
"a": "Starting at the top of the image next to the right ventricle and moving clockwise: anteroseptal, anterior, anterolateral, inferolateral, inferior, and inferoseptal. The septal segments touch the RV, the anterior segment is closest to the transducer, and the inferior segment lies nearest the diaphragm. Remembering the clock order matters because the LAD feeds the anterior and anteroseptal wedges, the circumflex feeds the anterolateral and inferolateral wedges, and the RCA feeds the inferior and inferoseptal wedges."
}
],
"numbers": [
{
"label": "Segments per basal or mid short-axis ring",
"value": "6",
"unit": "segments"
},
{
"label": "Segments in the apical ring",
"value": "4",
"unit": "segments"
},
{
"label": "Total ASE model segments",
"value": "17",
"unit": "segments"
}
],
"delta": null,
"pearl": "6 + 6 + 4 + 1 cap = 17; the short-axis views show the two sets of six.",
"lookalike": null,
"related": [
"Q12",
"Q13",
"Q17"
],
"widgets": [
"bullseye"
],
"reviewed": "2026-08-26"
},
{
"id": "Q12",
"orig": 12,
"title": "Walls in the apical views",
"lesions": [
"ANATOMY",
"VIEWS"
],
"lens": "anatomy",
"items": [
{
"id": "Q12.1",
"q": "Which two left ventricular walls are displayed in the apical four-chamber view?",
"a": "The inferoseptal wall on the left of the screen (next to the RV) and the anterolateral wall on the right. The four-chamber plane cuts obliquely through the ventricle so that the septal portion you see is the inferior part of the septum, which is RCA territory at the base and mid levels, while the opposite wall is circumflex territory. This is why an inferior infarct can show basal septal hypokinesis in the four-chamber view even though the anterior septum looks normal in the long axis."
},
{
"id": "Q12.2",
"q": "Which two left ventricular walls are displayed in the apical two-chamber view?",
"a": "The inferior wall on the left of the screen and the anterior wall on the right. Rotating the transducer counterclockwise about 60 degrees from the four-chamber view removes the right heart and brings the plane into the vertical long axis, which lies roughly perpendicular to the four-chamber plane. The two-chamber view is the best window for the inferior wall (RCA) and the anterior wall (LAD), and together the three apical views cover all six wall regions."
}
],
"numbers": [
{
"label": "Rotation from 4-chamber to 2-chamber",
"value": "~ 60",
"unit": "degrees counterclockwise"
}
],
"delta": null,
"pearl": "Four-chamber: inferoseptal and anterolateral. Two-chamber: inferior and anterior. Long-axis: anteroseptal and inferolateral.",
"lookalike": null,
"related": [
"Q11",
"Q13",
"Q21"
],
"reviewed": "2026-08-26"
},
{
"id": "Q13",
"orig": 13,
"title": "Walls and cusps in the long axis",
"lesions": [
"ANATOMY",
"VIEWS",
"AS"
],
"lens": "anatomy",
"items": [
{
"id": "Q13.1",
"q": "Which left ventricular walls are imaged in the parasternal long-axis and apical long-axis (three-chamber) views?",
"a": "The anteroseptal wall and the inferolateral wall. Both views cut the same anatomic plane through the LV outflow tract, differing only in transducer position, so the septum nearest the aorta is the anterior septum (LAD territory) and the opposite wall behind the mitral valve is the inferolateral wall (circumflex territory, sometimes RCA in a right-dominant system). The apical long-axis view adds the apex, which the parasternal view foreshortens."
},
{
"id": "Q13.2",
"q": "Which two aortic cusps are seen in the long-axis views, and which one is closer to the transducer?",
"a": "The right coronary cusp and the noncoronary cusp. The right coronary cusp is the anterior structure, so it appears at the top of the image nearest the transducer, adjacent to the RV outflow tract; the noncoronary cusp lies posteriorly next to the interatrial septum and the anterior mitral leaflet. The left coronary cusp sits out of the plane, which is why the short-axis view at the aortic level is needed to count all three cusps and diagnose a bicuspid valve."
}
],
"numbers": [],
"delta": null,
"pearl": "Long axis shows Right on top, Noncoronary on the bottom; the Left cusp hides until you go short axis.",
"lookalike": null,
"related": [
"Q11",
"Q12",
"Q21"
],
"reviewed": "2026-08-26"
},
{
"id": "Q14",
"orig": 14,
"title": "Locating the coronary sinus",
"lesions": [
"ANATOMY",
"VIEWS"
],
"lens": "anatomy",
"items": [
{
"id": "Q14.1",
"q": "Where does the coronary sinus appear in the parasternal long-axis view?",
"a": "It sits in the posterior atrioventricular groove, the fold between the left atrium and left ventricle just behind the mitral annulus. In the parasternal long-axis view it appears as a small, round, echo-free structure tucked into that groove on the posterior side of the heart, immediately in front of the pericardium. It is small in normal hearts and easy to overlook, but it becomes obvious when dilated."
},
{
"id": "Q14.2",
"q": "How is the coronary sinus positioned relative to the descending thoracic aorta, and why does this matter?",
"a": "The coronary sinus lies anterior to the descending aorta, inside the pericardial reflection, while the descending aorta lies posterior and outside the pericardium. Both are round echo-free structures behind the left atrium and LV in the long-axis view, so a dilated coronary sinus can be mistaken for the aorta. The pericardium runs between them, which is the anatomic basis for using these two landmarks to separate pericardial from pleural fluid."
},
{
"id": "Q14.3",
"q": "How would you adjust the transducer from the apical four-chamber view to display the coronary sinus?",
"a": "Tilt the transducer posteriorly (angle the beam toward the back) from the standard four-chamber position. The coronary sinus runs in the posterior AV groove, so dropping the plane below the mitral annulus brings it into view as a tubular structure that courses along the annulus and empties into the right atrium. A very slight tilt is enough; over-angling loses the LV apex and enters the coronary sinus long axis, which is actually the view you want when checking for dilation."
}
],
"numbers": [],
"delta": null,
"pearl": "Posterior AV groove, inside the pericardium, in front of the descending aorta: that is the coronary sinus.",
"lookalike": {
"vs": "descending thoracic aorta",
"discriminator": "The coronary sinus is intrapericardial and runs along the AV groove into the RA; the descending aorta is extrapericardial, pulsatile, and continues below the diaphragm."
},
"related": [
"Q15"
],
"reviewed": "2026-08-26"
},
{
"id": "Q15",
"orig": 15,
"title": "Landmarks for effusions and dilated CS",
"lesions": [
"EFFUSION",
"PLSVC",
"TR"
],
"lens": "pitfall",
"items": [
{
"id": "Q15.1",
"q": "Why do sonographers pay attention to the coronary sinus and descending aorta when fluid is seen behind the heart?",
"a": "Because they mark the pericardial boundary. The coronary sinus is inside the pericardium and the descending aorta is outside it, so a pericardial effusion collects between the two, lying behind the coronary sinus but in front of the descending aorta. A left pleural effusion collects behind and lateral to the descending aorta. Confusing the two fluid collections can lead to an unnecessary pericardiocentesis or a missed tamponade, so tracking where the fluid sits relative to these landmarks in the parasternal long-axis view is the fastest way to tell them apart."
},
{
"id": "Q15.2",
"q": "What conditions cause the coronary sinus to dilate?",
"a": "Anything that raises right atrial pressure or increases the volume draining through the sinus. High RA pressure, as in severe tricuspid regurgitation, right heart failure, or pulmonary hypertension, backs up into the coronary venous system and distends it. Increased flow occurs with a persistent left superior vena cava, which drains into the coronary sinus and is the most common cause of a markedly enlarged sinus; injecting agitated saline into a left arm vein confirms it because bubbles light up the coronary sinus before the right atrium. Rarer causes include an unroofed coronary sinus ASD and anomalous pulmonary or hepatic venous drainage."
}
],
"numbers": [],
"delta": null,
"pearl": "Fluid in front of the descending aorta is pericardial; fluid behind it is pleural.",
"lookalike": {
"vs": "pleural effusion",
"discriminator": "Pericardial fluid stops at the descending aorta and does not extend behind it; pleural fluid wraps posterior to the aorta and may contain compressed lung."
},
"related": [
"Q14",
"Q26",
"Q264"
],
"reviewed": "2026-08-26"
},
{
"id": "Q16",
"orig": 16,
"title": "The three major coronary arteries",
"lesions": [
"CAD",
"ANATOMY"
],
"lens": "anatomy",
"items": [
{
"id": "Q16.1",
"q": "Name the three major coronary arteries and explain where they originate.",
"a": "The right coronary artery, the left anterior descending artery, and the left circumflex artery. The RCA arises from the right sinus of Valsalva. The left main coronary artery arises from the left sinus and almost immediately bifurcates into the LAD and the circumflex, so the left main itself is treated as a short trunk rather than a fourth major artery, although a left main stenosis is the most dangerous single lesion because it jeopardizes both branches. No artery arises from the noncoronary (posterior) sinus."
},
{
"id": "Q16.2",
"q": "Describe the course of each major coronary artery along the surface of the heart.",
"a": "All three run in the epicardial fat along the grooves of the heart before sending branches into the muscle. The RCA travels in the right atrioventricular groove between the right atrium and right ventricle, wraps around the acute margin, and in a right-dominant heart continues as the posterior descending artery in the posterior interventricular groove. The LAD descends in the anterior interventricular groove toward the apex, giving diagonal branches to the anterior wall and septal perforators into the septum. The circumflex runs in the left atrioventricular groove between the left atrium and left ventricle, giving obtuse marginal branches to the lateral wall."
}
],
"numbers": [],
"delta": null,
"pearl": "AV grooves carry the RCA (right) and circumflex (left); interventricular grooves carry the LAD (front) and PDA (back).",
"lookalike": null,
"related": [
"Q17",
"Q18"
],
"reviewed": "2026-08-26"
},
{
"id": "Q17",
"orig": 17,
"title": "Coronary territories by wall",
"lesions": [
"CAD",
"ANATOMY"
],
"lens": "anatomy",
"items": [
{
"id": "Q17.1",
"q": "Using the ASE 17-segment model, which left ventricular walls does each coronary artery normally supply?",
"a": "The LAD supplies the anterior wall, the anteroseptal wall, and the apex, which is why an LAD occlusion produces the largest infarcts and apical aneurysms. The RCA supplies the inferior wall and the basal and mid inferoseptal segments, along with the RV free wall, so inferior infarcts often come with RV involvement and bradyarrhythmias from the AV nodal branch. The circumflex supplies the anterolateral and inferolateral walls. Territories overlap at the apex and inferolateral wall depending on dominance: in the roughly 85 percent of people who are right-dominant the RCA gives off the posterior descending artery and feeds the inferior wall, whereas in left-dominant hearts the circumflex does."
}
],
"numbers": [
{
"label": "Right-dominant circulation prevalence",
"value": "~ 85",
"unit": "%"
}
],
"delta": null,
"pearl": "LAD = front and apex, RCA = bottom and inferior septum, circumflex = side.",
"lookalike": null,
"related": [
"Q11",
"Q16",
"Q18",
"Q282"
],
"widgets": [
"bullseye"
],
"reviewed": "2026-08-26"
},
{
"id": "Q18",
"orig": 18,
"title": "Matching akinesis to an artery",
"lesions": [
"CAD"
],
"lens": "vignette",
"items": [
{
"id": "Q18.1",
"q": "A 47-year-old man with a remote myocardial infarction has an akinetic anterior wall on echo. Which coronary artery was most likely occluded?",
"a": "The left anterior descending artery. The anterior wall receives its blood from LAD diagonal branches, and after a transmural infarct the scarred muscle neither thickens nor moves inward, which is what akinesis means. Because the same vessel also feeds the anterior septum through septal perforators and the apex through its distal segment, look carefully at those regions too; an isolated anterior wall abnormality suggests a diagonal or mid-LAD lesion, whereas apical involvement indicates the occlusion was more proximal."
},
{
"id": "Q18.2",
"q": "In another patient, the apical four-chamber view shows hypokinesis of the distal septum and LV apex while the basal septum moves normally. Which artery is most likely diseased?",
"a": "Again the LAD, this time with a mid-to-distal lesion. The distal septum and apex are the terminal territory of the LAD, so reduced flow there hits those segments first. The basal inferoseptal segment seen in the four-chamber view gets its supply from RCA septal branches via the posterior descending artery, so it keeps contracting normally, and this sparing of the base with apical hypokinesis is a classic LAD pattern. Wall motion is scored 1 for normal, 2 for hypokinetic, 3 for akinetic, and 4 for dyskinetic, and averaging the scores across all 17 segments gives the wall motion score index."
}
],
"numbers": [
{
"label": "Wall motion score: normal",
"value": "1",
"unit": "score"
},
{
"label": "Wall motion score: hypokinetic",
"value": "2",
"unit": "score"
},
{
"label": "Wall motion score: akinetic",
"value": "3",
"unit": "score"
},
{
"label": "Wall motion score: dyskinetic",
"value": "4",
"unit": "score"
}
],
"delta": null,
"pearl": "Apex plus distal septum abnormal with a normal base equals distal LAD.",
"lookalike": {
"vs": "apical ballooning (takotsubo)",
"discriminator": "Takotsubo involves the apex circumferentially beyond any single coronary territory and recovers within weeks; LAD infarct scar is fixed and confined to LAD segments."
},
"related": [
"Q6",
"Q17",
"Q16"
],
"reviewed": "2026-08-26"
},
{
"id": "Q19",
"orig": 19,
"title": "Normal intracardiac pressures",
"lesions": [
"HEMODYNAMICS"
],
"lens": "numbers",
"items": [
{
"id": "Q19.1",
"q": "List the normal pressures in the right atrium, right ventricle, pulmonary artery, left ventricle, and aorta.",
"a": "Right atrial mean pressure is about 2 to 6 mmHg (typically 3 to 5). The right ventricle generates roughly 25 mmHg in systole with an end-diastolic pressure near 5 mmHg. The pulmonary artery runs about 25/10 mmHg with a mean of about 15 mmHg. The left ventricle produces about 120 mmHg in systole with an end-diastolic pressure near 8 mmHg, and the aorta is roughly 120/80 mmHg. Notice that RV and PA systolic pressures match because the pulmonic valve is open during ejection, just as LV and aortic systolic pressures match; the diastolic pressures differ because the semilunar valves close and the great vessels keep pressure while the ventricles relax."
},
{
"id": "Q19.2",
"q": "At what point in the cardiac cycle is left ventricular pressure at its lowest?",
"a": "In early diastole, just after the mitral valve opens. During isovolumic relaxation the ventricle actively relaxes with all valves closed, so pressure falls steeply; it reaches its nadir at the moment it drops below left atrial pressure and the mitral valve swings open. From there the ventricle fills and its pressure climbs gradually through diastasis and atrial contraction to the end-diastolic pressure just before the next QRS."
}
],
"numbers": [
{
"label": "RA mean pressure",
"value": "2–6",
"unit": "mmHg"
},
{
"label": "RV pressure",
"value": "25/5",
"unit": "mmHg"
},
{
"label": "PA pressure",
"value": "25/10",
"unit": "mmHg"
},
{
"label": "PA mean pressure",
"value": "15",
"unit": "mmHg"
},
{
"label": "LV pressure",
"value": "120/8",
"unit": "mmHg"
},
{
"label": "Aortic pressure",
"value": "120/80",
"unit": "mmHg"
}
],
"delta": {
"was": "2011 card taught a single RA mean of 6 mmHg and an LV end-diastolic pressure of 7 mmHg.",
"now": "Current teaching gives RA mean as a range of 2–6 mmHg (typically 3–5) and LV end-diastolic pressure of about 8 mmHg; PA mean is about 15 mmHg.",
"source": "ASE 2015 chamber quant"
},
"pearl": "25/5, 25/10, 120/8, 120/80: the systolic numbers pair across each open valve.",
"lookalike": null,
"related": [
"Q20",
"Q22"
],
"reviewed": "2026-08-26"
},
{
"id": "Q20",
"orig": 20,
"title": "Pulmonary capillary wedge pressure",
"lesions": [
"HEMODYNAMICS"
],
"lens": "definition",
"items": [
{
"id": "Q20.1",
"q": "What is the normal mean pulmonary capillary wedge pressure, and what does it represent?",
"a": "Normal mean wedge pressure is about 6 to 12 mmHg. It is a surrogate for left atrial pressure, and therefore for LV filling pressure when the mitral valve is normal. It is not the same as pulmonary artery pressure: PA pressure is generated by the RV upstream, while the wedge reflects the pressure downstream in the pulmonary veins and left atrium. A wedge above roughly 15 mmHg with pulmonary hypertension indicates a post-capillary (left heart) cause, whereas PH with a normal wedge is pre-capillary."
},
{
"id": "Q20.2",
"q": "How is the pulmonary capillary wedge pressure obtained?",
"a": "A balloon-tipped pulmonary artery (Swan-Ganz) catheter is floated from a central vein through the right heart into a pulmonary artery branch. Inflating the balloon occludes that branch so no forward flow reaches the catheter tip. With flow stopped, the tip senses a static column of blood that connects through the pulmonary capillaries and veins to the left atrium, so the pressure recorded is left atrial pressure transmitted backward. Echo estimates the same quantity noninvasively from E/e', where an average E/e' above 14 suggests elevated filling pressure."
}
],
"numbers": [
{
"label": "Normal mean PCWP",
"value": "6–12",
"unit": "mmHg"
},
{
"label": "PCWP indicating post-capillary PH",
"value": "> 15",
"unit": "mmHg"
},
{
"label": "Average E/e' suggesting elevated LAP",
"value": "> 14",
"unit": "ratio"
}
],
"delta": {
"was": "2011 card gave a single normal wedge value of 10 mmHg.",
"now": "Normal PCWP is quoted as a range of 6–12 mmHg; echo estimates the same pressure with E/e'.",
"source": "ASE 2016 diastolic"
},
"pearl": "Wedge equals left atrial pressure; PA pressure is what the RV makes upstream of it.",
"lookalike": null,
"related": [
"Q19",
"Q24"
],
"reviewed": "2026-08-26"
},
{
"id": "Q21",
"orig": 21,
"title": "Best view for each LV wall",
"lesions": [
"VIEWS",
"ANATOMY"
],
"lens": "best-method",
"items": [
{
"id": "Q21.1",
"q": "Which two-dimensional view best displays the anterior wall of the left ventricle?",
"a": "The apical two-chamber view. Its plane runs from the inferior wall on the left of the screen to the anterior wall on the right, with the whole length of each wall from base to apex visible, so regional thickening of the anterior segments is easy to judge. The anterior wall can also be seen in cross-section in the short-axis views, but the two-chamber view shows all three levels at once, which is why it is the standard for LAD-territory wall motion."
},
{
"id": "Q21.2",
"q": "Which two-dimensional view best displays the anterolateral wall of the left ventricle?",
"a": "The apical four-chamber view, where the anterolateral wall is the free wall on the right side of the screen opposite the septum. The short-axis views show the anterolateral segment as one wedge, but the four-chamber view lays out the basal, mid, and apical anterolateral segments in a single plane, which is better for grading circumflex-territory wall motion."
}
],
"numbers": [],
"delta": null,
"pearl": "Two-chamber for anterior and inferior; four-chamber for anterolateral and inferoseptal.",
"lookalike": null,
"related": [
"Q12",
"Q13"
],
"reviewed": "2026-08-26"
},
{
"id": "Q22",
"orig": 22,
"title": "Valve timing against the ECG",
"lesions": [
"HEMODYNAMICS",
"ARRHYTHMIA"
],
"lens": "numbers",
"items": [
{
"id": "Q22.1",
"q": "At what point on the ECG does the mitral valve normally close?",
"a": "Roughly 60 milliseconds after the QRS begins, which lands around the middle of the QRS complex. Depolarization must spread through the ventricle before pressure starts to rise, and once LV pressure exceeds left atrial pressure the leaflets are pushed shut. On M-mode this is the C point of the mitral trace, and the interval from the Q wave to mitral closure lengthens when contraction is delayed or filling pressure is high."
},
{
"id": "Q22.2",
"q": "At what point on the ECG does the aortic valve normally open?",
"a": "At about the end of the QRS complex. After mitral closure the ventricle contracts with both valves shut (isovolumic contraction) until LV pressure reaches aortic diastolic pressure, at which point the aortic cusps swing open. The electromechanical delay plus the isovolumic contraction time together place aortic opening at the end of the QRS, and the interval from aortic opening to closure (measured at the S2 or the aortic M-mode box) is the LV ejection time."
}
],
"numbers": [
{
"label": "QRS onset to mitral closure",
"value": "~ 60",
"unit": "ms"
}
],
"delta": null,
"pearl": "Mitral shuts mid-QRS; aortic opens at the end of QRS; the gap between them is isovolumic contraction.",
"lookalike": null,
"related": [
"Q19",
"Q23",
"Q24"
],
"reviewed": "2026-08-26"
},
{
"id": "Q23",
"orig": 23,
"title": "Electromechanical delay and diastasis",
"lesions": [
"HEMODYNAMICS",
"ARRHYTHMIA"
],
"lens": "definition",
"items": [
{
"id": "Q23.1",
"q": "What is the relationship between electrical systole and mechanical systole?",
"a": "Electrical events precede the mechanical events they trigger. Roughly 12 milliseconds pass between the start of ventricular depolarization on the ECG and the onset of myocardial contraction, because calcium must enter the myocytes and activate the contractile proteins before tension develops. This electromechanical delay is easiest to see on M-mode, where valve motion can be lined up against the simultaneous ECG trace. Conditions such as bundle branch block or severe LV dysfunction prolong the delay, which is the basis for dyssynchrony assessment."
},
{
"id": "Q23.2",
"q": "What is diastasis?",
"a": "Diastasis is the quiet middle phase of diastole between the end of early rapid filling and the onset of atrial contraction. During this period LV and LA pressures are nearly equal, so almost no blood moves across the mitral valve, and the leaflets drift toward a semi-closed position. Its length is set by the heart rate: at slow rates diastasis is long, while at fast rates it shrinks and eventually disappears, causing the E and A waves to fuse."
}
],
"numbers": [
{
"label": "Electromechanical delay",
"value": "~ 12",
"unit": "ms"
}
],
"delta": null,
"pearl": "Diastasis is the pause between E and A; tachycardia deletes it and fuses the waves.",
"lookalike": null,
"related": [
"Q22",
"Q24"
],
"reviewed": "2026-08-26"
},
{
"id": "Q24",
"orig": 24,
"title": "Phases of diastole and filling split",
"lesions": [
"HEMODYNAMICS",
"MS",
"HCM"
],
"lens": "numbers",
"items": [
{
"id": "Q24.1",
"q": "What proportion of ventricular filling occurs passively, before atrial contraction?",
"a": "In a normal heart at rest about 70 to 80 percent of filling occurs passively during early rapid filling and diastasis, driven by ventricular relaxation and suction, and atrial contraction contributes the remaining 20 to 30 percent. The balance shifts with disease: a stiff ventricle from hypertrophy or infiltration depends more on the atrial kick, which is why these patients decompensate when atrial fibrillation removes it, whereas mitral stenosis slows filling throughout diastole and makes the ventricle dependent on a long diastolic period."
},
{
"id": "Q24.2",
"q": "Name the four phases of diastole in order.",
"a": "Isovolumic relaxation, from aortic valve closure to mitral valve opening, during which LV pressure falls with both valves shut; early rapid filling, when the mitral valve opens and blood rushes in down the atrioventricular pressure gradient (the E wave); diastasis, the mid-diastolic pause when pressures equalize; and atrial contraction, the active late-filling phase that produces the A wave. The four phases map directly onto the Doppler and tissue Doppler measurements used to grade diastolic function."
}
],
"numbers": [
{
"label": "Passive filling fraction (normal)",
"value": "70–80",
"unit": "%"
},
{
"label": "Atrial contribution (normal)",
"value": "20–30",
"unit": "%"
}
],
"delta": null,
"pearl": "IVRT, E, diastasis, A: the four beats of diastole.",
"lookalike": null,
"related": [
"Q20",
"Q22",
"Q23",
"Q6"
],
"reviewed": "2026-08-26"
},
{
"id": "Q25",
"orig": 25,
"title": "Side-lobe artifacts",
"lesions": [
"INSTRUMENTATION"
],
"lens": "pitfall",
"items": [
{
"id": "Q25.1",
"q": "What produces a side-lobe artifact?",
"a": "Every transducer emits weaker secondary beams that fan out at angles to the main beam. Normally these side lobes return too little energy to display, but a very strong reflector lying off-axis, such as the pericardium, a calcified annulus, a prosthetic valve, or a catheter, can send back enough signal through a side lobe to be registered. The machine assumes all echoes come from the main beam, so it paints the reflector along the central line at the correct depth, producing a curved or smeared echo where no structure exists, often across the aortic root, left atrium, or an LV cavity, where it can mimic a mass or dissection flap."
},
{
"id": "Q25.2",
"q": "How can side-lobe artifacts be reduced?",
"a": "Reduce the sensitivity that lets weak off-axis echoes register: turn down overall gain, raise the reject threshold, and lower the time gain compensation at the depth of the strong reflector. Changing the transducer angle or window also helps, because an artifact moves or disappears when the beam geometry changes while a true structure stays put and can be confirmed in a second orthogonal view. Modern apodized and phased-array transducers suppress side lobes by design, but the artifact still appears around highly reflective targets."
}
],
"numbers": [],
"delta": null,
"pearl": "An echo that vanishes when you lower gain or change windows was never there.",
"lookalike": {
"vs": "true intracardiac mass or dissection flap",
"discriminator": "A real structure persists in multiple views with independent motion; a side-lobe artifact arcs at the depth of a strong reflector, crosses anatomic boundaries, and fades with reduced gain."
},
"related": [
"Q8"
],
"reviewed": "2026-08-26"
},
{
"id": "Q26",
"orig": 26,
"title": "Agitated saline contrast study",
"lesions": [
"CONTRAST",
"ASD"
],
"lens": "procedure",
"items": [
{
"id": "Q26.1",
"q": "What abnormalities are detected by injecting agitated saline into a peripheral vein during echo?",
"a": "Primarily intracardiac shunts at the atrial level, including patent foramen ovale and atrial septal defect, along with intrapulmonary shunts. The microbubbles opacify the right heart, and their appearance in the left atrium proves a communication. The same injection also maps abnormal venous return, such as a persistent left SVC when left-arm bubbles fill the coronary sinus first, and it outlines right-sided masses or thrombi as filling defects within the opacified right atrium or ventricle."
},
{
"id": "Q26.2",
"q": "Why does agitated saline normally fail to reach the left heart, and what timing suggests a shunt when it does?",
"a": "The bubbles are larger than the pulmonary capillaries, so in a normal circulation they are trapped and absorbed in the lungs and never reach the pulmonary veins. Bubbles appearing in the left atrium within about three cardiac cycles of right atrial opacification indicate an intracardiac (atrial-level) communication, because the only route that fast is directly across the septum. Bubbles that arrive later, after roughly five beats, and enter through the pulmonary veins point to an intrapulmonary shunt such as a pulmonary arteriovenous malformation. A Valsalva release during the injection transiently raises right atrial pressure and improves detection of a PFO."
}
],
"numbers": [
{
"label": "LA bubbles indicating atrial-level shunt",
"value": "≤ 3",
"unit": "cardiac cycles"
},
{
"label": "LA bubbles suggesting intrapulmonary shunt",
"value": "> 5",
"unit": "cardiac cycles"
}
],
"delta": null,
"pearl": "Early bubbles through the septum; late bubbles through the pulmonary veins.",
"lookalike": {
"vs": "intrapulmonary shunt",
"discriminator": "Atrial shunt bubbles appear within about three beats and cross the septum; pulmonary AVM bubbles appear after five or more beats and emerge from the pulmonary veins."
},
"related": [
"Q4",
"Q10",
"Q15",
"Q27",
"Q388",
"Q393"
],
"reviewed": "2026-08-26"
},
{
"id": "Q27",
"orig": 27,
"title": "Valsalva maneuver physiology",
"lesions": [
"HEMODYNAMICS",
"HCM"
],
"lens": "procedure",
"items": [
{
"id": "Q27.1",
"q": "How is the Valsalva maneuver performed during an echo?",
"a": "Ask the patient to take a moderate breath in, then bear down as if straining against a closed glottis, keeping the mouth and nose shut and the effort steady for about 10 seconds while you record, and then release and breathe normally. The two phases that matter to the echo are the strain and the release. Coaching matters: a half-hearted strain fails to change preload, and a full inspiration first can shift the heart out of the imaging window."
},
{
"id": "Q27.2",
"q": "How does the Valsalva maneuver change cardiac hemodynamics, and what is it used for on echo?",
"a": "During the strain, high intrathoracic pressure squeezes the great veins and cuts venous return, so right and then left ventricular filling falls, stroke volume drops, and a reflex tachycardia follows. On release, pooled venous blood rushes back into the chest, right-sided pressures and stroke volume rebound, and a reflex bradycardia occurs. On echo the reduced preload during strain shrinks the LV cavity, which provokes or worsens a dynamic LVOT gradient in hypertrophic cardiomyopathy and increases mitral valve prolapse. It also unmasks pseudonormal diastolic filling by dropping E and revealing a hidden E/A reversal (a fall of 0.5 or more in E/A is significant), and the release phase improves PFO detection during a bubble study."
}
],
"numbers": [
{
"label": "Strain duration",
"value": "~ 10",
"unit": "s"
},
{
"label": "E/A decrease unmasking pseudonormal filling",
"value": "≥ 0.5",
"unit": "ratio"
}
],
"delta": null,
"pearl": "Strain lowers preload: HCM gradients rise, MVP worsens, and pseudonormal E/A drops below 1.",
"lookalike": null,
"related": [
"Q5",
"Q26",
"Q30"
],
"reviewed": "2026-08-26"
},
{
"id": "Q28",
"orig": 28,
"title": "Causes of jugular venous distension",
"lesions": [
"HEMODYNAMICS",
"EFFUSION",
"CONSTRICTION"
],
"lens": "physical-exam",
"items": [
{
"id": "Q28.1",
"q": "What is the underlying cause of jugular venous distension?",
"a": "Elevated right atrial pressure. The internal jugular vein has no valves between it and the right atrium, so it acts as a manometer: when right atrial pressure rises, the column of blood backs up into the neck and the veins remain visibly distended above the clavicle with the patient sitting at 45 degrees. On echo the equivalent sign is a dilated inferior vena cava (more than 2.1 cm) that collapses less than 50 percent with a sniff, which assigns an estimated RA pressure of 15 mmHg."
},
{
"id": "Q28.2",
"q": "Name four cardiac conditions that commonly produce jugular venous distension, and explain the mechanism in each.",
"a": "Cardiac tamponade, in which pericardial fluid compresses the right atrium and raises the pressure needed to fill it. Constrictive pericarditis, in which a rigid pericardium stops diastolic filling early and venous pressure climbs. Pulmonary hypertension, in which the failing, pressure-loaded right ventricle cannot empty and transmits high end-diastolic pressure back to the atrium. Tricuspid stenosis, in which the narrowed valve holds blood in the right atrium and raises its pressure directly. Severe tricuspid regurgitation and right ventricular infarction do the same thing by other mechanisms."
}
],
"numbers": [
{
"label": "IVC diameter suggesting high RA pressure",
"value": "> 2.1",
"unit": "cm"
},
{
"label": "IVC sniff collapse considered normal",
"value": "> 50",
"unit": "%"
},
{
"label": "RA pressure when IVC dilated and non-collapsing",
"value": "15",
"unit": "mmHg"
},
{
"label": "RA pressure when IVC normal",
"value": "3",
"unit": "mmHg"
}
],
"delta": null,
"pearl": "The neck veins read right atrial pressure; the IVC reads the same number on echo.",
"lookalike": null,
"related": [
"Q3",
"Q4",
"Q254"
],
"reviewed": "2026-08-26"
},
{
"id": "Q29",
"orig": 29,
"title": "Doppler window and PHT constant for MS",
"lesions": [
"MS",
"DOPPLER_PHYSICS"
],
"lens": "formula",
"items": [
{
"id": "Q29.1",
"q": "From which window should pulsed or continuous wave Doppler be recorded to evaluate mitral stenosis, and why?",
"a": "From the apex, using the apical four-chamber or long-axis view. The stenotic mitral jet is directed from the left atrium toward the LV apex, so an apical transducer position aligns the Doppler beam nearly parallel to flow. Because measured velocity falls with the cosine of the intercept angle, keeping that angle within 20 degrees limits underestimation to less than 6 percent, which is what makes the peak velocity, mean gradient, and pressure half-time reliable. Use color Doppler to find the jet direction first, since a rheumatic jet is often eccentric."
},
{
"id": "Q29.2",
"q": "What constant is used in the mitral pressure half-time formula, and what does the result mean?",
"a": "The empiric constant is 220: mitral valve area in cm² equals 220 divided by the pressure half-time in milliseconds. Pressure half-time is the time for the peak transmitral gradient to fall by half, and a stenotic valve empties the atrium slowly so the half-time lengthens. A half-time of 220 ms therefore corresponds to an area of 1.0 cm², which is now graded as very severe stenosis; the severe threshold of 1.5 cm² corresponds to a half-time of roughly 150 ms. The formula is unreliable immediately after balloon valvuloplasty and with significant aortic regurgitation or abnormal LV compliance, because those change how fast the gradient decays independent of orifice size."
}
],
"numbers": [
{
"label": "Pressure half-time constant",
"value": "220",
"unit": "ms·cm²"
},
{
"label": "PHT for MVA 1.0 cm²",
"value": "220",
"unit": "ms"
},
{
"label": "Severe MS valve area",
"value": "≤ 1.5",
"unit": "cm²"
},
{
"label": "Very severe MS valve area",
"value": "≤ 1.0",
"unit": "cm²"
},
{
"label": "Maximum Doppler intercept angle",
"value": "≤ 20",
"unit": "degrees"
}
],
"delta": {
"was": "2011 card called a valve area under 1.0 cm² (PHT over 220 ms) severe mitral stenosis.",
"now": "Severe MS is defined as MVA ≤1.5 cm² (PHT roughly ≥150 ms), and MVA ≤1.0 cm² is very severe.",
"source": "ASE 2009 MS (valve stenosis guideline)"
},
"pearl": "220 over the half-time gives the area; 220 ms itself is a 1.0 cm² valve, which is very severe.",
"lookalike": null,
"related": [
"Q8",
"Q30"
],
"reviewed": "2026-08-26"
},
{
"id": "Q30",
"orig": 30,
"title": "Amyl nitrite and respiration effects",
"lesions": [
"HEMODYNAMICS",
"AS",
"MR"
],
"lens": "physical-exam",
"items": [
{
"id": "Q30.1",
"q": "What does inhaled amyl nitrite do to the circulation, and how does it change common murmurs?",
"a": "Amyl nitrite is a rapid, short-acting vasodilator. Within seconds it drops systemic vascular resistance and blood pressure, producing flushing and a reflex tachycardia, and the fall in afterload lets the ventricle eject faster with a higher stroke volume. Murmurs generated by forward flow across a stenotic semilunar valve, such as aortic or pulmonic stenosis, get louder because more blood is pushed across the obstruction. Murmurs that depend on a pressure gradient back into a lower-pressure chamber, such as mitral regurgitation, aortic regurgitation, and a VSD, get softer because the lower aortic pressure reduces the driving gradient. In HCM the smaller, faster-emptying ventricle worsens dynamic obstruction, so the outflow murmur and Doppler gradient increase."
},
{
"id": "Q30.2",
"q": "How does respiration alter venous return, and what is the clinical use of this?",
"a": "Inspiration lowers intrathoracic pressure, which pulls blood from the abdominal and peripheral veins into the chest and increases right heart filling; expiration raises intrathoracic pressure and reduces venous return. Right-sided murmurs and Doppler velocities, such as tricuspid regurgitation, therefore intensify with inspiration (Carvallo sign), whereas left-sided events change little. Exaggeration of this normal variation underlies pulsus paradoxus in tamponade and the respirophasic mitral and tricuspid inflow changes used to diagnose tamponade and constriction."
}
],
"numbers": [
{
"label": "Tamponade mitral E respiratory variation",
"value": "> 30",
"unit": "%"
},
{
"label": "Tamponade tricuspid E respiratory variation",
"value": "> 60",
"unit": "%"
}
],
"delta": null,
"pearl": "Amyl nitrite: forward-flow murmurs louder, backward-flow murmurs softer; inspiration makes right-sided murmurs louder.",
"lookalike": null,
"related": [
"Q5",
"Q27",
"Q29"
],
"reviewed": "2026-08-26"
},
{
"id": "Q31",
"orig": 31,
"title": "Optimizing gray scale and far field",
"lesions": [
"INSTRUMENTATION"
],
"lens": "procedure",
"items": [
{
"id": "Q31.1",
"q": "Your 2D image looks flat and binary, with almost no gray-scale gradation. Which controls should you adjust?",
"a": "Gray-scale richness is governed by how the machine maps the wide range of returning echo amplitudes onto the limited shades the monitor can display. Widening the dynamic range (compression) keeps more of the weak-to-strong amplitude spread instead of clipping it, and lowering the reject threshold stops low-level echoes from being discarded. The post-processing (gray map) curve selects how amplitudes are assigned to shades, so choosing a softer map adds mid-tones. Before blaming the scanner, confirm that overall transmit power and receiver gain are sensible and that monitor brightness and contrast have not been pushed to extremes, since a badly set display will look binary no matter what the processor does."
},
{
"id": "Q31.2",
"q": "Structures deep in the sector are faint and hard to resolve. What can you change to see them better?",
"a": "Deep echoes are weak because attenuation grows with both distance and frequency. Raising the far-field time-gain compensation sliders selectively amplifies late-returning signals without brightening the near field. If that is not enough, drop to a lower transmit frequency: attenuation is roughly proportional to frequency, so a lower-frequency probe or harmonic setting penetrates farther at the cost of some axial resolution. Moving the focal zone deeper and making sure the depth setting is not excessive also help concentrate acoustic energy where you need it."
}
],
"numbers": [],
"delta": null,
"pearl": "Flat image: think dynamic range and gray map; faint far field: think TGC and lower frequency.",
"lookalike": null,
"related": [
"Q32",
"Q34"
],
"reviewed": "2026-08-26"
},
{
"id": "Q32",
"orig": 32,
"title": "Apical thrombus versus artifact",
"lesions": [
"CAD",
"MASS",
"INSTRUMENTATION"
],
"lens": "pitfall",
"items": [
{
"id": "Q32.1",
"q": "In the apical four-chamber view you see an echodense blob at the LV apex and cannot decide whether it is a thrombus or an artifact. List three maneuvers that help separate the two.",
"a": "A real thrombus has a fixed anatomic relationship to the myocardium, whereas reverberation and near-field artifacts are tied to the beam geometry. First, change the depth and the imaging plane: an artifact often shifts, disappears, or fails to appear in a second view (apical two-chamber, off-axis apical, or a high parasternal short axis at the apex), while a thrombus persists in every plane. Second, switch to a higher-frequency transducer with a shallow focal zone, or use a short-axis apical sweep, because the near-field resolution of the standard apical window is poor exactly where the apex sits. Third, lower the near-field gain and TGC to suppress chest-wall reverberations; a true clot keeps a distinct border and usually sits over an akinetic or aneurysmal segment. When doubt remains, an ultrasound enhancing agent is the current standard: thrombus appears as a filling defect against opacified blood, and artifact vanishes."
}
],
"numbers": [],
"delta": null,
"pearl": "Thrombus lives on an akinetic wall and survives every view; artifact moves with the beam and dies with contrast.",
"lookalike": {
"vs": "near-field reverberation artifact",
"discriminator": "Persistence in two orthogonal views plus an underlying wall-motion abnormality favors thrombus; contrast shows a filling defect."
},
"related": [
"Q31",
"Q328",
"Q331",
"Q333",
"Q375"
],
"reviewed": "2026-08-26"
},
{
"id": "Q33",
"orig": 33,
"title": "Adult single-rescuer CPR basics",
"lesions": [
"PROCEDURE"
],
"lens": "procedure",
"items": [
{
"id": "Q33.1",
"q": "You are alone with an adult who has collapsed in the echo lab. What compression-to-ventilation ratio do you use?",
"a": "For a lone rescuer treating an adult, deliver 30 chest compressions followed by 2 breaths and keep cycling. Compress at 100 to 120 per minute to a depth of 5 to 6 cm, allowing full recoil, because coronary perfusion depends on uninterrupted, adequately deep compressions. Minimize pauses; the ratio exists to keep compressions dominant while still providing some oxygenation."
},
{
"id": "Q33.2",
"q": "After confirming that the patient is unresponsive and not breathing normally, what is the first action in the CPR sequence?",
"a": "Start chest compressions immediately after activating the emergency response and calling for a defibrillator. The sequence is C-A-B: circulation first, then airway, then breathing. The reasoning is that most adult arrests are cardiac, blood is still oxygenated at the moment of collapse, and every second spent on airway maneuvers before compressions lowers coronary and cerebral perfusion. Open the airway with a head-tilt chin-lift only after the first set of compressions, then give breaths."
}
],
"numbers": [
{
"label": "Compression:ventilation, single rescuer adult",
"value": "30:2",
"unit": ""
},
{
"label": "Compression rate",
"value": "100–120",
"unit": "/min"
},
{
"label": "Compression depth",
"value": "5–6",
"unit": "cm"
}
],
"delta": {
"was": "2011 card taught that the first step after deciding CPR is needed is to open the airway (head tilt, chin lift) and clear foreign material.",
"now": "Current guideline: begin chest compressions first (C-A-B), then airway, then breathing; airway opening is no longer the initial step.",
"source": "AHA 2020 CPR"
},
"pearl": "Push first, breathe second: C-A-B, 30:2, 100–120/min, 5–6 cm.",
"lookalike": null,
"related": [],
"reviewed": "2026-08-26"
},
{
"id": "Q34",
"orig": 34,
"title": "Apical two-chamber and color gain",
"lesions": [
"VIEWS",
"DOPPLER_PHYSICS"
],
"lens": "procedure",
"items": [
{
"id": "Q34.1",
"q": "Starting from a well-aligned apical four-chamber view, how do you get to the apical two-chamber view?",
"a": "Keep the transducer at the apex and rotate it counterclockwise by roughly 60 degrees while holding the apex in the same spot on the screen. The right heart drops out and you should see only the left ventricle, mitral valve, and left atrium, with the inferior wall on the left of the sector and the anterior wall on the right. If the LVOT or aortic valve comes into view you have rotated past the two-chamber plane into the apical long axis (about 120 degrees from the four-chamber view), so back off slightly."
},
{
"id": "Q34.2",
"q": "What is the quickest practical way to set color Doppler gain correctly?",
"a": "Turn the color gain up until random speckles of color appear in tissue and in the background, then lower it just to the point where that noise vanishes. At that setting the color map is as sensitive as it can be without painting artifact, so jet sizes are neither inflated by overgain nor shrunk by undergain. If the color still looks weak, improve the Doppler signal rather than adding gain: narrow the color sector and reduce depth to raise frame rate, and use a lower-frequency setting for better Doppler penetration."
}
],
"numbers": [
{
"label": "Rotation A4C to A2C",
"value": "~60",
"unit": "degrees counterclockwise"
},
{
"label": "Rotation A4C to apical long axis",
"value": "~120",
"unit": "degrees counterclockwise"
}
],
"delta": {
"was": "2011 card taught rotating approximately 30 degrees counterclockwise from the four-chamber view to obtain the two-chamber view.",
"now": "Current teaching: the apical two-chamber plane lies about 60 degrees counterclockwise from the four-chamber plane, with the apical long axis at about 120 degrees.",
"source": "ASE 2019 comprehensive TTE examination"
},
"pearl": "Color gain: raise until it snows, then back off until it stops.",
"lookalike": null,
"related": [
"Q31"
],
"reviewed": "2026-08-26"
},
{
"id": "Q35",
"orig": 35,
"title": "Normal mitral valve anatomy",
"lesions": [
"ANATOMY",
"MS"
],
"lens": "anatomy",
"items": [
{
"id": "Q35.1",
"q": "Describe the structure of a normal mitral valve.",
"a": "The mitral valve is the two-leaflet inlet valve between the left atrium and left ventricle. The anterior leaflet is tall and roughly semicircular, shares fibrous continuity with the aortic root, and although it occupies only about a third of the annular circumference it covers most of the orifice. The posterior leaflet is shorter but wraps around the remaining two thirds of the annulus and is typically indented into three scallops (P1, P2, P3, with matching A1 to A3 regions on the anterior leaflet). Chordae tendineae from both papillary muscles insert into both leaflets, and the annulus is a saddle-shaped fibrous ring rather than a flat circle, which matters when judging prolapse."
}
],
"numbers": [
{
"label": "Anterior leaflet share of annular circumference",
"value": "~1/3",
"unit": ""
},
{
"label": "Posterior leaflet scallops",
"value": "3",
"unit": ""
}
],
"delta": null,
"pearl": "Anterior leaflet: tall and narrow; posterior leaflet: short and wide with three scallops.",
"lookalike": null,
"related": [
"Q49",
"Q52",
"Q55"
],
"reviewed": "2026-08-26"
},
{
"id": "Q36",
"orig": 36,
"title": "M-mode and 2D signs of MS",
"lesions": [
"MS",
"PH"
],
"lens": "m-mode",
"items": [
{
"id": "Q36.1",
"q": "What are the four classic M-mode features of rheumatic mitral stenosis?",
"a": "Thickened, fused leaflets produce a dense, layered echo during diastole rather than a thin line. The E-F slope flattens because the stenotic orifice lets the ventricle fill slowly, so the anterior leaflet does not drift back toward the closed position. The E-wave excursion is reduced because the fused commissures limit how far the leaflet can open. Finally, the posterior leaflet moves anteriorly in diastole, dragged along by the anterior leaflet, instead of moving in the normal opposite direction."
},
{
"id": "Q36.2",
"q": "What does 2D echocardiography show in mitral stenosis?",
"a": "The leaflets are thickened, with commissural fusion that tethers the tips so that the body of the anterior leaflet bows forward in diastole (the 'hockey stick' or doming appearance) while the tips stay fixed. The short-axis view shows a fish-mouth orifice that can be planimetered. The left atrium enlarges from chronic pressure overload, and with long-standing disease you may see signs of pulmonary hypertension such as right ventricular and right atrial dilation."
}
],
"numbers": [],
"delta": null,
"pearl": "Hockey-stick doming plus a dilated LA behind a normal-sized LV says rheumatic MS.",
"lookalike": null,
"related": [
"Q37",
"Q42",
"Q53",
"Q39",
"Q366"
],
"reviewed": "2026-08-26"
},
{
"id": "Q37",
"orig": 37,
"title": "Mitral inflow velocities and MS",
"lesions": [
"MS",
"HEMODYNAMICS"
],
"lens": "numbers",
"items": [
{
"id": "Q37.1",
"q": "What is the normal Doppler velocity across the mitral valve in adults, and how does it differ in children?",
"a": "Adult mitral inflow peaks at about 0.9 m/s, with a normal range of roughly 0.6 to 1.3 m/s. Children run slightly faster, averaging about 1.0 m/s with a range near 0.7 to 1.4 m/s, because their faster heart rates and smaller hearts move a similar stroke volume through a smaller orifice. Measure at the leaflet tips with pulsed Doppler in the apical four-chamber view."
},
{
"id": "Q37.2",
"q": "How does the spectral Doppler trace change when the mitral valve is stenotic?",
"a": "A narrowed orifice forces the same stroke volume through a smaller area, so peak velocity rises and the pulsed trace shows spectral broadening from turbulence. Because the atrium empties slowly through the obstruction, the atrioventricular pressure difference persists through diastole and the velocity envelope decays gradually rather than dropping quickly, which lengthens the pressure half-time. Continuous-wave Doppler then gives a mean gradient (severe if above about 10 mmHg at a normal heart rate) and the PHT used for valve area."
}
],
"numbers": [
{
"label": "Normal adult mitral E velocity",
"value": "~0.9 (0.6–1.3)",
"unit": "m/s"
},
{
"label": "Normal pediatric mitral velocity",
"value": "~1.0 (0.7–1.4)",
"unit": "m/s"
},
{
"label": "Severe MS mean gradient",
"value": "> 10",
"unit": "mmHg"
}
],
"delta": {
"was": "2011 card gave the adult mitral range as 0.6 to 1.4 m/s.",
"now": "Current reference range for adult mitral inflow is about 0.6 to 1.3 m/s (mean ~0.9).",
"source": "ASE 2016 diastolic"
},
"pearl": "Faster, broader, slower-decaying: that is the MS spectral triad.",
"lookalike": null,
"related": [
"Q36",
"Q43",
"Q54"
],
"reviewed": "2026-08-26"
},
{
"id": "Q38",
"orig": 38,
"title": "Left atrial consequences of MS",
"lesions": [
"MS",
"ARRHYTHMIA"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q38.1",
"q": "What happens to the left atrium in mitral stenosis?",
"a": "The obstructed valve forces the atrium to generate a higher pressure to fill the ventricle, so the chamber is chronically pressure-loaded and dilates. Because the atrium is thin-walled, it stretches rather than hypertrophies. As the disease becomes severe, the elevated atrial pressure is transmitted backward into the pulmonary veins and pulmonary circulation, leading to pulmonary hypertension and eventually right ventricular strain and right atrial enlargement."
},
{
"id": "Q38.2",
"q": "Why is atrial fibrillation so common in mitral stenosis?",
"a": "Chronic stretch and elevated wall stress in the dilated atrium disrupt the normal myocyte architecture and promote fibrosis, creating a substrate of slowed, heterogeneous conduction that supports re-entrant circuits. Rheumatic inflammation adds direct atrial injury. Once fibrillation starts, the loss of atrial contraction and further remodeling perpetuate it, and the enlarged, poorly emptying atrium and appendage become a major site of thrombus formation."
}
],
"numbers": [],
"delta": null,
"pearl": "Pressure overload stretches the LA, the stretched LA fibrillates, and the fibrillating LA clots.",
"lookalike": null,
"related": [
"Q40",
"Q47",
"Q367",
"Q371"
],
"reviewed": "2026-08-26"
},
{
"id": "Q39",
"orig": 39,
"title": "Physical findings of mitral stenosis",
"lesions": [
"MS"
],
"lens": "physical-exam",
"items": [
{
"id": "Q39.1",
"q": "Name seven typical clinical findings in a patient with mitral stenosis.",
"a": "Auscultation gives a loud first heart sound, an opening snap after S2, and a low-pitched diastolic rumble at the apex, best heard in the left lateral position. Symptoms come from elevated left atrial and pulmonary pressures: exertional dyspnea, orthopnea, fatigue from a fixed low cardiac output, and hemoptysis from ruptured bronchial or pulmonary venules. An irregularly irregular pulse from atrial fibrillation is common, and long-standing cases may show a malar flush or signs of right heart failure."
},
{
"id": "Q39.2",
"q": "What produces the mitral opening snap?",
"a": "In rheumatic disease the leaflets are still pliable but the commissures are fused. When left atrial pressure exceeds ventricular pressure in early diastole, the doming leaflets are flung open and stop abruptly at the limit imposed by the fused tips, and that sudden halt generates a sharp, high-pitched sound shortly after S2. A shorter S2-to-snap interval implies higher left atrial pressure and more severe stenosis, and the snap disappears when the leaflets become heavily calcified and immobile."
}
],
"numbers": [],
"delta": null,
"pearl": "Shorter S2-opening snap interval means higher LA pressure and tighter stenosis.",
"lookalike": null,
"related": [
"Q36",
"Q42"
],
"reviewed": "2026-08-26"
},
{
"id": "Q40",
"orig": 40,
"title": "MS effects on ventricles and vessels",
"lesions": [
"MS",
"PH",
"TR"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q40.1",
"q": "How does isolated mitral stenosis affect the two ventricles?",
"a": "The left ventricle sits downstream of the obstruction, so it is underfilled rather than overloaded; it stays normal in size and function unless there is coexisting mitral regurgitation or another lesion. The right ventricle bears the consequences: chronically raised left atrial pressure is transmitted back to the pulmonary circulation, pulmonary artery pressure rises, and the right ventricle hypertrophies and then dilates. Right ventricular dilation stretches the tricuspid annulus, producing functional tricuspid regurgitation and right atrial enlargement."
},
{
"id": "Q40.2",
"q": "What happens to the aorta and pulmonary artery in mitral stenosis?",
"a": "The aorta is unaffected because forward output through the left ventricle is normal or reduced, not increased. The pulmonary artery, by contrast, is exposed to the pulmonary hypertension of severe long-standing disease and may dilate, and you may see a shortened pulmonary acceleration time (under about 105 ms) and a high-velocity TR jet reflecting elevated pulmonary pressure."
}
],
"numbers": [
{
"label": "PA acceleration time suggesting PH",
"value": "< 105",
"unit": "ms"
}
],
"delta": null,
"pearl": "MS spares the LV and aorta; the damage flows backward to the LA, lungs, and right heart.",
"lookalike": null,
"related": [
"Q38",
"Q47",
"Q367"
],
"reviewed": "2026-08-26"
},
{
"id": "Q41",
"orig": 41,
"title": "Most accurate mitral valve area method",
"lesions": [
"MS"
],
"lens": "best-method",
"items": [
{
"id": "Q41.1",
"q": "Which is the most accurate echocardiographic way to determine mitral valve area: M-mode E-F slope, 2D planimetry in the parasternal short-axis view, or Doppler pressure half-time?",
"a": "Direct 2D planimetry of the orifice in the parasternal short-axis view is the reference method, because it measures the anatomic orifice itself rather than inferring it from flow or leaflet motion, and it is independent of heart rate, compliance, and associated regurgitation. Accuracy depends on technique: scan from the base toward the apex to find the smallest orifice at the leaflet tips, keep the plane perpendicular to the funnel, and use the highest frequency and lowest gain that still outline the edges, since excess gain shrinks the traced area. The E-F slope is only qualitative, and pressure half-time is the easiest routine method but is confounded by ventricular compliance, aortic regurgitation, and atrial fibrillation. If a question asks for the simplest method, the answer is pressure half-time."
}
],
"numbers": [],
"delta": null,
"pearl": "Most accurate: planimetry. Easiest: PHT. Least useful: E-F slope.",
"lookalike": null,
"related": [
"Q43",
"Q53",
"Q54"
],
"reviewed": "2026-08-26"
},
{
"id": "Q42",
"orig": 42,
"title": "Rheumatic MS vignette",
"lesions": [
"MS"
],
"lens": "vignette",
"items": [
{
"id": "Q42.1",
"q": "A 48-year-old woman is referred for a diastolic murmur with a sharp sound after S2. Echo shows a dilated left atrium, thickened mitral leaflets that dome in diastole with restricted tip motion, and a normal-sized left ventricle. What is the most likely diagnosis?",
"a": "This is rheumatic mitral stenosis. Doming with tethered leaflet tips is the signature of commissural fusion, which is a rheumatic process rather than a degenerative one, and she is younger than the typical patient with calcific annular disease. The opening snap and the isolated left atrial enlargement with a normal left ventricle fit the same picture. Many patients never recall the childhood episode of rheumatic fever, so the absence of that history should not deter you."
},
{
"id": "Q42.2",
"q": "What further noninvasive assessment should follow to grade her lesion?",
"a": "Complete the Doppler examination: trace the continuous-wave mitral inflow to obtain the mean gradient and pressure half-time, calculate valve area as 220 divided by the PHT, and confirm it with planimetry in the short axis. Severe stenosis is a valve area of 1.5 cm² or less (very severe 1.0 cm² or less) or a mean gradient above about 10 mmHg at a normal heart rate. Estimate pulmonary pressure from the TR jet and assess leaflet morphology, since those findings determine whether she is a candidate for balloon valvuloplasty."
}
],
"numbers": [
{
"label": "PHT valve-area formula",
"value": "220 / PHT",
"unit": "cm²"
},
{
"label": "Severe MS valve area",
"value": "≤ 1.5",
"unit": "cm²"
},
{
"label": "Very severe MS valve area",
"value": "≤ 1.0",
"unit": "cm²"
},
{
"label": "Severe MS mean gradient",
"value": "> 10",
"unit": "mmHg"
}
],
"delta": null,
"pearl": "Doming leaflets in a young woman with a snap: rheumatic until proven otherwise.",
"lookalike": {
"vs": "degenerative mitral annular calcification",
"discriminator": "Calcific disease restricts the base of the leaflets and spares the tips; rheumatic disease fuses the tips and leaves the body mobile."
},
"related": [
"Q36",
"Q39",
"Q43",
"Q52",
"Q366"
],
"reviewed": "2026-08-26"
},
{
"id": "Q43",
"orig": 43,
"title": "Mitral valve area thresholds",
"lesions": [
"MS"
],
"lens": "numbers",
"items": [
{
"id": "Q43.1",
"q": "What is the area of a normal adult mitral valve?",
"a": "A normal mitral orifice measures about 4 to 6 cm². Because the orifice is large relative to the diastolic flow it carries, there is essentially no gradient across it at rest, and symptoms typically do not appear until the area has fallen by more than half."
},
{
"id": "Q43.2",
"q": "Which valve areas define mild, moderate, and severe mitral stenosis?",
"a": "Current grading collapses the old mild and moderate categories into 'progressive' disease with an area above 1.5 cm², while severe stenosis is 1.5 cm² or less and very severe stenosis is 1.0 cm² or less. The thresholds are lower than the corresponding aortic numbers because the mitral orifice starts larger and the diastolic flow through it is at lower pressure. Always pair the area with the mean gradient and pulmonary pressure, because a heart rate that shortens diastole can make a moderate lesion behave severely."
}
],
"numbers": [
{
"label": "Normal mitral valve area",
"value": "4–6",
"unit": "cm²"
},
{
"label": "Severe MS",
"value": "≤ 1.5",
"unit": "cm²"
},
{
"label": "Very severe MS",
"value": "≤ 1.0",
"unit": "cm²"
}
],
"delta": {
"was": "2011 card taught a normal area of 4 to 5 cm², moderate stenosis at 1.0 to 1.5 cm², and severe only below 1.0 cm².",
"now": "Current guideline: normal 4 to 6 cm²; severe stenosis is 1.5 cm² or less and very severe is 1.0 cm² or less.",
"source": "ASE 2009 valve stenosis / ACC-AHA 2020 valvular heart disease"
},
"pearl": "Mitral 1.5 is severe; aortic 1.0 is severe.",
"lookalike": null,
"related": [
"Q37",
"Q42",
"Q56",
"Q41"
],
"reviewed": "2026-08-26"
},
{
"id": "Q44",
"orig": 44,
"title": "Chronic versus acute MR findings",
"lesions": [
"MR",
"ENDOCARDITIS",
"CAD"
],
"lens": "2d",
"items": [
{
"id": "Q44.1",
"q": "What does the echocardiogram typically show in chronic mitral regurgitation?",
"a": "Mild chronic regurgitation may leave the chambers entirely normal. When the leak is moderate or severe and has been present for years, the volume returned to the atrium each beat dilates the left atrium and, because it comes back to the ventricle in diastole, dilates the left ventricle as well. The ventricle compensates with eccentric hypertrophy and typically looks vigorous or even hyperdynamic until it begins to fail. You will usually find the structural cause, such as myxomatous leaflets with prolapse, rheumatic thickening, annular calcification, or tethering from a dilated ventricle."
},
{
"id": "Q44.2",
"q": "What does the echocardiogram typically show in acute mitral regurgitation?",
"a": "Because there has been no time for remodeling, the chambers are normal in size even though the jet is severe, and the tell-tale finding is the mechanical lesion itself: a flail segment or ruptured chordae, a vegetation eroding the leaflet, or a ruptured papillary muscle. In ischemic cases the ventricle shows a regional wall-motion abnormality, most often inferior or inferolateral, matching the posteromedial papillary muscle territory. A normal-sized atrium with a large eccentric jet and high pulmonary pressure is the acute-MR pattern."
}
],
"numbers": [],
"delta": null,
"pearl": "Big jet with big chambers is chronic; big jet with normal chambers is acute.",
"lookalike": null,
"related": [
"Q47",
"Q50",
"Q51",
"Q365"
],
"reviewed": "2026-08-26"
},
{
"id": "Q45",
"orig": 45,
"title": "Pulsed Doppler appearance of MR",
"lesions": [
"MR",
"DOPPLER_PHYSICS"
],
"lens": "doppler",
"items": [
{
"id": "Q45.1",
"q": "How does mitral regurgitation appear when you place a pulsed-wave sample volume in the left atrium?",
"a": "You record a systolic signal of turbulent flow filling the spectral display, and because the regurgitant velocity (typically 4 to 6 m/s) far exceeds the Nyquist limit of pulsed Doppler, the signal aliases and wraps around the baseline. The spectral broadening reflects the disorganized, multidirectional flow of a high-velocity jet entering a low-pressure chamber. Pulsed Doppler cannot quantify the velocity, but it can localize where in the atrium the jet is present."
},
{
"id": "Q45.2",
"q": "How was mitral regurgitation graded with pulsed Doppler alone, and how is it graded today?",
"a": "The historical method moved the sample volume systematically through the left atrium to map how far and how wide the turbulent systolic signal extended, on the principle that a bigger disturbed-flow region meant more regurgitation. That approach is only semiquantitative and is heavily influenced by jet direction and driving pressure. Current grading integrates specific measures instead: vena contracta width of 0.7 cm or more, effective regurgitant orifice area of 0.4 cm² or more, regurgitant volume of 60 mL or more, regurgitant fraction of 50 percent or more, systolic flow reversal in the pulmonary veins, and structural findings such as a flail leaflet all indicate severe regurgitation."
}
],
"numbers": [
{
"label": "Severe MR vena contracta",
"value": "≥ 0.7",
"unit": "cm"
},
{
"label": "Severe MR EROA",
"value": "≥ 0.4",
"unit": "cm²"
},
{
"label": "Severe MR regurgitant volume",
"value": "≥ 60",
"unit": "mL"
},
{
"label": "Severe MR regurgitant fraction",
"value": "≥ 50",
"unit": "%"
}
],
"delta": {
"was": "2011 card taught that MR is quantified by pulsed Doppler mapping of the extent of systolic turbulence in the left atrium, with a larger mapped area meaning more severe regurgitation.",
"now": "Current guideline: jet extent mapping is at most semiquantitative; severity is graded by vena contracta, EROA, regurgitant volume and fraction, pulmonary vein flow, and structural findings.",
"source": "ASE 2017 regurgitation"
},
"pearl": "Pulsed Doppler tells you where the jet is; CW and PISA tell you how bad it is.",
"lookalike": null,
"related": [
"Q46"
],
"reviewed": "2026-08-26"
},
{
"id": "Q46",
"orig": 46,
"title": "Color Doppler grading of MR",
"lesions": [
"MR"
],
"lens": "doppler",
"items": [
{
"id": "Q46.1",
"q": "How is mitral regurgitation assessed with color flow Doppler?",
"a": "Color Doppler paints the regurgitant jet in the left atrium in real time, so within a single beat you see its origin, direction, and extent. Jet area was once the main severity index, but it is misleading: eccentric jets that hug the atrial wall lose energy and look small, while central jets look large, and gain, Nyquist setting, and atrial pressure all change the apparent size. Color is therefore used today to measure the vena contracta (the narrowest neck of the jet at the leaflet level, 0.7 cm or more being severe) and to generate a proximal isovelocity surface area for calculating EROA and regurgitant volume. A large jet area should prompt quantification, not stand alone as a grade."
}
],
"numbers": [
{
"label": "Severe MR vena contracta",
"value": "≥ 0.7",
"unit": "cm"
},
{
"label": "Severe MR EROA",
"value": "≥ 0.4",
"unit": "cm²"
}
],
"delta": {
"was": "2011 card taught that the size, length, and width of the color jet determine MR severity.",
"now": "Current guideline: color jet area alone is insufficient; grade with vena contracta, PISA-derived EROA and regurgitant volume, and supportive signs.",
"source": "ASE 2017 regurgitation"
},
"pearl": "Wall-hugging jets lie small; measure the neck, not the cloud.",
"lookalike": null,
"related": [
"Q45"
],
"reviewed": "2026-08-26"
},
{
"id": "Q47",
"orig": 47,
"title": "Chamber effects of mitral regurgitation",
"lesions": [
"MR",
"MS"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q47.1",
"q": "How does mitral regurgitation change the atria?",
"a": "Each systole sends part of the stroke volume backward, so the left atrium is volume-loaded and dilates roughly in proportion to the regurgitant volume; trivial or mild leaks rarely enlarge it. This differs from mitral stenosis, where the atrium dilates from pressure rather than volume. Only with severe chronic regurgitation and secondary pulmonary hypertension does the right atrium enlarge as well."
},
{
"id": "Q47.2",
"q": "How does chronic mitral regurgitation change the ventricles?",
"a": "Mild regurgitation leaves both ventricles unchanged. With moderate or severe chronic leakage the left ventricle receives the regurgitant volume back in diastole and adapts by dilating with eccentric hypertrophy. Because it ejects into the low-pressure atrium, afterload is low and the ejection fraction appears supranormal, which is why an EF drifting down to 60 percent already signals early dysfunction. Prolonged severe regurgitation raises pulmonary pressure and eventually dilates and hypertrophies the right ventricle."
}
],
"numbers": [
{
"label": "LVEF threshold suggesting early LV dysfunction in chronic severe MR",
"value": "≤ 60",
"unit": "%"
}
],
"delta": null,
"pearl": "In severe MR a 'normal' EF of 55 percent is already abnormal.",
"lookalike": null,
"related": [
"Q38",
"Q40",
"Q44"
],
"reviewed": "2026-08-26"
},
{
"id": "Q48",
"orig": 48,
"title": "Defining mitral valve prolapse",
"lesions": [
"MVP",
"MR"
],
"lens": "definition",
"items": [
{
"id": "Q48.1",
"q": "How is mitral valve prolapse defined on M-mode?",
"a": "On M-mode the leaflets normally trace a smooth line between the C point (closure) and the D point (opening). Prolapse is diagnosed when one or both leaflets bow posteriorly below that C-D line during systole by more than 2 to 3 mm. The displacement can be holosystolic (a hammock shape) or begin in mid-to-late systole after the leaflet buckles, which corresponds to the mid-systolic click heard clinically."
},
{
"id": "Q48.2",
"q": "How is mitral valve prolapse defined on 2D echocardiography?",
"a": "Prolapse is systolic displacement of one or both leaflets beyond the plane of the mitral annulus into the left atrium, judged in the parasternal long-axis view (or apical long-axis view), with more than 2 mm of displacement being the accepted cutoff. Classic myxomatous prolapse also shows thickened, redundant leaflets of 5 mm or more. The long-axis views are chosen because they cut through the high points of the saddle-shaped annulus, so leaflet excursion above that line is genuine rather than geometric."
}
],
"numbers": [
{
"label": "M-mode prolapse displacement below C-D line",
"value": "> 2–3",
"unit": "mm"
},
{
"label": "2D prolapse displacement beyond annulus",
"value": "> 2",
"unit": "mm"
},
{
"label": "Classic MVP leaflet thickness",
"value": "≥ 5",
"unit": "mm"
}
],
"delta": null,
"pearl": "Diagnose prolapse in the long axis, where the saddle is highest.",
"lookalike": null,
"related": [
"Q49"
],
"reviewed": "2026-08-26"
},
{
"id": "Q49",
"orig": 49,
"title": "False prolapse pitfalls",
"lesions": [
"MVP",
"EFFUSION",
"VIEWS"
],
"lens": "pitfall",
"items": [
{
"id": "Q49.1",
"q": "Why should you hesitate before calling mitral valve prolapse in a patient with a large pericardial effusion?",
"a": "A heart floating in a large effusion swings within the pericardial sac, and in late systole the whole heart moves posteriorly. On M-mode, which records motion relative to the fixed transducer, that whole-heart translation drags the mitral echoes posteriorly below the C-D line and mimics late-systolic prolapse. 2D imaging is less vulnerable because you can judge the leaflets relative to the annulus, which moves with them. Reassess after the effusion is treated."
},
{
"id": "Q49.2",
"q": "Why is the apical four-chamber view unreliable for diagnosing prolapse?",
"a": "The mitral annulus is saddle-shaped: its high points lie anteriorly and posteriorly and its low points lie medially and laterally. The four-chamber plane cuts through the low points, so a normal leaflet closing at the true annular level appears to rise above the line joining those low points and looks as though it prolapses. Use the parasternal or apical long-axis views, which pass through the saddle's high points, so that leaflet displacement above that line is real."
}
],
"numbers": [],
"delta": null,
"pearl": "Saddle high points are in the long axis; the four-chamber view sees the valley and overcalls prolapse.",
"lookalike": {
"vs": "true mitral valve prolapse",
"discriminator": "True prolapse persists in the parasternal long-axis view and is not explained by effusion-related cardiac swinging."
},
"related": [
"Q35",
"Q48"
],
"reviewed": "2026-08-26"
},
{
"id": "Q50",
"orig": 50,
"title": "Ruptured chordae tendineae",
"lesions": [
"MR",
"ENDOCARDITIS",
"MASS"
],
"lens": "etiology",
"items": [
{
"id": "Q50.1",
"q": "Does rupture of a few chordae cause serious trouble?",
"a": "Usually not. Each leaflet is anchored by many chordae, so losing a few secondary or tertiary cords leaves the leaflet edge supported and produces little or no regurgitation. The clinical picture changes when a primary (marginal) chord to the free edge ruptures, because the unsupported segment flails into the atrium and causes acute severe regurgitation. Chordal rupture occurs in myxomatous degeneration, infective endocarditis, and ischemic disease, and sometimes spontaneously."
},
{
"id": "Q50.2",
"q": "In which clinical setting can a ruptured chord be mistaken for something else?",
"a": "During an endocarditis workup, a torn chord whipping around in the atrium in systole can look like a mobile vegetation on the leaflet. A vegetation is usually a shaggy, irregular mass with independent motion attached to the upstream side of the leaflet, whereas a ruptured chord is a thin linear echo that is continuous with the leaflet tip and moves with it. Prior studies for comparison and, when needed, TEE clarify the distinction."
}
],
"numbers": [],
"delta": null,
"pearl": "A thin string that moves with the leaflet is a chord; a shaggy lump with its own motion is a vegetation.",
"lookalike": {
"vs": "mitral vegetation",
"discriminator": "Vegetations are irregular, independently mobile masses on the atrial side; a ruptured chord is linear and tethered to the leaflet tip."
},
"related": [
"Q44",
"Q51",
"Q318"
],
"reviewed": "2026-08-26"
},
{
"id": "Q51",
"orig": 51,
"title": "Flail leaflet and papillary rupture",
"lesions": [
"MR",
"CAD"
],
"lens": "etiology",
"items": [
{
"id": "Q51.1",
"q": "What are the hemodynamic consequences and typical presentation of a flail mitral leaflet?",
"a": "A flail leaflet loses coaptation completely, so the regurgitation is severe and, because it develops suddenly, the small unadapted left atrium cannot buffer the volume. Left atrial and pulmonary venous pressures spike, and the patient presents with acute pulmonary edema: abrupt breathlessness, orthopnea, pink frothy sputum, and often hypotension. If the cause is a papillary muscle rupture after infarction, chest pain precedes the collapse. On echo a flail segment is a leaflet tip pointing into the atrium in systole with an eccentric jet directed away from the affected leaflet."
},
{
"id": "Q51.2",
"q": "Which papillary muscle ruptures more often, and why?",
"a": "The posteromedial papillary muscle ruptures far more often than the anterolateral one. It is perfused by a single vessel, the posterior descending branch (from the right coronary artery in most people), so one inferior infarct can devascularize it entirely. The anterolateral muscle draws blood from both the left anterior descending and circumflex systems, which protects it. Rupture typically occurs several days after an inferior or inferolateral infarction."
}
],
"numbers": [],
"delta": null,
"pearl": "Posteromedial: one artery, one infarct, one ruptured muscle.",
"lookalike": null,
"related": [
"Q44",
"Q50",
"Q279",
"Q365",
"Q369"
],
"reviewed": "2026-08-26"
},
{
"id": "Q52",
"orig": 52,
"title": "Annular calcification and MR",
"lesions": [
"MR",
"ANATOMY"
],
"lens": "etiology",
"items": [
{
"id": "Q52.1",
"q": "A patient has heavy mitral annular calcification with structurally normal leaflets and mitral regurgitation. What is the mechanism?",
"a": "The normal annulus is a pliable fibromuscular ring that shrinks in systole by roughly a quarter of its diastolic area, helping the leaflets meet. When the annulus becomes calcified or fibrosed it turns into a rigid ring that can no longer contract or change shape with the ventricle, so the leaflets are asked to close a larger orifice than they were designed for and a central gap appears. The calcific bar can also lift the base of the posterior leaflet and restrict its motion, further impairing coaptation. The same rigid, narrowed inflow may produce a modest diastolic gradient, a form of degenerative stenosis."
}
],
"numbers": [],
"delta": null,
"pearl": "A rigid annulus cannot help the leaflets close.",
"lookalike": null,
"related": [
"Q35",
"Q42",
"Q368"
],
"reviewed": "2026-08-26"
},
{
"id": "Q53",
"orig": 53,
"title": "Why the E-F slope flattens",
"lesions": [
"MS"
],
"lens": "m-mode",
"items": [
{
"id": "Q53.1",
"q": "Flattening of the mitral E-F slope is a classic M-mode sign of mitral stenosis. What produces it?",
"a": "After the leaflet opens fully at the E point, it normally drifts back toward closure (the F point) as rapid early filling equalizes atrial and ventricular pressures. In mitral stenosis the narrow orifice keeps the atrium from emptying quickly, the transmitral gradient persists throughout diastole, and the leaflet is held open by continuing flow, so its descent is slow and the slope flattens. The slope is only a rough guide because it also depends on leaflet stiffness, ventricular compliance, heart rate, and annular motion; the same flattening occurs with a poorly compliant left ventricle without any stenosis, which is why the E-F slope has been abandoned for grading."
}
],
"numbers": [],
"delta": null,
"pearl": "A flat E-F slope says the atrium empties slowly, not necessarily that the valve is narrow.",
"lookalike": {
"vs": "flattened E-F slope from poor LV compliance",
"discriminator": "Look for thickened doming leaflets and a prolonged pressure half-time; stiff-ventricle flattening shows normal leaflets."
},
"related": [
"Q36",
"Q41"
],
"reviewed": "2026-08-26"
},
{
"id": "Q54",
"orig": 54,
"title": "MR effects on MS Doppler measures",
"lesions": [
"MS",
"MR"
],
"lens": "pitfall",
"items": [
{
"id": "Q54.1",
"q": "When mitral stenosis and regurgitation coexist, how does the regurgitation alter the peak inflow velocity?",
"a": "Mild regurgitation adds negligible volume and leaves the peak velocity essentially unchanged. Moderate or severe regurgitation returns a large volume to the atrium every beat, so the diastolic flow crossing the narrowed orifice is larger than the forward stroke volume alone. More flow through the same area means a higher peak velocity and a higher mean gradient, so the gradient overestimates the anatomic stenosis."
},
{
"id": "Q54.2",
"q": "Does coexisting mitral regurgitation invalidate the pressure half-time estimate of valve area?",
"a": "For mild to moderate regurgitation, no: PHT measures how fast the gradient decays, not its absolute size, and although the peak velocity climbs, the ratio between the peak and the decay is preserved, so the 220/PHT estimate remains reasonable. With severe regurgitation the larger diastolic volume load and higher atrial pressure can distort the decay curve, and the method becomes unreliable. In that setting rely on planimetry, and remember that aortic regurgitation and a stiff ventricle also shorten the PHT and underestimate stenosis."
}
],
"numbers": [
{
"label": "PHT valve-area formula",
"value": "220 / PHT",
"unit": "cm²"
}
],
"delta": null,
"pearl": "MR raises the mitral gradient but leaves PHT alone until it becomes severe.",
"lookalike": null,
"related": [
"Q37",
"Q41"
],
"reviewed": "2026-08-26"
},
{
"id": "Q55",
"orig": 55,
"title": "Normal aortic valve anatomy",
"lesions": [
"ANATOMY",
"AR"
],
"lens": "anatomy",
"items": [
{
"id": "Q55.1",
"q": "Describe the anatomy of a normal aortic valve.",
"a": "The aortic valve has three semilunar cusps, named for the coronary arteries that arise above them: the right coronary cusp, the left coronary cusp, and the noncoronary cusp, which sits posteriorly against the interatrial septum. Behind each cusp the aortic wall bulges outward to form a sinus of Valsalva, and the right and left coronary ostia open from their respective sinuses. The cusps meet along three commissures, and their free edges carry small central nodules (of Arantius) that seal the center of the valve in diastole. In the parasternal short-axis view the closed valve forms a Y-shaped pattern."
},
{
"id": "Q55.2",
"q": "The aortic cusps have no chordae. Why does the valve resist regurgitation so well?",
"a": "Competence comes from geometry rather than from tendinous support. Each cusp is cup-shaped, so diastolic aortic pressure pushes the cusps together rather than apart, and the free edges overlap by a few millimeters along the lunulae so the load is shared among all three. The sinuses of Valsalva generate vortices that help the cusps close gently before flow reverses, and the annulus is reinforced by the fibrous skeleton of the heart. Regurgitation appears when this geometry is disturbed, either by cusp disease or by dilation of the root that pulls the commissures apart."
}
],
"numbers": [
{
"label": "Number of aortic cusps",
"value": "3",
"unit": ""
}
],
"delta": null,
"pearl": "The noncoronary cusp is the posterior one next to the atrial septum.",
"lookalike": null,
"related": [
"Q35",
"Q57"
],
"reviewed": "2026-08-26"
},
{
"id": "Q56",
"orig": 56,
"title": "Normal aortic valve numbers",
"lesions": [
"AS",
"HEMODYNAMICS"
],
"lens": "numbers",
"items": [
{
"id": "Q56.1",
"q": "What is the normal aortic valve area?",
"a": "A normal adult aortic valve opens to about 3 to 4 cm². Because the area is large relative to systolic flow, velocity across it stays low and hemodynamically important obstruction does not appear until the area is below about 1.5 cm², with severe stenosis defined at less than 1.0 cm²."
},
{
"id": "Q56.2",
"q": "What are the normal systolic gradient and flow velocity across the aortic valve?",
"a": "The normal transaortic velocity is roughly 1.0 to 1.7 m/s in adults, which by the simplified Bernoulli equation (4v²) corresponds to a peak gradient of only a few millimeters of mercury, typically 2 to 4 mmHg, and children run slightly faster at about 1.5 m/s. A velocity above 2.5 m/s is the point at which stenosis is considered present; mild stenosis is 2.6 to 2.9 m/s, moderate 3.0 to 3.9 m/s, and severe 4.0 m/s or more."
}
],
"numbers": [
{
"label": "Normal aortic valve area",
"value": "3–4",
"unit": "cm²"
},
{
"label": "Normal adult aortic velocity",
"value": "1.0–1.7",
"unit": "m/s"
},
{
"label": "Normal peak aortic gradient",
"value": "2–4",
"unit": "mmHg"
},
{
"label": "Pediatric aortic velocity",
"value": "~1.5",
"unit": "m/s"
},
{
"label": "Severe AS Vmax",
"value": "≥ 4",
"unit": "m/s"
}
],
"delta": {
"was": "2011 card gave a normal aortic valve area of 2.5 to 3.5 cm² and a normal velocity range of 0.9 to 1.8 m/s.",
"now": "Current reference values: normal aortic valve area 3 to 4 cm² and normal velocity about 1.0 to 1.7 m/s.",
"source": "ASE 2017 valve stenosis"
},
"pearl": "Normal AVA 3 to 4; severe below 1.0. Normal velocity near 1; severe at 4.",
"lookalike": null,
"related": [
"Q43",
"Q59",
"Q60"
],
"reviewed": "2026-08-26"
},
{
"id": "Q57",
"orig": 57,
"title": "Aortic arch branches",
"lesions": [
"AORTA",
"ANATOMY"
],
"lens": "anatomy",
"items": [
{
"id": "Q57.1",
"q": "Name the branches of the aortic arch in order, beginning with the one nearest the aortic valve.",
"a": "Proceeding from proximal to distal along the top of the arch, the first branch is the brachiocephalic (innominate) artery, which soon divides into the right common carotid and right subclavian arteries. The second is the left common carotid artery, and the third is the left subclavian artery. The left subclavian marks the end of the arch; the descending aorta begins just beyond it at the isthmus, which is why coarctation and traumatic transection cluster there. In the suprasternal long-axis view you can see all three vessels leaving the arch and the right pulmonary artery passing beneath it."
}
],
"numbers": [
{
"label": "Number of arch branches",
"value": "3",
"unit": ""
}
],
"delta": null,
"pearl": "Innominate, left carotid, left subclavian: the right side shares one trunk, the left gets two.",
"lookalike": null,
"related": [
"Q55"
],
"reviewed": "2026-08-26"
},
{
"id": "Q58",
"orig": 58,
"title": "M-mode and 2D signs of AS",
"lesions": [
"AS",
"AORTA"
],
"lens": "m-mode",
"items": [
{
"id": "Q58.1",
"q": "What does M-mode show in valvular aortic stenosis?",
"a": "Thickened, calcified cusps return multiple dense echoes throughout systole and diastole, replacing the thin box-shaped opening pattern. Cusp separation is reduced (normal separation is about 1.5 to 2.6 cm; below roughly 1.5 cm suggests stenosis but is unreliable if the cusps are eccentrically calcified). Because the ventricle works against a fixed obstruction, the septum and posterior wall thicken symmetrically, which is concentric hypertrophy. M-mode cannot grade severity."
},
{
"id": "Q58.2",
"q": "What does 2D echocardiography show in valvular aortic stenosis?",
"a": "The cusps are thickened and echodense with restricted systolic excursion, and in rheumatic disease the commissures are fused so the valve domes. The short-axis view shows a reduced triangular or slit-like orifice and lets you count cusps to identify a bicuspid valve, the most common cause in younger adults. Downstream, the high-velocity jet striking the aortic wall produces poststenotic dilation of the ascending aorta, and upstream the left ventricle shows concentric hypertrophy. The 2D picture establishes the etiology; Doppler supplies the severity."
}
],
"numbers": [
{
"label": "Normal aortic cusp separation",
"value": "1.5–2.6",
"unit": "cm"
}
],
"delta": null,
"pearl": "Imaging tells you why the valve is tight; Doppler tells you how tight.",
"lookalike": null,
"related": [
"Q59",
"Q60"
],
"reviewed": "2026-08-26"
},
{
"id": "Q59",
"orig": 59,
"title": "Aortic stenosis Doppler and gradients",
"lesions": [
"AS",
"HEMODYNAMICS"
],
"lens": "doppler",
"items": [
{
"id": "Q59.1",
"q": "What changes do you see in the spectral Doppler trace in aortic stenosis?",
"a": "Continuous-wave Doppler through the valve shows a high-velocity, spectrally broadened systolic envelope, since a small orifice accelerates and disorganizes the flow. As stenosis worsens, the envelope becomes more rounded and its peak occurs later in systole, because a severely obstructed ventricle takes longer to build enough pressure to reach maximal flow; an acceleration time above about 100 ms and a ratio of acceleration time to ejection time above 0.35 point to severe disease. Interrogate from several windows, including the right parasternal and suprasternal, because the highest velocity is the true one."
},
{
"id": "Q59.2",
"q": "How well does the peak transaortic gradient track the severity of stenosis?",
"a": "Only as well as flow is normal. With a normal cardiac output, a peak velocity of 4 m/s or more (peak gradient about 64 mmHg) or a mean gradient of 40 mmHg or more indicates severe stenosis, and velocity of 3.0 to 3.9 m/s is moderate. When stroke volume is low, whether from a weak ventricle or a small stiff one (stroke volume index under 35 mL/m²), a critically small valve can generate a velocity of only 3 m/s (36 mmHg), so the gradient underestimates the lesion. That is why the valve area from the continuity equation, and dimensionless index below 0.25, are always interpreted alongside the gradient."
}
],
"numbers": [
{
"label": "Severe AS Vmax",
"value": "≥ 4",
"unit": "m/s"
},
{
"label": "Severe AS mean gradient",
"value": "≥ 40",
"unit": "mmHg"
},
{
"label": "Moderate AS Vmax",
"value": "3.0–3.9",
"unit": "m/s"
},
{
"label": "Low-flow stroke volume index",
"value": "< 35",
"unit": "mL/m²"
},
{
"label": "Severe AS dimensionless index",
"value": "< 0.25",
"unit": ""
},
{
"label": "Bernoulli constant",
"value": "4",
"unit": "× v²"
}
],
"delta": {
"was": "2011 card taught that a peak gradient above 100 mmHg denotes severe stenosis when output is normal.",
"now": "Current guideline: severe AS is Vmax 4 m/s or more, mean gradient 40 mmHg or more, and AVA under 1.0 cm²; low-flow states (SVi under 35 mL/m²) can hide severe stenosis behind a low gradient.",
"source": "ASE 2017 valve stenosis"
},
"pearl": "Low flow, low gradient does not mean mild; check the area and the DVI.",
"lookalike": null,
"related": [
"Q56",
"Q58",
"Q60"
],
"reviewed": "2026-08-26"
},
{
"id": "Q60",
"orig": 60,
"title": "Continuity equation and AVA grades",
"lesions": [
"AS"
],
"lens": "formula",
"items": [
{
"id": "Q60.1",
"q": "What is the best noninvasive method for quantifying aortic stenosis?",
"a": "The continuity equation is the reference Doppler method. Flow through the outflow tract must equal flow through the valve, so AVA = (LVOT area × LVOT VTI) / (aortic valve VTI), with LVOT area taken as π(d/2)² from the diameter measured in the parasternal long-axis view. The result is flow-independent, which is what makes it superior to gradients alone. The chief error source is the LVOT diameter, which is squared, so measure it carefully in mid-systole just below the cusps. When the LVOT is hard to measure, the dimensionless index (LVOT VTI divided by aortic VTI) sidesteps the problem, with values below 0.25 indicating severe stenosis."
},
{
"id": "Q60.2",
"q": "Which valve areas correspond to mild, moderate, and severe aortic stenosis?",
"a": "Mild stenosis is an area above 1.5 cm², moderate is 1.0 to 1.5 cm², and severe is below 1.0 cm², or below 0.6 cm²/m² when indexed to body surface area for very small or large patients. These cutoffs are calibrated so that they agree with a peak velocity of 4 m/s and mean gradient of 40 mmHg in patients with normal flow; when area and gradient disagree, check for measurement error, low flow, or high flow before assigning a grade."
}
],
"numbers": [
{
"label": "Continuity equation",
"value": "AVA = (LVOT area × LVOT VTI) / AV VTI",
"unit": "cm²"
},
{
"label": "Mild AS AVA",
"value": "> 1.5",
"unit": "cm²"
},
{
"label": "Moderate AS AVA",
"value": "1.0–1.5",
"unit": "cm²"
},
{
"label": "Severe AS AVA",
"value": "< 1.0",
"unit": "cm²"
},
{
"label": "Severe AS indexed AVA",
"value": "< 0.6",
"unit": "cm²/m²"
},
{
"label": "Severe AS DVI",
"value": "< 0.25",
"unit": ""
}
],
"delta": {
"was": "2011 card graded moderate stenosis at 0.7 to 1.5 cm² and severe below 0.7 cm².",
"now": "Current guideline: moderate 1.0 to 1.5 cm², severe below 1.0 cm² (indexed below 0.6 cm²/m²), DVI below 0.25.",
"source": "ASE 2017 valve stenosis"
},
"pearl": "LVOT diameter is squared, so a 1 mm error moves the AVA by about 10 percent.",
"lookalike": null,
"related": [
"Q56",
"Q59",
"Q58",
"Q354"
],
"reviewed": "2026-08-26"
},
{
"id": "Q61",
"orig": 61,
"title": "LV response to aortic stenosis",
"lesions": [
"AS",
"HCM"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q61.1",
"q": "Describe how the ventricles respond to chronic aortic stenosis.",
"a": "A fixed obstruction at the aortic valve forces the left ventricle to generate a higher systolic pressure to push the same stroke volume forward, which raises wall stress. By Laplace's law the ventricle lowers that stress by adding sarcomeres in parallel, producing concentric hypertrophy with a small cavity and thick walls. Early on this keeps ejection fraction normal, but with years of pressure loading and subendocardial ischemia the myocardium fibroses, the cavity dilates, and systolic function falls. The right ventricle is spared unless post-capillary pulmonary hypertension develops late in the course."
}
],
"numbers": [],
"delta": null,
"pearl": "Pressure overload = concentric hypertrophy (thick walls, small cavity); volume overload = eccentric dilatation.",
"lookalike": {
"vs": "hypertensive heart disease",
"discriminator": "Both give concentric LVH; look for a restricted, calcified valve with Vmax above 2.5 m/s to attribute it to AS."
},
"related": [
"Q62",
"Q73",
"Q66",
"Q364"
],
"reviewed": "2026-08-26"
},
{
"id": "Q62",
"orig": 62,
"title": "AS effects on atria and vessels",
"lesions": [
"AS",
"AORTA"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q62.1",
"q": "How does aortic stenosis change the atria?",
"a": "The hypertrophied, stiff left ventricle needs a higher filling pressure to reach the same end-diastolic volume, so left ventricular end-diastolic pressure and left atrial pressure climb. The left atrium responds to that chronic pressure load by enlarging, and its size on echo is a useful marker of how long and how severely diastolic function has been impaired. The right atrium is unaffected unless the disease has progressed to pulmonary hypertension and right heart failure."
},
{
"id": "Q62.2",
"q": "How does aortic stenosis change the great vessels?",
"a": "The high-velocity, eccentric jet leaving a stenotic valve strikes the wall of the ascending aorta and creates turbulent shear, which over time can produce poststenotic dilatation just above the sinotubular junction. In bicuspid valves an intrinsic aortopathy adds to this, so always measure the root and ascending aorta. The pulmonary artery is normally unaffected."
}
],
"numbers": [],
"delta": null,
"pearl": "Left atrial size is the 'hemoglobin A1c' of chronically elevated LV filling pressure.",
"lookalike": null,
"related": [
"Q61",
"Q65",
"Q68",
"Q72",
"Q81",
"Q361"
],
"reviewed": "2026-08-26"
},
{
"id": "Q63",
"orig": 63,
"title": "Best method for aortic valve area",
"lesions": [
"AS",
"DOPPLER_PHYSICS"
],
"lens": "best-method",
"items": [
{
"id": "Q63.1",
"q": "Of M-mode cusp separation, 2D short-axis planimetry, and the Doppler continuity equation, which gives the most reliable aortic valve area, and why do the others fall short?",
"a": "The continuity equation is the method of choice because it is derived from flow conservation rather than from visualizing a calcified orifice, and it works regardless of leaflet geometry. M-mode cusp separation samples only two cusps along a single line, so it says nothing about a third cusp or about a domed orifice, and is not a valve area at all. Transthoracic planimetry is limited because heavy calcium causes acoustic shadowing and reverberation that hide the true orifice edge and because the imaging plane often misses the smallest orifice at the leaflet tips; it is more feasible on TEE. Report AVA together with Vmax and mean gradient, and add the dimensionless index (DVI, LVOT VTI over AV VTI) when the LVOT measurement is doubtful."
}
],
"numbers": [
{
"label": "Severe AS AVA",
"value": "< 1.0",
"unit": "cm²"
},
{
"label": "Severe AS DVI",
"value": "< 0.25",
"unit": "ratio"
}
],
"delta": null,
"pearl": "When LVOT diameter is uncertain, DVI below 0.25 flags severe AS without needing an area.",
"lookalike": null,
"related": [
"Q64",
"Q69",
"Q66",
"Q357"
],
"reviewed": "2026-08-26"
},
{
"id": "Q64",
"orig": 64,
"title": "Continuity equation for AVA",
"lesions": [
"AS",
"DOPPLER_PHYSICS"
],
"lens": "formula",
"items": [
{
"id": "Q64.1",
"q": "State the continuity equation for aortic valve area and explain what each term represents.",
"a": "Because blood is incompressible, the volume crossing the outflow tract each beat must equal the volume crossing the valve: LVOT area times LVOT VTI equals AVA times aortic VTI. Rearranged, AVA = (LVOT area × LVOT VTI) / AV VTI. LVOT area is calculated as 0.785 times the LVOT diameter squared, measured in the parasternal long axis in mid-systole; LVOT VTI comes from pulsed-wave Doppler with the sample volume just proximal to the valve, and AV VTI from continuous-wave Doppler through the jet. Peak velocities can be substituted for VTIs in the simplified version, and any error in LVOT diameter is squared, so that measurement dominates the accuracy."
}
],
"numbers": [
{
"label": "LVOT area factor",
"value": "0.785",
"unit": "× d²"
},
{
"label": "Normal AVA",
"value": "3–4",
"unit": "cm²"
},
{
"label": "Severe AS AVA",
"value": "< 1.0",
"unit": "cm²"
}
],
"delta": null,
"pearl": "Diameter error is squared: a 2 mm LVOT error shifts AVA by roughly 20%.",
"lookalike": null,
"related": [
"Q63",
"Q69",
"Q354",
"Q357"
],
"reviewed": "2026-08-26"
},
{
"id": "Q65",
"orig": 65,
"title": "Systolic doming vignette",
"lesions": [
"AS",
"CONGENITAL"
],
"lens": "vignette",
"items": [
{
"id": "Q65.1",
"q": "A 52-year-old man is referred for a harsh crescendo-decrescendo systolic murmur. The parasternal long-axis view shows concentric left ventricular hypertrophy, moderately thickened aortic leaflets with restricted excursion, and leaflets that bow into the aortic root in systole rather than opening flat against the wall. What is the most likely diagnosis?",
"a": "This is stenosis of a congenital bicuspid aortic valve. Leaflet thickening and concentric hypertrophy occur in any form of aortic stenosis, but systolic doming, where the fused leaflets balloon upward with a restricted central opening, points to congenital fusion rather than degenerative calcification. Confirm in the parasternal short axis by looking for a single elliptical 'fish-mouth' orifice, a raphe, and only two commissures during systole, and then measure the aortic root and ascending aorta for the associated aortopathy. A bicuspid valve is the usual cause of significant AS presenting in the fifth or sixth decade, a couple of decades before calcific trileaflet disease."
}
],
"numbers": [],
"delta": null,
"pearl": "Doming = congenital; count commissures in systole, not diastole, because a raphe mimics a third commissure when the valve is closed.",
"lookalike": {
"vs": "degenerative calcific AS",
"discriminator": "Calcific AS shows nodular calcium with poor excursion but no doming; bicuspid valves dome and show a two-commissure orifice in systole."
},
"related": [
"Q67",
"Q73",
"Q62",
"Q361"
],
"reviewed": "2026-08-26"
},
{
"id": "Q66",
"orig": 66,
"title": "Sclerosis versus stenosis",
"lesions": [
"AS"
],
"lens": "definition",
"items": [
{
"id": "Q66.1",
"q": "Define aortic valve sclerosis.",
"a": "Aortic sclerosis is focal thickening and calcification of the leaflets without a hemodynamically important obstruction, defined by a peak transaortic velocity of 2.5 m/s or less. The leaflets look irregular and bright but still open adequately. It can generate an ejection murmur and mild regurgitation, is common after age 65, and matters because it progresses to stenosis in a minority of patients and marks higher cardiovascular risk."
},
{
"id": "Q66.2",
"q": "Define aortic valve stenosis and explain how it differs from sclerosis.",
"a": "Aortic stenosis is a fixed narrowing of the valve (or, in supravalvular and subvalvular forms, of the outflow tract) that produces a pressure gradient across it during ejection. The distinction from sclerosis is hemodynamic, not anatomic: once peak velocity exceeds 2.5 m/s the process is graded as stenosis, with mild disease at 2.6 to 2.9 m/s, moderate at 3.0 to 3.9 m/s, and severe at 4.0 m/s or more with a mean gradient of 40 mmHg or above and an area under 1.0 cm²."
}
],
"numbers": [
{
"label": "Sclerosis upper Vmax",
"value": "≤ 2.5",
"unit": "m/s"
},
{
"label": "Mild AS Vmax",
"value": "2.6–2.9",
"unit": "m/s"
},
{
"label": "Moderate AS Vmax",
"value": "3.0–3.9",
"unit": "m/s"
},
{
"label": "Severe AS Vmax",
"value": "≥ 4",
"unit": "m/s"
},
{
"label": "Severe AS mean gradient",
"value": "≥ 40",
"unit": "mmHg"
},
{
"label": "Severe AS AVA",
"value": "< 1.0",
"unit": "cm²"
}
],
"delta": {
"was": "2011 card defined the difference qualitatively as presence or absence of a gradient.",
"now": "Current guideline: sclerosis is Vmax ≤ 2.5 m/s; stenosis graded mild 2.6–2.9, moderate 3.0–3.9, severe ≥ 4.0 m/s (mean ≥ 40 mmHg, AVA < 1.0 cm²).",
"source": "ASE 2017 valve stenosis"
},
"pearl": "2.5 m/s is the fence between sclerosis and stenosis.",
"lookalike": null,
"related": [
"Q61",
"Q63",
"Q67"
],
"reviewed": "2026-08-26"
},
{
"id": "Q67",
"orig": 67,
"title": "Bicuspid, degenerative, rheumatic AS",
"lesions": [
"AS",
"MS",
"CONGENITAL"
],
"lens": "2d",
"items": [
{
"id": "Q67.1",
"q": "What 2D findings characterize stenosis of a congenital bicuspid aortic valve?",
"a": "Look for systolic doming of thickened leaflets in the parasternal long axis, an eccentric closure line in diastole, and in the short axis a single oval orifice with two commissures, often with a raphe on the larger conjoined cusp. The left ventricle shows concentric hypertrophy from the pressure load. Because the aortopathy travels with the valve, measure the sinuses, sinotubular junction, and ascending aorta, and check for coarctation from the suprasternal notch."
},
{
"id": "Q67.2",
"q": "On 2D imaging, what separates rheumatic aortic stenosis from degenerative calcific stenosis?",
"a": "The valves themselves can look alike: both show thickened, restricted leaflets, although rheumatic disease tends to fuse the commissures and thicken leaflet edges while degenerative disease deposits calcium in the leaflet bodies and leaves the commissures free. The decisive clue is the mitral valve. Rheumatic aortic involvement essentially never occurs in isolation, so hockey-stick doming of the anterior mitral leaflet and commissural fusion with mitral stenosis point to rheumatic etiology, whereas an isolated calcified aortic valve in an older adult is degenerative."
}
],
"numbers": [],
"delta": null,
"pearl": "Rheumatic AS without mitral involvement should make you re-examine the mitral valve, not accept the diagnosis.",
"lookalike": {
"vs": "degenerative AS",
"discriminator": "Commissural fusion plus rheumatic mitral stenosis = rheumatic; free commissures with nodular body calcium and a normal mitral valve = degenerative."
},
"related": [
"Q65",
"Q66",
"Q366"
],
"reviewed": "2026-08-26"
},
{
"id": "Q68",
"orig": 68,
"title": "Takayasu arteritis on echo",
"lesions": [
"AORTA",
"AS",
"COARCT"
],
"lens": "etiology",
"items": [
{
"id": "Q68.1",
"q": "What is Takayasu arteritis?",
"a": "Takayasu arteritis is a large-vessel granulomatous vasculitis of the aorta and its major branches, sometimes called pulseless disease or aortic arch syndrome. Inflammation of the vessel wall heals with fibrosis and intimal thickening, producing long segmental stenoses, occlusions, and occasionally aneurysms. It preferentially affects women under 40, with the highest incidence in East and South Asia, and presents with absent or unequal pulses, limb claudication, and bruits."
},
{
"id": "Q68.2",
"q": "What should you look for on the echocardiogram of a patient with Takayasu arteritis?",
"a": "Image the aorta from the suprasternal and high parasternal windows for diffuse wall thickening and narrowed segments of the arch and descending aorta, which can behave like multiple coarctations with turbulent continuous-wave flow and diastolic run-off. Involvement of the ascending aorta can produce supravalvular narrowing or, more often, root dilatation with aortic regurgitation from annular stretching. Also assess the left ventricle for hypertrophy from hypertension, which is frequent because renal artery stenosis is common, and check the pulmonary artery, which is involved in a substantial minority."
}
],
"numbers": [],
"delta": null,
"pearl": "Young Asian woman, absent radial pulse, aortic arch narrowing on suprasternal imaging: think Takayasu.",
"lookalike": {
"vs": "aortic coarctation",
"discriminator": "Congenital coarctation is a single discrete shelf distal to the left subclavian; Takayasu produces long, multiple, thick-walled segments and often branch-vessel disease."
},
"related": [
"Q62",
"Q77"
],
"reviewed": "2026-08-26"
},
{
"id": "Q69",
"orig": 69,
"title": "AR effects on AS gradient and area",
"lesions": [
"AR",
"AS",
"DOPPLER_PHYSICS"
],
"lens": "formula",
"items": [
{
"id": "Q69.1",
"q": "How does coexisting aortic regurgitation alter the Doppler gradient of a stenotic aortic valve?",
"a": "The transvalvular gradient depends on flow as well as orifice size, since pressure drop rises with the square of velocity. Regurgitant volume returns to the left ventricle in diastole and must be ejected again in systole, so moderate or severe AR raises total forward stroke volume and drives velocity and gradient higher than the orifice alone would predict. Mild AR adds too little volume to matter. In mixed disease, therefore, gradients overstate the stenosis and valve area is the more trustworthy severity measure."
},
{
"id": "Q69.2",
"q": "Does aortic regurgitation change the valve area calculated by the continuity equation?",
"a": "No. The extra regurgitant volume passes through both the outflow tract and the valve in systole, so the LVOT velocity and the transvalvular velocity rise in proportion. Their ratio, and therefore the calculated area, is unchanged. This flow independence is exactly why the continuity equation is preferred over gradients whenever forward flow is abnormal, whether high (AR, anemia) or low (poor LV function)."
}
],
"numbers": [],
"delta": null,
"pearl": "Gradients follow flow; the continuity area follows the orifice.",
"lookalike": null,
"related": [
"Q63",
"Q64"
],
"reviewed": "2026-08-26"
},
{
"id": "Q70",
"orig": 70,
"title": "Chronic versus acute AR findings",
"lesions": [
"AR",
"ENDOCARDITIS",
"AORTA"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q70.1",
"q": "What are the principal echocardiographic findings in chronic aortic regurgitation?",
"a": "Mild chronic AR may show nothing beyond a small color jet and slightly thickened leaflets. With moderate or severe chronic leakage the ventricle has years to adapt: it dilates eccentrically to accommodate the extra diastolic volume, and because the enlarged chamber ejects a large total stroke volume, wall motion looks vigorous with a normal or supranormal ejection fraction. Late in the course wall stress outstrips the compensation and ejection fraction falls, which is why guidelines trigger surgery on an LV end-systolic dimension above 50 mm or an ejection fraction of 55% or less even in asymptomatic patients."
},
{
"id": "Q70.2",
"q": "What are the principal echocardiographic findings in acute aortic regurgitation?",
"a": "In acute AR the ventricle has no time to dilate, so a normal-sized, hyperdynamic left ventricle is filled by a sudden large regurgitant volume and its diastolic pressure soars. Echo shows premature diastolic closure of the mitral valve and sometimes diastolic mitral regurgitation as LV pressure exceeds LA pressure before systole, a short pressure half-time on the AR continuous-wave signal, and an unimpressive color jet because the pressure gradient equalizes quickly. Nearly always there is a structural cause to find: a vegetation or leaflet perforation from endocarditis, a dissection flap prolapsing through the valve, a flail cusp from trauma, or prosthetic dehiscence."
}
],
"numbers": [
{
"label": "Surgical trigger LVESD chronic AR",
"value": "> 50",
"unit": "mm"
},
{
"label": "Surgical trigger LVEF chronic AR",
"value": "≤ 55",
"unit": "%"
}
],
"delta": null,
"pearl": "Acute severe AR can look mild by color: a small jet, normal-sized LV, but a closed mitral valve before the QRS.",
"lookalike": null,
"related": [
"Q73",
"Q75",
"Q76"
],
"reviewed": "2026-08-26"
},
{
"id": "Q71",
"orig": 71,
"title": "Color Doppler grading of AR",
"lesions": [
"AR",
"DOPPLER_PHYSICS"
],
"lens": "doppler",
"items": [
{
"id": "Q71.1",
"q": "How is color flow Doppler used to grade aortic regurgitation, and what are its limits?",
"a": "Color Doppler displays the regurgitant jet in real time so you can see its origin, direction, and size within a single beat. The useful color measurements are made at the valve, not downstream: the vena contracta (the narrowest neck of the jet just below the leaflets) and the ratio of jet width to LVOT diameter in the parasternal long axis, plus the proximal flow convergence used for PISA. A vena contracta above 0.6 cm or a jet occupying 65% or more of the outflow tract indicates severe AR. Jet length and area into the ventricle are unreliable because they depend on gain, Nyquist limit, driving pressure, and eccentricity, so guidelines require integrating color with pressure half-time, descending aortic flow reversal, and LV size."
}
],
"numbers": [
{
"label": "Severe AR vena contracta",
"value": "> 0.6",
"unit": "cm"
},
{
"label": "Severe AR jet width / LVOT",
"value": "≥ 65",
"unit": "%"
},
{
"label": "Severe AR EROA",
"value": "≥ 0.3",
"unit": "cm²"
},
{
"label": "Severe AR regurgitant volume",
"value": "≥ 60",
"unit": "mL"
}
],
"delta": {
"was": "2011 card taught that the bigger the color jet (total size, length, width), the more severe the AR.",
"now": "Current guideline: jet length and area are not used for grading; use vena contracta > 0.6 cm, jet width/LVOT ≥ 65%, PISA-derived EROA ≥ 0.3 cm² and RVol ≥ 60 mL, integrated with PHT and descending aortic reversal.",
"source": "ASE 2017 regurgitation"
},
"pearl": "Grade AR at the neck of the jet, never by how far it travels.",
"lookalike": null,
"related": [
"Q74",
"Q75",
"Q85"
],
"reviewed": "2026-08-26"
},
{
"id": "Q72",
"orig": 72,
"title": "AR effects on atria and aorta",
"lesions": [
"AR",
"AORTA"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q72.1",
"q": "How does aortic regurgitation affect the atria?",
"a": "The regurgitant volume lands in the left ventricle, not the left atrium, so the atria are secondary bystanders. Only when chronic volume overload has dilated the ventricle and raised its filling pressure, or when functional mitral regurgitation appears from annular dilatation, does the left atrium enlarge, and usually only modestly. The right atrium is unaffected in the absence of pulmonary hypertension."
},
{
"id": "Q72.2",
"q": "How does aortic regurgitation affect the great vessels?",
"a": "The causal arrow points from the aorta to the valve, not the reverse: aortic root dilatation from Marfan syndrome, hypertension, bicuspid aortopathy, or dissection stretches the annulus and prevents leaflet coaptation, producing AR. Regurgitation itself does not dilate the aorta. The pulmonary artery is uninvolved. Because root pathology is so often the cause, every AR study should include measured sinus, sinotubular junction, and ascending aortic dimensions."
}
],
"numbers": [],
"delta": null,
"pearl": "A dilated aorta causes AR; AR does not cause a dilated aorta.",
"lookalike": null,
"related": [
"Q62",
"Q77"
],
"reviewed": "2026-08-26"
},
{
"id": "Q73",
"orig": 73,
"title": "AR and the left ventricle",
"lesions": [
"AR",
"DCM",
"CONGENITAL"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q73.1",
"q": "How does aortic regurgitation affect the ventricles?",
"a": "Mild AR leaves the ventricle unchanged. Moderate to severe chronic AR imposes both volume and pressure overload: the diastolic leak enlarges end-diastolic volume, and the resulting large stroke volume raises systolic pressure and afterload. The ventricle responds with eccentric hypertrophy, dilating while wall thickness keeps pace, and early on ejection fraction is normal or high. Decompensation follows when wall stress exceeds the ability of the myocardium to hypertrophy, leading to declining ejection fraction and, if unrepaired, irreversible fibrosis. The right ventricle is not directly affected."
},
{
"id": "Q73.2",
"q": "What is the most common congenital cause of aortic regurgitation?",
"a": "A bicuspid aortic valve. The unequal conjoined cusp prolapses below the plane of the smaller cusp, and the accompanying aortopathy dilates the root, so leakage arises from both leaflet malcoaptation and annular stretch. Ventricular septal defects with prolapse of the right coronary cusp into the defect are a second, less common congenital cause."
}
],
"numbers": [],
"delta": null,
"pearl": "AR is the one valve lesion that loads the LV with both volume and pressure, so the ventricle gets big and thick.",
"lookalike": null,
"related": [
"Q61",
"Q65",
"Q70"
],
"reviewed": "2026-08-26"
},
{
"id": "Q74",
"orig": 74,
"title": "Descending aortic flow reversal",
"lesions": [
"AR",
"AORTA",
"DOPPLER_PHYSICS"
],
"lens": "doppler",
"items": [
{
"id": "Q74.1",
"q": "What term describes flow moving backward toward the heart in the descending aorta during diastole?",
"a": "Retrograde flow. When the aortic valve leaks, part of the blood that entered the aorta in systole runs back toward the ventricle in diastole, and pulsed-wave Doppler in the descending thoracic aorta from the suprasternal notch, or the abdominal aorta from the subcostal window, records that reversal as a diastolic signal on the opposite side of the baseline from the systolic forward flow. In a normal aorta only a brief early-diastolic reversal from aortic recoil is seen."
},
{
"id": "Q74.2",
"q": "How is diastolic flow reversal used to grade aortic regurgitation?",
"a": "Sample the proximal descending aorta just distal to the left subclavian artery with pulsed Doppler. Brief early-diastolic reversal is normal or mild; reversal that persists through the whole of diastole (holodiastolic) with an end-diastolic velocity of 20 cm/s or more is a specific sign of severe AR. Reversal detected in the abdominal aorta is even more specific for severe leakage. The sign is less reliable with a stiff, poorly compliant aorta in the elderly, which can prolong reversal on its own, and with high heart rates that shorten diastole."
}
],
"numbers": [
{
"label": "Holodiastolic reversal end-diastolic velocity severe AR",
"value": "≥ 20",
"unit": "cm/s"
}
],
"delta": {
"was": "2011 card graded reversal qualitatively: none for mild, early-diastolic for moderate, holodiastolic for severe.",
"now": "Current guideline: holodiastolic reversal with end-diastolic velocity ≥ 20 cm/s in the proximal descending aorta is a specific criterion for severe AR; brief early-diastolic reversal is normal or mild and is not a moderate criterion.",
"source": "ASE 2017 regurgitation"
},
"pearl": "Reversal that outlasts diastole and still runs at 20 cm/s at the R wave means severe AR.",
"lookalike": {
"vs": "normal aortic recoil",
"discriminator": "Physiologic reversal is brief and early-diastolic; severe AR reversal is holodiastolic and still ≥ 20 cm/s at end-diastole."
},
"related": [
"Q71",
"Q75"
],
"reviewed": "2026-08-26"
},
{
"id": "Q75",
"orig": 75,
"title": "M-mode signs of aortic regurgitation",
"lesions": [
"AR",
"MR"
],
"lens": "m-mode",
"items": [
{
"id": "Q75.1",
"q": "Name the classic M-mode findings of aortic regurgitation and explain their mechanism.",
"a": "First, high-frequency diastolic fluttering of the anterior mitral leaflet, because the regurgitant jet strikes the leaflet and vibrates it; the same jet can flutter the interventricular septum when it is directed that way. Second, an enlarged left ventricle with vigorous wall excursion in chronic disease, reflecting volume overload with preserved contractility (excursion falls once the ventricle decompensates). Third, in severe acute AR, premature closure of the mitral valve before the QRS complex, because the rapidly rising LV diastolic pressure exceeds left atrial pressure early. Diastolic fluttering of the aortic leaflets themselves suggests a flail or torn cusp, and an Austin Flint rumble corresponds to the fluttering mitral leaflet."
}
],
"numbers": [],
"delta": null,
"pearl": "Mitral leaflet flutter = AR jet hitting the leaflet; mitral preclosure = acute severe AR with very high LVEDP.",
"lookalike": {
"vs": "mitral leaflet flutter from a flail mitral chord",
"discriminator": "AR flutters the anterior mitral leaflet in diastole; a flail mitral segment flutters in systole within the left atrium."
},
"related": [
"Q70",
"Q71",
"Q74"
],
"reviewed": "2026-08-26"
},
{
"id": "Q76",
"orig": 76,
"title": "Aortic endocarditis and flail cusp",
"lesions": [
"ENDOCARDITIS",
"AR"
],
"lens": "physical-exam",
"items": [
{
"id": "Q76.1",
"q": "What clinical presentation is typical of aortic valve endocarditis?",
"a": "Patients present with persistent fever, chills, drenching night sweats, fatigue, and weight loss from bacteremia, often with a new or changing murmur; leaflet destruction produces a decrescendo diastolic murmur of AR along the left sternal border. Tachycardia, dyspnea, and orthopnea signal acute regurgitation and pulmonary congestion. Embolic and immunologic phenomena (stroke, splinter hemorrhages, Janeway lesions, Osler nodes, glomerulonephritis) and a new PR prolongation or heart block from an aortic root abscess round out the picture. Blood cultures plus echo showing a vegetation, abscess, or new dehiscence form the Duke criteria."
},
{
"id": "Q76.2",
"q": "What is the most common cause of a flail aortic cusp?",
"a": "Infective endocarditis. Bacterial destruction erodes or perforates a leaflet or ruptures its attachment so that the cusp swings freely into the outflow tract in diastole, causing severe, usually acute AR. Blunt chest trauma, iatrogenic injury during catheter procedures, and spontaneous cusp tear in myxomatous or bicuspid valves are much less frequent causes."
}
],
"numbers": [],
"delta": null,
"pearl": "New AR plus fever plus PR prolongation: look for a root abscess with TEE.",
"lookalike": {
"vs": "Lambl excrescence",
"discriminator": "Lambl excrescences are thin, filamentous, on the closure line, without destruction or fever; vegetations are irregular, mobile, on the upstream side, with tissue damage."
},
"related": [
"Q70",
"Q83",
"Q318"
],
"reviewed": "2026-08-26"
},
{
"id": "Q77",
"orig": 77,
"title": "Marfan syndrome and the valves",
"lesions": [
"AORTA",
"MVP",
"AR"
],
"lens": "definition",
"items": [
{
"id": "Q77.1",
"q": "Define Marfan syndrome.",
"a": "Marfan syndrome is an autosomal dominant connective tissue disorder caused by mutations in the fibrillin-1 gene, which weakens the elastic microfibrils of the aortic media, ligaments, and ocular zonules. Patients are tall with long limbs and fingers, joint hypermobility, pectus deformity, and ectopia lentis. The revised Ghent criteria diagnose it from a combination of aortic root dilatation, lens dislocation, family history, genetic testing, and a systemic feature score, and the cardiovascular features determine prognosis."
},
{
"id": "Q77.2",
"q": "How does Marfan syndrome affect the aortic valve and the mitral valve?",
"a": "The aortic valve is affected indirectly. Cystic medial degeneration dilates the sinuses of Valsalva first, giving the root a flask or pear shape that effaces the sinotubular junction; as the annulus stretches, the normal leaflets fail to coapt and central AR develops, and the weakened wall is prone to type A dissection, which is the main cause of death. The mitral valve is affected directly by myxomatous thickening with prolapse of one or both leaflets and variable mitral regurgitation. Root diameter is the key surveillance measurement, with prophylactic surgery advised at about 50 mm, or earlier with rapid growth, family history of dissection, or planned pregnancy."
}
],
"numbers": [
{
"label": "Marfan prophylactic root surgery threshold",
"value": "≈ 50",
"unit": "mm"
}
],
"delta": null,
"pearl": "Marfan root dilatation starts at the sinuses (pear-shaped root); atherosclerotic dilatation starts above the sinotubular junction.",
"lookalike": {
"vs": "bicuspid aortopathy",
"discriminator": "Bicuspid disease dilates the tubular ascending aorta with a bicuspid valve; Marfan dilates the sinuses with a trileaflet valve and mitral prolapse."
},
"related": [
"Q72",
"Q68",
"Q89",
"Q283",
"Q284",
"Q363"
],
"reviewed": "2026-08-26"
},
{
"id": "Q78",
"orig": 78,
"title": "Tricuspid valve anatomy",
"lesions": [
"TR",
"ANATOMY"
],
"lens": "anatomy",
"items": [
{
"id": "Q78.1",
"q": "Describe the anatomy of the tricuspid valve and name and locate each leaflet.",
"a": "The tricuspid valve guards the right atrioventricular orifice and is the largest and most apically positioned of the four valves. It has three leaflets: the anterior leaflet, the largest, attached to the anterior free wall; the posterior leaflet, attached to the inferior free wall; and the septal leaflet, which inserts directly on the interventricular septum with short chordae to the septum itself. Its annulus is a non-planar oval, three papillary muscle groups support the chordae, and the septal leaflet's hinge sits about 5 to 10 mm closer to the apex than the anterior mitral leaflet hinge, a normal offset that becomes pathologic beyond 8 mm/m² in Ebstein anomaly. In the apical four-chamber view you see the anterior and septal leaflets; the parasternal RV inflow view shows the anterior and posterior leaflets."
}
],
"numbers": [
{
"label": "Normal apical offset of septal tricuspid leaflet",
"value": "5–10",
"unit": "mm"
},
{
"label": "Ebstein displacement threshold",
"value": "≥ 8",
"unit": "mm/m²"
}
],
"delta": null,
"pearl": "The septal tricuspid leaflet sits lower than the mitral; that offset is why a primum ASD (no offset) and Ebstein (huge offset) are recognized in the four-chamber view.",
"lookalike": null,
"related": [
"Q79",
"Q89",
"Q90"
],
"reviewed": "2026-08-26"
},
{
"id": "Q79",
"orig": 79,
"title": "M-mode and 2D of tricuspid stenosis",
"lesions": [
"TS",
"MS"
],
"lens": "m-mode",
"items": [
{
"id": "Q79.1",
"q": "What are the three classic M-mode findings of tricuspid stenosis?",
"a": "The M-mode changes mirror those of rheumatic mitral stenosis because the mechanism, commissural fusion, is the same. The E-to-F slope flattens because the fused valve cannot close back after early filling while the atrium keeps pushing blood through a fixed orifice; the diastolic opening amplitude is reduced because the tethered leaflets cannot separate fully; and the leaflet echoes appear thick and multilayered in diastole from fibrosis and calcium. The posterior leaflet may also move anteriorly with the anterior leaflet."
},
{
"id": "Q79.2",
"q": "What are the characteristic 2D echocardiographic findings in tricuspid stenosis?",
"a": "Two-dimensional imaging shows thickened leaflets that dome into the right ventricle in diastole with restricted tip excursion, the right-sided equivalent of the mitral hockey stick. The right atrium and inferior vena cava dilate from chronic pressure loading. Because rheumatic tricuspid stenosis virtually never occurs alone, the mitral valve shows stenosis too, and you should also consider carcinoid disease, which thickens and immobilizes the leaflets in a semi-open position."
}
],
"numbers": [],
"delta": null,
"pearl": "Tricuspid stenosis is the mitral stenosis picture shifted one chamber to the right, and it almost never comes without mitral disease.",
"lookalike": {
"vs": "carcinoid tricuspid disease",
"discriminator": "Carcinoid leaflets are thickened, retracted, and fixed half-open causing combined TR and TS; rheumatic leaflets dome with commissural fusion and coexisting MS."
},
"related": [
"Q78",
"Q80",
"Q88",
"Q89"
],
"reviewed": "2026-08-26"
},
{
"id": "Q80",
"orig": 80,
"title": "Tricuspid inflow Doppler in stenosis",
"lesions": [
"TS",
"DOPPLER_PHYSICS"
],
"lens": "numbers",
"items": [
{
"id": "Q80.1",
"q": "What is the normal Doppler velocity of flow through the tricuspid valve?",
"a": "Normal tricuspid inflow peaks at roughly 0.5 to 0.8 m/s, lower than mitral inflow because the right-sided driving pressures are smaller and the orifice is larger. Velocity rises with inspiration as venous return increases, so tricuspid Doppler should be averaged over a respiratory cycle rather than taken at a single beat."
},
{
"id": "Q80.2",
"q": "How does the spectral Doppler trace change in tricuspid stenosis?",
"a": "The narrowed orifice forces blood through at higher velocity, so the E wave often exceeds 1 m/s and the mean gradient rises, with a mean of 5 mmHg or more indicating hemodynamically significant stenosis. The deceleration of early filling is prolonged, giving a pressure half-time of 190 ms or longer, and the color and pulsed Doppler show turbulence with spectral broadening. Valve area by the continuity equation of 1.0 cm² or less is consistent with severe stenosis. Because right-sided flow is respirophasic, average at least five beats, and remember that heart rate and coexisting TR raise the gradient independently of orifice size."
}
],
"numbers": [
{
"label": "Normal tricuspid inflow velocity",
"value": "0.5–0.8",
"unit": "m/s"
},
{
"label": "Significant TS mean gradient",
"value": "≥ 5",
"unit": "mmHg"
},
{
"label": "Significant TS pressure half-time",
"value": "≥ 190",
"unit": "ms"
},
{
"label": "Significant TS valve area",
"value": "≤ 1.0",
"unit": "cm²"
}
],
"delta": {
"was": "2011 card gave normal tricuspid velocity as a mean of 0.6 m/s with a range of 0.4 to 0.8 m/s.",
"now": "Current reference range for normal tricuspid inflow is 0.5–0.8 m/s; significant TS is defined by mean gradient ≥ 5 mmHg, PHT ≥ 190 ms, and area ≤ 1.0 cm².",
"source": "ASE 2017 valve stenosis"
},
"pearl": "Tricuspid stenosis numbers are the mitral numbers halved: mean gradient 5 instead of 10, PHT 190 instead of 220-based.",
"lookalike": null,
"related": [
"Q79",
"Q81",
"Q90"
],
"reviewed": "2026-08-26"
},
{
"id": "Q81",
"orig": 81,
"title": "Chamber effects of tricuspid stenosis",
"lesions": [
"TS",
"HEMODYNAMICS"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q81.1",
"q": "How does tricuspid stenosis affect the atria?",
"a": "Mild stenosis causes little change. As the orifice narrows, the right atrium must generate a higher pressure to fill the ventricle, and the chronic pressure load dilates it, often massively, with a dilated inferior vena cava and hepatic veins and large a waves in the jugular pulse. Systemically the venous hypertension produces hepatomegaly, ascites, and peripheral edema out of proportion to dyspnea. The left atrium is not affected by tricuspid stenosis itself, although it is usually enlarged from the coexisting rheumatic mitral disease."
},
{
"id": "Q81.2",
"q": "How does tricuspid stenosis affect the ventricles?",
"a": "The right ventricle sits downstream of the obstruction, so it is underfilled rather than overloaded and may look small with normal wall thickness. The reduced right-sided output limits pulmonary blood flow, which can paradoxically protect the patient from the pulmonary congestion of accompanying mitral stenosis. The left ventricle is not affected."
}
],
"numbers": [],
"delta": null,
"pearl": "Stenosis loads the chamber upstream: TS enlarges the right atrium and leaves the right ventricle small.",
"lookalike": null,
"related": [
"Q80",
"Q86",
"Q62"
],
"reviewed": "2026-08-26"
},
{
"id": "Q82",
"orig": 82,
"title": "Chronic tricuspid regurgitation findings",
"lesions": [
"TR",
"PH"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q82.1",
"q": "What are the main echocardiographic findings in chronic tricuspid regurgitation?",
"a": "Trivial or mild TR is common and the study is otherwise normal. With chronic moderate to severe leakage the right ventricle carries a volume overload: it dilates, its apex shares or takes over the cardiac apex in the four-chamber view, and the septum flattens in diastole to give the left ventricle a D shape in short axis. The right atrium enlarges, the tricuspid annulus dilates (4 cm or more in the four-chamber view supports severe TR), and the inferior vena cava and hepatic veins become plethoric with systolic flow reversal. Most chronic TR is functional, so look for the driver: annular dilatation, pulmonary hypertension, or a pacemaker lead."
}
],
"numbers": [
{
"label": "Severe TR annulus diameter",
"value": "≥ 4",
"unit": "cm"
},
{
"label": "Severe TR vena contracta",
"value": "≥ 0.7",
"unit": "cm"
}
],
"delta": null,
"pearl": "Diastolic septal flattening = RV volume overload (TR, ASD); systolic flattening = RV pressure overload (PH).",
"lookalike": null,
"related": [
"Q83",
"Q86",
"Q87",
"Q230",
"Q231",
"Q267",
"Q384"
],
"reviewed": "2026-08-26"
},
{
"id": "Q83",
"orig": 83,
"title": "Acute tricuspid regurgitation findings",
"lesions": [
"TR",
"ENDOCARDITIS",
"TRAUMA"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q83.1",
"q": "What are the main echocardiographic findings in acute tricuspid regurgitation?",
"a": "Acute TR almost always has a visible structural cause, so the diagnostic yield is in the valve rather than the chambers: a flail leaflet from chordal or papillary rupture after blunt chest trauma or endomyocardial biopsy, a vegetation in an intravenous drug user, or leaflet damage from a pacemaker lead. Because the right ventricle has not had time to remodel, it remains near normal in size but contracts vigorously as it handles the sudden extra volume, with mild dilatation of the right atrium and a distended inferior vena cava. The regurgitant continuous-wave signal is dense and often low velocity with an early peak and rapid decline, since right atrial pressure rises quickly and the pressures equalize."
}
],
"numbers": [],
"delta": null,
"pearl": "A normal-sized, hyperdynamic RV with a flail tricuspid leaflet means acute TR; look for trauma, drug use, or a lead.",
"lookalike": {
"vs": "chronic severe TR",
"discriminator": "Chronic TR shows a dilated RV and RA with diastolic septal flattening; acute TR shows a near-normal RV with an obvious leaflet lesion."
},
"related": [
"Q82",
"Q76"
],
"reviewed": "2026-08-26"
},
{
"id": "Q84",
"orig": 84,
"title": "Pulsed Doppler of tricuspid regurgitation",
"lesions": [
"TR",
"DOPPLER_PHYSICS"
],
"lens": "doppler",
"items": [
{
"id": "Q84.1",
"q": "How does tricuspid regurgitation appear on a pulsed-wave Doppler spectral trace?",
"a": "With the sample volume placed in the right atrium just above the leaflets, TR appears as a systolic signal below the baseline, moving away from an apical transducer, with spectral broadening because the jet is turbulent. Its peak velocity is only 2 to 3 m/s in patients with normal pulmonary pressure, because the RV-to-RA gradient is much smaller than the LV-to-LA gradient that drives mitral regurgitation at 5 to 6 m/s. So, unlike MR, a TR jet often stays within the Nyquist limit and may not alias; it aliases when pulmonary hypertension raises the jet velocity."
},
{
"id": "Q84.2",
"q": "How is tricuspid regurgitation graded with pulsed and continuous-wave Doppler?",
"a": "Mapping how far into the right atrium a pulsed Doppler signal can be found was the classic semi-quantitative method, but it depends on gain, driving pressure, and jet direction and is no longer used alone. Current grading combines several Doppler signs: the density and shape of the continuous-wave signal (a dense, triangular, early-peaking envelope indicates severe TR), systolic flow reversal in the hepatic veins, a dominant tricuspid E wave above 1 m/s, a vena contracta of 0.7 cm or wider, and a PISA-derived effective orifice of 0.4 cm² or more. Integrate these with RV, RA, annular, and IVC dimensions."
}
],
"numbers": [
{
"label": "TR peak velocity with normal PA pressure",
"value": "2–3",
"unit": "m/s"
},
{
"label": "Severe TR vena contracta",
"value": "≥ 0.7",
"unit": "cm"
},
{
"label": "Severe TR EROA",
"value": "≥ 0.4",
"unit": "cm²"
},
{
"label": "Severe TR tricuspid E velocity",
"value": "> 1",
"unit": "m/s"
}
],
"delta": {
"was": "2011 card taught grading TR by mapping the area of systolic turbulence in the right atrium: the larger the mapped area, the more severe.",
"now": "Current guideline: jet mapping alone is insufficient; grade with vena contracta ≥ 0.7 cm, EROA ≥ 0.4 cm², dense triangular CW signal, systolic hepatic vein reversal, and annular dilatation ≥ 4 cm.",
"source": "ASE 2017 regurgitation"
},
"pearl": "A TR jet that is dense, triangular, and peaks early is severe regardless of how it maps.",
"lookalike": null,
"related": [
"Q85",
"Q87",
"Q86"
],
"reviewed": "2026-08-26"
},
{
"id": "Q85",
"orig": 85,
"title": "Color Doppler grading of TR",
"lesions": [
"TR",
"DOPPLER_PHYSICS"
],
"lens": "doppler",
"items": [
{
"id": "Q85.1",
"q": "How is tricuspid regurgitation graded with color flow Doppler, and why is jet area alone unreliable?",
"a": "Color Doppler shows the regurgitant jet within one cardiac cycle so its origin, direction, and neck can be seen at a glance. The reliable color measurements are made at the valve: the vena contracta width in the four-chamber view, with 0.7 cm or more indicating severe TR, and the proximal flow convergence radius used for PISA (a radius above 0.9 cm at a 28 cm/s Nyquist suggests severe). Jet area is affected by gain, Nyquist setting, frame rate, atrial size, and wall impingement of eccentric jets, so a large central jet over 10 cm² only supports severe TR and a small eccentric jet can hide it. Always combine color with continuous-wave signal density, hepatic vein flow, and RV and annular size."
}
],
"numbers": [
{
"label": "Severe TR vena contracta",
"value": "≥ 0.7",
"unit": "cm"
},
{
"label": "Severe TR PISA radius at Nyquist 28 cm/s",
"value": "> 0.9",
"unit": "cm"
},
{
"label": "Supportive severe TR central jet area",
"value": "> 10",
"unit": "cm²"
}
],
"delta": {
"was": "2011 card taught that TR severity is judged by the overall size, length, and width of the color jet.",
"now": "Current guideline: jet area is only supportive; use vena contracta ≥ 0.7 cm, PISA/EROA ≥ 0.4 cm², CW density, and hepatic vein systolic reversal.",
"source": "ASE 2017 regurgitation"
},
"pearl": "Measure the neck, not the plume.",
"lookalike": null,
"related": [
"Q84",
"Q71",
"Q232"
],
"reviewed": "2026-08-26"
},
{
"id": "Q86",
"orig": 86,
"title": "Chamber effects of tricuspid regurgitation",
"lesions": [
"TR",
"HEMODYNAMICS"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q86.1",
"q": "How does tricuspid regurgitation affect the atria?",
"a": "Each systole a portion of the RV stroke volume is pushed backward into the right atrium, so the atrium receives both the normal venous return and the regurgitant volume. This volume overload dilates the right atrium in proportion to the leak, and the rise in atrial pressure during systole produces the large v wave, systolic hepatic vein reversal, and a plethoric inferior vena cava seen in severe cases. Trivial or mild TR does not enlarge the atrium. The mechanism differs from tricuspid stenosis, where atrial enlargement reflects pressure rather than volume. The left atrium is unaffected."
},
{
"id": "Q86.2",
"q": "How does tricuspid regurgitation affect the ventricles?",
"a": "Mild TR leaves the ventricles normal. Moderate to severe TR returns the regurgitant volume to the right ventricle in diastole, and the chronically volume-loaded ventricle dilates eccentrically, becomes hyperdynamic while its function is preserved, and flattens the septum in diastole. Dilatation stretches the annulus and worsens the leak, a self-perpetuating cycle, and eventually RV systolic function declines, marked by falling TAPSE and S' velocity. The left ventricle is affected only indirectly, through septal shift that impairs its filling."
}
],
"numbers": [],
"delta": null,
"pearl": "TR begets TR: RV dilatation stretches the annulus, which worsens the regurgitation.",
"lookalike": null,
"related": [
"Q81",
"Q82",
"Q84",
"Q88",
"Q230",
"Q231",
"Q384"
],
"reviewed": "2026-08-26"
},
{
"id": "Q87",
"orig": 87,
"title": "RVSP from the TR jet",
"lesions": [
"TR",
"PH",
"HEMODYNAMICS"
],
"lens": "formula",
"items": [
{
"id": "Q87.1",
"q": "Given the peak tricuspid regurgitant velocity, how do you estimate right ventricular systolic pressure?",
"a": "The TR jet velocity reflects the systolic pressure difference between the right ventricle and right atrium. The simplified Bernoulli equation converts velocity to gradient: pressure drop equals 4 times velocity squared. Adding an estimate of right atrial pressure to that gradient gives RVSP: RVSP = 4v² + RAP. Right atrial pressure comes from the subcostal IVC: a diameter of 2.1 cm or less that collapses more than 50% with a sniff means 3 mmHg, a diameter above 2.1 cm with less than 50% collapse means 15 mmHg, and any intermediate combination is assigned 8 mmHg. Use the densest complete envelope from several windows and avoid tracing faint fringes, which overestimate the pressure."
},
{
"id": "Q87.2",
"q": "Why is this calculation clinically important?",
"a": "It is the standard noninvasive estimate of pulmonary artery systolic pressure, because in the absence of pulmonic stenosis or RVOT obstruction the ventricle and pulmonary artery share the same systolic pressure. A TR velocity above 2.8 m/s raises intermediate probability of pulmonary hypertension and above 3.4 m/s high probability; the hemodynamic definition itself is a mean PA pressure above 20 mmHg at right heart catheterization. The number guides work-up for pulmonary vascular disease, tracks left heart disease and hypoxic lung disease, and is limited when the TR signal is weak, when RAP is misjudged, or when severe TR with a rapidly equalizing gradient underestimates the pressure."
}
],
"numbers": [
{
"label": "Bernoulli constant",
"value": "4",
"unit": "× v²"
},
{
"label": "RAP low: IVC ≤ 2.1 cm and > 50% collapse",
"value": "3",
"unit": "mmHg"
},
{
"label": "RAP intermediate",
"value": "8",
"unit": "mmHg"
},
{
"label": "RAP high: IVC > 2.1 cm and < 50% collapse",
"value": "15",
"unit": "mmHg"
},
{
"label": "TR Vmax intermediate PH probability",
"value": "> 2.8",
"unit": "m/s"
},
{
"label": "TR Vmax high PH probability",
"value": "> 3.4",
"unit": "m/s"
},
{
"label": "Hemodynamic PH definition mPAP",
"value": "> 20",
"unit": "mmHg"
}
],
"delta": {
"was": "2011 card added the converted TR gradient to an estimated RA pressure without a standardized IVC-based RAP scheme, and PH thresholds were not tied to a TR velocity or mPAP definition.",
"now": "Current guideline: RVSP = 4v² + RAP with RAP 3/8/15 mmHg from IVC size and collapsibility; TR Vmax > 2.8 m/s intermediate and > 3.4 m/s high probability of PH; PH defined as mPAP > 20 mmHg.",
"source": "ESC-ERS 2022 PH / ASE 2015 chamber quant"
},
"pearl": "A 3 m/s TR jet with a normal IVC gives 36 + 3 = 39 mmHg; memorize 4v² for 2.5, 3, 3.5, and 4 m/s (25, 36, 49, 64).",
"lookalike": null,
"related": [
"Q84",
"Q90",
"Q82",
"Q233",
"Q237",
"Q269",
"Q270",
"Q271"
],
"widgets": [
{
"id": "calc",
"opts": {
"k": "rvsp"
}
}
],
"reviewed": "2026-08-26"
},
{
"id": "Q88",
"orig": 88,
"title": "Carcinoid heart disease",
"lesions": [
"TR",
"PS",
"MASS"
],
"lens": "etiology",
"items": [
{
"id": "Q88.1",
"q": "What is carcinoid syndrome?",
"a": "Carcinoid syndrome is the clinical picture of flushing, secretory diarrhea, and bronchospasm produced when a neuroendocrine tumor, usually of the small bowel, releases serotonin and other vasoactive amines into the systemic circulation. Because the liver normally inactivates these substances, the syndrome nearly always signals hepatic metastases that let the hormones bypass first-pass clearance. About half of affected patients develop carcinoid heart disease, and elevated urinary 5-HIAA confirms the diagnosis."
},
{
"id": "Q88.2",
"q": "How does carcinoid syndrome damage the tricuspid valve?",
"a": "Serotonin bathing the right heart stimulates fibroblasts to lay down white, plaque-like fibrous tissue on the endocardium and the ventricular side of the tricuspid and pulmonic leaflets. The leaflets thicken, shorten, and retract until they are fixed in a semi-open position, so they neither coapt in systole nor open fully in diastole. The result is dominant, often severe tricuspid regurgitation with a dagger-shaped, early-peaking continuous-wave signal, frequently combined with tricuspid and pulmonic stenosis. The lungs metabolize serotonin, so left-sided valves are spared unless there is a right-to-left shunt, a bronchial carcinoid, or a very high hormone load."
}
],
"numbers": [
{
"label": "Proportion of carcinoid syndrome patients with cardiac involvement",
"value": "≈ 50",
"unit": "%"
}
],
"delta": null,
"pearl": "Thickened, retracted, immobile tricuspid leaflets stuck half-open with flushing and diarrhea: carcinoid until proven otherwise.",
"lookalike": {
"vs": "rheumatic tricuspid disease",
"discriminator": "Rheumatic leaflets dome with commissural fusion and coexisting mitral stenosis; carcinoid leaflets are retracted and fixed, with pulmonic involvement and a normal mitral valve."
},
"related": [
"Q79",
"Q86",
"Q385"
],
"reviewed": "2026-08-26"
},
{
"id": "Q89",
"orig": 89,
"title": "Tricuspid prolapse and rheumatic TS",
"lesions": [
"TR",
"MVP",
"TS"
],
"lens": "definition",
"items": [
{
"id": "Q89.1",
"q": "Define tricuspid valve prolapse.",
"a": "Tricuspid valve prolapse is the systolic bowing of one or more tricuspid leaflets back beyond the annular plane into the right atrium, usually from myxomatous degeneration that thickens and elongates the leaflets and chordae. Diagnose it in the parasternal RV inflow or apical four-chamber views and confirm coaptation failure with color Doppler, since prolapse produces tricuspid regurgitation of variable severity. The anterior and septal leaflets prolapse more often than the posterior leaflet."
},
{
"id": "Q89.2",
"q": "How does tricuspid valve prolapse relate to mitral valve prolapse?",
"a": "The two share the same myxomatous substrate, so tricuspid prolapse rarely occurs alone: roughly 90% of patients with tricuspid prolapse also have mitral prolapse, whereas only a minority of mitral prolapse patients have tricuspid involvement. Finding one should prompt a careful look at the other, and both cluster in connective tissue disorders such as Marfan and Ehlers-Danlos syndromes."
},
{
"id": "Q89.3",
"q": "How often does rheumatic heart disease involve the tricuspid valve with stenosis?",
"a": "Around 15% of patients with rheumatic heart disease have some degree of tricuspid stenosis, but it is almost never isolated; it accompanies mitral stenosis and often aortic involvement. Because the mitral lesion dominates the symptoms, tricuspid stenosis is easily overlooked, so interrogate the tricuspid inflow with Doppler in every rheumatic mitral patient and be suspicious when right atrial enlargement or venous congestion seem excessive for the degree of pulmonary hypertension."
}
],
"numbers": [
{
"label": "Tricuspid prolapse patients with coexisting MVP",
"value": "≈ 90",
"unit": "%"
},
{
"label": "Rheumatic heart disease with tricuspid stenosis",
"value": "≈ 15",
"unit": "%"
}
],
"delta": null,
"pearl": "Tricuspid prolapse is a marker for mitral prolapse; rheumatic TS is a stowaway on mitral stenosis.",
"lookalike": null,
"related": [
"Q78",
"Q79",
"Q77",
"Q366"
],
"reviewed": "2026-08-26"
},
{
"id": "Q90",
"orig": 90,
"title": "Pulmonic valve anatomy and velocity",
"lesions": [
"PS",
"ANATOMY",
"DOPPLER_PHYSICS"
],
"lens": "anatomy",
"items": [
{
"id": "Q90.1",
"q": "Describe the anatomy of the pulmonic valve and name and locate its cusps.",
"a": "The pulmonic valve is the most anterior and superior of the four valves, sitting at the top of the right ventricular outflow tract, anterior and slightly to the left of the aortic valve, so the two semilunar valves lie roughly at right angles to each other. It is a trileaflet semilunar valve with anterior, left, and right cusps; because the right cusp faces the aorta and lies posteriorly relative to the transducer, older M-mode texts call it the posterior cusp. Unlike the aortic valve it has no fibrous continuity with an atrioventricular valve, being separated from the tricuspid valve by muscular infundibulum, and it is imaged in the parasternal short axis at the aortic level and the RV outflow view, where usually only two cusps are seen."
},
{
"id": "Q90.2",
"q": "What is the normal Doppler velocity across the pulmonic valve in adults and in children?",
"a": "Normal adult pulmonic flow peaks at about 0.6 to 0.9 m/s, corresponding to a trivial gradient of only 1 to 3 mmHg, because a wide valve delivers the entire RV stroke volume into a low-pressure pulmonary circuit. Children run a little faster, with a mean near 0.8 m/s and an upper normal of roughly 1.0 m/s, reflecting their smaller orifice and higher cardiac index. Velocity above this suggests obstruction or increased flow (as with an atrial septal defect), and pulmonic stenosis is graded from the peak gradient: mild below 36 mmHg, moderate 36 to 64, and severe above 64 mmHg (Vmax above 4 m/s)."
}
],
"numbers": [
{
"label": "Normal adult pulmonic velocity",
"value": "0.6–0.9",
"unit": "m/s"
},
{
"label": "Normal pulmonic gradient",
"value": "1–3",
"unit": "mmHg"
},
{
"label": "Normal pediatric pulmonic velocity (mean)",
"value": "≈ 0.8",
"unit": "m/s"
},
{
"label": "Mild PS peak gradient",
"value": "< 36",
"unit": "mmHg"
},
{
"label": "Moderate PS peak gradient",
"value": "36–64",
"unit": "mmHg"
},
{
"label": "Severe PS peak gradient",
"value": "> 64",
"unit": "mmHg"
}
],
"delta": {
"was": "2011 card gave the normal adult pulmonic velocity as a mean of 0.7 m/s with a range of 0.5 to 0.9 m/s.",
"now": "Current reference range for normal pulmonic velocity is 0.6–0.9 m/s; PS is graded by peak gradient < 36 mild, 36–64 moderate, > 64 mmHg severe.",
"source": "ASE 2017 valve stenosis"
},
"pearl": "Pulmonic is the front-most valve: the first thing the ultrasound beam meets and the one whose gradient should be nearly nothing.",
"lookalike": null,
"related": [
"Q78",
"Q80",
"Q87",
"Q236"
],
"reviewed": "2026-08-26"
},
{
"id": "Q91",
"orig": 91,
"title": "Pulmonic stenosis on M-mode and 2D",
"lesions": [
"PS"
],
"lens": "m-mode",
"items": [
{
"id": "Q91.1",
"q": "Which M-mode sign points to valvular pulmonic stenosis, and what causes it?",
"a": "On an M-mode sweep through the pulmonic leaflet, atrial contraction produces a small posterior deflection just before systole, the so-called \"a\" dip. When the valve is stenotic, the RV becomes stiff and hypertrophied, so the right atrial kick generates an unusually large late-diastolic pressure pulse that briefly forces the doming leaflets open. That exaggerated \"a\" dip, deeper than about 7 mm, is the classic M-mode clue. It disappears when pulmonary pressures are high, which is one way M-mode helps separate valvular PS from pulmonary hypertension."
},
{
"id": "Q91.2",
"q": "What 2D findings should you look for when pulmonic stenosis is suspected?",
"a": "Look first at the leaflets: they are thickened, their opening is reduced, and in systole they bow toward the pulmonary artery in a dome rather than folding flat against the wall. Then look at the consequences of chronic pressure load: the RV free wall thickens, and the main pulmonary artery just beyond the valve is dilated because the high-velocity jet strikes and stretches its wall. A dilated main PA is more typical of PS than of pulmonary hypertension from other causes, where the branches also enlarge."
}
],
"numbers": [
{
"label": "Exaggerated pulmonic a-dip in PS",
"value": "> 7",
"unit": "mm"
}
],
"delta": null,
"pearl": "Big a-dip means a big atrial kick against a stiff, doming valve; a-dip vanishes when PA pressure is high.",
"lookalike": {
"vs": "pulmonary hypertension",
"discriminator": "PH flattens the a-dip and shows mid-systolic notching; PS exaggerates the a-dip and domes the leaflets."
},
"related": [
"Q92",
"Q93",
"Q94",
"Q235"
],
"reviewed": "2026-08-26"
},
{
"id": "Q92",
"orig": 92,
"title": "Doppler grading of pulmonic stenosis",
"lesions": [
"PS"
],
"lens": "doppler",
"items": [
{
"id": "Q92.1",
"q": "How does pulmonic stenosis change the spectral Doppler trace across the valve?",
"a": "A narrowed orifice forces blood to accelerate, so the CW envelope shows a peak velocity well above the normal 0.6 to 0.9 m/s, and the flow downstream is disorganized, which fills in the envelope with spectral broadening. As stenosis worsens, the time from flow onset to peak velocity lengthens and the contour becomes more rounded, mirroring the prolonged ejection of a pressure-loaded RV. Sample from the parasternal short-axis or subcostal RVOT view where the jet is parallel to the beam."
},
{
"id": "Q92.2",
"q": "What peak gradient separates mild, moderate, and severe pulmonic stenosis, and when does the gradient mislead?",
"a": "Using 4v², a peak gradient under 36 mmHg (Vmax under 3 m/s) is mild, 36 to 64 mmHg is moderate, and above 64 mmHg (Vmax above 4 m/s) is severe. The gradient depends on flow as much as on orifice size, so a failing RV with low output can push only a modest velocity, perhaps 3 m/s, through a critically narrow valve. In that setting a low gradient underestimates severity, and you should weigh RV hypertrophy, leaflet doming, and RV function alongside the number."
}
],
"numbers": [
{
"label": "Mild PS peak gradient",
"value": "< 36",
"unit": "mmHg"
},
{
"label": "Moderate PS peak gradient",
"value": "36–64",
"unit": "mmHg"
},
{
"label": "Severe PS peak gradient",
"value": "> 64",
"unit": "mmHg"
},
{
"label": "Severe PS Vmax",
"value": "> 4",
"unit": "m/s"
},
{
"label": "Normal pulmonic velocity",
"value": "0.6–0.9",
"unit": "m/s"
}
],
"delta": {
"was": "2011 card taught that a peak gradient above 75 mmHg denotes severe pulmonic stenosis.",
"now": "Current guideline: severe PS is a peak gradient >64 mmHg (Vmax >4 m/s); moderate 36–64 mmHg; mild <36 mmHg.",
"source": "ASE 2017 valve stenosis"
},
"pearl": "PS is graded by peak gradient, not mean: 36 and 64 are the fences (3 m/s and 4 m/s).",
"lookalike": {
"vs": "infundibular (subvalvular) stenosis",
"discriminator": "Subvalvular obstruction gives a late-peaking dagger-shaped jet that starts below the leaflets; valvular PS has doming leaflets with the jet at the valve plane."
},
"related": [
"Q91",
"Q93",
"Q234",
"Q236",
"Q237",
"Q238"
],
"reviewed": "2026-08-26"
},
{
"id": "Q93",
"orig": 93,
"title": "Chamber effects of pulmonic stenosis",
"lesions": [
"PS"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q93.1",
"q": "What does chronic pulmonic stenosis do to the ventricles?",
"a": "The RV must generate a much higher systolic pressure to push blood across the narrowed valve, and it answers that wall stress by adding muscle: concentric RV hypertrophy is the hallmark. Hypertrophy compensates for years, but eventually the chamber dilates and contractility falls, sometimes with paradoxical septal motion from the high RV pressure. The LV is a bystander; it is neither loaded nor enlarged unless the flattened septum interferes with its filling."
},
{
"id": "Q93.2",
"q": "How are the atria affected by pulmonic stenosis?",
"a": "A thick RV is a stiff RV, so its end-diastolic pressure rises and the RA must work harder to fill it. That raises RA pressure and, over time, enlarges the right atrium; with a patent foramen ovale, right-to-left shunting and cyanosis can occur. The left atrium is usually spared because LV filling is not directly affected."
},
{
"id": "Q93.3",
"q": "How does pulmonic stenosis affect the great vessels?",
"a": "The main pulmonary artery dilates just beyond the valve. The eccentric high-velocity jet repeatedly strikes the vessel wall, and the resulting turbulence and shear weaken and stretch it, producing post-stenotic dilatation of the main PA, often extending into the left branch. The aorta is unaffected."
}
],
"numbers": [],
"delta": null,
"pearl": "PS is a pressure-load lesion: RV thickens first, RA enlarges second, PA balloons beyond the jet.",
"lookalike": null,
"related": [
"Q91",
"Q92",
"Q97",
"Q234",
"Q239"
],
"reviewed": "2026-08-26"
},
{
"id": "Q94",
"orig": 94,
"title": "Etiology of pulmonic stenosis and carcinoid",
"lesions": [
"PS",
"PR",
"TR"
],
"lens": "etiology",
"items": [
{
"id": "Q94.1",
"q": "What is the most common cause of pulmonic stenosis?",
"a": "Nearly all pulmonic stenosis is congenital, either as an isolated doming valve with fused commissures or as part of syndromes such as Noonan (dysplastic leaflets) and tetralogy of Fallot. Acquired PS is rare; rheumatic disease almost never selects the pulmonic valve, so when an adult presents with new PS think of carcinoid or external compression by a mass."
},
{
"id": "Q94.2",
"q": "By what mechanism does carcinoid heart disease produce pulmonic stenosis?",
"a": "Neuroendocrine tumors, usually with hepatic metastases, release serotonin and related vasoactive substances into the venous blood. These reach the right heart first and stimulate fibroblasts to lay down plaques of fibrous tissue on the endocardium and the tricuspid and pulmonic leaflets. The leaflets become thick, retracted, and rigid; when the fibrosis narrows the orifice, stenosis results. The left side is usually spared because the lungs inactivate serotonin."
},
{
"id": "Q94.3",
"q": "Why does carcinoid more often cause pulmonic regurgitation than stenosis?",
"a": "The same fibrous plaques shorten and stiffen the leaflets so they can neither open nor close fully. Because the leaflets are retracted, the dominant lesion is usually a fixed, half-open valve, which produces regurgitation, often severe, with lesser stenosis. The tricuspid valve is affected in the same way and TR usually dominates the clinical picture."
}
],
"numbers": [],
"delta": null,
"pearl": "Carcinoid = right-sided valves frozen half open: regurgitation first, stenosis second.",
"lookalike": {
"vs": "rheumatic valve disease",
"discriminator": "Rheumatic disease attacks the mitral and aortic valves and spares the pulmonic; carcinoid attacks the tricuspid and pulmonic and spares the left side."
},
"related": [
"Q91",
"Q96",
"Q235",
"Q385"
],
"reviewed": "2026-08-26"
},
{
"id": "Q95",
"orig": 95,
"title": "Echo findings of chronic pulmonic regurgitation",
"lesions": [
"PR"
],
"lens": "2d",
"items": [
{
"id": "Q95.1",
"q": "What echocardiographic findings accompany chronic pulmonic regurgitation?",
"a": "A trivial or mild leak, which most healthy people have, produces no structural change and the study looks normal apart from a thin diastolic color jet in the RVOT. When regurgitation is moderate or severe, the RV takes on a large diastolic volume load: it dilates, its free wall moves vigorously early on, and the septum flattens in diastole and moves paradoxically. With years of overload the RV ultimately weakens and its systolic function declines. Doppler clues to severity include a wide jet filling the RVOT, a dense CW signal with rapid deceleration that ends before diastole is over (PHT under 100 ms), and diastolic flow reversal in the branch pulmonary arteries."
}
],
"numbers": [
{
"label": "PR pressure half-time suggesting severe PR",
"value": "< 100",
"unit": "ms"
}
],
"delta": null,
"pearl": "Severe PR: short, steep, early-terminating diastolic signal plus a big, bouncy RV.",
"lookalike": null,
"related": [
"Q96",
"Q97",
"Q240",
"Q242",
"Q243",
"Q244",
"Q246",
"Q385"
],
"reviewed": "2026-08-26"
},
{
"id": "Q96",
"orig": 96,
"title": "Causes of PR and effect of PH",
"lesions": [
"PR",
"PH"
],
"lens": "etiology",
"items": [
{
"id": "Q96.1",
"q": "What is the most common cause of pulmonic regurgitation?",
"a": "Most PR occurs across a structurally normal valve, and roughly 60 percent of healthy adults have a small physiologic leak detectable with color Doppler. Two features of the right side explain this: the low diastolic pressure in the pulmonary artery does not press the leaflets tightly together, and the main PA wraps around the aorta so its cross-section is slightly oval rather than round, which leaves a tiny central gap at closure. Pathologic PR is usually secondary to annular dilatation from pulmonary hypertension or is iatrogenic after balloon valvotomy or tetralogy repair."
},
{
"id": "Q96.2",
"q": "How does pulmonary hypertension alter the pulmonic regurgitant signal?",
"a": "The velocity of a regurgitant jet reflects the pressure difference driving it, here PA diastolic pressure minus RV diastolic pressure. With normal PA pressures that difference is small, so PR velocity is only about 1 m/s. When PA pressure climbs, the same valve leaks faster; velocities above 4 m/s are not unusual. This is clinically useful: 4 times the end-diastolic PR velocity squared plus RA pressure estimates PA diastolic pressure, and the early-diastolic peak estimates mean PA pressure."
}
],
"numbers": [
{
"label": "Prevalence of physiologic PR in adults",
"value": "~60",
"unit": "%"
},
{
"label": "Normal PR jet velocity",
"value": "~1",
"unit": "m/s"
},
{
"label": "PR velocity with pulmonary hypertension",
"value": "> 4",
"unit": "m/s"
}
],
"delta": null,
"pearl": "PR end-diastolic velocity gives PA diastolic pressure; PR peak velocity gives mean PA pressure.",
"lookalike": {
"vs": "coronary artery flow in the RVOT",
"discriminator": "Coronary flow is low-velocity and biphasic; PR is a diastolic jet aimed at the RV that begins with pulmonic closure."
},
"related": [
"Q94",
"Q95",
"Q240",
"Q241",
"Q244"
],
"reviewed": "2026-08-26"
},
{
"id": "Q97",
"orig": 97,
"title": "Chamber effects of pulmonic regurgitation",
"lesions": [
"PR"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q97.1",
"q": "How does pulmonic regurgitation affect the ventricles?",
"a": "Mild PR adds so little volume that the RV is unchanged. When the leak is moderate or severe, each diastole returns extra blood into the RV, so the chamber dilates and, by the Frank-Starling mechanism, contracts vigorously; this is a volume load, so the wall stays thin rather than thickening as in stenosis. The septum flattens in diastole and may move paradoxically. After many years the overloaded RV can decompensate with falling systolic function, which is why repaired tetralogy patients are followed serially for RV size. The LV is not directly involved."
},
{
"id": "Q97.2",
"q": "How does pulmonic regurgitation affect the atria?",
"a": "The right atrium is only modestly affected: as the dilated RV becomes less compliant, its filling pressure rises and the RA enlarges slightly, more so once functional TR develops from annular stretch. The left atrium is untouched because PR does not alter LV filling."
},
{
"id": "Q97.3",
"q": "Does pulmonic regurgitation change the great vessels?",
"a": "Isolated PR does not enlarge the pulmonary artery or aorta. When the PA is dilated in a patient with PR, the dilatation is usually the cause of the leak, from pulmonary hypertension or idiopathic PA dilatation stretching the annulus, rather than the result of it."
}
],
"numbers": [],
"delta": null,
"pearl": "Volume load dilates, pressure load thickens: PR gives a big thin RV, PS gives a thick one.",
"lookalike": null,
"related": [
"Q93",
"Q95",
"Q240",
"Q246"
],
"reviewed": "2026-08-26"
},
{
"id": "Q98",
"orig": 98,
"title": "M-mode appearance of vegetations",
"lesions": [
"ENDOCARDITIS",
"MR",
"AR"
],
"lens": "m-mode",
"items": [
{
"id": "Q98.1",
"q": "What does mitral valve endocarditis look like on M-mode?",
"a": "A vegetation is a friable clump of fibrin, platelets, and organisms attached to the leaflet but not restricting it, so the leaflet's M-mode excursion remains normal, unlike rheumatic thickening which stiffens the valve. What you see is a dense, irregular, shaggy echo riding on the anterior or posterior leaflet line, most conspicuous in systole when the closed leaflets bring the mass into the beam. A large pedunculated vegetation moves with a chaotic pattern of its own, out of phase with the leaflet, and may show high-frequency diastolic flutter."
},
{
"id": "Q98.2",
"q": "What does aortic valve endocarditis look like on M-mode?",
"a": "The aortic vegetation behaves the same way but with opposite timing: it hangs on the ventricular surface of the cusps and prolapses toward the LVOT in diastole, so the shaggy echoes appear within the aortic root box in diastole and are swept out of the beam when the cusps open in systole. A large mobile mass may prolapse through the closed valve into the LVOT, where a sweep across the mitral level shows it in diastole just above the anterior mitral leaflet. Associated AR may cause fine diastolic flutter of the anterior mitral leaflet."
}
],
"numbers": [],
"delta": null,
"pearl": "Vegetations follow the flow: mitral vegetations sit atrial-side and show in systole; aortic ones sit ventricular-side and show in diastole.",
"lookalike": {
"vs": "myxomatous leaflet thickening",
"discriminator": "Myxomatous leaflets are diffusely thick and move with the leaflet; vegetations are focal, shaggy, and move independently."
},
"related": [
"Q99",
"Q100",
"Q319",
"Q320"
],
"reviewed": "2026-08-26"
},
{
"id": "Q99",
"orig": 99,
"title": "2D location of valvular vegetations",
"lesions": [
"ENDOCARDITIS",
"MR",
"AR"
],
"lens": "2d",
"items": [
{
"id": "Q99.1",
"q": "Where do mitral vegetations form and how do they appear on 2D imaging?",
"a": "Vegetations grow where a high-velocity jet damages endothelium, which is on the low-pressure downstream side of a leak; for the mitral valve that is the atrial surface of the leaflets. On 2D you see a mobile, irregularly textured mass attached to the leaflet, often with thickened, redundant leaflet tissue nearby. In systole the closed leaflets push the mass into the left atrium; in diastole it swings back toward the LV inflow. Large mobile vegetations over 10 mm carry higher embolic risk, and any new perforation, flail, or abscess should be sought at the same time."
},
{
"id": "Q99.2",
"q": "Where do aortic vegetations form and how do they appear on 2D imaging?",
"a": "For the aortic valve, the low-pressure side is the ventricular surface of the cusps, so the mass sits on the LVOT side and prolapses into the outflow tract in diastole when the cusps are closed. In systole the opening cusps carry it up into the aortic root. Because the AV lies near the mitral-aortic fibrous continuity, infection can extend into a root abscess or a mycotic aneurysm of the anterior mitral leaflet, which is why TEE is favored for aortic endocarditis."
}
],
"numbers": [
{
"label": "Vegetation size with high embolic risk",
"value": "> 10",
"unit": "mm"
}
],
"delta": null,
"pearl": "Vegetations sit on the side the jet lands on: atrial for mitral, ventricular for aortic.",
"lookalike": {
"vs": "Lambl's excrescence",
"discriminator": "Lambl's strands are thin, filamentous, on the closure line of an otherwise normal valve, without clinical infection or regurgitation."
},
"related": [
"Q98",
"Q100",
"Q101",
"Q318",
"Q319",
"Q320",
"Q328",
"Q369",
"Q391",
"Q392"
],
"reviewed": "2026-08-26"
},
{
"id": "Q100",
"orig": 100,
"title": "Right-sided endocarditis in injection drug use",
"lesions": [
"ENDOCARDITIS",
"TR"
],
"lens": "etiology",
"items": [
{
"id": "Q100.1",
"q": "Why does injection drug use predispose to right-sided endocarditis?",
"a": "Injected material carries skin flora and particulate contaminants directly into the venous system, and the tricuspid valve is the first valve that bacteria-laden blood meets. Repeated bombardment by particles and organisms injures the tricuspid endothelium, giving bacteria a platelet-fibrin nidus to colonize. Tricuspid vegetations tend to be large, often shed septic emboli to the lungs, and cause TR; the pulmonic valve is involved far less often."
},
{
"id": "Q100.2",
"q": "Which organism most often causes endocarditis in people who inject drugs?",
"a": "Staphylococcus aureus, a skin commensal, is by far the most common isolate and is characteristically aggressive, able to infect a previously normal valve and destroy tissue quickly. Its virulence explains the acute presentation with fever, septic pulmonary emboli, and rapid leaflet damage. Other organisms in this group include streptococci, Pseudomonas, and fungi such as Candida."
}
],
"numbers": [],
"delta": null,
"pearl": "Tricuspid vegetation plus cavitating lung nodules in a young febrile patient: think S. aureus from injection drug use.",
"lookalike": null,
"related": [
"Q98",
"Q99",
"Q101",
"Q321",
"Q392"
],
"reviewed": "2026-08-26"
},
{
"id": "Q101",
"orig": 101,
"title": "Acute versus subacute endocarditis",
"lesions": [
"ENDOCARDITIS",
"MVP",
"PROSTHETIC"
],
"lens": "definition",
"items": [
{
"id": "Q101.1",
"q": "What is meant by acute bacterial endocarditis?",
"a": "Acute endocarditis is a fulminant infection caused by a virulent organism, classically Staphylococcus aureus, that can seed and rapidly destroy a valve that was structurally normal beforehand. Patients present within days with high fever, systemic toxicity, and early valve damage or abscess. In the pre-antibiotic era this course was almost uniformly fatal within about six weeks, which is where the historical label came from."
},
{
"id": "Q101.2",
"q": "What is meant by subacute bacterial endocarditis?",
"a": "Subacute endocarditis is an indolent infection by a low-virulence organism, typically viridans streptococci from the mouth, that settles on a valve already damaged or abnormal. Turbulent flow across a prolapsing, rheumatic, congenitally malformed, or prosthetic valve creates a sterile platelet-fibrin thrombus that transient bacteremia colonizes. Symptoms evolve over weeks to months with low-grade fever, fatigue, and embolic or immunologic signs, and the vegetation is found on a valve with a recognizable underlying lesion."
}
],
"numbers": [
{
"label": "Historical untreated survival in acute endocarditis",
"value": "~6",
"unit": "weeks"
}
],
"delta": null,
"pearl": "Acute: virulent bug, normal valve, days. Subacute: gentle bug, abnormal valve, weeks.",
"lookalike": null,
"related": [
"Q99",
"Q100",
"Q111",
"Q321"
],
"reviewed": "2026-08-26"
},
{
"id": "Q102",
"orig": 102,
"title": "Mechanical versus bioprosthetic valves",
"lesions": [
"PROSTHETIC",
"INSTRUMENTATION"
],
"lens": "2d",
"items": [
{
"id": "Q102.1",
"q": "On 2D echo, how do mechanical and bioprosthetic valves differ in appearance?",
"a": "Metal and pyrolytic carbon reflect nearly all incident ultrasound, so a mechanical valve casts a dense acoustic shadow behind its sewing ring and occluders and throws bright reverberation and comet-tail artifacts from the disc or leaflets. Structures behind the valve, such as the left atrium behind a mitral prosthesis, are masked. A bioprosthesis still shadows from its sewing ring and stent posts, but the tissue leaflets between the posts are only mildly echogenic, so they can be seen opening and closing and generate few reverberations."
},
{
"id": "Q102.2",
"q": "From the patient's perspective, what are the main trade-offs between mechanical and bioprosthetic valves?",
"a": "A mechanical valve is essentially permanent, often functioning for more than 20 years, but its surfaces are thrombogenic and require lifelong warfarin with its bleeding risk, and some patients hear the closing click. A bioprosthetic valve needs no long-term anticoagulation, but its leaflets calcify and degenerate over roughly 10 to 15 years, sooner in young patients, so reintervention is likely. Age, bleeding risk, and pregnancy plans drive the choice; valve-in-valve TAVR has made bioprosthetic degeneration easier to treat."
}
],
"numbers": [
{
"label": "Mechanical valve durability",
"value": "> 20",
"unit": "years"
},
{
"label": "Bioprosthetic valve durability",
"value": "~10–15",
"unit": "years"
}
],
"delta": null,
"pearl": "Mechanical: lasts, but needs warfarin and shadows everything. Tissue: no warfarin, but wears out.",
"lookalike": null,
"related": [
"Q106",
"Q110",
"Q112",
"Q322",
"Q359"
],
"reviewed": "2026-08-26"
},
{
"id": "Q103",
"orig": 103,
"title": "Starr-Edwards caged-ball valve",
"lesions": [
"PROSTHETIC"
],
"lens": "definition",
"items": [
{
"id": "Q103.1",
"q": "Which prosthesis is the classic caged-ball valve?",
"a": "The Starr-Edwards valve, introduced in 1960, is the prototype caged-ball prosthesis: a silicone ball moves within a metal cage, rising to open and seating on the ring to close. It is no longer implanted, but many recipients are still alive, so you may encounter one in an older patient and should recognize it on echo."
},
{
"id": "Q103.2",
"q": "What were the advantages and drawbacks of caged-ball valves?",
"a": "Their great strength was durability; many Starr-Edwards valves functioned for 15 to 30 years or longer. The costs were hemodynamic and thrombotic. Blood has to flow around a central ball, so the effective orifice is small and the transvalvular gradient is higher than any other design, and the tall cage can obstruct the LVOT in the mitral position. The large foreign surface is thrombogenic, so lifelong anticoagulation is mandatory, and hemolysis was common. Modern bileaflet valves replaced them."
}
],
"numbers": [
{
"label": "Starr-Edwards functional lifespan",
"value": "15–30",
"unit": "years"
}
],
"delta": {
"was": "2011 card described the Starr-Edwards caged-ball valve as a commonly used prosthesis.",
"now": "Caged-ball valves are historical; bileaflet mechanical valves (St. Jude, On-X), stented or stentless bioprostheses, and TAVR are the current options.",
"source": "Prosthetic valves anchor (ASE prosthetic valve guideline)"
},
"pearl": "Ball in a cage: most durable, highest gradient, tallest profile.",
"lookalike": null,
"related": [
"Q104",
"Q105",
"Q108",
"Q109"
],
"reviewed": "2026-08-26"
},
{
"id": "Q104",
"orig": 104,
"title": "Beall caged-disc valve",
"lesions": [
"PROSTHETIC"
],
"lens": "definition",
"items": [
{
"id": "Q104.1",
"q": "Name a caged-disc prosthesis and describe its status today.",
"a": "The Beall valve is the best-known caged-disc design: a flat disc, rather than a ball, moves up and down inside a short cage. It was used mainly in the mitral position in the 1960s and 1970s and was withdrawn because of disc wear and hemolysis, so it is now encountered only in rare long-term survivors."
},
{
"id": "Q104.2",
"q": "What were the advantages and disadvantages of caged-disc valves?",
"a": "Replacing the ball with a disc shortened the cage, giving a low profile that protruded far less into the LVOT than a Starr-Edwards in the mitral position, and the valve was mechanically durable. But flow still had to detour around a central occluder, so gradients remained high, and the disc's abrasive travel and turbulent flow caused more hemolysis and disc wear than other designs. Those problems ended the design."
}
],
"numbers": [],
"delta": null,
"pearl": "Caged-disc = low profile, high gradient, high hemolysis; now historical.",
"lookalike": null,
"related": [
"Q103",
"Q105"
],
"reviewed": "2026-08-26"
},
{
"id": "Q105",
"orig": 105,
"title": "Bjork-Shiley tilting-disc valve",
"lesions": [
"PROSTHETIC",
"AR"
],
"lens": "definition",
"items": [
{
"id": "Q105.1",
"q": "Which prosthesis is the classic tilting-disc valve and why did it improve on caged designs?",
"a": "The Bjork-Shiley valve is the classic single tilting-disc prosthesis; the Medtronic-Hall is another. A disc pivots on struts to open at an angle of roughly 60 to 70 degrees, creating a large major orifice and a small minor orifice through which blood flows nearly centrally. Because there is no ball or disc sitting in the middle of the stream, gradients and turbulence are far lower than with caged occluders."
},
{
"id": "Q105.2",
"q": "What are the advantages and disadvantages of tilting-disc valves?",
"a": "The advantages are good hemodynamics: low transvalvular gradient, less turbulence, and a low profile. The disadvantages are mechanical and regurgitant. Certain Bjork-Shiley convexo-concave models suffered strut fracture with disc escape, a catastrophic failure that led to recall, and all tilting-disc valves have a built-in closing and leakage backflow that is larger than in caged designs. Every mechanical valve has some physiologic regurgitation and some obstruction; the task on echo is distinguishing these normal washing jets from pathologic leaks."
}
],
"numbers": [
{
"label": "Tilting-disc opening angle",
"value": "~60–70",
"unit": "degrees"
}
],
"delta": {
"was": "2011 card described the Bjork-Shiley tilting-disc valve as commonly used.",
"now": "Single tilting-disc valves are historical; bileaflet mechanical valves (St. Jude, On-X) are the standard mechanical prosthesis today, with strut fracture of certain Bjork-Shiley models a known failure mode.",
"source": "Prosthetic valves anchor (ASE prosthetic valve guideline)"
},
"pearl": "Tilting disc: one large and one small orifice, good flow, but remember strut fracture.",
"lookalike": {
"vs": "pathologic prosthetic regurgitation",
"discriminator": "Normal washing jets are brief, narrow, symmetric, and originate inside the ring; pathologic leaks are broad, eccentric, or paravalvular."
},
"related": [
"Q103",
"Q104",
"Q110",
"Q323"
],
"reviewed": "2026-08-26"
},
{
"id": "Q106",
"orig": 106,
"title": "Porcine bioprosthetic valves",
"lesions": [
"PROSTHETIC",
"AS"
],
"lens": "definition",
"items": [
{
"id": "Q106.1",
"q": "How is a porcine bioprosthesis constructed?",
"a": "A pig aortic valve is harvested, fixed in glutaraldehyde to crosslink its collagen and kill the cells, and then sewn onto a flexible stent frame carrying a fabric sewing ring. Because fixation leaves no viable cells, the tissue does not provoke immune rejection, and the stent gives the valve a shape that can be sutured into either the aortic or mitral position. Stentless versions mount the pig root directly to the patient's aorta for a larger orifice."
},
{
"id": "Q106.2",
"q": "What are the advantages and disadvantages of porcine valves?",
"a": "The main advantage is low thrombogenicity: after the first few months of endothelialization, most patients need no anticoagulation. Central flow through tissue leaflets gives low gradients except in the smallest sizes, where the stent and ring occupy a large fraction of the annulus and patient-prosthesis mismatch can occur (indexed EOA under 0.85 cm²/m² in the aortic position). The disadvantage is limited durability: leaflets calcify, stiffen, and tear, so stenosis or regurgitation appears over roughly 10 to 15 years, and sooner in younger patients or those on dialysis."
}
],
"numbers": [
{
"label": "Aortic patient-prosthesis mismatch indexed EOA",
"value": "< 0.85",
"unit": "cm²/m²"
},
{
"label": "Porcine bioprosthesis durability",
"value": "~10–15",
"unit": "years"
}
],
"delta": null,
"pearl": "Bioprosthesis: no warfarin, central flow, but plan on structural degeneration in 10 to 15 years.",
"lookalike": null,
"related": [
"Q102",
"Q107",
"Q112"
],
"reviewed": "2026-08-26"
},
{
"id": "Q107",
"orig": 107,
"title": "Imaging a porcine mitral prosthesis",
"lesions": [
"PROSTHETIC",
"VIEWS"
],
"lens": "2d",
"items": [
{
"id": "Q107.1",
"q": "What does a normally functioning porcine mitral valve look like on 2D echo?",
"a": "In the parasternal long-axis view the stent posts appear as two bright, parallel echoes projecting into the LV, and the sewing ring is a dense band at the annulus. Because tissue leaflets reflect little sound, you can usually see thin leaflets opening between the posts during diastole. Apical views often show leaflet morphology and motion better, since the beam then meets the leaflets closer to perpendicular and the sewing ring's shadow falls on the atrium rather than on the leaflets."
},
{
"id": "Q107.2",
"q": "How does normal inflow through a porcine mitral prosthesis appear on color Doppler?",
"a": "Use the apical views, where diastolic inflow travels toward the transducer and is encoded red. A normal bioprosthesis passes a single central column of relatively laminar flow directed at the apex, without significant aliasing or a proximal convergence zone on the atrial side. Because the stent shadows part of the atrium, small physiologic regurgitation may be missed from the chest wall, and TEE is needed if a leak is suspected."
}
],
"numbers": [],
"delta": null,
"pearl": "Two bright posts, one central red jet: that is a healthy tissue mitral valve from the apex.",
"lookalike": null,
"related": [
"Q106",
"Q110",
"Q112",
"Q324"
],
"reviewed": "2026-08-26"
},
{
"id": "Q108",
"orig": 108,
"title": "M-mode of a caged-ball prosthesis",
"lesions": [
"PROSTHETIC",
"VIEWS"
],
"lens": "procedure",
"items": [
{
"id": "Q108.1",
"q": "Where should the transducer be placed to record M-mode motion of a caged-ball mitral prosthesis?",
"a": "Image from the LV apex. The ball travels along the long axis of the valve, from the ring toward the apex when it opens, so only a beam parallel to that axis captures its full excursion. From the apex you record the ball's opening and closing timing and any sluggish or incomplete travel that would suggest thrombus or variance. From the parasternal window the ball moves across the beam and its excursion is underestimated."
},
{
"id": "Q108.2",
"q": "For a caged-ball aortic prosthesis, where should the M-mode transducer be placed?",
"a": "Position the transducer above the valve, from the suprasternal notch or the right supraclavicular fossa, so the beam is again parallel to ball travel. In the aortic position the ball rises into the ascending aorta during systole and reseats in diastole; imaging from above lets you document the amplitude and timing of that motion. This is largely historical technique, but the principle of aligning M-mode with the direction of occluder motion applies to any prosthesis."
}
],
"numbers": [],
"delta": null,
"pearl": "Align the beam with the occluder's travel: apex for mitral, suprasternal for aortic.",
"lookalike": null,
"related": [
"Q103",
"Q109",
"Q323"
],
"reviewed": "2026-08-26"
},
{
"id": "Q109",
"orig": 109,
"title": "Caged-ball valve artifact on 2D",
"lesions": [
"PROSTHETIC",
"INSTRUMENTATION"
],
"lens": "pitfall",
"items": [
{
"id": "Q109.1",
"q": "How does a caged-ball mitral prosthesis appear in the parasternal long-axis view, and why does the ball seem to sit in the left atrium?",
"a": "The cage is fixed at the annulus and its struts project as bright lines into the LV cavity, with the ball moving between them and the near surface of the ball clearly outlined. The far side of the ball, however, appears displaced posteriorly into the left atrium. This is a speed-of-sound artifact: the scanner assumes sound travels at 1540 m/s, but the silicone ball transmits sound more slowly, so echoes returning from its far wall arrive late and are plotted deeper than their true position. The stretched, mispositioned back wall should not be read as a mass or as valve dehiscence."
}
],
"numbers": [
{
"label": "Assumed speed of sound in soft tissue",
"value": "1540",
"unit": "m/s"
}
],
"delta": null,
"pearl": "Slow sound through the ball paints its back half in the atrium; it is propagation-speed error, not pathology.",
"lookalike": {
"vs": "left atrial mass",
"discriminator": "The artifact moves exactly with the ball and lies along the beam behind it; a true mass has its own attachment and motion."
},
"related": [
"Q103",
"Q108"
],
"reviewed": "2026-08-26"
},
{
"id": "Q110",
"orig": 110,
"title": "Color flow and shadowing in mitral prostheses",
"lesions": [
"PROSTHETIC",
"TEE",
"MR"
],
"lens": "best-method",
"items": [
{
"id": "Q110.1",
"q": "What is the normal color Doppler pattern through a caged-ball mitral valve?",
"a": "Because the ball occupies the center of the orifice, forward flow splits and streams around it on both sides, so a normal color image shows two symmetric red inflow jets flanking the ball rather than one central column. If inflow appears on only one side, something is blocking the other channel, and thrombus, pannus, or a vegetation should be sought. Gradients are expected to be higher than for central-flow designs, so compare against the valve's own baseline."
},
{
"id": "Q110.2",
"q": "What is the main limitation of transthoracic echo for mitral prostheses, and how is it overcome?",
"a": "From the chest wall the left atrium lies directly behind the prosthesis, so the sewing ring and occluder shadow exactly the region where a regurgitant jet would appear. Transthoracic color Doppler therefore misses or badly underestimates prosthetic mitral regurgitation, especially paravalvular leaks. Indirect clues such as a high E velocity with a normal pressure half-time, a large DVI, or systolic pulmonary vein flow reversal should raise suspicion. TEE places the transducer in the esophagus behind the atrium, on the unshadowed side, and is the method of choice for detecting and quantifying prosthetic mitral regurgitation."
}
],
"numbers": [],
"delta": null,
"pearl": "The shadow falls away from the probe: TTE hides mitral prosthetic leaks, TEE hides aortic ones.",
"lookalike": null,
"related": [
"Q102",
"Q107",
"Q112",
"Q105",
"Q111",
"Q324"
],
"reviewed": "2026-08-26"
},
{
"id": "Q111",
"orig": 111,
"title": "Complications of prosthetic valves",
"lesions": [
"PROSTHETIC",
"ENDOCARDITIS"
],
"lens": "etiology",
"items": [
{
"id": "Q111.1",
"q": "List the principal complications that cause prosthetic valve dysfunction.",
"a": "Prosthetic valves fail in a limited number of ways, and each has an echo signature. Paravalvular leak occurs when sutures pull through the annulus, producing a regurgitant jet outside the sewing ring; when a large portion separates, the valve dehisces and rocks. Thrombus or pannus ingrowth can obstruct the orifice or restrict occluder motion, raising gradients. Endocarditis produces vegetations and, particularly with mechanical valves, a ring abscess that may lead to dehiscence. Bioprosthetic leaflets undergo structural degeneration with stenosis or tears. Rarer problems are strut fracture with occluder escape, patient-prosthesis mismatch, and hemolysis from high-shear jets through small leaks."
}
],
"numbers": [],
"delta": null,
"pearl": "Leak, stuck, infected, worn out, broken: paravalvular leak, thrombus or pannus, endocarditis or abscess, degeneration, and structural failure.",
"lookalike": {
"vs": "pannus",
"discriminator": "Thrombus is softer, larger, and often mobile with a recent anticoagulation lapse; pannus is dense, small, fixed, and grows slowly from the ring."
},
"related": [
"Q101",
"Q110",
"Q112",
"Q322",
"Q323",
"Q326",
"Q391"
],
"reviewed": "2026-08-26"
},
{
"id": "Q112",
"orig": 112,
"title": "Assessing prosthetic valve stenosis",
"lesions": [
"PROSTHETIC",
"AS",
"MS"
],
"lens": "numbers",
"items": [
{
"id": "Q112.1",
"q": "How do you evaluate a prosthetic valve for obstruction, and what gradients are expected normally?",
"a": "Every prosthesis is mildly obstructive, and the normal gradient depends on valve type, size, position, and the flow across it, so a single number cannot be judged in isolation. The most reliable approach is comparison with the patient's own baseline study performed soon after implantation, at a similar heart rate and cardiac output. For a mitral prosthesis a normal mean gradient is only a few mmHg, and a mean gradient above 10 mmHg or a pressure half-time above 200 ms suggests obstruction; for an aortic prosthesis a peak gradient in the teens is typical, and the flow-independent Doppler velocity index (LVOT VTI over prosthetic VTI) below 0.25 with a small effective orifice area points to obstruction. Also inspect occluder motion, look for thrombus or pannus, and remember that an indexed EOA under 0.85 cm²/m² in the aortic position means mismatch rather than valve failure."
}
],
"numbers": [
{
"label": "Mitral prosthesis mean gradient suspicious for obstruction",
"value": "> 10",
"unit": "mmHg"
},
{
"label": "Mitral prosthesis PHT suspicious for obstruction",
"value": "> 200",
"unit": "ms"
},
{
"label": "Aortic prosthesis DVI suggesting obstruction",
"value": "< 0.25",
"unit": "ratio"
},
{
"label": "Aortic patient-prosthesis mismatch indexed EOA",
"value": "< 0.85",
"unit": "cm²/m²"
}
],
"delta": {
"was": "2011 card gave fixed normal gradients of 3–7 mmHg for mitral and 14–20 mmHg for aortic prostheses.",
"now": "Current guidance relies on comparison with a baseline study plus flow-independent indices: mitral mean gradient >10 mmHg or PHT >200 ms is suspicious; aortic DVI <0.25 with reduced EOA suggests obstruction; indexed EOA <0.85 cm²/m² indicates patient-prosthesis mismatch.",
"source": "Prosthetic valves anchor (ASE prosthetic valve guideline) / ASE 2017 valve stenosis"
},
"pearl": "Compare with the baseline, then use DVI and PHT because they do not depend on flow.",
"lookalike": {
"vs": "patient-prosthesis mismatch",
"discriminator": "Mismatch has a high gradient with normal leaflet motion and an EOA that matches the manufacturer's reference; obstruction has reduced EOA and abnormal occluder or leaflet motion."
},
"related": [
"Q102",
"Q106",
"Q110",
"Q111",
"Q107",
"Q322",
"Q324",
"Q325",
"Q326",
"Q359"
],
"reviewed": "2026-08-26"
},
{
"id": "Q113",
"orig": 113,
"title": "Layers of the pericardium",
"lesions": [
"EFFUSION",
"ANATOMY"
],
"lens": "anatomy",
"items": [
{
"id": "Q113.1",
"q": "What are the two layers of the pericardium described in most echo texts?",
"a": "The heart sits inside a double-walled sac. The inner visceral layer is a thin serous membrane adherent to the surface of the heart; because it is the outermost coat of the heart itself, it is also called the epicardium. The outer parietal layer is the tough, fibrous sac that anchors the heart to the diaphragm and great vessels. Between them lies the pericardial space, which normally holds about 15 to 50 mL of lubricating fluid; an effusion is an excess of that fluid, and it appears on echo as an echo-free space between the two layers."
},
{
"id": "Q113.2",
"q": "Anatomically, how many pericardial layers are there?",
"a": "Anatomists describe three. The serous pericardium is a single continuous membrane folded into two layers: the visceral layer on the heart's surface and the parietal layer lining the inside of the fibrous sac. The fibrous pericardium is the third, outermost layer. Echo texts collapse the parietal serous and fibrous layers into one \"parietal pericardium\" because they are fused and inseparable on imaging."
}
],
"numbers": [
{
"label": "Normal pericardial fluid volume",
"value": "15–50",
"unit": "mL"
}
],
"delta": null,
"pearl": "One serous membrane folded twice plus a fibrous shell: visceral, parietal serous, fibrous.",
"lookalike": null,
"related": [
"Q114",
"Q120"
],
"reviewed": "2026-08-26"
},
{
"id": "Q114",
"orig": 114,
"title": "Pericardial versus pleural effusion",
"lesions": [
"EFFUSION",
"AORTA"
],
"lens": "pitfall",
"items": [
{
"id": "Q114.1",
"q": "In the parasternal long-axis view, how do you tell a pericardial effusion from a left pleural effusion?",
"a": "Use the descending thoracic aorta as the landmark. The pericardium is attached to the posterior left atrium and lies in front of the descending aorta, so pericardial fluid collects between the posterior heart and the aorta, often lifting the aorta away from the LA. Pleural fluid lies outside the pericardium, so it appears posterior and lateral to the descending aorta and leaves the aorta in contact with the heart. Confirm by scanning to the subcostal or left lateral windows, where pleural fluid surrounds collapsed lung and pericardial fluid wraps the heart; posterior pericardial fluid also tends to taper at the AV groove, whereas pleural fluid extends beyond it."
},
{
"id": "Q114.2",
"q": "What does the pericardium do?",
"a": "The pericardium is not essential for life; its removal is well tolerated. Nevertheless it serves several purposes. It anchors the heart in the mediastinum, limits acute overdistension of the chambers and couples their filling to one another, and provides a lubricated surface so the heart moves without friction. It also forms a physical barrier that slows spread of infection or tumor from adjacent lung and mediastinum."
}
],
"numbers": [],
"delta": null,
"pearl": "Fluid in front of the descending aorta is pericardial; fluid behind it is pleural.",
"lookalike": {
"vs": "pleural effusion",
"discriminator": "Pericardial fluid sits between LA and descending aorta and stops at the AV groove; pleural fluid lies posterior to the aorta and may contain collapsed lung."
},
"related": [
"Q113",
"Q117",
"Q120",
"Q264"
],
"reviewed": "2026-08-26"
},
{
"id": "Q115",
"orig": 115,
"title": "Pericarditis and its physical signs",
"lesions": [
"EFFUSION"
],
"lens": "physical-exam",
"items": [
{
"id": "Q115.1",
"q": "What is pericarditis?",
"a": "Pericarditis is inflammation of the pericardial layers, most often viral or idiopathic. The inflamed serous membrane leaks fluid and fibrin into the pericardial space, so effusion frequently accompanies it, though a dry fibrinous form also occurs. It is more common in men and in adults than in young children, and it may recur. On echo the pericardium may look normal or slightly thickened and bright, with or without an effusion."
},
{
"id": "Q115.2",
"q": "What are the three classic physical findings of pericarditis or pericardial effusion?",
"a": "First is a sharp, pleuritic chest pain that is worst lying flat and eased by sitting up and leaning forward, because that posture lifts the inflamed pericardium off adjacent structures. Second is a pericardial friction rub, a scratchy high-pitched sound produced by the roughened layers sliding over each other; it classically has three components timed to atrial systole, ventricular systole, and early diastolic filling. Third is dyspnea, which reflects restricted filling as fluid accumulates. A rub can vanish when a large effusion separates the layers."
}
],
"numbers": [
{
"label": "Components of the pericardial friction rub",
"value": "3",
"unit": "phases"
}
],
"delta": null,
"pearl": "Positional pain, three-part rub, and dyspnea; the rub fades as the effusion grows.",
"lookalike": null,
"related": [
"Q116",
"Q118"
],
"reviewed": "2026-08-26"
},
{
"id": "Q116",
"orig": 116,
"title": "Etiologies of pericardial effusion",
"lesions": [
"EFFUSION",
"CAD"
],
"lens": "etiology",
"items": [
{
"id": "Q116.1",
"q": "What are the main causes of pericardial effusion?",
"a": "The pericardium responds to many insults by producing fluid. In developed countries the most common category is idiopathic, most of which is presumed viral. Other infections include bacterial (purulent) and, worldwide, tuberculous pericarditis. Metabolic causes include uremia in renal failure and hypothyroidism. Ischemic causes are acute myocardial infarction with early pericarditis, and Dressler syndrome, an immune-mediated pericarditis appearing weeks after infarction. Iatrogenic or physical causes include postpericardiotomy syndrome after cardiac surgery, mediastinal radiation, and catheter or device perforation. Malignancy (lung, breast, lymphoma) and connective tissue disease such as lupus round out the list."
}
],
"numbers": [],
"delta": null,
"pearl": "Infection, kidneys, infarction, surgery, radiation, tumor: most effusions fall into one of these bins.",
"lookalike": null,
"related": [
"Q115",
"Q117",
"Q120"
],
"reviewed": "2026-08-26"
},
{
"id": "Q117",
"orig": 117,
"title": "Loculated pericardial effusions",
"lesions": [
"EFFUSION",
"MASS"
],
"lens": "etiology",
"items": [
{
"id": "Q117.1",
"q": "What conditions produce a loculated pericardial effusion?",
"a": "Fluid normally distributes freely around the heart, so a loculated collection implies that adhesions have partitioned the pericardial space. The two classic settings are malignancy and prior cardiac surgery. Metastatic tumor, most often from lung or breast cancer, seeds the pericardium and walls off pockets of fluid that are frequently hemorrhagic and may contain visible nodules. After surgery, fibrinous adhesions between the layers trap fluid in compartments, often behind the atria or along the right heart, where even a small collection can compress a chamber and cause regional tamponade. Inflammatory or purulent pericarditis can also loculate through fibrin strands."
}
],
"numbers": [],
"delta": null,
"pearl": "A loculated effusion after surgery can tamponade one chamber without classic signs; scan every window.",
"lookalike": {
"vs": "epicardial fat",
"discriminator": "Fat is anterior, finely speckled, and moves with the heart; a loculated effusion is echo-free, has a defined wall, and may be posterior or compress a chamber."
},
"related": [
"Q114",
"Q116",
"Q120"
],
"reviewed": "2026-08-26"
},
{
"id": "Q118",
"orig": 118,
"title": "Cardiac tamponade definition and signs",
"lesions": [
"EFFUSION",
"HEMODYNAMICS"
],
"lens": "physical-exam",
"items": [
{
"id": "Q118.1",
"q": "What is cardiac tamponade?",
"a": "Tamponade is a hemodynamic state, not a fluid volume: it exists when intrapericardial pressure rises high enough to impede diastolic filling of the heart, so stroke volume and cardiac output fall. What matters is the relationship between the amount of fluid and the compliance of the pericardium. A slowly accumulating effusion stretches the sac and can reach over a liter before symptoms, whereas a rapid bleed of a few hundred milliliters, as after a catheter perforation or aortic dissection, overwhelms an unstretched pericardium within minutes."
},
{
"id": "Q118.2",
"q": "What are the classic physical findings of tamponade?",
"a": "Pulsus paradoxus is the key sign: an inspiratory fall in systolic blood pressure exceeding 10 mmHg, because inspiration fills the RV, which can expand only by pushing the septum into the LV and reducing LV stroke volume. Beck's triad describes the end stage: elevated jugular venous pressure, hypotension, and muffled heart sounds. Patients are tachycardic to compensate for a fixed low stroke volume, and dyspneic because filling is restricted."
}
],
"numbers": [
{
"label": "Pulsus paradoxus threshold",
"value": "> 10",
"unit": "mmHg inspiratory drop in systolic BP"
}
],
"delta": null,
"pearl": "Tamponade is about rate and compliance: 200 mL fast can kill, 1500 mL slow may not.",
"lookalike": {
"vs": "constrictive pericarditis",
"discriminator": "Both show ventricular interdependence, but tamponade has a compressible effusion and collapsing chambers; constriction has a thick rigid pericardium and no effusion."
},
"related": [
"Q115",
"Q119",
"Q265",
"Q266",
"Q363",
"Q380"
],
"reviewed": "2026-08-26"
},
{
"id": "Q119",
"orig": 119,
"title": "Echo and Doppler signs of tamponade",
"lesions": [
"EFFUSION",
"HEMODYNAMICS"
],
"lens": "doppler",
"items": [
{
"id": "Q119.1",
"q": "What 2D and M-mode findings indicate cardiac tamponade?",
"a": "The thin-walled right chambers buckle whenever pericardial pressure exceeds their internal pressure. Right atrial collapse occurs in late diastole and early systole, when RA pressure is lowest; it is sensitive but becomes specific only when it lasts more than one third of the cardiac cycle. RV free wall collapse in early diastole is more specific, and it may be absent when the RV is hypertrophied or pulmonary pressure is high. The IVC is plethoric, dilated with less than 50 percent inspiratory collapse, reflecting elevated RA pressure. M-mode across the ventricles shows reciprocal respiratory size changes, with the RV enlarging and the LV shrinking on inspiration, and a swinging heart in a large effusion."
},
{
"id": "Q119.2",
"q": "What Doppler findings indicate tamponade?",
"a": "Doppler exposes exaggerated ventricular interdependence. Normally mitral E velocity varies less than 10 percent with breathing. In tamponade the septum shifts leftward on inspiration, and the peak mitral E falls by more than 30 percent on the first inspiratory beat while tricuspid E rises by more than 60 percent; the pattern reverses on expiration. Hepatic vein flow shows diminished diastolic forward flow with expiratory diastolic reversal, and the IVC does not collapse."
},
{
"id": "Q119.3",
"q": "Which is more reliable for tamponade, 2D chamber collapse or Doppler flow variation?",
"a": "Doppler respiratory variation tracks the hemodynamics more closely than chamber collapse. Collapse signs depend on the pressure of the chamber being compressed and can be blunted by RV hypertrophy, pulmonary hypertension, or positive-pressure ventilation, and RA collapse is common with any sizeable effusion. Doppler interdependence appears early and parallels pulsus paradoxus, though it is nonspecific in patients with obstructive lung disease or on ventilators. Tamponade remains a clinical diagnosis supported by the whole echo picture."
}
],
"numbers": [
{
"label": "Normal respiratory variation of mitral E",
"value": "< 10",
"unit": "%"
},
{
"label": "Mitral E inspiratory decrease in tamponade",
"value": "> 30",
"unit": "%"
},
{
"label": "Tricuspid E inspiratory increase in tamponade",
"value": "> 60",
"unit": "%"
},
{
"label": "RA collapse duration suggesting tamponade",
"value": "> 1/3",
"unit": "of cardiac cycle"
},
{
"label": "IVC plethora inspiratory collapse",
"value": "< 50",
"unit": "%"
}
],
"delta": {
"was": "2011 card taught respiratory flow variation thresholds of >25% for mitral and >50% for tricuspid inflow.",
"now": "Current guideline: mitral E variation >30% and tricuspid E variation >60% support tamponade, alongside RA collapse >1/3 of the cycle, early-diastolic RV collapse, IVC plethora, and expiratory hepatic vein diastolic reversal.",
"source": "ASE 2013 pericardial disease (tamponade)"
},
"pearl": "Thirty and sixty: mitral falls by 30 percent, tricuspid rises by 60 percent on inspiration.",
"lookalike": {
"vs": "constrictive pericarditis",
"discriminator": "Both show >25–30% mitral respiratory variation, but constriction has annulus reversus, a septal bounce, and no effusion or chamber collapse."
},
"related": [
"Q118",
"Q120",
"Q264",
"Q265",
"Q266",
"Q376",
"Q380"
],
"reviewed": "2026-08-26"
},
{
"id": "Q120",
"orig": 120,
"title": "Anterior fat pad and pericardial thickening",
"lesions": [
"EFFUSION",
"CONSTRICTION"
],
"lens": "pitfall",
"items": [
{
"id": "Q120.1",
"q": "Why can an anterior echo-free space be mistaken for a pericardial effusion?",
"a": "Epicardial and pericardial fat accumulates preferentially over the anterior RV and in the AV grooves, especially in obese, older, or diabetic patients. Fat is hypoechoic and can look like an echo-free space in front of the heart. Because free pericardial fluid settles posteriorly by gravity and loculated anterior collections are uncommon, an isolated anterior space without any posterior fluid is almost always fat. Fat shows fine, brightly speckled echoes, moves in lockstep with the heart, and does not change with position, whereas fluid is truly echo-free and is usually also seen behind the LV."
},
{
"id": "Q120.2",
"q": "In which settings is pericardial thickening seen?",
"a": "The pericardium thickens when chronic inflammation is replaced by fibrosis. This occurs with chronic or recurrent pericarditis of any cause, after mediastinal radiation, after cardiac surgery, with tuberculous or purulent infection, and in patients with long-term corticosteroid exposure or connective tissue disease. Thickening matters because it can progress to constriction; echo is insensitive for measuring it, and CT or MRI, showing thickness above about 4 mm, is used to confirm."
}
],
"numbers": [
{
"label": "Pericardial thickness considered abnormal on CT or MRI",
"value": "> 4",
"unit": "mm"
}
],
"delta": null,
"pearl": "Anterior only means fat; posterior means fluid.",
"lookalike": {
"vs": "pericardial effusion",
"discriminator": "Fat is anterior, speckled, and moves with the heart; effusion is echo-free and appears posteriorly first."
},
"related": [
"Q113",
"Q114",
"Q117",
"Q119",
"Q116",
"Q260"
],
"reviewed": "2026-08-26"
},
{
"id": "Q121",
"orig": 121,
"title": "Measuring pericardial thickness",
"lesions": [
"CONSTRICTION",
"INSTRUMENTATION"
],
"lens": "best-method",
"items": [
{
"id": "Q121.1",
"q": "Is transthoracic echo a reliable way to measure pericardial thickness when constriction is suspected?",
"a": "No. The pericardium is an intensely specular reflector, so on a transthoracic image it blooms into a bright band whose apparent width depends more on gain, dynamic range, and beam width than on true thickness. It also sits far from the transducer, roughly 15 to 20 cm deep on the posterior surface, well beyond the focal zone where lateral resolution is best. Cardiac CT and cardiac MRI resolve the pericardial layers directly and are the preferred noninvasive tests for thickness; TEE does better than TTE because the probe is closer, but it is still not the reference standard. Remember that a normal-thickness pericardium does not exclude constriction, so the physiologic Doppler findings matter more than the measurement."
}
],
"numbers": [
{
"label": "Posterior pericardium depth on TTE",
"value": "15–20",
"unit": "cm"
}
],
"delta": null,
"pearl": "Bright does not mean thick: echo shows pericardial physiology, CT/MRI show pericardial anatomy.",
"lookalike": {
"vs": "Pericardial thickening vs. epicardial fat",
"discriminator": "Fat is anterior, hypoechoic, and moves with the heart; true thickening is a bright, immobile band, best confirmed on CT or MRI."
},
"related": [
"Q124",
"Q126",
"Q122",
"Q259",
"Q260"
],
"reviewed": "2026-08-26"
},
{
"id": "Q122",
"orig": 122,
"title": "Acting on tamponade findings",
"lesions": [
"EFFUSION",
"PROCEDURE"
],
"lens": "procedure",
"items": [
{
"id": "Q122.1",
"q": "Your study shows a large effusion with RA and RV collapse, IVC plethora, and marked respiratory inflow variation. What should you do before the patient leaves the lab?",
"a": "Treat this as a critical finding. Tamponade is a clinical and hemodynamic emergency, so the study must be interpreted immediately rather than queued for routine reading. Notify the interpreting echo physician while the patient is still on the table, and make sure the result reaches the ordering or treating clinician directly, documenting whom you told and when. Do not send the patient back to a waiting area or home; keep them monitored until a physician has taken over. The sonographer's role is to recognize and escalate, not to make the treatment decision."
}
],
"numbers": [],
"delta": null,
"pearl": "Collapse plus plethora plus inflow swings equals a phone call, not a worksheet.",
"lookalike": null,
"related": [
"Q121",
"Q123",
"Q265",
"Q266"
],
"reviewed": "2026-08-26"
},
{
"id": "Q123",
"orig": 123,
"title": "Fibrin strands in effusions",
"lesions": [
"EFFUSION"
],
"lens": "etiology",
"items": [
{
"id": "Q123.1",
"q": "What processes most often produce fibrin strands or adhesions within a pericardial effusion?",
"a": "Organized material inside the pericardial space appears when the fluid has been present long enough, or is inflammatory or bloody enough, to lay down fibrin. The three classic settings are a chronic effusion that has had time to organize, malignant involvement of the pericardium where tumor and inflammatory exudate seed the space, and a hemorrhagic effusion in which clot forms and then contracts into strands. On imaging these look like mobile echogenic threads bridging the epicardium and parietal pericardium or loculating the fluid. Their presence matters because loculated fluid can cause regional tamponade and is harder to drain percutaneously."
}
],
"numbers": [],
"delta": null,
"pearl": "Strands in the fluid mean it is old, malignant, or bloody.",
"lookalike": {
"vs": "Fibrin strands vs. epicardial fat pad",
"discriminator": "Fat is a fixed, granular layer that moves with the myocardium; strands are thin, mobile, and float within anechoic fluid."
},
"related": [
"Q122",
"Q124"
],
"reviewed": "2026-08-26"
},
{
"id": "Q124",
"orig": 124,
"title": "Constriction causes and exam",
"lesions": [
"CONSTRICTION"
],
"lens": "etiology",
"items": [
{
"id": "Q124.1",
"q": "What is the usual etiology of constrictive pericarditis?",
"a": "Constriction is the end result of repeated or severe pericardial inflammation. In most patients the trigger is idiopathic or presumed viral pericarditis, with each episode of inflammation healing by fibrosis until the sac becomes stiff and noncompliant. In modern practice prior cardiac surgery and chest irradiation are the other major causes, and tuberculosis dominates where it is endemic. The common pathway is a rigid shell that fixes total cardiac volume, so filling of one ventricle can only occur at the expense of the other."
},
{
"id": "Q124.2",
"q": "What physical findings suggest constrictive pericarditis?",
"a": "The findings are those of right-sided congestion with a preserved ventricle. Expect elevated jugular venous pressure that may rise with inspiration (Kussmaul sign), ascites and peripheral edema, and exertional dyspnea. An early diastolic pericardial knock is the characteristic auscultatory clue; it occurs when rapid early filling is halted abruptly by the stiff pericardium. Hepatomegaly and a paradoxical pulse are less specific but can be present."
}
],
"numbers": [],
"delta": null,
"pearl": "Constriction looks like right heart failure with a normal-sized, normally contracting ventricle.",
"lookalike": {
"vs": "Restrictive cardiomyopathy",
"discriminator": "Constriction has respirophasic septal shift and a normal or high medial e'; RCM has a low e' and no ventricular interdependence."
},
"related": [
"Q125",
"Q126",
"Q148",
"Q121",
"Q123",
"Q258",
"Q263"
],
"reviewed": "2026-08-26"
},
{
"id": "Q125",
"orig": 125,
"title": "Pericardial knock and definitive diagnosis",
"lesions": [
"CONSTRICTION",
"HEMODYNAMICS"
],
"lens": "physical-exam",
"items": [
{
"id": "Q125.1",
"q": "What produces a pericardial knock?",
"a": "In constriction the ventricle fills very quickly in early diastole because atrial pressure is high and the ventricle itself is compliant, but filling stops suddenly the moment the ventricular volume reaches the limit set by the rigid pericardium. That abrupt deceleration of inflow sets the ventricular walls and pericardium vibrating, producing a high-pitched early diastolic sound. It is earlier and sharper than an S3 and corresponds on Doppler to the tall E wave with a very short deceleration time."
},
{
"id": "Q125.2",
"q": "What is considered the definitive test for constrictive pericarditis, and what does it show?",
"a": "Invasive hemodynamic catheterization remains the reference standard when noninvasive testing is inconclusive. It documents elevated and nearly equal end-diastolic pressures in the right and left ventricles, the dip-and-plateau (square root) sign, and, most specifically, discordant respiratory changes in RV and LV systolic pressures that prove ventricular interdependence. Echo with Doppler is the first-line test and can establish the diagnosis in most patients using septal shift, medial e' above 7 cm/s (above 8 favors constriction), and hepatic vein expiratory diastolic flow reversal; catheterization is reserved for discordant or ambiguous cases."
}
],
"numbers": [
{
"label": "Medial e' supporting constriction",
"value": "> 7 (> 8 favors)",
"unit": "cm/s"
}
],
"delta": {
"was": "2011 card taught that catheterization is the definitive test because it documents equalization of right and left ventricular diastolic pressures. Constriction medial e' cut-off was taught as ≥ 9 cm/s (Mayo criteria, ASE 2013).",
"now": "Current guideline: echo with Doppler (septal shift, medial e' > 7 cm/s, > 8 favors, hepatic vein expiratory diastolic reversal) is the first-line and often sufficient test; catheterization is reserved for discordant cases, and its most specific finding is respiratory discordance of RV/LV systolic pressures (ventricular interdependence), not pressure equalization alone.",
"source": "ASE 2013; ASE 2025 diastolic function guideline"
},
"pearl": "The knock is the sound of filling hitting a wall.",
"lookalike": {
"vs": "Third heart sound",
"discriminator": "A knock is earlier, higher-pitched, and pairs with a normal or high e'; an S3 in cardiomyopathy pairs with a low e' and a dilated ventricle."
},
"related": [
"Q124",
"Q126",
"Q254",
"Q258",
"Q263"
],
"reviewed": "2026-08-26"
},
{
"id": "Q126",
"orig": 126,
"title": "Constriction imaging findings",
"lesions": [
"CONSTRICTION"
],
"lens": "doppler",
"items": [
{
"id": "Q126.1",
"q": "What M-mode and two-dimensional findings support constrictive pericarditis?",
"a": "On M-mode the posterior LV wall stops moving after early diastole and traces a flat line, because filling ends abruptly once the pericardial limit is reached. The septum shows an early diastolic notch or bounce, and the pericardium may appear as a dense double line. On 2D the same septal bounce is visible, along with a respirophasic shift of the septum toward the LV with inspiration, a bright immobile pericardium that tethers the epicardium, biatrial enlargement, and a plethoric IVC. Ventricular size and systolic function are typically normal, which is the key contrast with cardiomyopathy."
},
{
"id": "Q126.2",
"q": "What Doppler findings characterize constrictive pericarditis?",
"a": "Mitral inflow shows a restrictive-looking pattern with a tall E wave, short deceleration time, and small A wave, but with exaggerated respiratory variation: the mitral E falls by roughly 25 percent or more with inspiration while the tricuspid E rises, reflecting ventricular interdependence. Hepatic venous flow shows diastolic flow reversal that becomes most prominent on expiration, and an expiratory diastolic reversal ratio of at least 0.79 supports the diagnosis. Tissue Doppler is the discriminator from restriction: the medial e' is preserved or increased (above 7 cm/s, above 8 favors constriction) and may exceed the lateral e', the so-called annulus reversus. Functional mitral and tricuspid regurgitation are common but nonspecific."
}
],
"numbers": [
{
"label": "Mitral E respiratory variation in constriction",
"value": "≥ 25",
"unit": "%"
},
{
"label": "Medial e' in constriction",
"value": "> 7 (> 8 favors)",
"unit": "cm/s"
},
{
"label": "Hepatic vein expiratory diastolic reversal ratio",
"value": "≥ 0.79",
"unit": "ratio"
}
],
"delta": {
"was": "2011 card and the Mayo criteria (ASE 2013) set the constriction medial e' cut-off at ≥ 9 cm/s.",
"now": "ASE 2025 lowers the constriction medial e' cut-off to > 7 cm/s, with > 8 cm/s strongly favoring constriction; it pairs with respirophasic septal shift for about 80% sensitivity and 96% specificity.",
"source": "ASE 2025 diastolic function guideline"
},
"pearl": "Bounce, shift, high e', and expiratory hepatic reversal: the Mayo quartet for constriction.",
"lookalike": {
"vs": "Restrictive cardiomyopathy",
"discriminator": "Both have short deceleration times, but RCM has a low e' and minimal respiratory variation; constriction has a high medial e' and swings of 25 percent or more."
},
"related": [
"Q124",
"Q125",
"Q149",
"Q121",
"Q257",
"Q258",
"Q259",
"Q260",
"Q261",
"Q262",
"Q379"
],
"reviewed": "2026-08-26"
},
{
"id": "Q127",
"orig": 127,
"title": "Defining systemic hypertension",
"lesions": [
"HTN"
],
"lens": "definition",
"items": [
{
"id": "Q127.1",
"q": "How is systemic hypertension currently defined and staged?",
"a": "Under the 2017 ACC/AHA classification, normal blood pressure is below 120/80 mmHg. Elevated blood pressure is a systolic of 120 to 129 with a diastolic under 80. Stage 1 hypertension is 130 to 139 systolic or 80 to 89 diastolic, and stage 2 is 140 or higher systolic or 90 or higher diastolic. The diagnosis rests on an average of properly measured readings from two or more visits rather than a single value, and the threshold was lowered because cardiovascular risk rises continuously well below the old 140/90 cutoff."
},
{
"id": "Q127.2",
"q": "What symptoms or physical signs does hypertension produce?",
"a": "Usually none. Uncomplicated hypertension is silent, which is why it is found by screening rather than by symptoms. Headache, dizziness, and tinnitus are sometimes attributed to it but occur just as often in normotensive people. The physical signs that do appear are those of end-organ effect: a sustained, displaced apical impulse from LV hypertrophy, an S4 from a stiff ventricle, retinal arteriolar changes, and eventually signs of heart failure or vascular disease."
}
],
"numbers": [
{
"label": "Normal BP",
"value": "< 120/80",
"unit": "mmHg"
},
{
"label": "Elevated BP",
"value": "120–129 / < 80",
"unit": "mmHg"
},
{
"label": "Stage 1 hypertension",
"value": "130–139 / 80–89",
"unit": "mmHg"
},
{
"label": "Stage 2 hypertension",
"value": "≥ 140/90",
"unit": "mmHg"
}
],
"delta": {
"was": "2011 card taught hypertension as sustained BP above 140 systolic and/or 90 diastolic, confirmed on three occasions at least a week apart.",
"now": "Current guideline: stage 1 hypertension begins at 130/80 mmHg; 140/90 defines stage 2; diagnosis uses averaged readings over two or more visits.",
"source": "ACC-AHA 2017"
},
"pearl": "130/80 is the new line; 140/90 is stage 2, not the start.",
"lookalike": null,
"related": [
"Q128",
"Q129",
"Q272",
"Q277"
],
"reviewed": "2026-08-26"
},
{
"id": "Q128",
"orig": 128,
"title": "Hypertensive vascular complications",
"lesions": [
"HTN",
"AORTA",
"CAD"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q128.1",
"q": "What vascular and end-organ complications result from long-standing systemic hypertension?",
"a": "Sustained pressure load injures arteries at every caliber. In large vessels it accelerates atherosclerosis and weakens the media, leading to coronary artery disease, stroke, peripheral arterial disease, and aortic aneurysm or dissection. In small vessels it causes nephrosclerosis and chronic kidney disease and retinopathy. In the heart the afterload produces concentric LV hypertrophy, diastolic dysfunction, atrial fibrillation, and eventually heart failure. Hypertension is the single most important risk factor for aortic dissection, which is why blood pressure history matters when the aortic root looks dilated."
},
{
"id": "Q128.2",
"q": "What can happen to the left ventricle late in the course of hypertensive heart disease?",
"a": "After years of compensated concentric hypertrophy the ventricle can decompensate. Wall stress rises, the myocardium becomes fibrotic and loses contractility, and the chamber dilates and thins. At that stage the echo looks like any other dilated cardiomyopathy: a large, globally hypokinetic LV with reduced ejection fraction, functional MR, and elevated filling pressures. The hypertrophic history is often only inferred from an increased LV mass or from the patient's record."
}
],
"numbers": [],
"delta": null,
"pearl": "Hypertension is the leading preventable cause of dissection; ask about it whenever the aorta is big.",
"lookalike": null,
"related": [
"Q127",
"Q129",
"Q142",
"Q273"
],
"reviewed": "2026-08-26"
},
{
"id": "Q129",
"orig": 129,
"title": "Echo signs of hypertension",
"lesions": [
"HTN",
"AR"
],
"lens": "2d",
"items": [
{
"id": "Q129.1",
"q": "What two-dimensional and M-mode findings are typical of hypertensive heart disease?",
"a": "The signature is concentric LV hypertrophy: increased wall thickness with a normal or small cavity and increased LV mass, reflecting sarcomeres added in parallel to normalize wall stress. The left atrium enlarges, usually mildly at first, as a marker of chronically elevated filling pressure. The aortic root and ascending aorta may dilate, and hypertension is the setting in which dissection should be looked for. Systolic function is preserved until late in the disease."
},
{
"id": "Q129.2",
"q": "What Doppler findings accompany systemic hypertension?",
"a": "The earliest Doppler change is impaired relaxation. The mitral E wave becomes smaller than the A wave, the E deceleration time and isovolumic relaxation time lengthen, and tissue Doppler e' velocities fall, because the thick, stiff ventricle depends on atrial contraction for filling. As the disease progresses the pattern can pseudonormalize with a rising E/e' ratio. If the aortic root has dilated, mild aortic regurgitation may appear from annular stretch."
}
],
"numbers": [],
"delta": null,
"pearl": "Thick walls, small cavity, big atrium, E less than A: the hypertensive quartet.",
"lookalike": {
"vs": "Hypertrophic cardiomyopathy",
"discriminator": "Hypertensive LVH is usually concentric and symmetric with a matching pressure history; HCM is often asymmetric with SAM and a family history."
},
"related": [
"Q127",
"Q128",
"Q138",
"Q273",
"Q274",
"Q275",
"Q276"
],
"reviewed": "2026-08-26"
},
{
"id": "Q130",
"orig": 130,
"title": "Defining pulmonary hypertension",
"lesions": [
"PH"
],
"lens": "definition",
"items": [
{
"id": "Q130.1",
"q": "How is pulmonary hypertension defined hemodynamically, and what are its common causes?",
"a": "The 2022 ESC/ERS definition is a mean pulmonary artery pressure above 20 mmHg at rest measured by right heart catheterization; a pulmonary vascular resistance above 2 Wood units identifies the precapillary component. Causes are grouped into five categories: pulmonary arterial hypertension (idiopathic, heritable, connective tissue disease, and shunt-related including Eisenmenger physiology), left heart disease such as mitral stenosis, mitral regurgitation, or LV failure, lung disease and hypoxia, chronic thromboembolic disease, and miscellaneous or multifactorial causes. Left heart disease is by far the most common cause seen in the echo lab."
},
{
"id": "Q130.2",
"q": "What symptoms and signs point to pulmonary hypertension?",
"a": "Symptoms are nonspecific and reflect a right ventricle that cannot raise output on demand: exertional dyspnea early, dyspnea at rest later, fatigue, exertional chest pain, and exertional syncope when the RV can no longer maintain cardiac output. Physical signs include a loud pulmonic component of S2, an RV heave, elevated jugular pressure, a tricuspid regurgitation murmur, and peripheral edema or ascites in advanced disease."
}
],
"numbers": [
{
"label": "Pulmonary hypertension definition (mPAP)",
"value": "> 20",
"unit": "mmHg"
},
{
"label": "Precapillary PH (PVR)",
"value": "> 2",
"unit": "Wood units"
}
],
"delta": {
"was": "2011 card taught pulmonary hypertension as a pulmonary artery pressure greater than 30 mmHg.",
"now": "Current guideline: mPAP >20 mmHg at rest by right heart catheterization, with PVR >2 WU defining the precapillary component.",
"source": "ESC-ERS 2022"
},
"pearl": "Twenty and two: mPAP over 20, PVR over 2.",
"lookalike": null,
"related": [
"Q131",
"Q133",
"Q267",
"Q270",
"Q389"
],
"reviewed": "2026-08-26"
},
{
"id": "Q131",
"orig": 131,
"title": "Echo findings in PH",
"lesions": [
"PH",
"PR"
],
"lens": "m-mode",
"items": [
{
"id": "Q131.1",
"q": "What echocardiographic findings suggest pulmonary hypertension?",
"a": "Pressure overload remodels the right heart. The RV hypertrophies (free wall more than 5 mm) and then dilates, the RA enlarges, and the interventricular septum flattens in the short-axis view, giving the LV a D shape that persists through systole. The pulmonary artery dilates, the IVC becomes plethoric, and the TR jet velocity rises: above 2.8 m/s carries intermediate probability and above 3.4 m/s high probability of PH. Pulmonic valve M-mode shows loss of the a dip and a mid-systolic notch, the flying W, and the PA Doppler acceleration time shortens below 105 ms."
},
{
"id": "Q131.2",
"q": "Why does the pulmonic valve a wave disappear in pulmonary hypertension?",
"a": "Normally right atrial contraction transmits a small pressure rise into the RV just before systole, and because PA diastolic pressure is low that pressure bump is enough to push the closed pulmonic leaflets slightly open, creating the a dip on M-mode. In pulmonary hypertension the PA diastolic pressure is far above what atrial contraction can generate in the RV, so the leaflets do not move and the a wave vanishes. The same high afterload produces a reflected pressure wave that briefly pushes the leaflets closed in mid-systole, giving the notch."
}
],
"numbers": [
{
"label": "TR Vmax intermediate PH probability",
"value": "> 2.8",
"unit": "m/s"
},
{
"label": "TR Vmax high PH probability",
"value": "> 3.4",
"unit": "m/s"
},
{
"label": "PA acceleration time suggesting PH",
"value": "< 105",
"unit": "ms"
},
{
"label": "RV free wall thickness abnormal",
"value": "> 5",
"unit": "mm"
}
],
"delta": null,
"pearl": "No a dip and a flying W means the PA pressure has overpowered the atrium.",
"lookalike": {
"vs": "RV volume overload",
"discriminator": "In volume overload the septum flattens only in diastole and rounds up in systole; in pressure overload it stays flat through systole."
},
"related": [
"Q130",
"Q132",
"Q133",
"Q242",
"Q268",
"Q381"
],
"reviewed": "2026-08-26"
},
{
"id": "Q132",
"orig": 132,
"title": "Septal flattening: pressure vs volume",
"lesions": [
"PH",
"HEMODYNAMICS"
],
"lens": "pitfall",
"items": [
{
"id": "Q132.1",
"q": "The septum is flattened in the parasternal short-axis view. How do you decide whether the right ventricle is volume overloaded or pressure overloaded?",
"a": "Watch when in the cardiac cycle the septum is flat. The septum bows toward whichever ventricle has the lower pressure at that instant. In pure volume overload, as in an ASD or severe TR, RV pressure exceeds LV pressure only in late diastole when the overloaded RV is full, so the septum flattens at end-diastole and rounds back to a circular LV during systole. In pressure overload the RV pressure stays elevated through systole, so the D shape is most pronounced at end-systole and persists across the cycle. Most real patients have a mixture, so you are judging which component dominates; the eccentricity index measured at end-systole versus end-diastole formalizes the same idea."
}
],
"numbers": [],
"delta": null,
"pearl": "Flat in diastole means volume; flat in systole means pressure.",
"lookalike": {
"vs": "Paradoxical septal motion after cardiac surgery or with LBBB",
"discriminator": "Post-surgical and conduction-related septal motion is a timing abnormality with a round LV; overload flattening changes LV shape."
},
"related": [
"Q131",
"Q133",
"Q268",
"Q271",
"Q382"
],
"reviewed": "2026-08-26"
},
{
"id": "Q133",
"orig": 133,
"title": "PA pressure from TR and acceleration time",
"lesions": [
"PH",
"TR"
],
"lens": "formula",
"items": [
{
"id": "Q133.1",
"q": "How is pulmonary artery systolic pressure estimated from the tricuspid regurgitant jet?",
"a": "The TR jet velocity reflects the systolic pressure difference between the RV and the RA. Applying the simplified Bernoulli equation, the gradient equals four times the peak TR velocity squared. Adding an estimate of RA pressure to that gradient gives RV systolic pressure, which equals PA systolic pressure as long as there is no pulmonic stenosis or RVOT obstruction. RA pressure comes from the IVC: a diameter of 2.1 cm or less that collapses more than 50 percent with a sniff means 3 mmHg, an IVC that is dilated and collapses poorly means 15 mmHg, and any other combination is assigned 8 mmHg. A TR velocity of 3.0 m/s with an RA pressure of 8 gives an RVSP of 36 plus 8, or 44 mmHg."
},
{
"id": "Q133.2",
"q": "How does pulmonary artery Doppler acceleration time help estimate PA pressure?",
"a": "Acceleration time is measured on the pulsed Doppler RVOT trace from the onset of flow to peak velocity. A compliant, low-resistance pulmonary bed lets flow accelerate gradually, so the normal acceleration time is long, generally above 120 ms. As pulmonary pressure and resistance rise the RV reaches peak velocity earlier and the trace becomes sharp and often notched. An acceleration time below 105 ms suggests pulmonary hypertension, and below about 80 ms the mean PA pressure is usually above roughly 40 mmHg. This method is useful when the TR jet is absent or unmeasurable, but it is heart-rate dependent and less precise than the TR method."
}
],
"numbers": [
{
"label": "Bernoulli constant",
"value": "4",
"unit": "× v²"
},
{
"label": "RAP with IVC ≤ 2.1 cm and > 50% collapse",
"value": "3",
"unit": "mmHg"
},
{
"label": "RAP intermediate",
"value": "8",
"unit": "mmHg"
},
{
"label": "RAP with dilated, noncollapsing IVC",
"value": "15",
"unit": "mmHg"
},
{
"label": "Normal PA acceleration time",
"value": "> 120",
"unit": "ms"
},
{
"label": "PA acceleration time suggesting PH",
"value": "< 105",
"unit": "ms"
},
{
"label": "PA acceleration time implying mPAP > ~40",
"value": "< 80",
"unit": "ms"
}
],
"delta": {
"was": "2011 card taught that an acceleration time under 75 ms indicates at least moderate pulmonary hypertension.",
"now": "Current guideline: an acceleration time under 105 ms suggests PH; under 80 ms corresponds to a mean PAP above roughly 40 mmHg. RA pressure is graded 3, 8, or 15 mmHg from IVC size and collapse.",
"source": "ESC-ERS 2022"
},
"pearl": "Four v squared plus RAP; and if there is no TR jet, a short, notched RVOT trace tells the same story.",
"lookalike": null,
"related": [
"Q130",
"Q131",
"Q132",
"Q233",
"Q237",
"Q239",
"Q242",
"Q245",
"Q269",
"Q270"
],
"reviewed": "2026-08-26"
},
{
"id": "Q134",
"orig": 134,
"title": "Three cardiomyopathy phenotypes",
"lesions": [
"HCM",
"DCM",
"RCM"
],
"lens": "definition",
"items": [
{
"id": "Q134.1",
"q": "What are the three classic morphologic categories of cardiomyopathy?",
"a": "The traditional scheme sorts cardiomyopathies by what the ventricle does rather than by cause. Hypertrophic cardiomyopathy is unexplained wall thickening, with or without outflow obstruction. Dilated cardiomyopathy is chamber enlargement with reduced contractility. Restrictive cardiomyopathy is stiff, poorly filling ventricles of normal size, most often from infiltration. Contemporary classifications add arrhythmogenic and unclassified categories, but these three remain the exam framework."
},
{
"id": "Q134.2",
"q": "What is the characteristic echo appearance of each category?",
"a": "In HCM the walls are thick, often asymmetrically with the septum thickest, the cavity is small, and there may be SAM with a dynamic outflow gradient. In DCM the ventricles are enlarged and globally hypokinetic with a low ejection fraction, wide E-point septal separation, and functional regurgitation; one or both ventricles may be involved. In RCM the ventricles are normal in size with normal or mildly increased wall thickness, the atria are markedly enlarged, the myocardium often has a bright granular texture, and Doppler shows restrictive filling with low tissue velocities. Systolic function in RCM is preserved until late."
}
],
"numbers": [],
"delta": null,
"pearl": "HCM thick, DCM big, RCM stiff with huge atria.",
"lookalike": {
"vs": "Athlete's heart",
"discriminator": "Athletic remodeling has proportionate cavity enlargement, normal diastolic function, and regresses with deconditioning; HCM has a small cavity and impaired relaxation."
},
"related": [
"Q135",
"Q142",
"Q148",
"Q247",
"Q258"
],
"reviewed": "2026-08-26"
},
{
"id": "Q135",
"orig": 135,
"title": "HCM genetics and SAM",
"lesions": [
"HCM",
"MR"
],
"lens": "etiology",
"items": [
{
"id": "Q135.1",
"q": "What is the most common cause of hypertrophic cardiomyopathy?",
"a": "HCM is a genetic disease of the sarcomere. Pathogenic variants in genes such as MYBPC3 and MYH7 are inherited in an autosomal dominant pattern with variable penetrance, and a causal variant is identified in roughly half of probands; the rest are presumed genetic with an unidentified variant or arise as new mutations. First-degree relatives therefore need screening with echo, and phenocopies such as amyloid, Fabry disease, and hypertensive heart disease must be excluded before the label is applied."
},
{
"id": "Q135.2",
"q": "What causes systolic anterior motion of the mitral valve in HCM?",
"a": "Two mechanisms combine. Anatomically the papillary muscles and leaflets are displaced anteriorly and the leaflets are often elongated, so the coaptation point sits close to a hypertrophied septum inside the outflow tract. Hemodynamically, early systolic flow pushes and drags the leaflet tips into the outflow stream, and as blood accelerates through the narrowed tract the fall in local pressure (the Venturi effect) pulls the leaflet further toward the septum. The result is mitral-septal contact, a late-peaking outflow gradient, and a posteriorly directed jet of mitral regurgitation because the leaflets no longer coapt."
}
],
"numbers": [],
"delta": null,
"pearl": "SAM is drag plus Venturi on a valve that is already sitting in the wrong place.",
"lookalike": {
"vs": "Fixed subaortic membrane",
"discriminator": "A membrane gives an early-peaking, non-provocable gradient and no SAM; HCM gives a late-peaking dagger gradient that rises with Valsalva."
},
"related": [
"Q134",
"Q137",
"Q140",
"Q141",
"Q136",
"Q138",
"Q247",
"Q372"
],
"reviewed": "2026-08-26"
},
{
"id": "Q136",
"orig": 136,
"title": "HOCM symptoms and abbreviations",
"lesions": [
"HCM"
],
"lens": "physical-exam",
"items": [
{
"id": "Q136.1",
"q": "What symptoms and clinical findings are associated with obstructive hypertrophic cardiomyopathy?",
"a": "Exertional dyspnea is the most frequent complaint, reported by roughly 90 percent of symptomatic patients, because the stiff ventricle raises filling pressure with any increase in heart rate. Angina occurs in about three quarters, from supply-demand mismatch in thick muscle with small-vessel disease even when the epicardial coronaries are normal. Exertional syncope reflects dynamic outflow obstruction or arrhythmia, and sudden cardiac death, particularly in the young, is the feared complication. Examination shows a harsh systolic murmur at the left sternal border that intensifies with maneuvers reducing preload, and often a bifid carotid pulse."
},
{
"id": "Q136.2",
"q": "What do the abbreviations ASH, HCM, HOCM, and IHSS refer to?",
"a": "HCM is hypertrophic cardiomyopathy, the umbrella term for unexplained LV hypertrophy. HOCM is the obstructive subset in which a resting or provoked LVOT gradient of 30 mmHg or more is present. ASH stands for asymmetric septal hypertrophy, the morphologic finding of a septum disproportionately thicker than the posterior wall, classically at a ratio of 1.3 or more. IHSS, idiopathic hypertrophic subaortic stenosis, is the historical name for HOCM and is now considered obsolete."
}
],
"numbers": [
{
"label": "Dyspnea in symptomatic HOCM",
"value": "~90",
"unit": "%"
},
{
"label": "Angina in symptomatic HOCM",
"value": "~75",
"unit": "%"
},
{
"label": "Obstructive HCM gradient threshold",
"value": "≥ 30",
"unit": "mmHg"
},
{
"label": "ASH septal-to-posterior wall ratio",
"value": "≥ 1.3",
"unit": "ratio"
}
],
"delta": null,
"pearl": "Dyspnea, angina, syncope, sudden death: the HOCM tetrad in descending order of frequency.",
"lookalike": null,
"related": [
"Q135",
"Q137"
],
"reviewed": "2026-08-26"
},
{
"id": "Q137",
"orig": 137,
"title": "Provoking the HOCM murmur",
"lesions": [
"HCM"
],
"lens": "physical-exam",
"items": [
{
"id": "Q137.1",
"q": "How does amyl nitrite change the murmur of obstructive hypertrophic cardiomyopathy, and why?",
"a": "Amyl nitrite is a potent vasodilator that drops afterload and, through venous pooling, preload. A smaller LV cavity brings the mitral leaflet closer to the septum and a lower aortic pressure lets the outflow tract collapse more easily, so the dynamic gradient rises and the harsh crescendo-decrescendo murmur becomes louder. This is the opposite of what happens with fixed aortic stenosis or with mitral regurgitation, where afterload reduction diminishes the murmur, which is why the maneuver is used at the bedside."
},
{
"id": "Q137.2",
"q": "What happens to the murmur during the Valsalva maneuver?",
"a": "Straining against a closed glottis raises intrathoracic pressure and cuts venous return, shrinking the LV. With less volume to hold the leaflet away from the septum, SAM worsens, the gradient climbs, and the murmur intensifies. Almost every other systolic murmur softens during the strain phase, so a murmur that gets louder with Valsalva is nearly pathognomonic for dynamic obstruction. Standing has the same effect, while squatting and handgrip do the reverse."
}
],
"numbers": [],
"delta": null,
"pearl": "Anything that shrinks the ventricle makes HOCM louder: Valsalva, standing, nitrite, dehydration.",
"lookalike": {
"vs": "Valvular aortic stenosis",
"discriminator": "AS softens with Valsalva and does not change or falls with amyl nitrite; HOCM loudens with both."
},
"related": [
"Q135",
"Q136",
"Q140",
"Q373"
],
"reviewed": "2026-08-26"
},
{
"id": "Q138",
"orig": 138,
"title": "M-mode in obstructive HCM",
"lesions": [
"HCM"
],
"lens": "m-mode",
"items": [
{
"id": "Q138.1",
"q": "What does the M-mode tracing show in obstructive hypertrophic cardiomyopathy?",
"a": "Three findings define the tracing. The walls are thick, and when the septum is disproportionately thicker than the posterior wall (ratio 1.3 or more) the hypertrophy is asymmetric. The LV cavity is small, sometimes nearly obliterated at end-systole, with a hyperdynamic posterior wall. On the mitral M-mode the anterior leaflet moves forward toward the septum during systole and may contact it, the systolic anterior motion that marks obstruction. Aortic valve M-mode adds a fourth clue: mid-systolic partial closure or fluttering as the late-peaking gradient transiently reduces forward flow."
}
],
"numbers": [
{
"label": "ASH septal-to-posterior wall ratio",
"value": "≥ 1.3",
"unit": "ratio"
}
],
"delta": null,
"pearl": "Thick, small, SAM: the three-word M-mode of HOCM.",
"lookalike": {
"vs": "Hypertensive LVH",
"discriminator": "Hypertensive hypertrophy is symmetric and lacks SAM or mid-systolic aortic closure."
},
"related": [
"Q129",
"Q139",
"Q135",
"Q247"
],
"reviewed": "2026-08-26"
},
{
"id": "Q139",
"orig": 139,
"title": "2D versus M-mode in HCM",
"lesions": [
"HCM"
],
"lens": "best-method",
"items": [
{
"id": "Q139.1",
"q": "What does two-dimensional imaging add to M-mode in evaluating hypertrophic cardiomyopathy?",
"a": "M-mode samples only one line through the base of the heart, so it can miss hypertrophy that is regional or apical and can overestimate septal thickness when the beam crosses obliquely. Two-dimensional imaging maps the distribution and extent of thickening across all segments, detects apical and mid-cavity variants, and allows the maximal wall thickness to be measured in the right plane. It also shows the textural changes of fiber disarray, the speckled ground-glass myocardium, as well as papillary muscle abnormalities, elongated leaflets, mitral annular calcification, and a fibrous contact plaque on the septum where the anterior leaflet repeatedly strikes it. Maximal wall thickness of 15 mm or more in an adult without another explanation (13 mm or more with a family history) supports the diagnosis."
}
],
"numbers": [
{
"label": "HCM maximal wall thickness (sporadic)",
"value": "≥ 15",
"unit": "mm"
},
{
"label": "HCM wall thickness with family history",
"value": "≥ 13",
"unit": "mm"
}
],
"delta": null,
"pearl": "M-mode finds the thick septum; 2D finds the thick apex.",
"lookalike": {
"vs": "Apical foreshortening",
"discriminator": "A foreshortened apical view fakes apical thickening; confirm on a true long axis and consider contrast to define the apex."
},
"related": [
"Q138",
"Q140",
"Q247",
"Q372"
],
"reviewed": "2026-08-26"
},
{
"id": "Q140",
"orig": 140,
"title": "PW and CW Doppler in HCM",
"lesions": [
"HCM",
"DOPPLER_PHYSICS"
],
"lens": "doppler",
"items": [
{
"id": "Q140.1",
"q": "How does pulsed-wave Doppler help in evaluating hypertrophic cardiomyopathy?",
"a": "Pulsed Doppler is range-gated, so it tells you where a velocity occurs. From the apical window you march the sample volume from the apex toward the aortic valve; the point at which the velocity abruptly rises and the spectrum fills in with aliasing marks the level of obstruction, whether mid-cavity or in the outflow tract at the point of mitral-septal contact. This localization distinguishes HOCM from valvular or fixed subvalvular stenosis and helps separate an LVOT gradient from a coexisting MR jet. Pulsed Doppler of mitral inflow and tissue Doppler of the annulus also document the diastolic dysfunction that is universal in HCM."
},
{
"id": "Q140.2",
"q": "How is continuous-wave Doppler used in hypertrophic cardiomyopathy?",
"a": "Continuous-wave Doppler has no velocity limit, so it captures the full peak velocity of the outflow jet and the gradient from 4v squared. The HOCM trace is a dagger: velocity rises slowly and peaks late in systole because the obstruction develops as the ventricle empties. Gradients are recorded at rest and again after Valsalva, standing, or exercise, since a resting gradient below 30 mmHg may rise well above 50 mmHg with provocation, a threshold that changes management. Take care not to contaminate the trace with the MR jet, which is higher velocity, earlier peaking, and longer in duration."
}
],
"numbers": [
{
"label": "Obstructive HCM gradient",
"value": "≥ 30",
"unit": "mmHg"
},
{
"label": "Gradient threshold guiding septal reduction",
"value": "≥ 50",
"unit": "mmHg"
},
{
"label": "Bernoulli constant",
"value": "4",
"unit": "× v²"
}
],
"delta": null,
"pearl": "PW finds where, CW finds how much, and the dagger shape says the obstruction is dynamic.",
"lookalike": {
"vs": "Mitral regurgitation jet",
"discriminator": "MR is faster (often over 5 m/s), starts at mitral closure, and lasts through isovolumic periods; the LVOT jet is late-peaking and confined to ejection."
},
"related": [
"Q137",
"Q139",
"Q141",
"Q135",
"Q276",
"Q372",
"Q373"
],
"reviewed": "2026-08-26"
},
{
"id": "Q141",
"orig": 141,
"title": "Color Doppler in HCM",
"lesions": [
"HCM",
"MR"
],
"lens": "doppler",
"items": [
{
"id": "Q141.1",
"q": "What does color-flow Doppler contribute to the assessment of hypertrophic cardiomyopathy?",
"a": "Color Doppler shows the spatial pattern of flow in one glance. In the outflow tract it displays a mosaic of aliased, variance-coded color that begins at the level of mitral-septal contact, confirming where the obstruction lies and guiding placement of the CW cursor. It also detects the mitral regurgitation that accompanies SAM, typically a posteriorly and laterally directed jet that begins in mid-systole as the leaflets are pulled apart, and lets you grade it with vena contracta and other quantitative measures. A centrally or anteriorly directed MR jet suggests intrinsic leaflet disease rather than SAM alone, which changes the surgical plan."
}
],
"numbers": [],
"delta": null,
"pearl": "In HOCM the MR jet points posteriorly; if it points anteriorly, look for a second problem with the valve.",
"lookalike": null,
"related": [
"Q135",
"Q140",
"Q373"
],
"reviewed": "2026-08-26"
},
{
"id": "Q142",
"orig": 142,
"title": "Causes of dilated cardiomyopathy",
"lesions": [
"DCM",
"CAD"
],
"lens": "etiology",
"items": [
{
"id": "Q142.1",
"q": "List five categories of causes of dilated cardiomyopathy.",
"a": "Dilated cardiomyopathy is a final common pathway rather than a single disease. Major categories are idiopathic or genetic (a familial pattern is found in a substantial minority), ischemic damage from coronary disease, infectious myocarditis (most often viral, but also bacterial, fungal, or parasitic such as Chagas disease), toxic injury from alcohol, cocaine, anthracyclines such as doxorubicin, or heavy metals, and peripartum cardiomyopathy presenting in the last month of pregnancy or the months after delivery. Tachycardia-induced, metabolic, and nutritional causes round out the list."
},
{
"id": "Q142.2",
"q": "What is the most common cause of dilated cardiomyopathy in the United States?",
"a": "Ischemic heart disease is the leading identifiable cause of a dilated, poorly contracting ventricle in the United States, which is why coronary evaluation is part of any new DCM workup. Among nonischemic causes, alcohol is the classic and frequently tested answer: alcoholic cardiomyopathy typically appears in men in their thirties to fifties after more than a decade of heavy drinking and can partially reverse with abstinence. A large share of cases remain idiopathic even after full evaluation."
}
],
"numbers": [],
"delta": null,
"pearl": "Ask three questions of every new DCM: coronaries, alcohol, pregnancy.",
"lookalike": {
"vs": "Ischemic cardiomyopathy",
"discriminator": "Ischemic disease produces regional wall motion abnormalities in coronary territories; nonischemic DCM is globally hypokinetic."
},
"related": [
"Q128",
"Q143",
"Q144",
"Q134",
"Q249",
"Q253",
"Q377"
],
"reviewed": "2026-08-26"
},
{
"id": "Q143",
"orig": 143,
"title": "Chagas cardiomyopathy",
"lesions": [
"DCM"
],
"lens": "etiology",
"items": [
{
"id": "Q143.1",
"q": "What is Chagas disease and how does it affect the heart?",
"a": "Chagas disease is infection with the protozoan Trypanosoma cruzi, transmitted by the bite and feces of triatomine (reduviid or kissing) bugs and endemic in Central and South America, where several million people are infected. After an often unnoticed acute phase, a chronic inflammatory myocarditis develops over decades in a subset of patients, producing dilated cardiomyopathy, conduction disease such as right bundle branch block, ventricular arrhythmias, and thromboembolism. A history of residence in an endemic region is a key clue in an otherwise unexplained cardiomyopathy."
},
{
"id": "Q143.2",
"q": "What are the echocardiographic findings of Chagas heart disease?",
"a": "The late picture is a dilated, globally hypokinetic left ventricle indistinguishable from other DCM, often with biventricular involvement and functional regurgitation. What sets Chagas apart is its regional signature: an apical aneurysm, frequently thin-walled and harboring thrombus, and segmental hypokinesis of the inferior and inferolateral walls with relative sparing of the septum, all in the presence of normal coronary arteries. Diastolic dysfunction and RV dysfunction are common and carry prognostic weight."
}
],
"numbers": [],
"delta": null,
"pearl": "An apical aneurysm with clean coronaries in a patient from Latin America is Chagas until proven otherwise.",
"lookalike": {
"vs": "Ischemic apical aneurysm",
"discriminator": "Ischemic aneurysms follow an LAD territory with a documented infarct; Chagas aneurysms occur with normal coronaries and coexisting inferolateral involvement."
},
"related": [
"Q142",
"Q144",
"Q374"
],
"reviewed": "2026-08-26"
},
{
"id": "Q144",
"orig": 144,
"title": "M-mode signs of DCM",
"lesions": [
"DCM",
"HEMODYNAMICS"
],
"lens": "m-mode",
"items": [
{
"id": "Q144.1",
"q": "Name six classic M-mode findings in dilated cardiomyopathy.",
"a": "Each finding is a consequence of a large, weak ventricle with high filling pressure. The LV internal dimension is increased and the walls move poorly, giving a low fractional shortening. E-point septal separation widens beyond about 7 mm because the mitral leaflet opens only as far as the reduced stroke volume pushes it while the septum has moved away. The mitral valve shows a B notch, a shoulder on the A-C closure slope that reflects elevated LV end-diastolic pressure, and in some patients a double-diamond appearance from mid-diastolic closure and reopening when flow across the valve is slow and interrupted. The aortic root moves little and the aortic valve opens briefly with a gradual closure, both reflecting low stroke volume."
}
],
"numbers": [
{
"label": "Abnormal E-point septal separation",
"value": "> 7",
"unit": "mm"
}
],
"delta": null,
"pearl": "A wide EPSS is the M-mode shorthand for low ejection fraction.",
"lookalike": {
"vs": "Aortic regurgitation on M-mode",
"discriminator": "AR can also widen EPSS and flutter the anterior leaflet, but the ventricle is hyperdynamic rather than hypokinetic."
},
"related": [
"Q142",
"Q145",
"Q143",
"Q250",
"Q252"
],
"reviewed": "2026-08-26"
},
{
"id": "Q145",
"orig": 145,
"title": "2D and color in DCM",
"lesions": [
"DCM",
"MR",
"EFFUSION"
],
"lens": "best-method",
"items": [
{
"id": "Q145.1",
"q": "What advantages does two-dimensional imaging offer over M-mode in dilated cardiomyopathy?",
"a": "M-mode measures a single dimension, which overstates or understates function when the ventricle is distorted. Two-dimensional imaging permits volumetric assessment of ejection fraction with biplane Simpson's method, shows whether hypokinesis is truly global or has regional components suggesting ischemia, and measures atrial and RV size. It also screens the apex and the LV cavity for thrombus, excludes primary valve disease that could be the cause rather than the consequence of dilatation, and identifies pericardial effusion, which is common in heart failure. Contrast or 3D can be added when endocardial definition is poor."
},
{
"id": "Q145.2",
"q": "How does color-flow Doppler contribute in dilated cardiomyopathy?",
"a": "Annular dilatation and papillary muscle displacement pull the leaflets apart, so functional mitral and tricuspid regurgitation are almost universal. Color Doppler identifies the regurgitant jets quickly and provides the first estimate of their severity, which is then refined with vena contracta and PISA measurements. Documenting the degree of secondary MR matters because it drives symptoms, predicts outcome, and is now a treatment target with transcatheter repair."
}
],
"numbers": [],
"delta": null,
"pearl": "In DCM the valves leak because the ventricle is big, not because the valves are sick.",
"lookalike": null,
"related": [
"Q144",
"Q146",
"Q249",
"Q250",
"Q251"
],
"reviewed": "2026-08-26"
},
{
"id": "Q146",
"orig": 146,
"title": "Why chambers enlarge in DCM",
"lesions": [
"DCM",
"HEMODYNAMICS"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q146.1",
"q": "Why do many patients with dilated cardiomyopathy have enlargement of both ventricles?",
"a": "Most causes of DCM are diffuse rather than confined to the left side. A viral or toxic insult injures myocytes throughout the heart, so the right ventricle dilates and weakens along with the left. Even when the primary injury is left-sided, chronic elevation of left-sided filling pressure produces postcapillary pulmonary hypertension that loads the RV and drives secondary dilatation and tricuspid regurgitation. RV involvement is a strong marker of worse prognosis."
},
{
"id": "Q146.2",
"q": "Why are the atria enlarged in dilated cardiomyopathy?",
"a": "As the ventricle dilates and stiffens, its end-diastolic pressure rises, and the atrium must fill it against that pressure. Chronically elevated atrial pressure stretches the thin-walled atrium, and functional atrioventricular regurgitation adds a volume load on top. The enlarged atrium is therefore a cumulative record of high filling pressure over time, which is why left atrial volume index is used as a marker of chronic diastolic dysfunction and a predictor of atrial fibrillation."
}
],
"numbers": [],
"delta": null,
"pearl": "The atrium is the ventricle's pressure diary.",
"lookalike": null,
"related": [
"Q145",
"Q149",
"Q147",
"Q151",
"Q152",
"Q249",
"Q252",
"Q253",
"Q377"
],
"reviewed": "2026-08-26"
},
{
"id": "Q147",
"orig": 147,
"title": "The transplanted heart on echo",
"lesions": [
"ANATOMY",
"PROCEDURE"
],
"lens": "anatomy",
"items": [
{
"id": "Q147.1",
"q": "What is the most distinctive echocardiographic feature of a heart transplant recipient, and what explains it?",
"a": "With the classic biatrial (Shumway) technique the surgeon leaves the back walls of the recipient's atria in place, preserving the caval and pulmonary venous connections, and sews the donor atria onto them. The result is an enlarged, oddly shaped atrium with a ridge of suture line partway across it, which can look like a mass or a membrane; the atria contract asynchronously because the two portions have separate pacemaker tissue. Modern bicaval anastomosis preserves the donor RA intact, so the RA looks nearly normal and only the LA carries a suture ridge. Other expected features are a mildly thickened LV early after surgery, a small pericardial effusion, and paradoxical septal motion."
}
],
"numbers": [],
"delta": null,
"pearl": "A suture ridge in a giant atrium plus a fresh sternotomy scar is a transplant, not a tumor.",
"lookalike": {
"vs": "Atrial mass or cor triatriatum",
"discriminator": "The transplant ridge runs along the anastomosis line, is linear and echogenic, and fits the surgical history; a membrane in cor triatriatum divides the LA and has a flow gradient."
},
"related": [
"Q146"
],
"reviewed": "2026-08-26"
},
{
"id": "Q148",
"orig": 148,
"title": "Causes of restrictive cardiomyopathy",
"lesions": [
"RCM"
],
"lens": "etiology",
"items": [
{
"id": "Q148.1",
"q": "Name four causes of restrictive cardiomyopathy.",
"a": "Restriction arises when something stiffens the myocardium without necessarily dilating it. Infiltrative deposition diseases lead the list: amyloidosis (light-chain and transthyretin types), sarcoidosis, and hemochromatosis, in which iron loads the myocytes. Storage disorders such as Fabry and glycogen storage diseases, endomyocardial fibrosis and hypereosinophilic (Loeffler) endocarditis, radiation-induced fibrosis, and idiopathic or familial restrictive cardiomyopathy complete the differential."
},
{
"id": "Q148.2",
"q": "Which cause of restrictive cardiomyopathy is most common?",
"a": "Cardiac amyloidosis is the most frequent cause encountered in adults, and its recognized prevalence has grown with awareness of wild-type transthyretin amyloid in older patients with heart failure and preserved ejection fraction. Suspect it when the walls are thick but the ECG voltage is low, the atria are large, longitudinal strain is reduced with apical sparing, and there is no hypertension to explain the hypertrophy."
}
],
"numbers": [],
"delta": null,
"pearl": "Thick walls with low voltage is amyloid until proven otherwise.",
"lookalike": {
"vs": "Hypertrophic cardiomyopathy",
"discriminator": "HCM has high ECG voltage and often asymmetric hypertrophy; amyloid has low voltage, symmetric thickening including the RV and septum, and apical-sparing strain."
},
"related": [
"Q134",
"Q149",
"Q150",
"Q124",
"Q254",
"Q256",
"Q360",
"Q377"
],
"reviewed": "2026-08-26"
},
{
"id": "Q149",
"orig": 149,
"title": "Restrictive versus infiltrative",
"lesions": [
"RCM",
"HEMODYNAMICS"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q149.1",
"q": "Why is restrictive cardiomyopathy also called infiltrative cardiomyopathy?",
"a": "The two words describe different levels of the same disease. Restrictive is the physiology: the ventricle cannot expand normally in diastole, so filling pressures rise steeply after a brief early filling phase. Infiltrative is the pathology behind that stiffness in the most common cases, where abnormal material such as amyloid fibrils, sarcoid granulomas, or iron is deposited between or inside myocytes. Not every restrictive heart is infiltrated, however; endomyocardial fibrosis and idiopathic RCM restrict filling without deposition, so the terms overlap but are not synonyms."
},
{
"id": "Q149.2",
"q": "How does restrictive cardiomyopathy affect the atria, and why?",
"a": "Biatrial enlargement is more pronounced in RCM than in any other cardiomyopathy and is a diagnostic clue in itself. Because both ventricles are stiff, both atria face persistently high end-diastolic pressures and dilate in response, producing the picture of small or normal-sized ventricles flanked by huge atria. The same high pressures generate a restrictive Doppler pattern with a tall E wave, short deceleration time, small A wave, and low tissue e', and predispose to atrial fibrillation and atrial thrombus."
}
],
"numbers": [],
"delta": null,
"pearl": "Small ventricles, giant atria, tiny e': restriction.",
"lookalike": {
"vs": "Constrictive pericarditis",
"discriminator": "Constriction has normal or high medial e' with respiratory septal shift; restriction has low e' with little respiratory variation."
},
"related": [
"Q126",
"Q148",
"Q150",
"Q146",
"Q248",
"Q255",
"Q257",
"Q261",
"Q262"
],
"reviewed": "2026-08-26"
},
{
"id": "Q150",
"orig": 150,
"title": "Bright myocardium in RCM",
"lesions": [
"RCM",
"INSTRUMENTATION"
],
"lens": "pitfall",
"items": [
{
"id": "Q150.1",
"q": "Why does the myocardium look so bright in restrictive cardiomyopathy, and how reliable is that sign?",
"a": "Deposited material changes the acoustic impedance of the tissue. Amyloid fibrils, iron, or granulomas create countless small interfaces within the muscle, scattering ultrasound and producing a sparkling or granular texture that is brighter than normal myocardium. This ground-glass appearance is the classic exam answer for infiltrative disease. In practice it is unreliable: modern harmonic imaging and high-dynamic-range processing make normal myocardium look bright in thin, easily imaged patients, and gain settings alter it freely. A bright myocardium should prompt a look for the more specific companions of amyloid, namely thick walls with low ECG voltage, biatrial enlargement, thickened valves and interatrial septum, a small effusion, and apical-sparing longitudinal strain."
}
],
"numbers": [],
"delta": null,
"pearl": "Sparkling is suggestive, not diagnostic; let strain and the ECG make the call.",
"lookalike": {
"vs": "Normal myocardium with harmonic imaging and high gain",
"discriminator": "Turn down gain and compare with the pericardium; true infiltration stays granular and comes with thick walls, low voltage, and restrictive filling."
},
"related": [
"Q148",
"Q149",
"Q248",
"Q256",
"Q360"
],
"reviewed": "2026-08-26"
},
{
"id": "Q151",
"orig": 151,
"title": "2D appearance of restrictive cardiomyopathy",
"lesions": [
"RCM",
"EFFUSION"
],
"lens": "2d",
"items": [
{
"id": "Q151.1",
"q": "What does two-dimensional imaging typically show in restrictive cardiomyopathy, and why does the heart look this way?",
"a": "The underlying problem is a stiff, noncompliant ventricle, so the ventricular cavities stay normal or small while both atria dilate markedly from chronically elevated filling pressures. Wall thickness is often increased, and in infiltrative forms such as amyloid the myocardium takes on a granular, speckled, highly reflective texture. Systolic function is usually preserved until late in the disease, and a small to moderate pericardial effusion is common, although tamponade is uncommon. The combination of biatrial enlargement with small, thick, bright ventricles is the classic 2D picture."
}
],
"numbers": [],
"delta": {
"was": "2011 card and the Mayo criteria (ASE 2013) set the constriction medial e' cut-off at ≥ 9 cm/s.",
"now": "ASE 2025 lowers the constriction medial e' cut-off to > 7 cm/s, with > 8 cm/s strongly favoring constriction; it pairs with respirophasic septal shift for about 80% sensitivity and 96% specificity.",
"source": "ASE 2025 diastolic function guideline"
},
"pearl": "Big atria, small stiff ventricles, bright walls: think restriction, and ask about amyloid.",
"lookalike": {
"vs": "constrictive pericarditis",
"discriminator": "Constriction has normal wall thickness and texture with a thickened pericardium, septal bounce, and preserved or elevated medial e' (> 7 cm/s, > 8 favors constriction); restriction has low e' and high E/e'."
},
"related": [
"Q152",
"Q146",
"Q255",
"Q256",
"Q378"
],
"reviewed": "2026-08-26"
},
{
"id": "Q152",
"orig": 152,
"title": "Doppler pattern of restrictive filling",
"lesions": [
"RCM",
"MR",
"TR"
],
"lens": "doppler",
"items": [
{
"id": "Q152.1",
"q": "Which Doppler findings characterize restrictive cardiomyopathy?",
"a": "Because the ventricle is stiff and atrial pressure is high, early filling is driven by a large atrioventricular gradient that dissipates quickly, producing a tall E wave with a short deceleration time and a small A wave (E/A well above 2). Tissue Doppler shows low mitral annular e' velocities and a high E/e' ratio, reflecting impaired relaxation combined with high filling pressures. Mild mitral and tricuspid regurgitation are common because the annuli dilate with the atria. Pulmonary vein flow is systolic-blunted with a prominent, prolonged atrial reversal wave, and the pattern changes little with respiration."
}
],
"numbers": [
{
"label": "Restrictive E/A ratio",
"value": "> 2",
"unit": "ratio"
},
{
"label": "Restrictive deceleration time",
"value": "< 160",
"unit": "ms"
}
],
"delta": null,
"pearl": "Restriction = tall E, tiny A, short DT, and low e' — high pressure filling a stiff chamber.",
"lookalike": {
"vs": "constrictive pericarditis",
"discriminator": "Both show restrictive inflow, but constriction shows >25% respiratory E variation, preserved e', and expiratory hepatic vein diastolic reversal; RCM shows low e' and little respiratory change."
},
"related": [
"Q151",
"Q146",
"Q250",
"Q255",
"Q257",
"Q262"
],
"reviewed": "2026-08-26"
},
{
"id": "Q153",
"orig": 153,
"title": "Wall motion categories and scoring",
"lesions": [
"CAD"
],
"lens": "definition",
"items": [
{
"id": "Q153.1",
"q": "What categories of regional wall motion are recognized on echocardiography, and how are they scored?",
"a": "The ASE grades each of the 17 segments by its inward excursion and systolic thickening. Score 1 is normal motion and thickening; score 2 is hypokinesis, meaning reduced but present inward motion and thickening; score 3 is akinesis, in which the segment neither moves nor thickens; and score 4 is dyskinesis, where the segment bulges outward during systole. An aneurysmal segment is one that is deformed in both systole and diastole. Hyperkinesis (exaggerated motion) is also described, usually as compensation in noninfarcted walls, but it is not part of the numeric score. Summing the scores and dividing by the number of segments scored gives the wall motion score index, where 1.0 is normal."
}
],
"numbers": [
{
"label": "Segment model",
"value": "17",
"unit": "segments"
},
{
"label": "Normal wall motion score index",
"value": "1.0",
"unit": "index"
}
],
"delta": {
"was": "2011 card listed five descriptive types including hypercontractile motion, without a scoring scheme.",
"now": "Current guideline: ASE 17-segment model with numeric scoring 1 normal, 2 hypokinetic, 3 akinetic, 4 dyskinetic, plus aneurysmal; hyperkinesis is descriptive only.",
"source": "ASE 2015 chamber quant"
},
"pearl": "Score it 1-2-3-4: normal, hypo, a-, dys-kinetic; the index is the average.",
"lookalike": null,
"related": [
"Q158",
"Q164",
"Q280",
"Q282"
],
"widgets": [
"bullseye",
{
"id": "calc",
"opts": {
"k": "wmsi"
}
}
],
"reviewed": "2026-08-26"
},
{
"id": "Q154",
"orig": 154,
"title": "True aneurysm versus pseudoaneurysm",
"lesions": [
"CAD"
],
"lens": "2d",
"items": [
{
"id": "Q154.1",
"q": "How does a true left ventricular aneurysm differ from a pseudoaneurysm on echocardiography?",
"a": "A true aneurysm is a thinned, scarred segment of intact ventricular wall that still contains all three layers, so its neck is broad and the outpouching is wider at its mouth than deep in its sac. A pseudoaneurysm is a contained free-wall rupture: blood has escaped through the myocardium and is held only by adherent pericardium and thrombus, so the wall is not myocardium at all. On imaging, the pseudoaneurysm shows an abrupt, narrow neck (typically less than half the maximal sac diameter) with turbulent to-and-fro flow through it, and it nearly always contains layered thrombus. Both are most often seen after infarction, but true aneurysms favor the apex and anterior wall, while pseudoaneurysms favor the inferior and lateral walls."
},
{
"id": "Q154.2",
"q": "Which lesion carries the higher risk of rupture, and what does that mean for management?",
"a": "The pseudoaneurysm, because its wall is only pericardium and clot rather than scar. Free rupture into the pericardium can occur at any time, so a pseudoaneurysm is treated as a surgical emergency, whereas a chronic true aneurysm rarely ruptures and is managed for its complications such as thrombus, heart failure, and arrhythmia."
}
],
"numbers": [
{
"label": "Pseudoaneurysm neck-to-sac ratio",
"value": "< 0.5",
"unit": "ratio"
}
],
"delta": null,
"pearl": "Narrow neck, no myocardium, needs surgery: pseudoaneurysm. Wide mouth, scarred wall: true aneurysm.",
"lookalike": {
"vs": "true LV aneurysm",
"discriminator": "Neck width: pseudoaneurysm neck is narrow relative to the sac and shows bidirectional flow on color Doppler; true aneurysm has a wide neck in continuity with the ventricular contour."
},
"related": [
"Q155",
"Q158",
"Q159",
"Q374",
"Q376"
],
"reviewed": "2026-08-26"
},
{
"id": "Q155",
"orig": 155,
"title": "Complications of myocardial infarction",
"lesions": [
"CAD",
"VSD",
"EFFUSION"
],
"lens": "etiology",
"items": [
{
"id": "Q155.1",
"q": "What complications can follow an acute myocardial infarction, and which should the sonographer specifically screen for?",
"a": "Complications fall into electrical, mechanical, and pericardial groups. Electrical complications are arrhythmias and conduction block. Mechanical complications include true aneurysm, pseudoaneurysm, mural thrombus, papillary muscle dysfunction or rupture with acute mitral regurgitation, ventricular septal rupture, and free-wall rupture with tamponade; right ventricular infarction is a hemodynamic complication of inferior infarcts. Pericardial complications are early pericarditis with effusion and later Dressler syndrome. The sonographer should specifically look for new mitral regurgitation, a septal defect on color Doppler, apical thrombus, and effusion whenever a post-infarct patient deteriorates."
},
{
"id": "Q155.2",
"q": "Which structural complication is the most common?",
"a": "Left ventricular aneurysm is the most common structural complication, historically reported in roughly 8 to 15 percent of infarcts, most often after a large anterior infarct with persistent LAD occlusion. It forms because a full-thickness scar cannot resist ventricular pressure and stretches outward over weeks."
}
],
"numbers": [
{
"label": "Aneurysm incidence after MI",
"value": "8–15",
"unit": "%"
}
],
"delta": null,
"pearl": "After MI, three ruptures kill: papillary muscle, septum, free wall. Look for MR, VSD, and effusion.",
"lookalike": null,
"related": [
"Q154",
"Q158",
"Q160",
"Q161",
"Q157",
"Q162",
"Q279",
"Q281",
"Q376"
],
"reviewed": "2026-08-26"
},
{
"id": "Q156",
"orig": 156,
"title": "Coronary artery disease risk factors",
"lesions": [
"CAD"
],
"lens": "etiology",
"items": [
{
"id": "Q156.1",
"q": "Which risk factors predispose a patient to coronary artery disease?",
"a": "Risk factors are divided into those that cannot be changed and those that can. Nonmodifiable factors are advancing age, male sex (women catch up after menopause), and a family history of premature coronary disease. Modifiable factors include cigarette smoking, hypertension, dyslipidemia (high LDL, low HDL), diabetes mellitus, obesity, and physical inactivity. Each factor accelerates endothelial injury and lipid deposition, and the factors multiply rather than add, which is why risk calculators combine them."
}
],
"numbers": [],
"delta": null,
"pearl": "Three you cannot change (age, sex, family); the rest you can (smoke, pressure, lipids, sugar, weight).",
"lookalike": null,
"related": [
"Q164"
],
"reviewed": "2026-08-26"
},
{
"id": "Q157",
"orig": 157,
"title": "Dressler syndrome",
"lesions": [
"CAD",
"EFFUSION"
],
"lens": "definition",
"items": [
{
"id": "Q157.1",
"q": "What is Dressler syndrome, and how does it present?",
"a": "Dressler syndrome is a delayed, immune-mediated pericarditis that follows myocardial infarction (or cardiac surgery), thought to result from antibodies formed against injured myocardial tissue. It typically appears weeks after the event, classically 2 to 8 weeks, rather than in the first few days like early post-infarction pericarditis. Patients report pleuritic, positional chest pain that eases when sitting forward, with fever, a friction rub, and elevated inflammatory markers. Echocardiography shows a pericardial effusion, which is usually small but should be checked for tamponade physiology."
}
],
"numbers": [
{
"label": "Onset after MI",
"value": "2–8",
"unit": "weeks"
}
],
"delta": null,
"pearl": "Early post-MI pericarditis is days; Dressler is weeks and immune.",
"lookalike": {
"vs": "early post-infarction pericarditis",
"discriminator": "Timing: early pericarditis occurs within the first week and is due to direct epicardial inflammation; Dressler is delayed by weeks and is autoimmune."
},
"related": [
"Q155"
],
"reviewed": "2026-08-26"
},
{
"id": "Q158",
"orig": 158,
"title": "2D findings of old infarction",
"lesions": [
"CAD"
],
"lens": "2d",
"items": [
{
"id": "Q158.1",
"q": "Which two-dimensional findings indicate that a myocardial segment has previously infarcted?",
"a": "Healed infarction replaces muscle with scar, so the involved segments become thin (often under 6 mm at end-diastole), bright and echodense, and fail to thicken in systole; the wall motion abnormality is fixed and follows a coronary territory. Larger scars may deform into an aneurysm with diastolic bulging, seen in up to about 15 percent of cases, and any akinetic or aneurysmal apex should be examined for mural thrombus using an apical zoom and, if needed, contrast. Adjacent walls may be hyperkinetic as compensation. A small pericardial effusion may persist. Global function is summarized with ejection fraction and the wall motion score index."
}
],
"numbers": [
{
"label": "Scar wall thickness",
"value": "< 6",
"unit": "mm"
},
{
"label": "Aneurysm after MI",
"value": "up to 15",
"unit": "%"
}
],
"delta": null,
"pearl": "Thin, bright, and not thickening equals scar; thickening, not just motion, is the key.",
"lookalike": {
"vs": "stunned or hibernating myocardium",
"discriminator": "Viable myocardium keeps normal wall thickness and texture and may improve with low-dose dobutamine; scar is thin, bright, and fixed."
},
"related": [
"Q153",
"Q154",
"Q161",
"Q155",
"Q159",
"Q280",
"Q282",
"Q374"
],
"reviewed": "2026-08-26"
},
{
"id": "Q159",
"orig": 159,
"title": "Pre-aneurysmectomy echo checklist",
"lesions": [
"CAD",
"PROCEDURE"
],
"lens": "procedure",
"items": [
{
"id": "Q159.1",
"q": "What should the echo report contain before surgical repair of a left ventricular aneurysm?",
"a": "The surgeon needs the aneurysm's location and extent, its size and neck, whether it contains thrombus, and the status of any associated mitral regurgitation. Most important is the function of the remaining, nonaneurysmal walls, because surgical resection only helps if enough contracting myocardium remains to support the circulation; a ventricle that is globally akinetic will not benefit. Report the ejection fraction, the wall motion score index, and right ventricular function, and consider viability assessment of borderline segments. Also measure pulmonary pressures from the tricuspid jet, since pulmonary hypertension raises surgical risk."
}
],
"numbers": [],
"delta": null,
"pearl": "The surgeon's real question is not the aneurysm but what is left to contract.",
"lookalike": null,
"related": [
"Q154",
"Q158",
"Q374"
],
"reviewed": "2026-08-26"
},
{
"id": "Q160",
"orig": 160,
"title": "New murmur after inferior infarct",
"lesions": [
"CAD",
"MR"
],
"lens": "vignette",
"items": [
{
"id": "Q160.1",
"q": "A 58-year-old woman treated for an inferior ST-elevation infarction five days earlier develops sudden dyspnea, pulmonary edema, and a new harsh systolic murmur. What diagnosis should you suspect first, and why does the infarct location matter?",
"a": "Suspect rupture of the posteromedial papillary muscle causing acute severe mitral regurgitation. The posteromedial papillary muscle is supplied by a single vessel, usually the posterior descending branch of the right coronary (or circumflex in left-dominant anatomy), so an inferior or inferolateral infarct can render it ischemic and necrotic; the anterolateral papillary muscle has dual supply from the LAD and circumflex and rarely ruptures. Rupture usually occurs 2 to 7 days after infarction. Echo shows a flail leaflet with a mobile ruptured head, an eccentric MR jet, hyperdynamic LV, and often a surprisingly small infarct. Because the acute regurgitant volume enters a small, noncompliant atrium, the murmur may be soft and pulmonary edema dominates; urgent surgery is required."
}
],
"numbers": [
{
"label": "Posteromedial share of papillary ruptures",
"value": "~ 90",
"unit": "%"
},
{
"label": "Typical timing after MI",
"value": "2–7",
"unit": "days"
}
],
"delta": null,
"pearl": "Single supply, single point of failure: posteromedial muscle plus inferior MI equals rupture.",
"lookalike": {
"vs": "post-infarction ventricular septal rupture",
"discriminator": "VSR is more common after anterior infarcts and shows a color Doppler jet crossing the septum with RV volume overload; papillary rupture shows a flail mitral leaflet with an eccentric MR jet."
},
"related": [
"Q155",
"Q163",
"Q279",
"Q369"
],
"reviewed": "2026-08-26"
},
{
"id": "Q161",
"orig": 161,
"title": "Ventricular thrombus formation rule",
"lesions": [
"CAD",
"MASS"
],
"lens": "pitfall",
"items": [
{
"id": "Q161.1",
"q": "What is the basic rule linking ventricular thrombus to wall motion, and when does post-infarction thrombus usually form?",
"a": "Thrombus needs stasis, so it forms only in a region of the ventricle that is akinetic, dyskinetic, or aneurysmal; a mass sitting on a normally contracting wall is almost never a thrombus and should be reconsidered as artifact, trabeculation, or tumor. After infarction, thrombus most often develops in the first one to two weeks, particularly around days 6 to 10, and the apex is the usual site because anterior infarcts are largest and apical flow is slowest. Historically about 40 percent of large anterior infarcts developed mural thrombus, though modern reperfusion has lowered this. Use apical zoom, high frequency, off-axis views, and ultrasound enhancing agent when the apex is foreshortened or poorly seen."
}
],
"numbers": [
{
"label": "Historic thrombus rate after acute MI",
"value": "~ 40",
"unit": "%"
},
{
"label": "Peak thrombus formation",
"value": "6–10",
"unit": "days"
}
],
"delta": null,
"pearl": "No stasis, no thrombus: a clot on a normally moving wall is probably not a clot.",
"lookalike": {
"vs": "apical near-field artifact",
"discriminator": "Artifact fades with reduced gain, does not persist in orthogonal views, and lies on a normally thickening wall; thrombus is a discrete mass with defined borders over an akinetic segment and fills defect with contrast."
},
"related": [
"Q158",
"Q170",
"Q155",
"Q328",
"Q329",
"Q332",
"Q333",
"Q375"
],
"reviewed": "2026-08-26"
},
{
"id": "Q162",
"orig": 162,
"title": "Echo signs of RV infarction",
"lesions": [
"CAD",
"TR"
],
"lens": "2d",
"items": [
{
"id": "Q162.1",
"q": "How is a right ventricular infarction recognized on two-dimensional echocardiography, and how common is it?",
"a": "Right ventricular infarction complicates inferior infarction because the same right coronary artery supplies the RV free wall through acute marginal branches; pathologic series find RV involvement in a majority of inferior infarcts, yet only a small fraction become clinically apparent. The most sensitive 2D sign is akinesis or dyskinesis of the RV free wall, best seen in the subcostal and RV-focused apical views. Supporting but nonspecific findings are RV dilatation, reduced TAPSE and RV S' velocity, tricuspid regurgitation from annular dilatation, paradoxical septal motion, and a plethoric IVC with elevated right atrial pressure. Recognition matters because these patients are preload dependent and worsen with nitrates and diuretics."
}
],
"numbers": [
{
"label": "RV involvement in inferior MI at autopsy",
"value": "up to 70",
"unit": "%"
},
{
"label": "Clinically recognized RV infarct",
"value": "~ 3",
"unit": "%"
},
{
"label": "TAPSE lower limit of normal",
"value": "17",
"unit": "mm"
}
],
"delta": null,
"pearl": "Inferior MI plus hypotension and clear lungs: look at the RV free wall, not the LV.",
"lookalike": {
"vs": "acute pulmonary embolism",
"discriminator": "PE spares the RV apex (McConnell sign) and dilates the RV with normal LV inferior wall; RV infarct shows free-wall akinesis alongside an inferior LV wall motion abnormality."
},
"related": [
"Q155",
"Q163",
"Q383"
],
"reviewed": "2026-08-26"
},
{
"id": "Q163",
"orig": 163,
"title": "Ischemic versus nonischemic dilated ventricle",
"lesions": [
"CAD",
"DCM",
"MR"
],
"lens": "2d",
"items": [
{
"id": "Q163.1",
"q": "On two-dimensional imaging, how does an ischemic cardiomyopathy differ from a viral or idiopathic dilated cardiomyopathy?",
"a": "Both produce a dilated, poorly contracting left ventricle, so the distinction rests on the pattern of dysfunction. Ischemic disease typically shows regional abnormalities that follow coronary territories, with thin bright scar in some segments and preserved or hyperkinetic motion in others, and the right ventricle is often spared. A viral or idiopathic dilated cardiomyopathy shows global, uniform hypokinesis with normal wall thickness and texture, and the right ventricle is frequently dilated and hypocontractile as well. Regional variation in severe DCM can occur, so the pattern suggests rather than proves the etiology."
},
{
"id": "Q163.2",
"q": "What does Doppler add to the echo evaluation of ischemic heart disease?",
"a": "Doppler detects and grades the mechanical complications that 2D imaging may only hint at. Color and spectral Doppler quantify ischemic mitral regurgitation from tethering or a flail leaflet, identify a post-infarction septal rupture as a systolic jet crossing the septum with a calculable gradient, and estimate pulmonary pressures from tricuspid regurgitation. Mitral inflow and tissue Doppler grade diastolic dysfunction and filling pressures, which track prognosis. Tricuspid regurgitation frequently accompanies right ventricular infarction but is not specific for it."
}
],
"numbers": [],
"delta": null,
"pearl": "Regional plus spared RV points to ischemia; global plus RV involvement points to nonischemic DCM.",
"lookalike": {
"vs": "nonischemic dilated cardiomyopathy",
"discriminator": "Territorial scar with thin bright segments and a normal RV favors ischemic; uniform hypokinesis with RV involvement favors nonischemic."
},
"related": [
"Q160",
"Q162",
"Q251",
"Q377"
],
"reviewed": "2026-08-26"
},
{
"id": "Q164",
"orig": 164,
"title": "Stress echo versus exercise ECG",
"lesions": [
"CAD",
"STRESS"
],
"lens": "best-method",
"items": [
{
"id": "Q164.1",
"q": "Why does exercise echocardiography outperform exercise electrocardiography for detecting coronary disease?",
"a": "In the ischemic cascade, a regional wall motion abnormality appears before ST-segment change or angina, so imaging the ventricle at peak stress catches ischemia earlier and localizes it to a coronary territory. Exercise ECG alone has a sensitivity around 60 to 70 percent for single-vessel disease and is uninterpretable with baseline ST abnormalities, left bundle branch block, paced rhythm, or digoxin. Stress echo reaches roughly 85 to 90 percent sensitivity and specificity, with sensitivity rising further in multivessel disease because more territories become abnormal. It also provides resting function, valve assessment, and pulmonary pressures without radiation."
}
],
"numbers": [
{
"label": "Exercise ECG sensitivity (single vessel)",
"value": "~ 60",
"unit": "%"
},
{
"label": "Exercise echo sensitivity and specificity",
"value": "~ 85–90",
"unit": "%"
}
],
"delta": null,
"pearl": "Wall motion changes before the ECG does: imaging beats electricity in the ischemic cascade.",
"lookalike": null,
"related": [
"Q153",
"Q156",
"Q281"
],
"reviewed": "2026-08-26"
},
{
"id": "Q165",
"orig": 165,
"title": "Penetrating cardiac injury findings",
"lesions": [
"TRAUMA",
"EFFUSION",
"VSD"
],
"lens": "etiology",
"items": [
{
"id": "Q165.1",
"q": "What cardiac injuries can result from a penetrating wound to the chest, and what should the focused echo look for?",
"a": "A knife or bullet can lacerate any structure in its path, so the injuries include free-wall laceration with hemopericardium and tamponade, traumatic septal defects at the atrial or ventricular level, disruption of a valve leaflet, chordae, or papillary muscle with acute regurgitation, laceration of a coronary artery with a regional wall motion abnormality or infarct, and retained foreign bodies or fistulae between chambers and great vessels. The focused examination first asks whether there is a pericardial effusion and tamponade, then screens for new regurgitant jets, an abnormal color Doppler shunt across the septum, and new wall motion abnormalities. Findings can evolve, so a normal first study does not exclude injury."
}
],
"numbers": [],
"delta": null,
"pearl": "Trace the wound track: wall, septum, valve, coronary, pericardium.",
"lookalike": null,
"related": [
"Q166"
],
"reviewed": "2026-08-26"
},
{
"id": "Q166",
"orig": 166,
"title": "Effusion absent in cardiac trauma",
"lesions": [
"TRAUMA",
"EFFUSION"
],
"lens": "pitfall",
"items": [
{
"id": "Q166.1",
"q": "Why is the absence of a pericardial effusion unreliable for excluding cardiac injury after a penetrating wound?",
"a": "An effusion accumulates only if the pericardium holds the blood; when the wound also opens the pericardium, blood drains into the pleural space or mediastinum and the pericardial sac may look empty despite a cardiac laceration. Only about half to three quarters of patients with proven cardiac injury show an effusion, and the figure is lowest, near 50 percent, with gunshot wounds, which create larger pericardial defects than stab wounds. Therefore a negative FAST or echo in an unstable patient should prompt evaluation for hemothorax and surgical exploration rather than reassurance. Conversely, a positive effusion in this setting is highly specific and mandates urgent intervention."
}
],
"numbers": [
{
"label": "Effusion present in cardiac trauma",
"value": "50–75",
"unit": "%"
},
{
"label": "Effusion present with gunshot wounds",
"value": "~ 50",
"unit": "%"
}
],
"delta": null,
"pearl": "A torn pericardium cannot hold a tamponade: no effusion does not mean no heart injury.",
"lookalike": null,
"related": [
"Q165"
],
"reviewed": "2026-08-26"
},
{
"id": "Q167",
"orig": 167,
"title": "Cardiac myxoma basics",
"lesions": [
"MASS"
],
"lens": "definition",
"items": [
{
"id": "Q167.1",
"q": "What is a cardiac myxoma?",
"a": "A myxoma is the most common primary cardiac tumor in adults and is benign, arising from primitive mesenchymal cells in the subendocardium and producing a gelatinous, mucopolysaccharide-rich stroma. On echo it appears as a mobile, often heterogeneous mass attached by a stalk, most commonly to the fossa ovalis region of the interatrial septum; it may be smooth and encapsulated or friable and multilobulated. The friable type is the one that embolizes. Most are sporadic, but familial cases occur in Carney complex, where they are younger, multiple, and in unusual sites."
},
{
"id": "Q167.2",
"q": "Where do myxomas most commonly arise?",
"a": "About 75 percent grow in the left atrium, typically from the fossa ovalis; the right atrium is next at roughly 15 to 20 percent, and ventricular myxomas are rare. Multiple tumors are seen in about 5 percent of patients, more often in familial disease."
},
{
"id": "Q167.3",
"q": "How often do myxomas recur after surgical resection?",
"a": "Recurrence occurs in roughly 5 to 14 percent of cases, usually at or near the original attachment site from incomplete removal of the stalk base, but sometimes at other intracardiac locations, especially in familial disease. Because of this, follow-up echocardiography is recommended after resection."
}
],
"numbers": [
{
"label": "Left atrial location",
"value": "~ 75",
"unit": "%"
},
{
"label": "Multiple myxomas",
"value": "~ 5",
"unit": "%"
},
{
"label": "Recurrence after resection",
"value": "5–14",
"unit": "%"
}
],
"delta": null,
"pearl": "Stalk on the fossa ovalis in the left atrium is the classic myxoma; familial ones are multiple and come back.",
"lookalike": {
"vs": "left atrial thrombus",
"discriminator": "Thrombus favors the appendage or posterior wall, is broad-based, and occurs with AF or mitral stenosis; myxoma is pedunculated from the fossa ovalis and mobile with a stalk."
},
"related": [
"Q168",
"Q169",
"Q170",
"Q171",
"Q327",
"Q332"
],
"reviewed": "2026-08-26"
},
{
"id": "Q168",
"orig": 168,
"title": "Left atrial myxoma presentation",
"lesions": [
"MASS",
"MS"
],
"lens": "physical-exam",
"items": [
{
"id": "Q168.1",
"q": "What symptoms and examination findings does a left atrial myxoma produce?",
"a": "The tumor prolapses into the mitral orifice during diastole, so patients develop the symptoms of mitral inflow obstruction: exertional dyspnea, orthopnea, fatigue, and sometimes syncope that changes with body position as the mass shifts. Auscultation reveals a diastolic rumble and a loud first heart sound; a low-pitched early diastolic 'tumor plop' may replace the opening snap as the mass drops into the orifice. Constitutional features such as fever, weight loss, and elevated inflammatory markers result from interleukin-6 production, and embolic events, including stroke, occur in a third of patients."
},
{
"id": "Q168.2",
"q": "Which cardiac condition does a left atrial myxoma mimic?",
"a": "It mimics rheumatic mitral stenosis, because both obstruct the mitral orifice and produce dyspnea, a diastolic murmur, and elevated left atrial pressure. Echo settles the question: a myxoma is a mobile mass on a stalk with normal leaflets, whereas rheumatic stenosis shows thickened, doming leaflets with commissural fusion. Clues favoring myxoma are positional symptoms, constitutional symptoms, and a murmur that varies between examinations."
}
],
"numbers": [],
"delta": null,
"pearl": "Mitral stenosis that changes with position or comes with fever is a myxoma until proven otherwise.",
"lookalike": {
"vs": "rheumatic mitral stenosis",
"discriminator": "Rheumatic MS has thickened doming leaflets with fused commissures; myxoma has normal leaflets with a stalked mass prolapsing through them."
},
"related": [
"Q167",
"Q327",
"Q330"
],
"reviewed": "2026-08-26"
},
{
"id": "Q169",
"orig": 169,
"title": "Malignant and pediatric cardiac tumors",
"lesions": [
"MASS"
],
"lens": "etiology",
"items": [
{
"id": "Q169.1",
"q": "What is the most common primary malignant tumor of the heart?",
"a": "Sarcoma is the most common primary cardiac malignancy, accounting for roughly a quarter of all primary cardiac tumors and second only to myxoma in overall frequency. Angiosarcoma is the most frequent subtype and typically arises in the right atrium near the atrioventricular groove, often invading the pericardium and causing hemorrhagic effusion; rhabdomyosarcoma, fibrosarcoma, and undifferentiated sarcomas make up the rest. Echo features suggesting malignancy include a broad-based, infiltrative mass that crosses tissue planes, involvement of the right atrium or pericardium, and associated effusion. Metastatic tumors are far more common than any primary malignancy."
},
{
"id": "Q169.2",
"q": "What is the most common benign cardiac tumor in children?",
"a": "Rhabdomyoma, a hamartoma of cardiac myocytes, is the most common pediatric cardiac tumor and is strongly associated with tuberous sclerosis. These lesions are usually multiple, bright, well-circumscribed intramural or intracavitary masses in the ventricles that can obstruct inflow or outflow or cause arrhythmia, and most regress spontaneously in the first years of life. Fibroma is the second most common pediatric tumor; it is typically a solitary, large, intramural mass in the septum or free wall, often calcified, and does not regress."
}
],
"numbers": [
{
"label": "Sarcoma share of primary cardiac tumors",
"value": "~ 25",
"unit": "%"
}
],
"delta": null,
"pearl": "Adult primary malignancy: angiosarcoma in the right atrium. Child benign tumor: rhabdomyoma with tuberous sclerosis.",
"lookalike": {
"vs": "myxoma",
"discriminator": "Myxoma is pedunculated from the left atrial septum with a narrow stalk; sarcoma is broad-based and infiltrative, commonly right-sided with pericardial involvement."
},
"related": [
"Q167",
"Q330"
],
"reviewed": "2026-08-26"
},
{
"id": "Q170",
"orig": 170,
"title": "Separating masses from artifacts",
"lesions": [
"MASS",
"INSTRUMENTATION"
],
"lens": "procedure",
"items": [
{
"id": "Q170.1",
"q": "Which technical steps help distinguish a true intracardiac mass from an imaging artifact?",
"a": "Artifacts depend on the physics of the beam, so changing the physics makes them move or disappear while a real structure stays put. Lower the overall gain and adjust time gain compensation, because near-field clutter and noise fade while tissue persists. Image the finding from at least two independent windows; a true mass keeps the same location and attachment, whereas reverberation and side-lobe artifacts fail to reproduce. Change the depth and focal zone, which shifts range-related artifacts, and switch to a higher-frequency transducer or harmonic imaging to improve resolution. Ultrasound enhancing agent outlines a real mass as a filling defect and helps with the apex and right-sided structures. Finally, a real mass moves with the wall or valve it is attached to throughout the cardiac cycle."
}
],
"numbers": [
{
"label": "Minimum views to confirm a mass",
"value": "2",
"unit": "views"
}
],
"delta": null,
"pearl": "Change the physics: if it survives gain, depth, frequency, and a second window, it is real.",
"lookalike": {
"vs": "reverberation or side-lobe artifact",
"discriminator": "Artifacts cross anatomic boundaries, sit at multiples of a strong reflector's depth, and vanish when the window or depth changes; masses have defined borders and consistent attachment across views."
},
"related": [
"Q161",
"Q167",
"Q171",
"Q320",
"Q328",
"Q331"
],
"reviewed": "2026-08-26"
},
{
"id": "Q171",
"orig": 171,
"title": "Mass in the inferior vena cava",
"lesions": [
"MASS"
],
"lens": "pitfall",
"items": [
{
"id": "Q171.1",
"q": "A mobile mass is seen in the inferior vena cava extending into the right atrium. What diagnosis must you consider?",
"a": "A mass rising up the IVC into the right atrium should be considered tumor extension from renal cell carcinoma until proved otherwise, because this tumor characteristically grows along the renal vein into the cava and sometimes into the heart. Hepatocellular carcinoma and adrenal tumors can do the same. Bland thrombus from deep venous disease or a central line is the main alternative, and the two cannot be reliably separated by echo alone, so abdominal imaging and a search for a primary are required. Identifying caval extension is important because it changes the surgical approach and may require cardiopulmonary bypass."
}
],
"numbers": [],
"delta": null,
"pearl": "A mass climbing the IVC came from below: image the kidneys.",
"lookalike": {
"vs": "IVC thrombus",
"discriminator": "Thrombus is usually homogeneous and associated with venous stasis, a catheter, or DVT; tumor thrombus is often heterogeneous, continuous with a renal mass on abdominal imaging, and may show internal flow on Doppler."
},
"related": [
"Q167",
"Q170",
"Q330"
],
"reviewed": "2026-08-26"
},
{
"id": "Q172",
"orig": 172,
"title": "Atrial fibrillation on echo",
"lesions": [
"ARRHYTHMIA"
],
"lens": "m-mode",
"items": [
{
"id": "Q172.1",
"q": "What does M-mode imaging of the mitral valve show in atrial fibrillation?",
"a": "Without organized atrial contraction there is no late diastolic push of blood, so the mitral A wave (the second opening peak) disappears from the M-mode trace and the Doppler inflow. Instead, chaotic atrial activity produces fine fibrillatory undulations of the leaflets during diastole, most evident on the anterior leaflet. The diastolic intervals vary from beat to beat because the ventricular response is irregular, so the length of the leaflet-open period changes continuously. Doppler shows E waves only, with variable velocity, and any measurement should be averaged over several beats."
},
{
"id": "Q172.2",
"q": "How does atrial fibrillation affect the left ventricle on two-dimensional imaging?",
"a": "The changes are subtler than on M-mode. Because diastolic filling time varies with each beat, end-diastolic volume and therefore stroke volume fluctuate, and beats after a long pause eject more forcefully than those following a short interval; this is the Frank-Starling effect combined with postextrasystolic potentiation. Ejection fraction and Doppler indices should be averaged over at least five beats, or measured on beats with similar preceding intervals, to avoid misrepresenting function. Left atrial enlargement is common and may be cause or consequence."
}
],
"numbers": [
{
"label": "Beats to average in AF",
"value": "≥ 5",
"unit": "beats"
}
],
"delta": null,
"pearl": "No A wave, irregular filling, and fluttering leaflets: AF on M-mode.",
"lookalike": {
"vs": "atrial flutter",
"discriminator": "Flutter produces regular, rapid leaflet undulations at a fixed rate (about 300/min) with an often regular ventricular response; fibrillation produces irregular fine undulations and irregular RR intervals."
},
"related": [
"Q174",
"Q175",
"Q367"
],
"reviewed": "2026-08-26"
},
{
"id": "Q173",
"orig": 173,
"title": "Preexcitation on M-mode",
"lesions": [
"ARRHYTHMIA"
],
"lens": "m-mode",
"items": [
{
"id": "Q173.1",
"q": "How does Wolff-Parkinson-White syndrome alter wall motion on M-mode?",
"a": "An accessory pathway depolarizes part of the ventricle before the normal conduction system does, so the preexcited region contracts early and the M-mode trace shows an early systolic notch or abnormal motion at that site. With a left-sided (classically type A) pathway, the posterior left ventricular wall shows early systolic contraction or notching; with a right-sided (type B) pathway, the septum moves abnormally with early posterior motion, resembling a conduction delay pattern. The findings are subtle and vary with the pathway location and the degree of preexcitation, and modern practice localizes pathways with the ECG delta-wave vector and electrophysiology rather than M-mode."
}
],
"numbers": [],
"delta": null,
"pearl": "Early activation means early contraction: the notch sits where the pathway is.",
"lookalike": {
"vs": "left bundle branch block",
"discriminator": "LBBB produces early systolic septal beaking without a delta wave; WPW shows a short PR and delta wave on ECG and the notch localizes to the preexcited wall."
},
"related": [
"Q175"
],
"reviewed": "2026-08-26"
},
{
"id": "Q174",
"orig": 174,
"title": "PVCs and flutter on Doppler and M-mode",
"lesions": [
"ARRHYTHMIA",
"HEMODYNAMICS"
],
"lens": "doppler",
"items": [
{
"id": "Q174.1",
"q": "How do premature ventricular contractions alter the aortic Doppler spectral trace?",
"a": "A premature beat interrupts diastole early, so the ventricle has had little time to fill and ejects a small stroke volume: the aortic envelope for that beat is short and low in velocity, or absent if the aortic valve never opens. The compensatory pause that follows allows prolonged filling, and the next sinus beat ejects a larger volume through the Frank-Starling mechanism plus postextrasystolic potentiation, producing a taller, longer envelope. Neither the premature beat nor the beat after it represents steady state, so exclude both from velocity and gradient measurements and use beats with normal preceding intervals."
},
{
"id": "Q174.2",
"q": "What does atrial flutter look like on M-mode of the mitral valve?",
"a": "In flutter the atria contract regularly at roughly 250 to 350 times per minute, and each contraction nudges the mitral leaflets, so the M-mode shows rapid, regular, sawtooth-like undulations of the leaflets during diastole. These correspond one to one with the flutter waves on the ECG, distinguishing flutter from the irregular fine fibrillatory motion of atrial fibrillation. The ventricular response is often a fixed ratio, so RR intervals are more regular than in fibrillation."
}
],
"numbers": [
{
"label": "Atrial flutter rate",
"value": "250–350",
"unit": "beats/min"
}
],
"delta": null,
"pearl": "Measure neither the PVC nor the beat after it; both lie about stroke volume.",
"lookalike": {
"vs": "atrial fibrillation on M-mode",
"discriminator": "Flutter undulations are regular and rapid with a fixed rate; fibrillatory undulations are irregular and fine with irregular RR intervals."
},
"related": [
"Q172",
"Q175"
],
"reviewed": "2026-08-26"
},
{
"id": "Q175",
"orig": 175,
"title": "M-mode for conduction disturbances",
"lesions": [
"ARRHYTHMIA"
],
"lens": "best-method",
"items": [
{
"id": "Q175.1",
"q": "For timing subtle motion changes caused by arrhythmias and conduction disturbances, is M-mode or two-dimensional imaging preferred, and why?",
"a": "M-mode is preferred. It samples a single scan line at a very high rate, on the order of 1000 to 2000 lines per second, whereas 2D imaging builds a whole sector at typically 30 to 90 frames per second. Brief events such as an early systolic septal notch, fibrillatory leaflet undulations, or a delayed valve closure last only tens of milliseconds and are blurred or missed at 2D frame rates but resolved by M-mode. Color-guided M-mode and tissue Doppler extend the same temporal advantage to timing flow and wall velocities."
},
{
"id": "Q175.2",
"q": "What are the typical M-mode findings in bundle branch block?",
"a": "Bundle branch block alters the sequence of septal activation, so the abnormal motion is confined to the interventricular septum. In left bundle branch block the septum is activated late from the right side, producing an early systolic posterior beak or notch followed by paradoxical anterior motion later in systole, and on 2D this appears as septal flash. In right bundle branch block the septum still depolarizes normally from left to right, so septal motion on M-mode is essentially normal. Recognizing the LBBB pattern matters because it can mimic ischemic septal dyskinesis and confounds wall motion scoring."
}
],
"numbers": [
{
"label": "M-mode sampling rate",
"value": "1000–2000",
"unit": "lines/s"
},
{
"label": "Typical 2D frame rate",
"value": "30–90",
"unit": "frames/s"
}
],
"delta": null,
"pearl": "Time resolves with M-mode; LBBB beaks the septum, RBBB leaves it alone.",
"lookalike": {
"vs": "ischemic septal dyskinesis",
"discriminator": "LBBB septal motion is early and brief with preserved systolic thickening and a wide QRS; ischemic dyskinesis persists through systole with reduced thickening."
},
"related": [
"Q172",
"Q173",
"Q174"
],
"reviewed": "2026-08-26"
},
{
"id": "Q176",
"orig": 176,
"title": "Most common congenital lesions",
"lesions": [
"VSD",
"CONGENITAL"
],
"lens": "etiology",
"items": [
{
"id": "Q176.1",
"q": "What is the most common congenital heart defect?",
"a": "Ventricular septal defect is the most common congenital heart defect diagnosed at birth, making up roughly 20 to 30 percent of all congenital lesions, with the perimembranous type accounting for about 80 percent of VSDs. Bicuspid aortic valve is actually more prevalent, affecting about 1 to 2 percent of the population, but it is usually silent for decades and is often excluded from defect statistics or counted separately as a valve anomaly; it matters later because of stenosis, regurgitation, and aortopathy. Many small muscular VSDs close spontaneously in childhood."
},
{
"id": "Q176.2",
"q": "Which cyanotic congenital lesion is most prevalent?",
"a": "Tetralogy of Fallot is the most common cyanotic lesion overall, combining a large malalignment VSD, right ventricular outflow obstruction, an overriding aorta, and right ventricular hypertrophy; cyanosis results from right-to-left shunting across the VSD when outflow obstruction is severe. In the newborn period, transposition of the great arteries is the most common lesion presenting with cyanosis, because the parallel circulations produce cyanosis immediately."
}
],
"numbers": [
{
"label": "VSD share of congenital defects",
"value": "20–30",
"unit": "%"
},
{
"label": "Perimembranous share of VSDs",
"value": "≈ 80",
"unit": "%"
},
{
"label": "Bicuspid aortic valve prevalence",
"value": "1–2",
"unit": "%"
}
],
"delta": null,
"pearl": "Most common defect: VSD. Most common cyanotic: tetralogy. Most common valve anomaly: bicuspid aortic valve.",
"lookalike": null,
"related": [
"Q177",
"Q178",
"Q179",
"Q390"
],
"reviewed": "2026-08-26"
},
{
"id": "Q177",
"orig": 177,
"title": "Atrioventricular septal defect anatomy",
"lesions": [
"ASD",
"VSD",
"CONGENITAL"
],
"lens": "anatomy",
"items": [
{
"id": "Q177.1",
"q": "Which structural components can be involved in an atrioventricular septal defect?",
"a": "AV septal defects arise from failed endocardial cushion fusion, so the abnormalities cluster at the center of the heart. A complete defect has an ostium primum atrial septal defect, an inlet ventricular septal defect, and a single common atrioventricular valve; a partial defect has the primum ASD with a cleft in the anterior mitral leaflet and two separate valve orifices. In all forms the left and right AV valves insert at the same level on the septum, losing the normal apical offset of the tricuspid valve, and the left ventricular outflow tract is elongated ('gooseneck'). Echo should define the ASD, any VSD, the number of valve orifices, cleft-related regurgitation, and ventricular balance."
},
{
"id": "Q177.2",
"q": "Which patients are at particularly high risk for an atrioventricular septal defect?",
"a": "Children with Down syndrome (trisomy 21): roughly 40 percent have congenital heart disease, and AV septal defect, usually the complete form, is the most common lesion in this group. Conversely, a substantial share of patients with complete AVSD have trisomy 21. Heterotaxy syndromes are another association."
}
],
"numbers": [
{
"label": "Congenital heart disease in Down syndrome",
"value": "~ 40",
"unit": "%"
}
],
"delta": null,
"pearl": "Same-level AV valves in a four-chamber view: think endocardial cushion defect and check for trisomy 21.",
"lookalike": {
"vs": "secundum ASD",
"discriminator": "Primum defects abut the AV valves with loss of tricuspid offset and a cleft mitral leaflet; secundum defects sit mid-septum at the fossa ovalis with normal valves."
},
"related": [
"Q176",
"Q179",
"Q387"
],
"reviewed": "2026-08-26"
},
{
"id": "Q178",
"orig": 178,
"title": "Congenital lesion associations",
"lesions": [
"PS",
"COARCT",
"CONGENITAL"
],
"lens": "etiology",
"items": [
{
"id": "Q178.1",
"q": "Which congenital lesion commonly accompanies pulmonic stenosis?",
"a": "Ventricular septal defect is the usual companion, most conspicuously in tetralogy of Fallot, where infundibular and valvar pulmonic stenosis coexist with a large malalignment VSD. Isolated valvar pulmonic stenosis also occurs and is associated with Noonan syndrome, in which the valve is dysplastic and thick. When you find a VSD, interrogate the right ventricular outflow tract with color and continuous-wave Doppler, and when you find pulmonic stenosis, look for a septal defect."
},
{
"id": "Q178.2",
"q": "Which congenital lesion commonly accompanies a bicuspid aortic valve?",
"a": "Coarctation of the aorta: roughly half of patients with coarctation have a bicuspid aortic valve, and both are part of a broader left-sided obstructive spectrum that also includes aortic arch hypoplasia and ascending aortopathy. The association is also seen in Turner syndrome. Every bicuspid valve study should therefore include suprasternal imaging of the arch and descending aorta with Doppler, looking for a gradient with diastolic run-off, and every coarctation study should count aortic cusps in the short axis."
}
],
"numbers": [
{
"label": "Bicuspid valve among coarctation patients",
"value": "~ 50",
"unit": "%"
}
],
"delta": null,
"pearl": "PS travels with VSD; bicuspid travels with coarctation. Find one, hunt for the other.",
"lookalike": null,
"related": [
"Q176",
"Q235",
"Q303",
"Q361"
],
"reviewed": "2026-08-26"
},
{
"id": "Q179",
"orig": 179,
"title": "Four types of atrial septal defect",
"lesions": [
"ASD",
"CONGENITAL"
],
"lens": "anatomy",
"items": [
{
"id": "Q179.1",
"q": "Name and describe the four main types of atrial septal defect.",
"a": "Secundum defects, about 75 percent, lie in the central septum at the fossa ovalis from a deficient septum primum flap or an oversized foramen ovale; they are the type suitable for device closure. Primum defects, about 15 to 20 percent, occupy the lowest part of the septum adjacent to the AV valves, represent the partial form of AV septal defect, and are accompanied by a cleft mitral leaflet. Sinus venosus defects, 5 to 10 percent, sit high near the superior vena cava entry (rarely low near the IVC) and are nearly always paired with partial anomalous pulmonary venous return of the right upper pulmonary vein; they are easily missed transthoracically and often need TEE. Coronary sinus defects, under 1 percent, are an unroofed coronary sinus that lets it communicate with the left atrium, often with a persistent left superior vena cava."
}
],
"numbers": [
{
"label": "Secundum ASD",
"value": "~ 75",
"unit": "%"
},
{
"label": "Primum ASD",
"value": "15–20",
"unit": "%"
},
{
"label": "Sinus venosus ASD",
"value": "5–10",
"unit": "%"
},
{
"label": "Coronary sinus ASD",
"value": "< 1",
"unit": "%"
}
],
"delta": {
"was": "2011 card gave secundum 70%, primum 20%, sinus venosus 8%, coronary sinus 2%.",
"now": "Current teaching: secundum ~75%, primum 15–20%, sinus venosus 5–10%, coronary sinus <1%.",
"source": "REWRITE_SPEC anchor for ASD distribution (ASE congenital guidance)"
},
"pearl": "Middle, bottom, top, back: secundum, primum, sinus venosus, coronary sinus.",
"lookalike": {
"vs": "septal dropout artifact",
"discriminator": "Apical four-chamber dropout at the thin fossa ovalis has no color jet and disappears in the subcostal view; a true defect shows a color flow jet and T-shaped bright edges."
},
"related": [
"Q177",
"Q180",
"Q176",
"Q387"
],
"reviewed": "2026-08-26"
},
{
"id": "Q180",
"orig": 180,
"title": "Direction and detection of ASD flow",
"lesions": [
"ASD",
"HEMODYNAMICS"
],
"lens": "doppler",
"items": [
{
"id": "Q180.1",
"q": "In which direction does blood usually flow across an atrial septal defect, and why?",
"a": "Flow is predominantly left to right. The atria are low-pressure chambers, and the direction is set less by pressure than by relative ventricular compliance: the thin-walled right ventricle fills more easily than the left, so blood preferentially crosses to the right during diastole. A brief right-to-left component occurs normally in early systole and with the onset of inspiration. Sustained reversal to right-to-left flow implies that the right ventricle has become stiff or that pulmonary hypertension has developed (Eisenmenger physiology), which changes management."
},
{
"id": "Q180.2",
"q": "Which view is best for demonstrating shunt flow across an atrial septal defect with color Doppler?",
"a": "The subcostal four-chamber (or subcostal bicaval) view, because there the ultrasound beam strikes the atrial septum perpendicularly for imaging while the shunt flow runs nearly parallel to the beam, maximizing Doppler sensitivity. The apical four-chamber view is poor for this purpose since the beam is parallel to the thin septum, causing dropout that mimics a defect, and the shunt runs perpendicular to the beam so its Doppler signal is weak. Lower the color scale to catch the low-velocity shunt, and use agitated saline if the color study is equivocal."
}
],
"numbers": [],
"delta": null,
"pearl": "For the atrial septum go subcostal: perpendicular to the septum, parallel to the shunt.",
"lookalike": {
"vs": "apical dropout of the fossa ovalis",
"discriminator": "Dropout shows no color jet and vanishes subcostally; a real ASD shows a low-velocity left-to-right color jet in the subcostal view."
},
"related": [
"Q179"
],
"reviewed": "2026-08-26"
},
{
"id": "Q181",
"orig": 181,
"title": "Bubble study and ASD chamber effects",
"lesions": [
"ASD",
"CONTRAST"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q181.1",
"q": "An ASD shunts predominantly left-to-right. Why does an agitated-saline bubble study still detect it?",
"a": "Atrial pressures are nearly equal and cross over briefly during the cardiac cycle, so even a predominantly left-to-right ASD leaks a few bubbles right-to-left, typically in late diastole or with early ventricular contraction. Those bubbles show up in the left atrium within the first three beats of right-heart opacification, which is the hallmark of an intracardiac (rather than pulmonary) shunt. If a resting injection is negative, repeat it timed to the release of a Valsalva strain: venous return surges into the right atrium at release, transiently raising right atrial pressure above left and pushing contrast across the defect. Color Doppler across the septum in the subcostal view is a useful companion because it displays the dominant left-to-right jet that bubbles cannot show."
},
{
"id": "Q181.2",
"q": "What does an atrial septal defect do to the cardiac chambers?",
"a": "The extra left-to-right flow returns to the right atrium, so the right atrium and right ventricle dilate from chronic volume overload and pulmonary blood flow rises in proportion to the shunt. In the parasternal short-axis view the septum flattens in diastole (D-shaped LV), the classic sign of RV volume overload, and paradoxical septal motion appears on M-mode. The left ventricle is usually normal in size because the shunted blood bypasses it. With a long-standing large shunt, pulmonary hypertension can develop and the septum then flattens in systole as well."
}
],
"numbers": [
{
"label": "Bubble arrival in LA for intracardiac shunt",
"value": "≤ 3",
"unit": "beats"
}
],
"delta": null,
"pearl": "Negative bubble study? Inject again and have the patient release a Valsalva as the bubbles reach the RA.",
"lookalike": {
"vs": "pulmonary AV malformation",
"discriminator": "Intracardiac shunt bubbles reach the LA within 3 beats; a pulmonary shunt delivers them late (after 3–5 beats) via the pulmonary veins."
},
"related": [
"Q183",
"Q185",
"Q186",
"Q187",
"Q387",
"Q389"
],
"reviewed": "2026-08-26"
},
{
"id": "Q182",
"orig": 182,
"title": "Persistent left SVC",
"lesions": [
"PLSVC",
"ANATOMY"
],
"lens": "definition",
"items": [
{
"id": "Q182.1",
"q": "What is a persistent left superior vena cava?",
"a": "A persistent left superior vena cava is the most common thoracic venous anomaly, present in roughly 0.3–0.5% of the population, and results from failure of the left anterior cardinal vein to regress in fetal life. Blood from the left arm and left side of the head drains through this vessel, which runs down beside the left atrium and, in about 90% of cases, empties into the coronary sinus and then the right atrium. Because the venous blood still reaches the right atrium, the anomaly is hemodynamically silent by itself. It matters for line and pacemaker placement and can coexist with other congenital lesions, and rarely it drains directly into the left atrium, producing a right-to-left shunt."
}
],
"numbers": [
{
"label": "Prevalence of PLSVC in general population",
"value": "0.3–0.5",
"unit": "%"
},
{
"label": "PLSVC draining to coronary sinus",
"value": "~90",
"unit": "%"
}
],
"delta": null,
"pearl": "Left arm blood taking the scenic route through the coronary sinus.",
"lookalike": null,
"related": [
"Q183"
],
"reviewed": "2026-08-26"
},
{
"id": "Q183",
"orig": 183,
"title": "Dilated coronary sinus workup",
"lesions": [
"PLSVC",
"CONTRAST"
],
"lens": "2d",
"items": [
{
"id": "Q183.1",
"q": "What is the characteristic 2D finding of a persistent left SVC?",
"a": "A dilated coronary sinus is the clue, seen in the parasternal long-axis view as an enlarged circular echo-free space in the posterior atrioventricular groove behind the left atrium, just above the posterior mitral annulus. The sinus enlarges because it now carries the entire left-sided venous return in addition to coronary venous blood. A coronary sinus wider than about 1 cm should prompt a search for the vessel itself, which can be traced in a modified apical view or the suprasternal window. Other causes of a big coronary sinus, such as elevated right atrial pressure or anomalous pulmonary venous return to the sinus, need to be excluded."
},
{
"id": "Q183.2",
"q": "How do you confirm a persistent left SVC on echo?",
"a": "Inject agitated saline into a left arm vein while imaging the coronary sinus in the parasternal long-axis or apical view. With a persistent left SVC the bubbles opacify the coronary sinus first and only afterward appear in the right atrium and right ventricle. A right arm injection produces the normal sequence, right atrium first with the coronary sinus staying clear, so comparing the two injections proves the diagnosis. If bubbles enter the left atrium directly, the vessel drains to the left atrium, which is a right-to-left shunt."
}
],
"numbers": [
{
"label": "Coronary sinus diameter that is abnormal",
"value": "> 1",
"unit": "cm"
}
],
"delta": null,
"pearl": "Bubbles from the LEFT arm light up the coronary sinus BEFORE the RA.",
"lookalike": {
"vs": "descending thoracic aorta",
"discriminator": "The aorta lies posterior to the pericardium and does not move with the AV groove; the coronary sinus sits inside the pericardium in the AV groove and opacifies with left-arm saline."
},
"related": [
"Q182",
"Q181"
],
"reviewed": "2026-08-26"
},
{
"id": "Q184",
"orig": 184,
"title": "VSD types by location",
"lesions": [
"VSD",
"ANATOMY"
],
"lens": "anatomy",
"items": [
{
"id": "Q184.1",
"q": "Describe the main anatomic types of ventricular septal defect.",
"a": "Ventricular septal defects are classified by which part of the septum they occupy. Perimembranous defects sit in the thin membranous septum just beneath the aortic valve and adjacent to the septal tricuspid leaflet, and account for about 80% of VSDs. Muscular defects lie entirely within the trabecular muscular septum, often toward the apex, and can be multiple. Inlet defects occupy the posterior septum beneath the tricuspid valve and are typical of atrioventricular septal defects, while outlet (supracristal, subarterial) defects lie in the RV outflow tract under the pulmonary and aortic valves and may allow the right coronary cusp to prolapse into the hole, causing aortic regurgitation. Each type has a preferred imaging plane: parasternal short axis at the aortic level for perimembranous (near 10 o'clock) and outlet defects (near 1 o'clock), and apical or subcostal four-chamber for inlet and muscular defects."
}
],
"numbers": [
{
"label": "Perimembranous share of VSDs",
"value": "≈ 80",
"unit": "%"
}
],
"delta": {
"was": "2011 card taught perimembranous defects make up 75% of VSDs.",
"now": "Current teaching: perimembranous defects account for roughly 80% of ventricular septal defects.",
"source": "ASE 2015 chamber quant / current congenital echo teaching"
},
"pearl": "Short-axis clock face: perimembranous around 10 o'clock, supracristal near 1 o'clock.",
"lookalike": null,
"related": [
"Q185",
"Q186",
"Q187"
],
"reviewed": "2026-08-26"
},
{
"id": "Q185",
"orig": 185,
"title": "Finding a VSD: Doppler vs bubbles",
"lesions": [
"VSD",
"DOPPLER_PHYSICS"
],
"lens": "best-method",
"items": [
{
"id": "Q185.1",
"q": "Doppler or contrast echo: which is the better tool for detecting a ventricular septal defect, and why?",
"a": "Doppler wins. Because LV systolic pressure far exceeds RV pressure, flow through a VSD is almost entirely left-to-right, so agitated saline injected into a vein rarely crosses into the left ventricle and a bubble study is usually negative; at most you may see a negative-contrast washout in the RV. Color Doppler, by contrast, displays the high-velocity turbulent left-to-right jet entering the RV, which localizes even small defects, and pulsed Doppler confirms the timing. Continuous-wave Doppler across the defect then gives the peak systolic velocity, and 4v² converts it to the interventricular gradient, which is what you need to estimate RV pressure and judge whether the defect is restrictive."
}
],
"numbers": [
{
"label": "Bernoulli constant",
"value": "4",
"unit": "× v²"
}
],
"delta": null,
"pearl": "Bubbles need right-to-left flow; a VSD is left-to-right, so use color and CW instead.",
"lookalike": null,
"related": [
"Q181",
"Q196",
"Q184",
"Q186"
],
"reviewed": "2026-08-26"
},
{
"id": "Q186",
"orig": 186,
"title": "VSD flow direction and Eisenmenger",
"lesions": [
"VSD",
"PH"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q186.1",
"q": "In what direction does blood normally cross a ventricular septal defect?",
"a": "Left-to-right. The LV generates roughly 120 mmHg in systole while the RV generates about 25 mmHg, so during systole blood is driven through the defect into the right ventricle and on into the pulmonary circulation. A restrictive VSD maintains a large gradient with a high-velocity jet (often above 4 m/s), whereas a large unrestrictive defect equalizes pressures and produces a low-velocity, laminar bidirectional flow. Brief right-to-left flow can occur in early diastole or isovolumic periods even with a normal RV, which is why timing the jet with pulsed Doppler matters."
},
{
"id": "Q186.2",
"q": "Explain the physiology of Eisenmenger syndrome.",
"a": "A long-standing large left-to-right shunt (VSD, ASD, or PDA) floods the pulmonary bed with excess flow and, for post-tricuspid shunts, transmits systemic pressure into the pulmonary arteries. Over years the pulmonary arterioles remodel, pulmonary vascular resistance climbs, and pulmonary artery pressure eventually reaches or exceeds systemic pressure. At that point the shunt reverses and becomes right-to-left, deoxygenated blood enters the systemic circulation, and the patient becomes cyanotic. On echo you see a hypertrophied RV, systolic septal flattening, a low-velocity bidirectional or right-to-left jet across the defect, and a TR velocity consistent with high-probability pulmonary hypertension; a bubble study at this stage becomes positive."
}
],
"numbers": [
{
"label": "Normal LV systolic pressure",
"value": "120",
"unit": "mmHg"
},
{
"label": "Normal RV systolic pressure",
"value": "25",
"unit": "mmHg"
},
{
"label": "TR Vmax high probability of PH",
"value": "> 3.4",
"unit": "m/s"
}
],
"delta": null,
"pearl": "Low-velocity VSD jet is the worrisome one: no gradient means the RV pressure is near systemic.",
"lookalike": null,
"related": [
"Q187",
"Q196",
"Q185",
"Q181",
"Q184",
"Q389"
],
"reviewed": "2026-08-26"
},
{
"id": "Q187",
"orig": 187,
"title": "Chamber effects of a VSD",
"lesions": [
"VSD",
"HEMODYNAMICS"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q187.1",
"q": "How does a ventricular septal defect affect the cardiac chambers?",
"a": "A small restrictive VSD carries little flow and leaves chamber sizes normal; its only echo marker is the high-velocity jet. A moderate or large defect delivers extra volume to the pulmonary circulation, and that blood returns through the pulmonary veins, so the chambers that actually dilate are the left atrium and left ventricle, which handle the increased pulmonary venous return. The right ventricle receives the shunt during systole and ejects it immediately, so it dilates less than in an ASD, but it hypertrophies as pulmonary pressure rises with a nonrestrictive defect. Once pulmonary hypertension supervenes, RV pressure overload with systolic septal flattening dominates the picture."
}
],
"numbers": [],
"delta": null,
"pearl": "ASD dilates the right heart; VSD (and PDA) dilate the left heart, because the shunt returns through the lungs.",
"lookalike": {
"vs": "ASD volume overload",
"discriminator": "ASD: RA/RV dilation with diastolic septal flattening. VSD: LA/LV dilation with a normal-size RV until PH develops."
},
"related": [
"Q181",
"Q186",
"Q184",
"Q188"
],
"reviewed": "2026-08-26"
},
{
"id": "Q188",
"orig": 188,
"title": "Patent ductus arteriosus",
"lesions": [
"PDA",
"AORTA"
],
"lens": "best-method",
"items": [
{
"id": "Q188.1",
"q": "What is a patent ductus arteriosus?",
"a": "The ductus arteriosus is a fetal vessel connecting the proximal descending aorta, just beyond the left subclavian origin, to the main pulmonary artery near the left pulmonary artery. In utero it diverts right ventricular output away from the fluid-filled lungs into the aorta. It normally constricts within the first days of life as oxygen tension rises and prostaglandin levels fall; when it stays open it is called a patent ductus, and flow now runs from the high-pressure aorta into the pulmonary artery throughout the cardiac cycle. A significant PDA volume-loads the pulmonary circulation and therefore the left atrium and left ventricle."
},
{
"id": "Q188.2",
"q": "Which view and Doppler technique best show a PDA?",
"a": "The parasternal short-axis view at the aortic valve level, angled to open the pulmonary artery bifurcation, is the standard window; the ductus enters the main PA at its distal end near the left PA. Color Doppler is the key technique: it shows a continuous, turbulent left-to-right jet entering the main PA and running back toward the pulmonary valve, with flow persisting in diastole because aortic diastolic pressure still exceeds PA pressure. Continuous-wave Doppler of the jet gives a continuous systolic-diastolic signal; the peak systolic gradient subtracted from systolic blood pressure estimates PA systolic pressure. A suprasternal or high left parasternal ductal view can display the vessel directly."
}
],
"numbers": [],
"delta": null,
"pearl": "Continuous color jet in the main PA that never stops in diastole: think PDA.",
"lookalike": {
"vs": "pulmonary regurgitation",
"discriminator": "PR is a diastolic-only jet pointed from the valve into the RV; a PDA jet is continuous and travels from the distal PA back toward the valve."
},
"related": [
"Q187",
"Q189",
"Q193",
"Q305",
"Q307"
],
"reviewed": "2026-08-26"
},
{
"id": "Q189",
"orig": 189,
"title": "Coarctation site and severity",
"lesions": [
"COARCT",
"AORTA"
],
"lens": "doppler",
"items": [
{
"id": "Q189.1",
"q": "Where in the aorta does coarctation usually occur?",
"a": "Coarctation is a discrete narrowing of the aortic isthmus, the short segment between the origin of the left subclavian artery and the insertion of the ductus arteriosus. Ductal tissue extending into the aortic wall is thought to constrict at this site after birth, which explains the typical juxtaductal location. It is frequently accompanied by a bicuspid aortic valve, so any coarctation should trigger a careful look at the aortic valve, and vice versa. Less common variants involve the arch or the abdominal aorta."
},
{
"id": "Q189.2",
"q": "How is the severity of a coarctation quantified with echo?",
"a": "From the suprasternal notch, align continuous-wave Doppler with the descending aorta and record the peak velocity across the narrowing; 4v² gives the peak instantaneous gradient. Because flow proximal to the coarctation is often already accelerated, subtract the proximal velocity using the expanded Bernoulli equation (4[v2² − v1²]) to avoid overestimating. The most telling qualitative sign is persistent forward flow into diastole, the so-called diastolic runoff or sawtooth profile, which indicates a hemodynamically significant obstruction. Pulsed Doppler in the abdominal aorta from the subcostal window shows a dampened, delayed, low-pulsatility waveform, and 2D imaging of the arch shows the shelf-like narrowing with post-stenotic dilation."
}
],
"numbers": [
{
"label": "Bernoulli constant",
"value": "4",
"unit": "× v²"
}
],
"delta": null,
"pearl": "Diastolic runoff across the isthmus means the obstruction is significant, regardless of the exact gradient.",
"lookalike": {
"vs": "pseudocoarctation (kinked arch)",
"discriminator": "A kinked but unobstructed isthmus has no gradient and no diastolic runoff; the abdominal aortic Doppler remains pulsatile."
},
"related": [
"Q188",
"Q196",
"Q272",
"Q303",
"Q304",
"Q305",
"Q306",
"Q307",
"Q308",
"Q309",
"Q310"
],
"reviewed": "2026-08-26"
},
{
"id": "Q190",
"orig": 190,
"title": "Ebstein anomaly basics",
"lesions": [
"EBSTEIN",
"TR"
],
"lens": "definition",
"items": [
{
"id": "Q190.1",
"q": "What is Ebstein anomaly?",
"a": "Ebstein anomaly is a congenital malformation of the tricuspid valve in which the septal and posterior leaflets fail to delaminate from the RV wall and are displaced apically, while the anterior leaflet is typically large and sail-like. The annulus itself stays in its normal position, so the portion of the RV between the true annulus and the displaced leaflet hinge point becomes thin-walled and functionally part of the right atrium, an atrialized RV. The residual functional RV is small, and the malformed valve nearly always leaks, so moderate-to-severe tricuspid regurgitation with a large right atrium is the usual picture. Severity ranges from incidental to profound depending on the displacement and how much RV is left."
},
{
"id": "Q190.2",
"q": "Which congenital lesion commonly accompanies Ebstein anomaly?",
"a": "An interatrial communication, either a secundum ASD or a patent foramen ovale, is present in most patients. Because right atrial pressure is elevated by the massive TR and the small functional RV, the shunt frequently runs right-to-left, producing cyanosis and a positive bubble study. Other associations include pulmonary stenosis or atresia and, in the electrical domain, accessory pathways."
}
],
"numbers": [],
"delta": null,
"pearl": "Ebstein = leaflets slide toward the apex, annulus stays put, RV gets 'atrialized'.",
"lookalike": null,
"related": [
"Q191",
"Q311",
"Q312",
"Q313",
"Q314",
"Q315",
"Q316",
"Q317",
"Q386"
],
"reviewed": "2026-08-26"
},
{
"id": "Q191",
"orig": 191,
"title": "Imaging Ebstein anomaly",
"lesions": [
"EBSTEIN",
"ARRHYTHMIA"
],
"lens": "2d",
"items": [
{
"id": "Q191.1",
"q": "Which views are most useful for Ebstein anomaly, and what measurement makes the diagnosis?",
"a": "The apical four-chamber view is the workhorse, with the subcostal four-chamber view as a good alternative in children, because both display the mitral and tricuspid septal leaflet insertions side by side. Measure the distance from the septal mitral leaflet hinge point to the septal tricuspid leaflet hinge point; normal offset is small. Apical displacement of at least 8 mm/m² of body surface area, which works out to about 20 mm or more in an adult, is the accepted diagnostic threshold. The same view demonstrates the atrialized RV, the elongated anterior leaflet, right atrial enlargement, and the tethering that produces the regurgitant jet."
},
{
"id": "Q191.2",
"q": "What conduction abnormality is linked to Ebstein anomaly?",
"a": "Wolff-Parkinson-White syndrome is far more common in Ebstein patients than in the general population, and the accessory pathway is almost always right-sided, running along the malformed tricuspid annulus where the fibrous insulation between atrium and ventricle is deficient. Multiple pathways are frequent. The resulting AV reentrant tachycardias and atrial arrhythmias contribute substantially to symptoms, and the ECG typically also shows right bundle branch block and tall broad P waves."
}
],
"numbers": [
{
"label": "Ebstein septal leaflet displacement threshold (indexed)",
"value": "≥ 8",
"unit": "mm/m²"
},
{
"label": "Ebstein displacement threshold (adult)",
"value": "≥ 20",
"unit": "mm"
}
],
"delta": {
"was": "2011 card taught that a mitral-tricuspid leaflet insertion offset of more than 8 mm indicates tricuspid leaflet malposition.",
"now": "Current criterion: apical displacement of the septal tricuspid leaflet ≥ 8 mm/m² of body surface area (roughly ≥ 20 mm in an adult) relative to the mitral annulus.",
"source": "ASE 2015 chamber quant"
},
"pearl": "8 per square meter, 20 in an adult: the Ebstein offset numbers.",
"lookalike": null,
"related": [
"Q190",
"Q313",
"Q314",
"Q315",
"Q316",
"Q317",
"Q386"
],
"reviewed": "2026-08-26"
},
{
"id": "Q192",
"orig": 192,
"title": "Dissection classification and AR",
"lesions": [
"AORTA",
"AR"
],
"lens": "definition",
"items": [
{
"id": "Q192.1",
"q": "Describe the classification of aortic dissection.",
"a": "Two systems are in use. DeBakey type I starts in the ascending aorta and extends through the arch into the descending aorta; type II starts in and is confined to the ascending aorta; type III starts beyond the left subclavian artery in the descending aorta and extends distally, sometimes into the abdominal aorta, or rarely retrograde into the arch. The Stanford scheme simplifies management: type A includes any dissection involving the ascending aorta (DeBakey I and II) and is a surgical emergency, while type B spares the ascending aorta (DeBakey III) and is usually managed medically or endovascularly. The dividing line is whether the tear or flap involves the ascending aorta, because that is what threatens the coronaries, the aortic valve, and the pericardium."
},
{
"id": "Q192.2",
"q": "Which dissection types are associated with aortic regurgitation, and why?",
"a": "Aortic regurgitation accompanies dissections that involve the aortic root, meaning DeBakey I and II, or Stanford type A. The flap can dilate the root and prevent cusp coaptation, undermine a commissure so a cusp prolapses, or physically prolapse into the LVOT through the valve in diastole. Type B (DeBakey III) dissections begin beyond the arch vessels and normally leave the valve untouched. New AR in a chest-pain patient with a dilated root should therefore raise suspicion of a type A dissection."
}
],
"numbers": [],
"delta": null,
"pearl": "Stanford A = ascending involved = surgery now. AR travels with the A.",
"lookalike": null,
"related": [
"Q194",
"Q195",
"Q193",
"Q206",
"Q283"
],
"reviewed": "2026-08-26"
},
{
"id": "Q193",
"orig": 193,
"title": "Sinus of Valsalva aneurysm",
"lesions": [
"AORTA",
"CONGENITAL"
],
"lens": "2d",
"items": [
{
"id": "Q193.1",
"q": "Describe the 2D echo appearance of a sinus of Valsalva aneurysm.",
"a": "A sinus of Valsalva aneurysm is a thin-walled, windsock-like outpouching of one aortic sinus caused by a congenital (or occasionally infectious) weakness where the aortic media meets the annulus. The right coronary sinus is affected in about 70% of cases, the noncoronary sinus in roughly 25%, and the left in about 5%. The parasternal short-axis view at the aortic valve level shows all three sinuses at once, so you compare them directly: the abnormal sinus is enlarged and thin, often bulging toward the adjacent chamber (right sinus into the RV outflow tract or RA, noncoronary sinus into the RA). Rupture produces a continuous high-velocity jet into that chamber, and color Doppler shows its origin, direction, and timing, which distinguishes it from a VSD or coronary fistula. The parasternal long-axis view can show the sac protruding under the aortic valve."
}
],
"numbers": [
{
"label": "Sinus of Valsalva aneurysm in right coronary sinus",
"value": "~70",
"unit": "%"
},
{
"label": "Noncoronary sinus involvement",
"value": "~25",
"unit": "%"
},
{
"label": "Left coronary sinus involvement",
"value": "~5",
"unit": "%"
}
],
"delta": null,
"pearl": "Right sinus 70, noncoronary 25, left 5; a ruptured one gives a continuous jet into the right heart.",
"lookalike": {
"vs": "supracristal VSD with RCC prolapse",
"discriminator": "A ruptured sinus aneurysm jet is continuous (systole and diastole) and originates above the valve; a VSD jet is systolic and originates below the valve."
},
"related": [
"Q192",
"Q188",
"Q284"
],
"reviewed": "2026-08-26"
},
{
"id": "Q194",
"orig": 194,
"title": "Echo signs of aortic dissection",
"lesions": [
"AORTA",
"TEE"
],
"lens": "best-method",
"items": [
{
"id": "Q194.1",
"q": "What are the echocardiographic findings of aortic dissection?",
"a": "The defining sign is an intimal flap: a thin, linear, mobile echo inside the aortic lumen that moves independently of the wall and separates a true lumen from a false lumen. The true lumen expands in systole and shows brisk color flow, while the false lumen is often larger, expands in diastole, shows sluggish or reversed flow, spontaneous contrast, or thrombus. Color Doppler may show entry and re-entry tears with flow crossing the flap. Supporting findings include aortic dilation, aortic regurgitation, pericardial effusion or tamponade from leakage, regional LV wall-motion abnormality from coronary involvement, and pleural effusion. Always ask whether an apparent flap could be a reverberation artifact: a true flap moves out of phase with the wall and is seen in more than one plane."
},
{
"id": "Q194.2",
"q": "What is the best echocardiographic technique for evaluating dissection?",
"a": "Transesophageal echocardiography, with sensitivity around 98% and specificity in the mid-90s, is the echo method of choice because the esophagus lies directly against the thoracic aorta and allows high-frequency imaging of the root, arch, and descending aorta. It identifies the flap, the entry tear, the extent of the dissection, aortic regurgitation and its mechanism, pericardial effusion, and coronary ostial involvement, and can be done at the bedside in an unstable patient. The blind spot is the distal ascending aorta and proximal arch, where the trachea interposes. Transthoracic echo is a useful first look, especially for type A, but its sensitivity is much lower and a negative TTE never excludes dissection."
}
],
"numbers": [
{
"label": "TEE sensitivity for aortic dissection",
"value": "≈ 98",
"unit": "%"
}
],
"delta": null,
"pearl": "True lumen expands in systole; the false lumen is bigger, slower, and clots.",
"lookalike": {
"vs": "reverberation artifact in the ascending aorta",
"discriminator": "Artifacts move in phase with the aortic wall, lie at exactly twice the depth of a strong reflector, and lack flow crossing them on color Doppler; a real flap moves independently and persists in multiple planes."
},
"related": [
"Q192",
"Q195",
"Q283",
"Q363"
],
"reviewed": "2026-08-26"
},
{
"id": "Q195",
"orig": 195,
"title": "Marfan root vs other dilation",
"lesions": [
"AORTA"
],
"lens": "pitfall",
"items": [
{
"id": "Q195.1",
"q": "What echocardiographic feature helps distinguish Marfan syndrome from other causes of aortic dilation?",
"a": "The pattern of dilation is the clue. In Marfan syndrome the medial defect is most severe at the aortic root, so the sinuses of Valsalva balloon out symmetrically while the sinotubular junction is effaced and the tubular ascending aorta is comparatively spared, producing a pear- or flask-shaped root (annuloaortic ectasia). Hypertensive, atherosclerotic, or age-related dilation and the poststenotic dilation of a bicuspid valve involve the tubular ascending aorta above a preserved sinotubular junction, with the sinuses relatively normal. Measure the annulus, sinuses, sinotubular junction, and ascending aorta separately in the parasternal long-axis view, leading edge to leading edge at end-diastole, and index to body size; a young tall patient with a dilated root and a normal ascending aorta should raise the question of Marfan. Mitral valve prolapse with a myxomatous valve, and a family history of dissection, support the diagnosis."
}
],
"numbers": [],
"delta": null,
"pearl": "Marfan blows out the sinuses (pear-shaped root); hypertension and bicuspid disease blow out the tube above them.",
"lookalike": {
"vs": "bicuspid aortopathy",
"discriminator": "Bicuspid disease dilates the tubular ascending aorta with a preserved sinotubular junction; Marfan effaces the junction with maximal dilation at the sinuses."
},
"related": [
"Q192",
"Q194",
"Q284",
"Q363"
],
"reviewed": "2026-08-26"
},
{
"id": "Q196",
"orig": 196,
"title": "RVSP from a VSD jet",
"lesions": [
"VSD",
"HEMODYNAMICS"
],
"lens": "formula",
"items": [
{
"id": "Q196.1",
"q": "How do you estimate right ventricular systolic pressure from a ventricular septal defect?",
"a": "The VSD jet velocity reflects the systolic pressure difference between the two ventricles. Record the peak velocity with continuous-wave Doppler aligned to the jet and convert it with the simplified Bernoulli equation, gradient = 4v². Because LV systolic pressure equals systemic systolic pressure when there is no LVOT or aortic obstruction, take the brachial cuff systolic pressure as the LV pressure and subtract the gradient: RVSP = SBP − 4v². A 4.5 m/s jet with a cuff pressure of 120 mmHg means an 81 mmHg gradient and an RVSP of about 39 mmHg. The method fails when aortic stenosis or LVOT obstruction is present, since LV pressure then exceeds cuff pressure, and it should be cross-checked against the TR-derived RVSP whenever both jets are available."
}
],
"numbers": [
{
"label": "Bernoulli constant",
"value": "4",
"unit": "× v²"
},
{
"label": "Worked example: RVSP with 4.5 m/s jet and SBP 120",
"value": "~39",
"unit": "mmHg"
}
],
"delta": null,
"pearl": "A screaming VSD jet is reassuring: big gradient means low RV pressure.",
"lookalike": null,
"related": [
"Q185",
"Q186",
"Q189",
"Q389"
],
"reviewed": "2026-08-26"
},
{
"id": "Q197",
"orig": 197,
"title": "Color flow Doppler defined",
"lesions": [
"DOPPLER_PHYSICS",
"INSTRUMENTATION"
],
"lens": "definition",
"items": [
{
"id": "Q197.1",
"q": "What is color flow Doppler?",
"a": "Color flow Doppler is a pulsed-wave technique that samples Doppler shifts at thousands of points across a region of interest and paints a color-coded map of mean velocity over the grayscale 2D (or M-mode) image. Because it is pulsed, it obeys the same Nyquist limit as pulsed Doppler and therefore aliases at high velocities, which is why turbulent jets show a mosaic pattern. By convention flow toward the transducer is red and flow away is blue, with brighter or lighter shades representing faster mean velocities; some maps add green to flag variance. It displays direction, relative velocity, and spatial extent of flow, but it does not give a peak velocity, which still requires spectral pulsed or continuous-wave Doppler."
}
],
"numbers": [
{
"label": "Nyquist limit",
"value": "PRF/2",
"unit": ""
}
],
"delta": null,
"pearl": "BART: Blue Away, Red Toward. Color is pulsed Doppler, so it aliases.",
"lookalike": null,
"related": [
"Q198",
"Q199"
],
"widgets": [
"nyquist"
],
"reviewed": "2026-08-26"
},
{
"id": "Q198",
"orig": 198,
"title": "Packet size and frame rate",
"lesions": [
"DOPPLER_PHYSICS",
"INSTRUMENTATION"
],
"lens": "pitfall",
"items": [
{
"id": "Q198.1",
"q": "In color Doppler, what is a pulse packet (ensemble length)?",
"a": "A single pulse cannot reveal motion, so the system fires a series of pulses down each scan line and compares the returning echoes for phase shift from pulse to pulse; that series of pulses, typically 8 to 16, is the packet or ensemble. Autocorrelation across the packet yields the mean velocity, its direction, and the variance for every pixel along the line. The packet is the color-Doppler equivalent of the sample volume dwell time in spectral Doppler."
},
{
"id": "Q198.2",
"q": "Why does packet size matter, and how do you balance it?",
"a": "More pulses per packet give a better estimate of mean velocity and greater sensitivity to slow flow, because the autocorrelator has more samples to average. The cost is time: every scan line must wait for the entire packet, so frame rate falls as packet size, color sector width, or depth increases. In practice you keep the packet large enough for good sensitivity and recover frame rate by narrowing the color box, reducing the depth, or lowering line density, rather than sacrificing accuracy. A very small packet gives a fast but noisy, flickering color map that underestimates low-velocity flow."
}
],
"numbers": [
{
"label": "Typical color packet size",
"value": "8–16",
"unit": "pulses"
}
],
"delta": null,
"pearl": "Bigger packet = better color, slower frames. Narrow the color box instead of shrinking the packet.",
"lookalike": null,
"related": [
"Q197",
"Q199"
],
"reviewed": "2026-08-26"
},
{
"id": "Q199",
"orig": 199,
"title": "Continuous wave vs pulsed Doppler",
"lesions": [
"DOPPLER_PHYSICS",
"INSTRUMENTATION"
],
"lens": "doppler",
"items": [
{
"id": "Q199.1",
"q": "What is continuous wave Doppler?",
"a": "In continuous wave Doppler one transducer element (or group) transmits ultrasound without interruption while a separate element receives continuously. The returned signal is mixed with the transmitted frequency to extract the Doppler shift, which is displayed as a spectral trace. Because transmission never pauses, there is no pulse repetition frequency and no range gating: every moving reflector along the entire beam contributes to the signal, and the tracing therefore shows a filled-in envelope rather than the narrow band of a single sample volume."
},
{
"id": "Q199.2",
"q": "What are the main advantages and disadvantages of continuous wave compared with pulsed wave Doppler?",
"a": "The advantage is the absence of a Nyquist limit, so CW measures the very high velocities of aortic stenosis, tricuspid regurgitation, and VSD jets (often 4 to 6 m/s) without aliasing, which pulsed Doppler cannot do at cardiac depths. The disadvantage is range ambiguity: CW tells you the peak velocity somewhere along the beam but not where, so it cannot localize the flow, and the spectrum can be contaminated by other jets in the beam path (for example, MR mimicking AS). Pulsed Doppler is the mirror image, precise localization at the cost of aliasing. The practical rule is to locate and time flow with PW and color, then quantify high velocities with CW."
}
],
"numbers": [
{
"label": "Nyquist limit for pulsed Doppler",
"value": "PRF/2",
"unit": ""
}
],
"delta": null,
"pearl": "PW knows where but not how fast; CW knows how fast but not where.",
"lookalike": null,
"related": [
"Q197",
"Q198",
"Q200"
],
"widgets": [
"nyquist"
],
"reviewed": "2026-08-26"
},
{
"id": "Q200",
"orig": 200,
"title": "Angle theta in the Doppler equation",
"lesions": [
"DOPPLER_PHYSICS"
],
"lens": "formula",
"items": [
{
"id": "Q200.1",
"q": "Which term in the Doppler equation matters most in practice, and why?",
"a": "The Doppler equation, Δf = 2 f₀ v cosθ / c, contains several constants (transmit frequency, speed of sound), but the term the operator controls is cosθ, the angle between the ultrasound beam and the direction of blood flow. The machine assumes θ = 0 (cos = 1); any real angle makes the measured shift smaller, so velocity is always underestimated, never overestimated, by misalignment. Up to 20 degrees the cosine stays above 0.94 and the error is under 6%, which is acceptable; at 30 degrees the error grows to 13%, and at 60 degrees you have lost half the velocity. That is why you interrogate a stenotic jet from several windows and report the highest velocity, and why angle correction is not used in cardiac Doppler."
}
],
"numbers": [
{
"label": "Acceptable Doppler angle",
"value": "≤ 20",
"unit": "degrees"
},
{
"label": "Velocity error at 20 degrees",
"value": "< 6",
"unit": "%"
}
],
"delta": null,
"pearl": "Angle error only goes one way: it makes velocities and gradients smaller, so the highest reading is the truest.",
"lookalike": null,
"related": [
"Q199",
"Q201",
"Q210"
],
"reviewed": "2026-08-26"
},
{
"id": "Q201",
"orig": 201,
"title": "VTI vs peak velocity in the continuity equation",
"lesions": [
"AS",
"AR"
],
"lens": "pitfall",
"items": [
{
"id": "Q201.1",
"q": "When calculating aortic valve area by the continuity equation, when should you use VTI rather than peak velocity for V1 and V2?",
"a": "The continuity equation assumes that the ratio of LVOT to aortic velocities is the same whether you use peak velocity or the velocity-time integral, which holds only when the two flow curves have the same shape. Peak velocities are acceptable in a normal-flow state, but when the stroke volume is low (reduced ejection fraction, low-flow low-gradient AS with SVi below 35 mL/m²) or when significant aortic regurgitation increases and prolongs LVOT flow, the LVOT and transvalvular curves diverge in shape and timing, and peak-velocity ratios can misestimate the area. In those settings use VTI for both V1 and V2, which integrates the whole ejection period; the VTI ratio (DVI) below 0.25 is itself a severity marker independent of LVOT diameter. Guidelines recommend the VTI-based equation as the default for clinical reporting."
}
],
"numbers": [
{
"label": "DVI suggesting severe AS",
"value": "< 0.25",
"unit": ""
},
{
"label": "Low-flow stroke volume index",
"value": "< 35",
"unit": "mL/m²"
},
{
"label": "Severe AS AVA",
"value": "< 1.0",
"unit": "cm²"
}
],
"delta": null,
"pearl": "Low EF or more than mild AR: switch the continuity equation to VTIs.",
"lookalike": null,
"related": [
"Q200",
"Q204",
"Q210",
"Q357"
],
"reviewed": "2026-08-26"
},
{
"id": "Q202",
"orig": 202,
"title": "Components of an MR jet",
"lesions": [
"MR"
],
"lens": "doppler",
"items": [
{
"id": "Q202.1",
"q": "What are the four Doppler components of a mitral regurgitant jet?",
"a": "Regurgitant flow across the mitral valve passes through four zones. Upstream, on the LV side, is the proximal flow convergence zone, where blood accelerates in hemispheric shells toward the orifice and forms the basis of the PISA method. At the orifice itself is the vena contracta, the narrowest neck of the jet just distal to the leaflets. Beyond it the jet expands into the left atrium as the color jet area, which depends heavily on gain, Nyquist limit, and atrial pressure. Finally, the jet's effect on the pulmonary veins can be read with pulsed Doppler as blunting or reversal of systolic venous inflow."
},
{
"id": "Q202.2",
"q": "Which component gives the most robust hemodynamic evidence of severity?",
"a": "Systolic flow reversal in the pulmonary veins is the most specific hemodynamic marker: a regurgitant volume large enough to push blood backward into the veins during systole reflects severe MR and a high LA v wave, and it is nearly unaffected by machine settings. Its weakness is sensitivity, since eccentric jets may reverse flow in only one vein and atrial fibrillation or elevated LA pressure blunts systolic flow for other reasons. Current guidelines therefore combine it with the quantitative measures, a vena contracta of 0.7 cm or greater and an EROA of at least 0.4 cm² (regurgitant volume ≥ 60 mL, fraction ≥ 50%), and explicitly state that color jet area alone should not be used to grade MR."
}
],
"numbers": [
{
"label": "Severe MR vena contracta",
"value": "≥ 0.7",
"unit": "cm"
},
{
"label": "Severe MR EROA",
"value": "≥ 0.4",
"unit": "cm²"
},
{
"label": "Severe MR regurgitant volume",
"value": "≥ 60",
"unit": "mL"
},
{
"label": "Severe MR regurgitant fraction",
"value": "≥ 50",
"unit": "%"
}
],
"delta": {
"was": "2011 card presented jet size by color flow as one of four coequal components used to judge MR severity.",
"now": "ASE 2017 states color jet area alone is insufficient for grading; integrate vena contracta ≥ 0.7 cm, EROA ≥ 0.4 cm², RVol ≥ 60 mL, RF ≥ 50%, and pulmonary vein systolic reversal.",
"source": "ASE 2017 regurgitation"
},
"pearl": "Systolic reversal in the pulmonary veins is specific but not sensitive; one vein may miss an eccentric jet.",
"lookalike": null,
"related": [
"Q203"
],
"reviewed": "2026-08-26"
},
{
"id": "Q203",
"orig": 203,
"title": "The vena contracta",
"lesions": [
"MR",
"AR",
"TR"
],
"lens": "numbers",
"items": [
{
"id": "Q203.1",
"q": "What is the vena contracta?",
"a": "The vena contracta is the narrowest cross-section of a regurgitant jet, located at or just downstream of the regurgitant orifice, after the proximal flow convergence and before the jet expands into the receiving chamber. Its width is a direct surrogate for the effective regurgitant orifice, so it is relatively independent of driving pressure, chamber size, and, to a large extent, color gain and Nyquist settings. Measure it perpendicular to the jet in a zoomed view with the Nyquist limit at 50 to 60 cm/s, using a plane that shows all three components (convergence, neck, jet) in a single image."
},
{
"id": "Q203.2",
"q": "How is vena contracta width used to grade regurgitation?",
"a": "It is one of the core quantitative parameters in the ASE 2017 integrative approach. For mitral regurgitation a width of 0.7 cm or more indicates severe MR and under 0.3 cm mild; for tricuspid regurgitation the severe threshold is also 0.7 cm or more; for aortic regurgitation a width greater than 0.6 cm is severe and under 0.3 cm mild. Values in the intermediate range require confirmation with PISA-derived EROA and regurgitant volume. Because the neck of an eccentric or wall-hugging jet is measured as easily as a central one, the vena contracta is especially valuable when color jet area is misleading; its limitations are multiple jets, where widths cannot be summed, and elliptical orifices, where a single-plane width may under- or overestimate."
}
],
"numbers": [
{
"label": "Severe MR vena contracta",
"value": "≥ 0.7",
"unit": "cm"
},
{
"label": "Severe TR vena contracta",
"value": "≥ 0.7",
"unit": "cm"
},
{
"label": "Severe AR vena contracta",
"value": "> 0.6",
"unit": "cm"
},
{
"label": "Mild MR/AR vena contracta",
"value": "< 0.3",
"unit": "cm"
},
{
"label": "Nyquist setting for VC measurement",
"value": "50–60",
"unit": "cm/s"
}
],
"delta": null,
"pearl": "Seven for mitral and tricuspid, six for aortic: the severe vena contracta cutoffs in millimeters.",
"lookalike": null,
"related": [
"Q202",
"Q232"
],
"reviewed": "2026-08-26"
},
{
"id": "Q204",
"orig": 204,
"title": "Pulse pressure in AS and AR",
"lesions": [
"HEMODYNAMICS",
"AS",
"AR"
],
"lens": "physical-exam",
"items": [
{
"id": "Q204.1",
"q": "What is pulse pressure?",
"a": "Pulse pressure is the arithmetic difference between systolic and diastolic arterial pressure, about 40 mmHg for a normal 120/80 reading. It is determined by the stroke volume ejected into the arterial tree and by the compliance of the aorta: a larger stroke volume or a stiffer aorta widens it, while a smaller stroke volume or a slowed ejection narrows it. Pulse pressure therefore offers a bedside hint about valve disease before the echo is done."
},
{
"id": "Q204.2",
"q": "In which conditions is pulse pressure abnormal?",
"a": "Severe aortic stenosis narrows the pulse pressure because the fixed obstruction limits and slows ejection, giving the small, late-peaking pulsus parvus et tardus. Chronic severe aortic regurgitation widens it dramatically, since a large total stroke volume drives systolic pressure up while diastolic runoff back into the LV drives diastolic pressure down, producing readings such as 160/50 and the bounding water-hammer pulse. A wide pulse pressure also occurs with a large PDA or a stiff atherosclerotic aorta in the elderly, and a narrow one occurs in cardiac tamponade, cardiogenic shock, and severe heart failure. A normal pulse pressure in a patient with a dilated LV argues against severe AR."
}
],
"numbers": [
{
"label": "Normal pulse pressure",
"value": "~40",
"unit": "mmHg"
},
{
"label": "Normal aortic pressure",
"value": "120/80",
"unit": "mmHg"
}
],
"delta": null,
"pearl": "Narrow pulse pressure = fixed obstruction (AS, tamponade); wide = leak or stiff pipe (AR, PDA, old aorta).",
"lookalike": null,
"related": [
"Q201"
],
"reviewed": "2026-08-26"
},
{
"id": "Q205",
"orig": 205,
"title": "Why order an exercise stress echo",
"lesions": [
"STRESS",
"CAD"
],
"lens": "procedure",
"items": [
{
"id": "Q205.1",
"q": "What are four indications for exercise stress echocardiography?",
"a": "Exercise stress echo compares regional wall motion at rest and immediately after peak exercise, so it is used wherever the question is inducible ischemia. Typical indications are: diagnosing coronary disease in a patient with chest pain and an intermediate pretest probability, particularly when the baseline ECG is uninterpretable; establishing the extent and location of ischemia in known coronary disease to guide revascularization; risk stratification and functional assessment after myocardial infarction or before entering a cardiac rehabilitation program; and evaluating symptoms or arrhythmias that occur with exertion. It also has non-ischemic uses, such as unmasking symptoms or gradients in moderate valve disease, hypertrophic cardiomyopathy, and exercise-induced pulmonary hypertension, and assessing diastolic reserve."
}
],
"numbers": [],
"delta": null,
"pearl": "Stress echo answers one question: does a wall that moves at rest stop moving with stress?",
"lookalike": null,
"related": [
"Q206",
"Q207",
"Q281",
"Q355"
],
"reviewed": "2026-08-26"
},
{
"id": "Q206",
"orig": 206,
"title": "When not to stress a patient",
"lesions": [
"STRESS",
"AS",
"AORTA"
],
"lens": "procedure",
"items": [
{
"id": "Q206.1",
"q": "Name four contraindications to exercise stress echocardiography.",
"a": "Exercise should not be used to provoke ischemia when the provocation itself could be lethal. Absolute contraindications include acute myocardial infarction within the first 48 hours or ongoing unstable angina, acute aortic dissection, symptomatic severe aortic stenosis, and uncontrolled arrhythmias, decompensated heart failure, acute myocarditis or pericarditis, and acute pulmonary embolism. Relative contraindications include known left main stenosis, severe hypertension above roughly 200/110 mmHg, hypertrophic obstructive cardiomyopathy, high-grade AV block, and any inability to exercise, in which case pharmacologic stress with dobutamine or a vasodilator is used instead. Asymptomatic severe AS can be exercised under physician supervision to unmask symptoms, but symptomatic severe AS is off limits."
}
],
"numbers": [
{
"label": "Acute MI: no exercise testing within",
"value": "48",
"unit": "hours"
},
{
"label": "Severe hypertension relative contraindication",
"value": "> 200/110",
"unit": "mmHg"
}
],
"delta": null,
"pearl": "Don't stress the acutely torn, the acutely infarcted, the unstable, or the tightly stenosed.",
"lookalike": null,
"related": [
"Q205",
"Q192"
],
"reviewed": "2026-08-26"
},
{
"id": "Q207",
"orig": 207,
"title": "Defining akinesis",
"lesions": [
"CAD"
],
"lens": "definition",
"items": [
{
"id": "Q207.1",
"q": "In wall motion analysis, what does akinesis mean?",
"a": "Akinesis describes a myocardial segment that shows neither inward endocardial excursion nor systolic thickening. Both criteria matter because a segment can be dragged inward by its neighbors (tethering) while still failing to thicken, and thickening is the more reliable sign of living, contracting muscle. In the ASE 17-segment scoring scheme akinesis scores 3, between hypokinesis (score 2, reduced but present thickening) and dyskinesis (score 4, paradoxical outward systolic motion, often with thinning); aneurysmal segments are noted separately. Acute akinesis usually reflects transmural ischemia or infarction in a single coronary territory, whereas chronic akinesis with wall thinning below about 6 mm and increased echogenicity indicates scar."
}
],
"numbers": [
{
"label": "Wall motion score: akinesis",
"value": "3",
"unit": ""
},
{
"label": "Wall motion score: hypokinesis",
"value": "2",
"unit": ""
},
{
"label": "Wall motion score: dyskinesis",
"value": "4",
"unit": ""
},
{
"label": "ASE LV segment model",
"value": "17",
"unit": "segments"
}
],
"delta": null,
"pearl": "Watch thickening, not just motion: a tethered scar moves but never thickens.",
"lookalike": {
"vs": "dyskinesis",
"discriminator": "Akinetic wall stays still; dyskinetic wall bulges outward in systole."
},
"related": [
"Q205",
"Q280"
],
"reviewed": "2026-08-26"
},
{
"id": "Q208",
"orig": 208,
"title": "Tuberous sclerosis and cardiac rhabdomyoma",
"lesions": [
"MASS",
"CONGENITAL"
],
"lens": "etiology",
"items": [
{
"id": "Q208.1",
"q": "What cardiac problem are children with tuberous sclerosis prone to?",
"a": "Tuberous sclerosis complex, caused by TSC1 or TSC2 mutations, produces hamartomas in many organs, and in the heart the lesion is the rhabdomyoma, the most common primary cardiac tumor of infancy and childhood. Rhabdomyomas appear on echo as multiple, well-circumscribed, homogeneous, brightly echogenic masses within the ventricular myocardium or protruding into the ventricular cavity, and finding more than one strongly suggests tuberous sclerosis. Most are asymptomatic and regress spontaneously over the first years of life, so surgery is reserved for lesions that obstruct inflow or outflow or provoke arrhythmias. In adults, by contrast, the most common primary tumor is the myxoma, a mobile left atrial mass attached to the fossa ovalis."
}
],
"numbers": [],
"delta": null,
"pearl": "Multiple bright ventricular masses in a baby: rhabdomyomas until proven otherwise, and check for tuberous sclerosis.",
"lookalike": {
"vs": "fibroma",
"discriminator": "Fibroma is usually a single, large, often calcified intramural mass that does not regress; rhabdomyomas are multiple and shrink with age."
},
"related": [
"Q330"
],
"reviewed": "2026-08-26"
},
{
"id": "Q209",
"orig": 209,
"title": "Positioning for TEE probe insertion",
"lesions": [
"TEE",
"PROCEDURE"
],
"lens": "procedure",
"items": [
{
"id": "Q209.1",
"q": "How should an outpatient be positioned before the TEE probe is inserted?",
"a": "Place the patient in the left lateral decubitus position with the head flexed forward toward the chest and a bite block in place. Lying on the left side lets saliva and any regurgitated material drain out of the mouth rather than pooling near the airway, and chin flexion straightens the path into the esophagus so the probe passes the cricopharyngeus more easily. Before insertion confirm fasting for at least 4 to 6 hours, review for esophageal disease or dysphagia, remove dentures, apply topical pharyngeal anesthesia, establish IV access for sedation, and attach ECG, pulse oximetry, and blood pressure monitoring. The same lateral position is maintained throughout the study and during recovery."
}
],
"numbers": [
{
"label": "Fasting before TEE",
"value": "4–6",
"unit": "hours"
}
],
"delta": null,
"pearl": "Left side, chin down, bite block in, nothing by mouth for 4 to 6 hours.",
"lookalike": null,
"related": [
"Q210"
],
"reviewed": "2026-08-26"
},
{
"id": "Q210",
"orig": 210,
"title": "Right parasternal Pedoff for AS",
"lesions": [
"AS",
"PROCEDURE"
],
"lens": "procedure",
"items": [
{
"id": "Q210.1",
"q": "How do you position a patient with aortic stenosis to record the AS jet with a Pedoff probe from the right sternal border?",
"a": "Roll the patient into a right lateral decubitus position, with the right arm raised over the head if possible. In many patients the stenotic aortic jet is directed anteriorly and rightward toward the right upper sternal border, and lying on the right side brings the ascending aorta closer to the chest wall and moves lung tissue out of the path. Place the nonimaging continuous-wave (Pedoff) probe in the second or third right intercostal space and angle it toward the left shoulder, hunting for the clean, high-pitched signal with a sharp envelope. The right parasternal window yields the highest velocity in a substantial fraction of AS patients, so ASE 2017 recommends interrogating from multiple windows including this one and reporting the highest value obtained."
}
],
"numbers": [
{
"label": "Right parasternal intercostal space for Pedoff",
"value": "2nd–3rd",
"unit": "interspace"
},
{
"label": "Severe AS Vmax",
"value": "≥ 4",
"unit": "m/s"
}
],
"delta": null,
"pearl": "Turn the patient onto the right side to open the right parasternal window; the highest velocity from any window is the one you report.",
"lookalike": null,
"related": [
"Q209",
"Q200",
"Q201"
],
"reviewed": "2026-08-26"
},
{
"id": "Q211",
"orig": 211,
"title": "Causes of mitral valve prolapse",
"lesions": [
"MVP",
"MR"
],
"lens": "etiology",
"items": [
{
"id": "Q211.1",
"q": "What is the underlying pathology in primary mitral valve prolapse, and what are the two phenotypes you should be able to name?",
"a": "Primary MVP is a myxomatous degeneration of the leaflets: proteoglycan accumulates in the spongiosa, collagen in the fibrosa becomes disorganized, and the leaflets and chordae stretch and thicken. The two ends of the spectrum are Barlow disease (diffuse, thick, redundant tissue involving multiple scallops, large annulus, long chordae, usually younger patients) and fibroelastic deficiency (thin, translucent leaflets with a single ruptured or elongated chord causing one prolapsing or flail segment, usually older patients). The distinction matters because it predicts the repair strategy and how much of the valve the surgeon must address."
},
{
"id": "Q211.2",
"q": "Which systemic conditions are associated with secondary or syndromic prolapse?",
"a": "Heritable connective tissue disorders are the classic associations: Marfan syndrome, Ehlers-Danlos, osteogenesis imperfecta, and Loeys-Dietz. Prolapse can also be acquired when chordae rupture from endocarditis, ischemic papillary muscle dysfunction, or trauma, and a small hypovolemic left ventricle (for example in a secundum ASD or with pectus excavatum) can create apparent leaflet displacement without myxomatous change. Familial non-syndromic MVP is common and is inherited mainly in an autosomal dominant pattern with variable penetrance."
}
],
"numbers": [],
"delta": null,
"pearl": "Barlow = big, billowing, bilateral, young. Fibroelastic deficiency = thin, focal, flail, older.",
"lookalike": {
"vs": "Flail leaflet",
"discriminator": "In prolapse the leaflet tip still points toward the LV apex; in flail the tip everts into the left atrium in systole, usually with a visible ruptured chord."
},
"related": [
"Q212",
"Q214"
],
"reviewed": "2026-08-26"
},
{
"id": "Q212",
"orig": 212,
"title": "Click, murmur and bedside maneuvers",
"lesions": [
"MVP",
"MR"
],
"lens": "physical-exam",
"items": [
{
"id": "Q212.1",
"q": "Describe the auscultatory findings of mitral valve prolapse and explain what produces each sound.",
"a": "The hallmark is a mid-systolic click followed by a late systolic murmur. The click is generated when the elongated chordae snap taut as the redundant leaflet balloons past the annular plane; the murmur begins at that instant because regurgitation starts only once the leaflet has lost coaptation. As the degree of regurgitation increases the murmur starts earlier and lengthens, and in a flail leaflet it can become holosystolic and lose the click entirely."
},
{
"id": "Q212.2",
"q": "How do standing, Valsalva and squatting change the timing of the click and murmur, and why?",
"a": "Anything that shrinks the left ventricle makes the chordae reach their limit sooner, so the click and murmur move earlier and the murmur lengthens: standing and the strain phase of Valsalva reduce venous return and LV volume. Squatting, leg raise, and handgrip increase preload or afterload, enlarge the LV, delay leaflet displacement, and push the click and murmur later toward S2 with a shorter murmur. This is the opposite of hypertrophic cardiomyopathy only in mechanism, not direction: both get louder on standing, so the click is the discriminating feature."
}
],
"numbers": [],
"delta": null,
"pearl": "Smaller ventricle = earlier click. Stand up, click moves up (earlier); squat down, click moves down (later).",
"lookalike": {
"vs": "HCM systolic murmur",
"discriminator": "Both intensify with standing or Valsalva, but MVP has a mid-systolic click and a murmur that radiates to the axilla; HCM has no click and a crescendo-decrescendo murmur at the left sternal border."
},
"related": [
"Q211",
"Q213"
],
"reviewed": "2026-08-26"
},
{
"id": "Q213",
"orig": 213,
"title": "M-mode signs of mitral prolapse",
"lesions": [
"MVP"
],
"lens": "m-mode",
"items": [
{
"id": "Q213.1",
"q": "What does mitral valve prolapse look like on M-mode, and why is M-mode no longer the basis of the diagnosis?",
"a": "On an M-mode through the leaflet tips, prolapse appears as posterior (upward on the trace toward the transducer, away from the left atrium is downward) buckling of the closed CD segment: either a late-systolic hammock-shaped dip or a pansystolic bowing of at least 2 to 3 mm posterior to the C-D line. Because M-mode samples one line through a saddle-shaped annulus, angulation of the beam and the transducer position on the chest can create or hide the sign, so it produced many false positives in the 1980s. Today it is a supporting finding; the diagnosis rests on a 2D long-axis measurement of leaflet displacement."
}
],
"numbers": [
{
"label": "M-mode posterior CD-segment displacement",
"value": "≥ 2–3",
"unit": "mm"
}
],
"delta": null,
"pearl": "Hammock in late systole = classic; pansystolic bowing = more redundant leaflet; but confirm it on 2D PLAX.",
"lookalike": {
"vs": "Pericardial effusion motion artifact",
"discriminator": "With a large effusion the whole heart swings and the C-D line drifts; true prolapse shows buckling of the leaflet echo only, with the annulus stationary."
},
"related": [
"Q214",
"Q212"
],
"reviewed": "2026-08-26"
},
{
"id": "Q214",
"orig": 214,
"title": "2D diagnosis of mitral prolapse",
"lesions": [
"MVP",
"MR"
],
"lens": "2d",
"items": [
{
"id": "Q214.1",
"q": "State the 2D criterion for mitral valve prolapse and explain which view must be used.",
"a": "Prolapse is present when any part of one or both leaflets is displaced 2 mm or more beyond the plane of the mitral annulus into the left atrium during systole, measured in the parasternal long-axis view. The annulus is saddle-shaped, with its high points anterior and posterior and its low points medial and lateral; the PLAX cuts through the high points, so a leaflet that reaches the annular line in that view is truly above the ring. In the apical four-chamber view the plane runs through the low points, and a normal leaflet can appear to bow above that line, which is why A4C over-diagnoses prolapse."
},
{
"id": "Q214.2",
"q": "How do you distinguish Barlow disease from fibroelastic deficiency on the 2D images?",
"a": "Barlow valves have leaflets thicker than 5 mm with excess, billowing tissue involving several scallops, a dilated annulus, elongated chordae, and often chordal or annular calcification; prolapse is typically bileaflet and the valve looks like a parachute. In fibroelastic deficiency the leaflets are thin and nearly normal apart from one segment, most often P2, that prolapses or flails because a single chord has ruptured or stretched; the annulus is only mildly dilated. Barlow patients tend to be young with a long murmur history, whereas fibroelastic deficiency presents abruptly in older adults."
}
],
"numbers": [
{
"label": "Prolapse displacement beyond annulus (PLAX)",
"value": "≥ 2",
"unit": "mm"
},
{
"label": "Barlow leaflet thickness",
"value": "> 5",
"unit": "mm"
}
],
"delta": null,
"pearl": "Measure prolapse only in PLAX; the A4C plane sits at the saddle's low points and fakes it.",
"lookalike": {
"vs": "Normal leaflet in A4C",
"discriminator": "Apparent displacement seen only in A4C but not in PLAX is the saddle-shape artifact, not prolapse."
},
"related": [
"Q211",
"Q213",
"Q215",
"Q217",
"Q218"
],
"reviewed": "2026-08-26"
},
{
"id": "Q215",
"orig": 215,
"title": "Doppler features of prolapse regurgitation",
"lesions": [
"MVP",
"MR"
],
"lens": "doppler",
"items": [
{
"id": "Q215.1",
"q": "What is characteristic about the timing and direction of the regurgitant jet in mitral valve prolapse, and how does that affect grading?",
"a": "Because coaptation is lost only after the leaflet has displaced, the jet in classic prolapse is late-systolic, and the color jet and CW envelope may occupy only the second half of systole. The jet is eccentric and travels away from the prolapsing leaflet: posterior leaflet prolapse produces an anteriorly directed jet that hugs the anterior leaflet and interatrial septum, while anterior leaflet prolapse sends the jet posterolaterally. Eccentric, wall-hugging jets lose energy against the atrial wall (the Coanda effect) and look smaller than a central jet of the same volume, so jet area underestimates severity; quantify with vena contracta, PISA, and the pulmonary vein pattern instead."
},
{
"id": "Q215.2",
"q": "What pitfall arises when you calculate regurgitant volume in late-systolic prolapse?",
"a": "PISA and the CW envelope give instantaneous values at one moment, but in late-systolic MR the regurgitation lasts only part of systole, so an EROA that looks severe can correspond to a modest regurgitant volume. Use the CW VTI of the actual regurgitant signal, not a full-systole extrapolation, and cross-check with LA and LV size; a truly severe lesion should have enlarged the chambers. Also confirm which leaflet prolapses by following the jet direction, because it will point away from the diseased side."
}
],
"numbers": [
{
"label": "Severe MR vena contracta",
"value": "≥ 0.7",
"unit": "cm"
},
{
"label": "Severe MR EROA",
"value": "≥ 0.4",
"unit": "cm²"
}
],
"delta": null,
"pearl": "The jet points away from the culprit leaflet: posterior prolapse, anterior jet.",
"lookalike": null,
"related": [
"Q214",
"Q216",
"Q218",
"Q365",
"Q369"
],
"reviewed": "2026-08-26"
},
{
"id": "Q216",
"orig": 216,
"title": "Chamber consequences of prolapse",
"lesions": [
"MVP",
"MR"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q216.1",
"q": "What chamber changes should you look for in a patient with mitral valve prolapse, and what do they tell you?",
"a": "Uncomplicated prolapse with trivial regurgitation leaves the chambers normal. Once regurgitation becomes significant the left atrium enlarges from the systolic volume load, and the left ventricle dilates with an increased end-diastolic volume because it must eject the regurgitant volume plus forward stroke volume. Surgical timing for primary MR hinges on these chamber effects: an LVEF of 60% or less or an LV end-systolic diameter of 40 mm or more signals early ventricular decompensation even in an asymptomatic patient. Look also for a dilated, saddle-flattened annulus, mitral annular disjunction, and pulmonary hypertension from chronic LA pressure elevation."
},
{
"id": "Q216.2",
"q": "What is mitral annular disjunction and why has it attracted attention?",
"a": "Mitral annular disjunction is a separation between the atrial wall-mitral leaflet hinge and the crest of the LV myocardium, so the posterior annulus appears to detach from the ventricle in systole; it is measured in PLAX at end-systole. It is associated with bileaflet myxomatous prolapse, papillary muscle traction, and ventricular arrhythmias, and it has been linked with sudden death in a small subset (often called arrhythmic MVP), so report it when present and note any inferolateral wall or papillary muscle scar seen on cardiac MRI."
}
],
"numbers": [
{
"label": "LVEF trigger for surgery in primary MR",
"value": "≤ 60",
"unit": "%"
},
{
"label": "LVESD trigger for surgery in primary MR",
"value": "≥ 40",
"unit": "mm"
}
],
"delta": null,
"pearl": "EF 60 and ESD 40: in primary MR those are already abnormal, not normal.",
"lookalike": null,
"related": [
"Q215",
"Q217",
"Q218"
],
"reviewed": "2026-08-26"
},
{
"id": "Q217",
"orig": 217,
"title": "Best approach to prolapse assessment",
"lesions": [
"MVP",
"MR",
"TEE"
],
"lens": "best-method",
"items": [
{
"id": "Q217.1",
"q": "Which imaging approach best confirms prolapse and defines the anatomy for repair?",
"a": "Transthoracic PLAX is the diagnostic view for prolapse itself, using the 2 mm displacement criterion, and the parasternal short-axis at the leaflet tips plus the apical two-chamber help assign the scallop. For surgical planning, transesophageal echo is superior: the mid-esophageal views at 0, 60, 90 and 120 degrees sweep the segments systematically, and 3D en-face imaging from the atrial side (the surgeon's view) shows the whole valve so each prolapsing or flail scallop, cleft, and chordal rupture can be labeled by the Carpentier A1-A3, P1-P3 system. TEE also quantifies regurgitation more reliably in eccentric jets and confirms the mechanism intraoperatively before and after repair."
}
],
"numbers": [],
"delta": null,
"pearl": "TTE PLAX diagnoses it; TEE 3D surgeon's view maps it segment by segment.",
"lookalike": null,
"related": [
"Q214",
"Q216",
"Q365"
],
"reviewed": "2026-08-26"
},
{
"id": "Q218",
"orig": 218,
"title": "Key numbers in mitral prolapse",
"lesions": [
"MVP",
"MR"
],
"lens": "numbers",
"items": [
{
"id": "Q218.1",
"q": "List the numbers examiners expect you to know about mitral valve prolapse.",
"a": "Diagnosis requires 2 mm or more of leaflet displacement above the annular plane in PLAX; leaflet thickness above 5 mm defines classic or myxomatous prolapse and separates Barlow disease from fibroelastic deficiency. The prevalence with the modern PLAX criterion is roughly 2 to 3% of adults, far lower than the older estimates that came from A4C or M-mode. Prolapse is the leading cause of surgical primary MR in the United States, and severe MR is graded by the same thresholds as any other etiology: vena contracta 0.7 cm or more, EROA 0.4 cm² or more, regurgitant volume 60 mL or more, and regurgitant fraction 50% or more."
}
],
"numbers": [
{
"label": "Prolapse displacement (PLAX)",
"value": "≥ 2",
"unit": "mm"
},
{
"label": "Classic (myxomatous) leaflet thickness",
"value": "> 5",
"unit": "mm"
},
{
"label": "Adult prevalence",
"value": "2–3",
"unit": "%"
},
{
"label": "Severe MR vena contracta",
"value": "≥ 0.7",
"unit": "cm"
},
{
"label": "Severe MR EROA",
"value": "≥ 0.4",
"unit": "cm²"
},
{
"label": "Severe MR regurgitant volume",
"value": "≥ 60",
"unit": "mL"
},
{
"label": "Severe MR regurgitant fraction",
"value": "≥ 50",
"unit": "%"
}
],
"delta": null,
"pearl": "2 mm up, 5 mm thick, 2 to 3% of people.",
"lookalike": null,
"related": [
"Q214",
"Q215",
"Q216"
],
"reviewed": "2026-08-26"
},
{
"id": "Q219",
"orig": 219,
"title": "Rheumatic versus calcific mitral stenosis",
"lesions": [
"MS"
],
"lens": "etiology",
"items": [
{
"id": "Q219.1",
"q": "Contrast the two major causes of mitral stenosis in terms of where the valve is affected.",
"a": "Rheumatic disease attacks the leaflet tips and commissures: post-streptococcal inflammation fuses the commissures, thickens the leaflet edges, and shortens and fuses the chordae, so the leaflet bodies stay mobile and dome in diastole, giving the hockey-stick anterior leaflet on PLAX and the fish-mouth orifice on PSAX. Degenerative mitral annular calcification is the opposite pattern: calcium builds up at the base of the posterior leaflet and annulus in elderly patients, those with renal failure, and after radiation; the commissures remain open, the leaflet tips are spared, and the orifice narrows because the annulus can no longer expand rather than because the tips are fused. Rheumatic MS remains the dominant cause worldwide, while MAC-related stenosis is the more common form in older Western patients."
},
{
"id": "Q219.2",
"q": "What is the Wilkins score and how is it used?",
"a": "The Wilkins score grades four features of a rheumatic valve on a 1 to 4 scale each: leaflet mobility, leaflet thickening, leaflet calcification, and subvalvular thickening, giving a total of 4 to 16. A score of 8 or less predicts a good result from percutaneous balloon mitral commissurotomy, while scores above 8, especially with heavy commissural calcification or more than mild MR, favor surgery. The score does not apply to MAC-related stenosis, which is not amenable to balloon commissurotomy because there are no fused commissures to split."
}
],
"numbers": [
{
"label": "Wilkins score range",
"value": "4–16",
"unit": ""
},
{
"label": "Wilkins score favorable for balloon commissurotomy",
"value": "≤ 8",
"unit": ""
}
],
"delta": null,
"pearl": "Rheumatic fuses the tips; MAC calcifies the base. Only fused commissures can be split by a balloon.",
"lookalike": {
"vs": "Mitral annular calcification without stenosis",
"discriminator": "MAC alone shows a bright posterior annulus with freely moving tips and a normal gradient; stenosis from MAC produces a raised mean gradient with a small planimetered or continuity-derived area."
},
"related": [
"Q220",
"Q223",
"Q366",
"Q368"
],
"reviewed": "2026-08-26"
},
{
"id": "Q220",
"orig": 220,
"title": "Doppler grading of mitral stenosis",
"lesions": [
"MS",
"HEMODYNAMICS"
],
"lens": "doppler",
"items": [
{
"id": "Q220.1",
"q": "How do you grade mitral stenosis severity with Doppler, and what are the ASE cutoffs?",
"a": "Trace the diastolic CW inflow envelope to obtain the mean gradient, which is the most direct hemodynamic measure: above 10 mmHg is severe, 5 to 10 moderate, below 5 mild, but always report the heart rate because the gradient rises steeply as diastole shortens. Valve area is graded as severe at 1.5 cm² or less and very severe at 1.0 cm² or less, against a normal 4 to 6 cm². Estimate the area by pressure half-time (MVA = 220 / PHT), by planimetry in PSAX at the leaflet tips, by continuity equation using LVOT stroke volume, or by PISA, and check that the methods agree."
},
{
"id": "Q220.2",
"q": "Explain the pressure half-time method and its limitations.",
"a": "PHT is the time for the peak transmitral gradient to fall to half, which on the velocity trace means the time to reach peak velocity divided by 1.41. A tight orifice empties the atrium slowly so the slope is flat and the PHT long; dividing 220 by the PHT in milliseconds gives the area in cm². The method assumes normal LA and LV compliance, so it is unreliable immediately after balloon commissurotomy, in significant AR, in restrictive LV filling, with a stiff hypertrophied ventricle, and in atrial fibrillation where you must average several beats; it also should not be used for prosthetic valves."
},
{
"id": "Q220.3",
"q": "How is PISA applied to calculate mitral valve area in stenosis?",
"a": "In diastole flow converges on the atrial side of the stenotic orifice, and shifting the color baseline toward the LV creates a hemispheric aliasing shell. Area = 2πr² × aliasing velocity ÷ peak inflow velocity, multiplied by the angle correction α/180, where α is the angle between the leaflets because the funnel-shaped leaflets subtend less than a full hemisphere. It is independent of LA compliance and heart rate, which makes it valuable when PHT is unreliable, but the radius is measured near the leaflet tips and small errors are squared."
}
],
"numbers": [
{
"label": "Severe MS valve area",
"value": "≤ 1.5",
"unit": "cm²"
},
{
"label": "Very severe MS valve area",
"value": "≤ 1.0",
"unit": "cm²"
},
{
"label": "Normal mitral valve area",
"value": "4–6",
"unit": "cm²"
},
{
"label": "Severe MS mean gradient",
"value": "> 10",
"unit": "mmHg"
},
{
"label": "PHT constant",
"value": "220",
"unit": "ms·cm²"
},
{
"label": "PHT from deceleration time",
"value": "0.29 × DT",
"unit": ""
}
],
"delta": null,
"pearl": "MVA = 220 / PHT, but PHT lies when compliance changes; PISA and planimetry do not care about compliance.",
"lookalike": null,
"related": [
"Q219",
"Q226"
],
"reviewed": "2026-08-26"
},
{
"id": "Q221",
"orig": 221,
"title": "Causes of aortic regurgitation",
"lesions": [
"AR",
"AORTA"
],
"lens": "etiology",
"items": [
{
"id": "Q221.1",
"q": "Organize the causes of aortic regurgitation by mechanism and explain why the distinction matters on echo.",
"a": "AR arises either from the leaflets or from the root. Leaflet disease includes bicuspid valve (the commonest cause in young Western adults), calcific degeneration, rheumatic retraction, infective endocarditis with perforation or flail, and radiation or drug-induced thickening. Root disease stretches the annulus and pulls the cusps apart even when they are normal: annuloaortic ectasia in Marfan, Loeys-Dietz or Ehlers-Danlos, hypertension-related dilatation, aortitis (syphilis, giant cell, Takayasu, ankylosing spondylitis), and acute dissection with prolapse of a cusp into the LVOT. The mechanism dictates the jet: cusp prolapse or perforation gives an eccentric jet, whereas root dilatation gives a central jet, and root pathology must be measured because the surgery may be a root replacement rather than a valve replacement."
},
{
"id": "Q221.2",
"q": "Which causes present as acute severe AR, and how does the echo differ from chronic AR?",
"a": "Endocarditis, type A dissection, and trauma cause acute AR. The unconditioned LV cannot dilate acutely, so diastolic pressure rises abruptly: you see a normal-sized hyperdynamic LV, premature mitral closure, diastolic mitral regurgitation, a short pressure half-time under 200 ms with early equalization of pressures, and a small forward stroke volume despite a color jet that may look modest because the driving gradient collapses. In chronic AR the ventricle has had time to enlarge eccentrically, so LV dilatation with preserved early function is the rule."
}
],
"numbers": [
{
"label": "Severe AR pressure half-time",
"value": "< 200",
"unit": "ms"
}
],
"delta": null,
"pearl": "Leaflet problem gives an eccentric jet; root problem gives a central jet. Acute AR: normal LV size, premature mitral closure.",
"lookalike": {
"vs": "Mitral stenosis inflow on CW",
"discriminator": "Both are diastolic signals from the apex, but AR is a high-velocity (4 to 5 m/s) signal starting right at aortic closure, whereas MS inflow is low velocity and begins after the isovolumic relaxation period."
},
"related": [
"Q222",
"Q370"
],
"reviewed": "2026-08-26"
},
{
"id": "Q222",
"orig": 222,
"title": "Integrative grading of aortic regurgitation",
"lesions": [
"AR"
],
"lens": "best-method",
"items": [
{
"id": "Q222.1",
"q": "What is the recommended approach to grading aortic regurgitation, and which single parameters are most reliable?",
"a": "No single measure is adequate; ASE 2017 asks for an integrated judgment across structural, color, spectral and quantitative data. Start with valve and root anatomy and LV size, then use the semi-quantitative measures: vena contracta width above 0.6 cm, jet width relative to LVOT diameter of 65% or more in PLAX, and holodiastolic flow reversal in the descending aorta with an end-diastolic velocity of 20 cm/s or more from the suprasternal notch. Add CW density and pressure half-time under 200 ms, then quantify when feasible with EROA of 0.3 cm² or more and regurgitant volume of 60 mL or more from PISA or the volumetric method comparing LVOT and mitral inflow stroke volumes. Grade severe when most specific criteria agree and the LV is dilated; if they conflict, say so and explain why."
},
{
"id": "Q222.2",
"q": "Which AR parameters mislead most often and how do you correct for them?",
"a": "Jet length into the LV is nearly useless because it depends on driving pressure and LV compliance. Jet width to LVOT ratio overestimates eccentric jets that spread along the anterior mitral leaflet; measure at the origin with a Nyquist of 50 to 60 cm/s. Pressure half-time shortens in any condition that raises LV diastolic pressure, so a stiff hypertrophied ventricle can show a short PHT with only moderate AR, and chronic compensated severe AR can show a long PHT. Descending aortic reversal is also seen with a stiff, non-compliant aorta in the elderly, and the volumetric method fails if there is more than mild MR."
}
],
"numbers": [
{
"label": "Severe AR vena contracta",
"value": "> 0.6",
"unit": "cm"
},
{
"label": "Severe AR jet width / LVOT",
"value": "≥ 65",
"unit": "%"
},
{
"label": "Severe AR pressure half-time",
"value": "< 200",
"unit": "ms"
},
{
"label": "Severe AR descending aorta end-diastolic velocity",
"value": "≥ 20",
"unit": "cm/s"
},
{
"label": "Severe AR EROA",
"value": "≥ 0.3",
"unit": "cm²"
},
{
"label": "Severe AR regurgitant volume",
"value": "≥ 60",
"unit": "mL"
}
],
"delta": null,
"pearl": "Vena contracta at the origin, reversal in the descending aorta, and LV dilatation are your three anchors; jet length is not one of them.",
"lookalike": null,
"related": [
"Q221",
"Q370"
],
"reviewed": "2026-08-26"
},
{
"id": "Q223",
"orig": 223,
"title": "Causes of tricuspid stenosis",
"lesions": [
"TS",
"MS"
],
"lens": "etiology",
"items": [
{
"id": "Q223.1",
"q": "What causes tricuspid stenosis, and what should you look for on the left side when you find it?",
"a": "Rheumatic disease is by far the leading cause, and rheumatic TS almost never occurs in isolation; it accompanies mitral stenosis in the great majority of cases, so finding a thickened, doming tricuspid valve should send you back to the mitral valve. Less common causes are carcinoid heart disease, where serotonin-induced plaques thicken and fix the leaflets in a semi-open position producing mixed stenosis and regurgitation, congenital tricuspid atresia or hypoplasia, and obstruction that mimics stenosis: right atrial myxoma, large vegetations, pacemaker lead fibrosis, and metastatic tumor. Other rare causes include Fabry disease, Whipple disease, and endomyocardial fibrosis."
}
],
"numbers": [],
"delta": null,
"pearl": "Rheumatic TS travels with rheumatic MS; carcinoid gives a stiff half-open valve with both TS and TR.",
"lookalike": {
"vs": "Right atrial mass obstructing the valve",
"discriminator": "A myxoma or vegetation prolapses through the orifice in diastole and the leaflets themselves are thin, whereas rheumatic TS shows thick, doming leaflets with a fixed small orifice."
},
"related": [
"Q219",
"Q224",
"Q225",
"Q229"
],
"reviewed": "2026-08-26"
},
{
"id": "Q224",
"orig": 224,
"title": "Bedside findings in tricuspid stenosis",
"lesions": [
"TS"
],
"lens": "physical-exam",
"items": [
{
"id": "Q224.1",
"q": "What are the auscultatory and venous findings of tricuspid stenosis, and how do you tell its murmur from mitral stenosis?",
"a": "TS produces a low-pitched diastolic rumble at the lower left sternal border, often with an opening snap, and because right-sided flow increases with inspiration the murmur gets louder on inspiration (Carvallo sign); the mitral stenosis rumble is heard at the apex and does not change with respiration, or softens. The jugular venous pulse shows a prominent a wave from forceful atrial contraction against the narrowed valve and a slow y descent because the atrium empties slowly; in sinus rhythm the a wave can be large enough to be visible from across the room. Systemic venous congestion, hepatomegaly with presystolic pulsation, ascites and edema out of proportion to lung congestion suggest that TS is limiting flow to the lungs and protecting the patient from pulmonary edema."
}
],
"numbers": [],
"delta": null,
"pearl": "Right-sided murmurs rise with inspiration; giant a wave with a slow y descent is the venous signature of TS.",
"lookalike": {
"vs": "Mitral stenosis murmur",
"discriminator": "MS rumbles at the apex and does not increase with inspiration; TS rumbles at the left lower sternal border and does."
},
"related": [
"Q223",
"Q225",
"Q229"
],
"reviewed": "2026-08-26"
},
{
"id": "Q225",
"orig": 225,
"title": "2D appearance of tricuspid stenosis",
"lesions": [
"TS",
"RV_FUNCTION"
],
"lens": "2d",
"items": [
{
"id": "Q225.1",
"q": "Describe the 2D findings of tricuspid stenosis and the views that show them best.",
"a": "The leaflets are thickened, especially at the tips, with restricted opening and diastolic doming of the anterior leaflet, best seen in the RV inflow view and the apical four-chamber; commissural fusion narrows the orifice, and the chordae are shortened. The right atrium and IVC enlarge from the chronic pressure load, while the RV is usually normal or small because it is underfilled. Planimetry of the tricuspid orifice is unreliable in 2D because the three leaflets rarely lie in one short-axis plane, but 3D en-face imaging can measure it. Always image the mitral valve too, since rheumatic TS almost always coexists with MS, and note any carcinoid-type retraction of the pulmonary valve."
}
],
"numbers": [],
"delta": null,
"pearl": "Doming tricuspid leaflets with a big right atrium and a small, underfilled RV.",
"lookalike": null,
"related": [
"Q223",
"Q226",
"Q224"
],
"reviewed": "2026-08-26"
},
{
"id": "Q226",
"orig": 226,
"title": "Doppler criteria for tricuspid stenosis",
"lesions": [
"TS",
"HEMODYNAMICS"
],
"lens": "doppler",
"items": [
{
"id": "Q226.1",
"q": "How do you assess tricuspid stenosis with Doppler, and what values indicate hemodynamically significant stenosis?",
"a": "Record CW inflow from the RV inflow or apical four-chamber view during quiet respiration and average at least five beats, because right-sided velocities vary with breathing and the patients are often in atrial fibrillation. Significant TS is indicated by a mean gradient of 5 mmHg or more, a pressure half-time of 190 ms or more, and an inflow VTI of 60 cm or more, with a valve area by continuity equation of 1 cm² or less. Because the normal right-sided gradient is tiny, a mean gradient that would be trivial across the mitral valve is significant here; a peak inflow velocity above 1 m/s is already abnormal for the tricuspid valve."
},
{
"id": "Q226.2",
"q": "How is tricuspid valve area calculated, and why is the pressure half-time constant different from the mitral valve?",
"a": "Use the continuity equation: stroke volume from the LVOT or RVOT divided by the tricuspid inflow VTI gives the area, valid only if there is no significant TR. The mitral constant of 220 was validated against catheter data for the mitral valve; the right atrium and ventricle are far more compliant so the decay of the gradient is different, and the constant of 190 was derived for the tricuspid valve, although in practice most laboratories rely on the mean gradient and the PHT threshold rather than a calculated area."
}
],
"numbers": [
{
"label": "Significant TS mean gradient",
"value": "≥ 5",
"unit": "mmHg"
},
{
"label": "Significant TS pressure half-time",
"value": "≥ 190",
"unit": "ms"
},
{
"label": "Significant TS inflow VTI",
"value": "≥ 60",
"unit": "cm"
},
{
"label": "Significant TS valve area (continuity)",
"value": "≤ 1.0",
"unit": "cm²"
},
{
"label": "Tricuspid PHT constant",
"value": "190",
"unit": "ms·cm²"
},
{
"label": "Beats to average for right-sided Doppler",
"value": "≥ 5",
"unit": ""
}
],
"delta": null,
"pearl": "Five, one-ninety, sixty, one: mean gradient 5, PHT 190, VTI 60, area 1.",
"lookalike": null,
"related": [
"Q220",
"Q225",
"Q227",
"Q228",
"Q229"
],
"reviewed": "2026-08-26"
},
{
"id": "Q227",
"orig": 227,
"title": "Best method for tricuspid stenosis",
"lesions": [
"TS"
],
"lens": "best-method",
"items": [
{
"id": "Q227.1",
"q": "What is the most reliable way to establish and grade tricuspid stenosis?",
"a": "Mean gradient from a respiration-averaged CW trace is the most reproducible and best validated single measure, so it is the primary grading number, with pressure half-time and continuity-derived area as supporting evidence. 2D confirms the mechanism (rheumatic doming versus carcinoid fixation versus obstructing mass) and the accompanying RA and IVC dilatation, and 3D planimetry can give an orifice area when the leaflets are well seen. Because TR frequently coexists, grade both lesions; TR invalidates the continuity area but not the mean gradient, though a large regurgitant volume will inflate the gradient by increasing forward flow. Catheterization is rarely needed and is itself insensitive for the small gradients that define TS."
}
],
"numbers": [
{
"label": "Significant TS mean gradient",
"value": "≥ 5",
"unit": "mmHg"
}
],
"delta": null,
"pearl": "Average the mean gradient across the respiratory cycle; that number carries the diagnosis.",
"lookalike": null,
"related": [
"Q226",
"Q228"
],
"reviewed": "2026-08-26"
},
{
"id": "Q228",
"orig": 228,
"title": "Pitfalls in tricuspid stenosis",
"lesions": [
"TS",
"TR",
"DOPPLER_PHYSICS"
],
"lens": "pitfall",
"items": [
{
"id": "Q228.1",
"q": "What errors most commonly lead to over- or under-diagnosis of tricuspid stenosis?",
"a": "Respiration is the first trap: a single inspiratory beat can show a gradient twice the expiratory value, so average five or more beats over a full cycle or record at end-expiratory apnea consistently. Severe TR increases the diastolic flow across the valve and raises the gradient without any true stenosis, and in the same way an ASD with a large left-to-right shunt or high-output states can produce a functional gradient; check for structural leaflet disease before calling stenosis. Under-diagnosis occurs when the sonographer skips right-sided CW altogether because the mitral findings dominate, or dismisses a 5 mmHg gradient as trivial by mitral standards. Beam misalignment in the four-chamber view underestimates velocity; use the RV inflow or subcostal window if the jet is eccentric."
}
],
"numbers": [
{
"label": "Significant TS mean gradient",
"value": "≥ 5",
"unit": "mmHg"
},
{
"label": "Beats to average",
"value": "≥ 5",
"unit": ""
}
],
"delta": null,
"pearl": "A high tricuspid gradient without thick doming leaflets is flow, not stenosis: think TR or shunt.",
"lookalike": {
"vs": "Functional gradient from severe TR or ASD",
"discriminator": "Increased forward flow raises the gradient with thin, freely opening leaflets and a short PHT; true TS has thick, doming leaflets and a PHT of 190 ms or more."
},
"related": [
"Q226",
"Q227"
],
"reviewed": "2026-08-26"
},
{
"id": "Q229",
"orig": 229,
"title": "Tricuspid stenosis vignette",
"lesions": [
"TS",
"MS"
],
"lens": "vignette",
"items": [
{
"id": "Q229.1",
"q": "A 52-year-old woman who emigrated from South Asia presents with fatigue, ankle swelling and abdominal distension but no orthopnea. Her neck veins show large a waves. Echo shows thickened doming mitral leaflets with a mean gradient of 9 mmHg at 78 bpm, a right atrium of 32 cm², and a tricuspid inflow with a peak velocity of 1.4 m/s, a respiration-averaged mean gradient of 6 mmHg and a pressure half-time of 215 ms. What is the diagnosis, and why are her symptoms mostly right-sided?",
"a": "She has rheumatic mitral stenosis with coexisting rheumatic tricuspid stenosis: the tricuspid mean gradient of 6 mmHg and PHT above 190 ms meet the criteria for significant TS, and the dilated right atrium with giant a waves fits a chronic obstruction to RA emptying. The tricuspid lesion throttles flow into the RV and lungs, so her pulmonary venous congestion and orthopnea are muted despite a moderate-to-severe mitral gradient, while systemic venous pressure rises and produces edema, hepatic congestion and ascites. Management should address both valves: isolated relief of the mitral stenosis would expose the previously protected lungs to the full flow through a still-stenotic tricuspid valve, and the surgeon or interventionalist needs to know the tricuspid valve is also diseased."
}
],
"numbers": [
{
"label": "Significant TS mean gradient",
"value": "≥ 5",
"unit": "mmHg"
},
{
"label": "Significant TS pressure half-time",
"value": "≥ 190",
"unit": "ms"
},
{
"label": "Dilated RA area",
"value": "> 18",
"unit": "cm²"
}
],
"delta": null,
"pearl": "Right-sided congestion out of proportion to dyspnea in a rheumatic patient means look for TS.",
"lookalike": null,
"related": [
"Q223",
"Q224",
"Q226",
"Q385"
],
"reviewed": "2026-08-26"
},
{
"id": "Q230",
"orig": 230,
"title": "Bedside signs of tricuspid regurgitation",
"lesions": [
"TR",
"PH"
],
"lens": "physical-exam",
"items": [
{
"id": "Q230.1",
"q": "Describe the murmur of tricuspid regurgitation and the maneuver that helps separate it from mitral regurgitation.",
"a": "TR produces a blowing holosystolic murmur heard best at the left lower sternal border, because the regurgitant jet runs from the RV into the RA throughout systole while RV pressure exceeds RA pressure. The Carvallo sign is the key discriminator: the murmur gets louder with inspiration, since negative intrathoracic pressure increases venous return to the right heart and therefore the volume regurgitated. A mitral regurgitation murmur, by contrast, is loudest at the apex, radiates to the axilla, and does not grow with inspiration. When TR is massive and the RV is failing, the murmur can be soft or even absent because the RV can no longer generate a high velocity across the leaky valve."
},
{
"id": "Q230.2",
"q": "What findings in the neck veins and abdomen accompany severe TR, and what is their mechanism?",
"a": "Severe TR transmits RV systolic pressure straight into the RA and venae cavae, so the normal x descent is replaced by a large systolic CV wave, a visible outward pulsation of the jugular veins that is sometimes called ventricularization of the venous pulse. The same pressure wave travels down the IVC into the hepatic veins, producing a pulsatile liver in systole that you can feel by palpating the right upper quadrant. On echo the counterparts are systolic flow reversal in the hepatic veins and a dilated, non-collapsing IVC, which is why the exam and the Doppler agree so well in severe disease."
}
],
"numbers": [],
"delta": null,
"pearl": "Louder on a deep breath in? Think right side. Carvallo sign marks the murmur as tricuspid.",
"lookalike": {
"vs": "mitral regurgitation murmur",
"discriminator": "MR is apical, radiates to the axilla, and is unchanged by inspiration; TR is parasternal and increases with inspiration (Carvallo sign)."
},
"related": [
"Q82",
"Q86"
],
"reviewed": "2026-08-26"
},
{
"id": "Q231",
"orig": 231,
"title": "M-mode clues in tricuspid regurgitation",
"lesions": [
"TR",
"RV_FUNCTION"
],
"lens": "m-mode",
"items": [
{
"id": "Q231.1",
"q": "Which M-mode findings suggest hemodynamically significant tricuspid regurgitation?",
"a": "M-mode does not show the leak itself, but it captures the consequences. The RV is volume overloaded, so the RV internal dimension is enlarged and the free wall moves briskly. The interventricular septum shows paradoxical motion: because the RV fills with an excess of blood in diastole, the septum is pushed toward the LV and then moves anteriorly during systole instead of thickening toward the LV cavity. Through the IVC, an M-mode cursor shows a plethoric vessel with little or no inspiratory collapse and, when the tracing is timed with the ECG, a systolic expansion that corresponds to the CV wave. A tricuspid annular M-mode (TAPSE) may still be normal or even supranormal early on, because the RV is unloading part of its stroke volume into the low-pressure RA."
},
{
"id": "Q231.2",
"q": "Why can TAPSE be misleading when TR is severe?",
"a": "TAPSE measures how far the lateral tricuspid annulus travels toward the apex in systole, and that excursion depends on both intrinsic RV contractility and the load the RV is working against. Severe TR gives the RV an easy low-pressure escape route into the RA, so the annulus moves well even when the myocardium is beginning to fail. A preserved TAPSE therefore does not exclude RV dysfunction in severe TR, and a falling TAPSE after the valve is repaired often reflects loss of that pop-off rather than new injury. Use it together with FAC, S', and free wall strain, and interpret all of them in the context of the regurgitant volume."
}
],
"numbers": [
{
"label": "TAPSE abnormal",
"value": "< 17",
"unit": "mm"
},
{
"label": "RV S' abnormal",
"value": "< 9.5",
"unit": "cm/s"
},
{
"label": "RV FAC abnormal",
"value": "< 35",
"unit": "%"
}
],
"delta": null,
"pearl": "Paradoxical septum plus a fat IVC on M-mode is a volume-loaded right heart; go find the TR.",
"lookalike": {
"vs": "atrial septal defect",
"discriminator": "Both give RV volume overload with paradoxical septal motion; ASD shows a shunt on color across the atrial septum and usually only mild functional TR, while primary TR shows a large jet with hepatic vein systolic reversal."
},
"related": [
"Q82",
"Q86"
],
"reviewed": "2026-08-26"
},
{
"id": "Q232",
"orig": 232,
"title": "Integrative grading of TR severity",
"lesions": [
"TR"
],
"lens": "best-method",
"items": [
{
"id": "Q232.1",
"q": "What is the best way to grade tricuspid regurgitation, and what are the specific criteria for severe TR?",
"a": "No single measurement is reliable, so ASE 2017 asks you to integrate structural, color, and spectral parameters and to state severity only when they agree. Structural clues are a flail or badly malcoapting leaflet, a tricuspid annulus of 4 cm or more, and a dilated RV, RA, and IVC. On color, a vena contracta of 0.7 cm or more and a PISA-derived EROA of 0.4 cm² or more (regurgitant volume ≥45 mL) define severe. Spectral clues are a dense, triangular, early-peaking CW signal, which tells you the RA pressure rises quickly as a large volume pours in, and systolic flow reversal in the hepatic veins on pulsed Doppler. If the vena contracta says moderate but the hepatic veins reverse and the CW is dense and triangular, believe the hemodynamic signs and call it severe."
},
{
"id": "Q232.2",
"q": "Why is the vena contracta preferred over jet area for TR, and what are its limitations?",
"a": "The vena contracta is the narrowest neck of the jet just distal to the orifice, so it approximates the regurgitant orifice and is largely independent of gain, Nyquist limit, and driving pressure. Jet area, on the other hand, shrinks when RV pressure is low or the jet is eccentric and hugs the atrial wall, so a big leak with a low-pressure RV can look deceptively small. The vena contracta still has weaknesses: the tricuspid orifice is often crescentic rather than round, so a single diameter can misjudge the true area, and multiple jets cannot simply be added. Measure it in the view where the neck is best seen, ideally from more than one plane, and use PISA or 3D when the orifice looks elliptical."
}
],
"numbers": [
{
"label": "Severe TR vena contracta",
"value": "≥ 0.7",
"unit": "cm"
},
{
"label": "Severe TR EROA",
"value": "≥ 0.4",
"unit": "cm²"
},
{
"label": "Severe TR regurgitant volume",
"value": "≥ 45",
"unit": "mL"
},
{
"label": "Dilated tricuspid annulus",
"value": "≥ 4",
"unit": "cm"
}
],
"delta": null,
"pearl": "Dense triangle on CW plus systolic reversal in the hepatic vein: the RA is being hammered, the TR is severe.",
"lookalike": {
"vs": "moderate TR with a low Nyquist setting",
"discriminator": "A low aliasing velocity inflates jet area but not the vena contracta or hepatic vein pattern; severe TR shows reversal and a dense CW envelope at any color setting."
},
"related": [
"Q85",
"Q203",
"Q384"
],
"reviewed": "2026-08-26"
},
{
"id": "Q233",
"orig": 233,
"title": "Pacemaker lead and worsening TR",
"lesions": [
"TR",
"RV_FUNCTION"
],
"lens": "vignette",
"items": [
{
"id": "Q233.1",
"q": "A 71-year-old man with a dual-chamber pacemaker placed three years ago presents with leg swelling and early satiety. On exam there is a holosystolic murmur at the left lower sternal border that gets louder with inspiration, and the liver edge pulsates. Echo shows a dilated RV, RA, and IVC, a tricuspid vena contracta of 0.9 cm, and a dense triangular CW envelope with a peak velocity of 2.3 m/s. What is the diagnosis, and how do you explain the low TR velocity?",
"a": "This is severe tricuspid regurgitation, most likely caused by the ventricular lead interfering with leaflet coaptation, either by pinning the septal or posterior leaflet or by perforating or tethering it. Every finding fits severe TR: the Carvallo-positive murmur, the pulsatile liver from the systolic pressure wave in the hepatic veins, a vena contracta well above the 0.7 cm cutoff, and a dense triangular CW signal. The TR velocity is low because severe regurgitation equalizes RV and RA pressure quickly, so the gradient across the valve is small even though the volume is huge. Do not conclude that pulmonary pressure is normal from this velocity: with a plethoric IVC you should assign an RAP of 15 mmHg, and even then the RVSP estimate is unreliable when TR is this severe."
},
{
"id": "Q233.2",
"q": "What additional imaging would clarify the mechanism, and why does it matter?",
"a": "Three-dimensional TEE from the RV side shows the lead's path across the valve and whether it crosses at a commissure, which is well tolerated, or impinges on a leaflet body, which is not. It also demonstrates leaflet perforation or adherence of the lead to the leaflet. The mechanism matters because lead-related TR can sometimes be treated by repositioning or extracting the lead, or by planning a repair that works around it, whereas functional TR from annular dilation is approached with annuloplasty. Document RV size and function carefully, since the RV will look better than it is while the TR provides a low-pressure outlet."
}
],
"numbers": [
{
"label": "Severe TR vena contracta",
"value": "≥ 0.7",
"unit": "cm"
},
{
"label": "RAP with dilated non-collapsing IVC",
"value": "15",
"unit": "mmHg"
}
],
"delta": null,
"pearl": "A low TR velocity with a huge jet is not reassuring; severe TR flattens the gradient it is measured from.",
"lookalike": {
"vs": "functional TR from pulmonary hypertension",
"discriminator": "PH-driven TR shows a high-velocity jet (>3.4 m/s) with a tethered but structurally intact valve; lead-related TR shows a low-velocity, high-volume jet with a leaflet visibly restrained by the wire."
},
"related": [
"Q87",
"Q133",
"Q384"
],
"reviewed": "2026-08-26"
},
{
"id": "Q234",
"orig": 234,
"title": "Auscultation in pulmonic stenosis",
"lesions": [
"PS"
],
"lens": "physical-exam",
"items": [
{
"id": "Q234.1",
"q": "What are the classic auscultatory features of valvular pulmonic stenosis?",
"a": "Valvular PS produces a crescendo-decrescendo systolic ejection murmur at the left upper sternal border that radiates toward the left shoulder and back, generated by turbulent flow through the narrowed orifice as the RV ejects. A pulmonic ejection click often precedes the murmur; it is the sound of the mobile, domed leaflets snapping to their maximal open position, and it is the only right-sided sound that gets softer with inspiration. The pulmonic component of S2 is delayed and soft because RV ejection is prolonged and the valve closes slowly at a low pressure, so S2 is widely split. In severe stenosis P2 can be inaudible and the murmur peaks late in systole, reflecting the long ejection time."
},
{
"id": "Q234.2",
"q": "Why does the pulmonic ejection click become softer with inspiration when most right-sided sounds get louder?",
"a": "Inspiration increases venous return, which raises RV end-diastolic volume and pressure. With the valve already partly pushed upward by that higher diastolic pressure, the leaflets have less distance to travel when ejection begins, so the click that marks their abrupt halt is muted or disappears. The murmur itself still intensifies with inspiration, because more blood is being forced through the stenosis. On expiration the RV fills less, the leaflets rest lower, and the click returns. This inspiratory fading distinguishes a pulmonic click from an aortic ejection click, which does not vary with respiration."
}
],
"numbers": [],
"delta": null,
"pearl": "The pulmonic click is the odd one out on the right side: it fades on inspiration while the murmur grows.",
"lookalike": {
"vs": "atrial septal defect murmur",
"discriminator": "ASD gives a soft pulmonic flow murmur with fixed splitting of S2 and no click; PS gives a louder, harsher murmur with an ejection click and wide but respiration-variable splitting."
},
"related": [
"Q92",
"Q93"
],
"reviewed": "2026-08-26"
},
{
"id": "Q235",
"orig": 235,
"title": "2D anatomy of pulmonic stenosis",
"lesions": [
"PS",
"CONGENITAL"
],
"lens": "2d",
"items": [
{
"id": "Q235.1",
"q": "What does valvular pulmonic stenosis look like on 2D imaging, and how do you tell it apart from subvalvular and supravalvular obstruction?",
"a": "In typical valvular PS the leaflets are thickened and their commissures partially fused, so in systole they do not open flat against the artery wall but bulge upward into the main PA as a dome, with a small central orifice. The main PA distal to the valve is often dilated because the high-velocity jet strikes the arterial wall. Subvalvular (infundibular) obstruction lives below the valve in the RVOT, where muscle bundles or a fibrous ridge narrow the outflow tract while the valve leaflets themselves look normal; the RVOT is often hypertrophied and the narrowing is dynamic, worsening in late systole. Supravalvular obstruction is a discrete narrowing of the main PA or its branches beyond a normal valve. Sweep the parasternal short axis and the subcostal RVOT view with color to localize the aliasing point, because that is where the obstruction is."
},
{
"id": "Q235.2",
"q": "How does a dysplastic pulmonic valve differ from a domed valve, and which syndrome should it make you think of?",
"a": "A dysplastic valve has three grossly thickened, immobile, myxomatous leaflets with little commissural fusion, so it does not dome; it simply fails to open well, and the annulus is often small. Post-stenotic PA dilation is usually absent. This morphology is characteristic of Noonan syndrome, which also brings short stature, a webbed neck, and hypertrophic cardiomyopathy in a subset of patients. The distinction matters clinically: a domed valve with fused commissures responds well to balloon valvuloplasty, whereas a dysplastic valve often does not and may need surgical replacement."
}
],
"numbers": [],
"delta": null,
"pearl": "Doming means fused commissures and a balloon will help; thick and immobile without doming means dysplastic and think Noonan.",
"lookalike": {
"vs": "infundibular stenosis",
"discriminator": "Infundibular obstruction shows a normal, freely opening valve with the aliasing point below it in a muscular RVOT and a late-peaking dagger-shaped CW profile; valvular PS shows doming with the aliasing at the leaflet tips."
},
"related": [
"Q91",
"Q94",
"Q178"
],
"reviewed": "2026-08-26"
},
{
"id": "Q236",
"orig": 236,
"title": "Best approach to quantifying PS",
"lesions": [
"PS",
"DOPPLER_PHYSICS"
],
"lens": "best-method",
"items": [
{
"id": "Q236.1",
"q": "What is the most reliable echo method for grading the severity of pulmonic stenosis, and how do you optimize it?",
"a": "Peak instantaneous gradient from continuous-wave Doppler across the pulmonic valve is the accepted standard, converted from peak velocity with the simplified Bernoulli equation, 4v². Alignment is everything: try the parasternal short axis at the aortic level, the modified high left parasternal view of the RVOT, and the subcostal RVOT view, and keep the best envelope. Use CW rather than pulsed Doppler because the velocity exceeds the Nyquist limit, and trace the envelope with the densest, clearest outline. Grade the result as mild below 36 mmHg, moderate 36 to 64, and severe above 64 mmHg, which corresponds to a peak velocity above 4 m/s. Complement the gradient with 2D assessment of leaflet mobility, RV hypertrophy, and RV systolic pressure from TR, because the ventricle's response to the obstruction confirms the severity."
},
{
"id": "Q236.2",
"q": "When would you add a mean gradient or the LVOT-style continuity approach, and why is the peak gradient still preferred?",
"a": "Mean gradient is useful when the peak is borderline or when the trace is noisy, and it is the number catheterization laboratories report, so it helps reconcile the two. Valve area by continuity is rarely used on the right side because the RVOT is hard to measure reproducibly and the pulsed Doppler sample is prone to contamination near the obstruction. Peak gradient stays preferred because the guideline thresholds and the outcome data behind intervention decisions are anchored to it, and because the pulmonic jet is easy to align from the parasternal window. Report RVSP alongside, since a high gradient with a high RVSP and RV hypertrophy is more convincing than a gradient alone."
}
],
"numbers": [
{
"label": "Bernoulli constant",
"value": "4",
"unit": "× v²"
},
{
"label": "Mild PS peak gradient",
"value": "< 36",
"unit": "mmHg"
},
{
"label": "Moderate PS peak gradient",
"value": "36–64",
"unit": "mmHg"
},
{
"label": "Severe PS peak gradient",
"value": "> 64",
"unit": "mmHg"
},
{
"label": "Severe PS peak velocity",
"value": "> 4",
"unit": "m/s"
}
],
"delta": null,
"pearl": "Same rule as aortic stenosis: 4 m/s is the line that separates severe from the rest.",
"lookalike": null,
"related": [
"Q92",
"Q90",
"Q238"
],
"reviewed": "2026-08-26"
},
{
"id": "Q237",
"orig": 237,
"title": "Traps in pulmonic gradient measurement",
"lesions": [
"PS",
"PR",
"DOPPLER_PHYSICS"
],
"lens": "pitfall",
"items": [
{
"id": "Q237.1",
"q": "How can a high velocity across the RVOT mislead you about the location and severity of pulmonic obstruction?",
"a": "Continuous-wave Doppler adds up every velocity along its line, so it cannot tell you whether the jet was generated at the valve or in the infundibulum below it. A patient with both a dynamic subvalvular narrowing and a mildly stenotic valve will give a single tall envelope that overstates the valve. Look at the shape: fixed valvular stenosis gives a symmetric, early-peaking envelope, whereas dynamic infundibular obstruction peaks late and is dagger shaped. Then walk a pulsed Doppler sample up the RVOT to find where the velocity jumps. In tetralogy repair or in RV hypertrophy from any cause, the infundibular component can be the main obstruction, and it will worsen with inotropes and improve with volume, the opposite of a fixed valve."
},
{
"id": "Q237.2",
"q": "Why is a pulmonic gradient flow dependent, and how do PR and cardiac output confound it?",
"a": "Bernoulli translates velocity into pressure, and velocity depends on how much blood crosses the orifice per unit time, not only on how small the orifice is. Significant pulmonic regurgitation adds the regurgitant volume back onto the next stroke, so the forward flow across the valve is larger and the gradient rises even though the anatomic stenosis is unchanged; this is why patients after tetralogy repair with free PR can carry a moderate-looking gradient across a mildly narrowed outflow. The reverse happens with low output or RV failure, where a severely stenotic valve produces a modest gradient. Sedation, anemia, fever, and pregnancy all shift the number the same way. When the gradient and the anatomy disagree, report both, comment on the flow state, and consider a cardiac MRI or catheterization before labeling the valve."
},
{
"id": "Q237.3",
"q": "What happens to the PR-derived pulmonary artery pressures when pulmonic stenosis is present?",
"a": "Pulmonary artery diastolic pressure from the PR end-diastolic velocity and mean PA pressure from the PR peak velocity assume that the pressure downstream of the valve is the pulmonary artery pressure, which holds. However, RVSP from the TR jet no longer equals PA systolic pressure, because the stenotic valve sits between them; the PA systolic pressure is the RVSP minus the transpulmonic gradient. If you forget this, a patient with severe PS and a 90 mmHg RVSP is mislabeled as having severe pulmonary hypertension when the PA pressure is actually normal. Always subtract the peak PS gradient from the RVSP before commenting on pulmonary pressure."
}
],
"numbers": [
{
"label": "PA systolic pressure with PS",
"value": "RVSP − peak PS gradient",
"unit": "mmHg"
}
],
"delta": null,
"pearl": "A tall TR jet plus a stenotic pulmonic valve says RV pressure, not PA pressure; subtract the gradient before you call PH.",
"lookalike": {
"vs": "double-chambered right ventricle",
"discriminator": "The obstruction in DCRV is a muscle band in the mid RV cavity, well below the infundibulum, with a normal RVOT and valve; the aliasing point on color is mid-ventricular rather than at the outflow."
},
"related": [
"Q92",
"Q133",
"Q87"
],
"reviewed": "2026-08-26"
},
{
"id": "Q238",
"orig": 238,
"title": "Pulmonic stenosis severity thresholds",
"lesions": [
"PS"
],
"lens": "numbers",
"items": [
{
"id": "Q238.1",
"q": "State the peak gradient and velocity cutoffs used to grade pulmonic stenosis, and explain why they are set higher than the equivalent mean-gradient thresholds for aortic stenosis.",
"a": "Pulmonic stenosis is graded by the peak instantaneous gradient: mild is below 36 mmHg, corresponding to a peak velocity under 3 m/s; moderate is 36 to 64 mmHg, or roughly 3 to 4 m/s; severe is above 64 mmHg, meaning a peak velocity above 4 m/s. Because these are peak instantaneous values, they are naturally larger than the mean gradients used for aortic stenosis, where 40 mmHg mean marks severe. The pulmonic thresholds also reflect the right ventricle's tolerance: the RV adapts to pressure load with hypertrophy for decades, so a higher bar is used before recommending intervention. Note that 64 mmHg is simply 4 × 4², so the severe cutoff is the same 4 m/s velocity used for aortic stenosis."
},
{
"id": "Q238.2",
"q": "What supporting numbers help confirm that a pulmonic gradient truly reflects severe disease?",
"a": "A severe fixed obstruction should raise RV systolic pressure, so expect a TR jet that reflects an RVSP far above the normal 25 mmHg; the PA pressure beyond the valve will be normal once you subtract the gradient. RV free wall thickness above 5 mm on the subcostal view indicates pressure-load hypertrophy. A normal RV and a normal RVSP with a gradient above 64 mmHg should prompt a search for a flow-driven artifact, such as significant PR or a high-output state, before the label is applied."
}
],
"numbers": [
{
"label": "Mild PS peak gradient",
"value": "< 36",
"unit": "mmHg"
},
{
"label": "Moderate PS peak gradient",
"value": "36–64",
"unit": "mmHg"
},
{
"label": "Severe PS peak gradient",
"value": "> 64",
"unit": "mmHg"
},
{
"label": "Severe PS peak velocity",
"value": "> 4",
"unit": "m/s"
},
{
"label": "Mild PS peak velocity",
"value": "< 3",
"unit": "m/s"
},
{
"label": "Normal RV systolic pressure",
"value": "25",
"unit": "mmHg"
},
{
"label": "RV hypertrophy free wall",
"value": "> 5",
"unit": "mm"
}
],
"delta": null,
"pearl": "36 and 64 are 4 × 3² and 4 × 4²: memorize the velocities 3 and 4 and the gradients follow.",
"lookalike": null,
"related": [
"Q92",
"Q236"
],
"reviewed": "2026-08-26"
},
{
"id": "Q239",
"orig": 239,
"title": "Young adult with a systolic murmur and click",
"lesions": [
"PS",
"CONGENITAL"
],
"lens": "vignette",
"items": [
{
"id": "Q239.1",
"q": "A 24-year-old woman is referred for a murmur noted at a pre-employment physical. She is asymptomatic. There is a harsh crescendo-decrescendo murmur at the left upper sternal border with a click that fades when she breathes in, and S2 is widely split. Echo shows thickened pulmonic leaflets that dome in systole, a dilated main PA, a CW peak velocity across the valve of 4.4 m/s, mild TR with a velocity of 4.0 m/s, and an IVC of 1.6 cm that collapses well. Grade the stenosis and calculate the pulmonary artery systolic pressure.",
"a": "The doming leaflets with post-stenotic dilation indicate congenital valvular pulmonic stenosis. A peak velocity of 4.4 m/s gives a peak gradient of 4 × 4.4² ≈ 77 mmHg, which is above 64 mmHg and therefore severe. RVSP from the TR jet is 4 × 4.0² + 3 ≈ 67 mmHg, using an RAP of 3 mmHg for a small, collapsing IVC. The PA systolic pressure is the RVSP minus the valve gradient, roughly 67 − 77, which cannot be negative in reality and simply tells you the PA pressure is low-normal and the two estimates carry measurement error; the point is that the RV is generating high pressure to push through the valve while the pulmonary circulation itself is unloaded. Report severe valvular PS with RV pressure overload and normal pulmonary artery pressure."
},
{
"id": "Q239.2",
"q": "What else should the report include, and what is the likely management?",
"a": "Describe RV wall thickness and systolic function, since chronic pressure load produces RV hypertrophy and eventually dysfunction; document the size of the annulus and main PA, because balloon sizing depends on them; and look for associated lesions, especially a secundum ASD or patent foramen ovale, which coexist with PS. Note leaflet morphology explicitly: a domed valve with fused commissures, as here, is an excellent candidate for percutaneous balloon valvuloplasty, which is the treatment of choice for severe valvular PS regardless of symptoms. A dysplastic valve would push the plan toward surgery. Mention any pulmonic regurgitation, because it is the expected trade-off after balloon dilation and needs a baseline."
}
],
"numbers": [
{
"label": "Severe PS peak gradient",
"value": "> 64",
"unit": "mmHg"
},
{
"label": "RAP with small collapsing IVC",
"value": "3",
"unit": "mmHg"
},
{
"label": "IVC normal cutoff",
"value": "≤ 2.1",
"unit": "cm"
}
],
"delta": null,
"pearl": "Severe valvular PS with doming leaflets is a balloon case; RV pressure is high but the lungs are not.",
"lookalike": {
"vs": "pulmonary hypertension with a normal valve",
"discriminator": "In PH the pulmonic valve opens normally, there is no transvalvular gradient, and the high TR velocity reflects true PA pressure; in PS the valve domes and the PA pressure beyond it is normal."
},
"related": [
"Q93",
"Q133"
],
"reviewed": "2026-08-26"
},
{
"id": "Q240",
"orig": 240,
"title": "Defining pulmonic regurgitation",
"lesions": [
"PR"
],
"lens": "definition",
"items": [
{
"id": "Q240.1",
"q": "Define pulmonic regurgitation and explain when it is physiologic versus pathologic.",
"a": "Pulmonic regurgitation is retrograde diastolic flow from the pulmonary artery into the right ventricle because the pulmonic leaflets fail to seal. A trivial or mild central jet is found in the majority of healthy adults, especially with modern color Doppler, because the valve closes against a low diastolic pressure and a small amount of leakage is normal; it produces no RV enlargement and no murmur. Pathologic PR occurs when the annulus is stretched by pulmonary hypertension or PA dilation, when the leaflets are absent or damaged after surgery or balloon valvuloplasty, or when they are destroyed by endocarditis or deformed by carcinoid. Significant PR is a volume load, so the RV dilates and, over years, fails; the clinical importance lies in the duration and volume of the leak rather than in its mere presence."
}
],
"numbers": [],
"delta": null,
"pearl": "A whisper of PR is normal; a wide jet with a dilated RV is disease.",
"lookalike": null,
"related": [
"Q95",
"Q96",
"Q97"
],
"reviewed": "2026-08-26"
},
{
"id": "Q241",
"orig": 241,
"title": "Auscultation of pulmonic regurgitation",
"lesions": [
"PR",
"PH"
],
"lens": "physical-exam",
"items": [
{
"id": "Q241.1",
"q": "What is the Graham Steell murmur, and how does it differ from the murmur of low-pressure pulmonic regurgitation?",
"a": "The Graham Steell murmur is a high-pitched, blowing, decrescendo early-diastolic murmur at the left upper sternal border produced by PR secondary to pulmonary hypertension. Because the PA diastolic pressure is high, the regurgitant velocity is high and the murmur is loud, begins immediately after a loud P2, and sounds very much like aortic regurgitation; it increases with inspiration, which is the clue that it is right sided. Low-pressure PR, as after tetralogy repair or valvuloplasty, sounds completely different: the PA diastolic pressure is near RV diastolic pressure, so the jet is slow and the murmur is low pitched, short, and rumbling, sometimes absent altogether even when the regurgitation is free. In that setting the loudest sign may be the flow murmur in systole from the large forward stroke volume."
},
{
"id": "Q241.2",
"q": "How do you distinguish a Graham Steell murmur from aortic regurgitation at the bedside?",
"a": "Both are decrescendo early-diastolic murmurs along the left sternal border, so location alone fails. Respiration helps: PR gets louder with inspiration while AR does not. The company it keeps is decisive. Pulmonary hypertension gives a loud, palpable P2, an RV heave, and sometimes a TR murmur, whereas AR gives a wide pulse pressure, a bounding carotid, and a displaced apical impulse. AR also produces the peripheral signs of aortic run-off, which PR never does. When the exam is equivocal, Doppler settles it by showing which valve the diastolic jet comes from."
}
],
"numbers": [],
"delta": null,
"pearl": "Graham Steell is AR's sound-alike with a loud P2 and no wide pulse pressure.",
"lookalike": {
"vs": "aortic regurgitation murmur",
"discriminator": "AR does not change with respiration and comes with a wide pulse pressure and bounding pulses; Graham Steell increases with inspiration and is accompanied by a loud P2 and RV heave."
},
"related": [
"Q96"
],
"reviewed": "2026-08-26"
},
{
"id": "Q242",
"orig": 242,
"title": "Doppler assessment of pulmonic regurgitation",
"lesions": [
"PR",
"PH",
"HEMODYNAMICS"
],
"lens": "doppler",
"items": [
{
"id": "Q242.1",
"q": "How is the PR jet used to estimate pulmonary artery pressures?",
"a": "In diastole the pulmonic valve separates the pulmonary artery from the right ventricle, so the velocity of the PR jet at any instant reflects the pressure difference between them. At end-diastole the RV pressure equals RA pressure, so 4 × (PR end-diastolic velocity)² plus RAP gives the pulmonary artery diastolic pressure. At the start of diastole the gradient is largest and corresponds closely to mean PA pressure, so 4 × (PR peak early-diastolic velocity)² plus RAP estimates mean PAP. An end-diastolic PR velocity above about 2.2 m/s therefore points to an elevated PA diastolic pressure. These numbers are valid only when the PR jet is well aligned and when there is no pulmonic stenosis interposed; align from the parasternal short axis at the aortic level and use CW."
},
{
"id": "Q242.2",
"q": "Which Doppler features indicate severe pulmonic regurgitation?",
"a": "Severe PR is recognized more by shape and width than by velocity. A jet width at its origin of 50 to 65 percent or more of the pulmonic annulus diameter on color indicates a large regurgitant orifice. On CW the envelope is dense and decelerates rapidly, with a pressure half-time under 100 ms, because the RV and PA pressures equalize quickly when a large volume returns to a compliant RV; in free PR the signal may end well before the next QRS, which is called early termination. Pulsed Doppler in the main or branch pulmonary arteries shows diastolic flow reversal, and the ratio of reverse to forward flow, or a regurgitant fraction by the RVOT VTI method, rises with severity. A dilated RV with paradoxical septal motion supports that the volume load is real."
}
],
"numbers": [
{
"label": "PA diastolic pressure",
"value": "4 × PR EDV² + RAP",
"unit": "mmHg"
},
{
"label": "Mean PA pressure",
"value": "4 × PR peak velocity² + RAP",
"unit": "mmHg"
},
{
"label": "Severe PR pressure half-time",
"value": "< 100",
"unit": "ms"
},
{
"label": "Severe PR jet width / annulus",
"value": "≥ 50–65",
"unit": "%"
},
{
"label": "PR end-diastolic velocity suggesting raised PADP",
"value": "> 2.2",
"unit": "m/s"
}
],
"delta": null,
"pearl": "PR peak gives mean PAP, PR end gives PADP; TR gives systolic. Three velocities, three pressures.",
"lookalike": {
"vs": "coronary artery flow in the RVOT",
"discriminator": "A right coronary or conus branch signal is low velocity, biphasic, and does not originate at the leaflets; PR arises at the valve line and tracks the PA-RV gradient."
},
"related": [
"Q95",
"Q133",
"Q131",
"Q243",
"Q245"
],
"widgets": [
{
"id": "calc",
"opts": {
"k": "pr"
}
}
],
"reviewed": "2026-08-26"
},
{
"id": "Q243",
"orig": 243,
"title": "Best method for grading PR",
"lesions": [
"PR",
"RV_FUNCTION"
],
"lens": "best-method",
"items": [
{
"id": "Q243.1",
"q": "What is the most reliable way to grade pulmonic regurgitation on echo, and when should you look beyond echo?",
"a": "No single parameter is robust, so combine them. Start with color jet width at the valve relative to the annulus, which is the most reproducible echo measure; add the CW envelope density and pressure half-time, with early termination and a half-time under 100 ms marking severe; and add pulsed Doppler diastolic flow reversal in the branch pulmonary arteries, which is specific for severe PR because reversal deep in the branches requires a large regurgitant volume. Weigh these against the RV response: a normal-sized RV with preserved function makes severe chronic PR unlikely. Echo consistently underestimates PR because the RVOT is hard to image in adults, so when the decision is whether to replace the pulmonic valve, cardiac MRI is the reference method, giving a regurgitant fraction and precise RV volumes that guide timing."
},
{
"id": "Q243.2",
"q": "Why is jet length a poor measure of PR severity?",
"a": "Jet length depends on the pressure driving the jet, not on the size of the hole. In pulmonary hypertension a small orifice produces a long, high-velocity jet that reaches deep into the RV, while after tetralogy repair a valve that is essentially absent can produce a short, broad, brief jet because the PA and RV pressures equalize almost immediately. Width at the origin and the hemodynamic signs, such as branch PA reversal and a short half-time, track the volume of regurgitation far better. This is the same principle that makes vena contracta superior to jet area for MR and TR."
}
],
"numbers": [
{
"label": "Severe PR pressure half-time",
"value": "< 100",
"unit": "ms"
},
{
"label": "Severe PR jet width / annulus",
"value": "≥ 50–65",
"unit": "%"
}
],
"delta": null,
"pearl": "Wide, brief, and reversing in the branches beats long and skinny; length is pressure, width is volume.",
"lookalike": null,
"related": [
"Q95",
"Q242"
],
"reviewed": "2026-08-26"
},
{
"id": "Q244",
"orig": 244,
"title": "Overcalling and undercalling PR",
"lesions": [
"PR",
"CONGENITAL"
],
"lens": "pitfall",
"items": [
{
"id": "Q244.1",
"q": "How common is physiologic pulmonic regurgitation, and how do you avoid reporting it as disease?",
"a": "Color Doppler detects a small central PR jet in roughly 60 to 80 percent of normal adults, and in young people with good windows the figure approaches nearly everyone. The jet is thin, central, brief, and low velocity, and it comes with a normal-sized RV, a normal pulmonic annulus, and a normal PA. Grade it as trivial or physiologic and say so, because a report that lists pulmonic regurgitation without qualification generates needless follow-up. The only time a small jet deserves attention is when the end-diastolic velocity is high, which signals pulmonary hypertension rather than valve disease."
},
{
"id": "Q244.2",
"q": "Why is pulmonic regurgitation after tetralogy of Fallot repair so easy to underestimate, and what should the report emphasize?",
"a": "After a transannular patch the valve is often functionally absent, so the PA and RV pressures equalize early in diastole. The jet is then short in duration and low in velocity, the color signal is brief and may look unimpressive, and the CW envelope can be faint and end early, all of which read as mild to an untrained eye when the regurgitation is actually free. A dilated RVOT also makes alignment difficult. Focus the report on the consequences: RV end-diastolic size and function, paradoxical septal motion, the width of the jet relative to the annulus, and diastolic flow reversal in the branch pulmonary arteries. Serial RV volumes by cardiac MRI drive the timing of pulmonic valve replacement, so echo's job is to flag progression and RV decline, not to stand alone."
}
],
"numbers": [
{
"label": "Prevalence of physiologic PR in normal adults",
"value": "60–80",
"unit": "%"
}
],
"delta": null,
"pearl": "In repaired tetralogy, a PR jet that is short and faint is not mild; it is so free the pressures equalize before you can see it.",
"lookalike": {
"vs": "pathologic PR",
"discriminator": "Physiologic PR is a thin central jet with normal RV size and a normal annulus; pathologic PR is wide relative to the annulus, reverses flow in the branch PAs, and enlarges the RV."
},
"related": [
"Q95",
"Q96",
"Q246",
"Q390"
],
"reviewed": "2026-08-26"
},
{
"id": "Q245",
"orig": 245,
"title": "Pulmonic regurgitation by the numbers",
"lesions": [
"PR",
"PH"
],
"lens": "numbers",
"items": [
{
"id": "Q245.1",
"q": "List the numeric criteria used to grade pulmonic regurgitation and to derive pulmonary pressures from the PR jet.",
"a": "For severity, the two most-cited echo numbers are a jet width at the origin of at least 50 to 65 percent of the pulmonic annulus diameter and a CW pressure half-time under 100 ms, both indicating severe PR; a regurgitant fraction by MRI of 40 percent or more is generally accepted as severe and is the reference number for surgical decisions. For pressures, the PR end-diastolic velocity gives PA diastolic pressure by 4v² plus RAP, and the PR peak early-diastolic velocity gives mean PA pressure the same way; a mean PAP above 20 mmHg at rest defines pulmonary hypertension in the current ESC/ERS definition. Use the same RAP you would for the TR jet: 3 mmHg when the IVC is 2.1 cm or less and collapses more than 50 percent, 15 when it is dilated and does not collapse, and 8 in between."
}
],
"numbers": [
{
"label": "Severe PR jet width / annulus",
"value": "≥ 50–65",
"unit": "%"
},
{
"label": "Severe PR pressure half-time",
"value": "< 100",
"unit": "ms"
},
{
"label": "Severe PR regurgitant fraction (MRI)",
"value": "≥ 40",
"unit": "%"
},
{
"label": "PA diastolic pressure",
"value": "4 × PR EDV² + RAP",
"unit": "mmHg"
},
{
"label": "Mean PA pressure",
"value": "4 × PR peak velocity² + RAP",
"unit": "mmHg"
},
{
"label": "Pulmonary hypertension mPAP",
"value": "> 20",
"unit": "mmHg"
},
{
"label": "RAP low / intermediate / high",
"value": "3 / 8 / 15",
"unit": "mmHg"
},
{
"label": "IVC size cutoff",
"value": "≤ 2.1",
"unit": "cm"
}
],
"delta": {
"was": "Older teaching defined pulmonary hypertension as a mean PA pressure of 25 mmHg or more.",
"now": "Current guideline: pulmonary hypertension is a resting mean PA pressure above 20 mmHg, with PVR above 2 Wood units for the precapillary form.",
"source": "ESC-ERS 2022 PH"
},
"pearl": "Half-time under 100 for the pulmonic, under 200 for the aortic: the right side equalizes twice as fast because the pressures are lower.",
"lookalike": null,
"related": [
"Q133",
"Q242"
],
"reviewed": "2026-08-26"
},
{
"id": "Q246",
"orig": 246,
"title": "Dilated RV decades after tetralogy repair",
"lesions": [
"PR",
"CONGENITAL",
"RV_FUNCTION"
],
"lens": "vignette",
"items": [
{
"id": "Q246.1",
"q": "A 34-year-old man who underwent tetralogy of Fallot repair with a transannular patch in infancy reports declining exercise tolerance. Echo shows a markedly dilated RV with a basal diameter of 52 mm, paradoxical septal motion, TAPSE 15 mm, a broad, brief color jet in the RVOT that fills the annulus in diastole, and pulsed Doppler diastolic flow reversal in both branch pulmonary arteries. There is a residual RVOT gradient of 20 mmHg. What is the diagnosis and the main concern?",
"a": "This is severe, essentially free pulmonic regurgitation after tetralogy repair, the expected long-term consequence of a transannular patch that leaves the valve incompetent. The jet width filling the annulus and reversal deep in the branch pulmonary arteries are the specific signs; the brevity of the jet reflects rapid pressure equalization rather than a small leak. The RV has responded with volume-overload dilation, well beyond the 41 mm basal diameter cutoff, and it is beginning to fail, as shown by a TAPSE below 17 mm and the exercise intolerance. The concern is irreversible RV dysfunction and ventricular arrhythmia, so the patient needs prompt referral for pulmonic valve replacement evaluation; the mild residual RVOT gradient is not the driver here."
},
{
"id": "Q246.2",
"q": "What further imaging and reporting details are needed, and why?",
"a": "Cardiac MRI is essential: it measures RV end-diastolic and end-systolic volume indices and the PR regurgitant fraction, and it is these numbers, together with symptoms and RV EF, that determine the timing of pulmonic valve replacement, since replacement after the RV has dilated too far does not restore function. On echo, document RV size and function with FAC and free wall strain in addition to TAPSE, measure the RVOT and annulus for possible transcatheter valve sizing, quantify any TR and the RVSP, look for residual VSD patch leaks with color, and assess the aortic root, which dilates in a subset of tetralogy patients. Comment on QRS duration if available, because a very wide QRS with a dilated RV raises arrhythmic risk."
}
],
"numbers": [
{
"label": "RV basal diameter dilated",
"value": "> 41",
"unit": "mm"
},
{
"label": "TAPSE abnormal",
"value": "< 17",
"unit": "mm"
},
{
"label": "RV FAC abnormal",
"value": "< 35",
"unit": "%"
},
{
"label": "RV free wall strain abnormal",
"value": "> −20",
"unit": "%"
}
],
"delta": null,
"pearl": "Repaired tetralogy plus a big RV: the diagnosis is free PR until proven otherwise, and MRI sets the surgical clock.",
"lookalike": {
"vs": "residual RVOT obstruction as the cause of RV dilation",
"discriminator": "Pressure load from residual PS produces RV hypertrophy with a preserved cavity size and a high, symmetric CW gradient; free PR produces a dilated, thin-walled RV with a low residual gradient and branch PA diastolic reversal."
},
"related": [
"Q95",
"Q97",
"Q244",
"Q390"
],
"reviewed": "2026-08-26"
},
{
"id": "Q247",
"orig": 247,
"title": "2D diagnostic criteria for HCM",
"lesions": [
"HCM"
],
"lens": "2d",
"items": [
{
"id": "Q247.1",
"q": "What 2D wall-thickness criteria establish a diagnosis of hypertrophic cardiomyopathy, and how does the septal-to-posterior ratio help?",
"a": "HCM is diagnosed when any LV segment measures 15 mm or more at end-diastole with no loading condition (hypertension, aortic stenosis) that could explain it. The threshold drops to 13 mm when a first-degree relative has proven HCM or the patient carries a pathogenic sarcomere variant, because pretest probability is higher. Asymmetric distribution is the classic clue: a septal-to-posterior (inferolateral) wall ratio of 1.3 or greater in a normotensive patient points to HCM rather than pressure-overload hypertrophy, which thickens the walls symmetrically. Measure in PSAX or PLAX at end-diastole and avoid including RV trabeculations or the moderator band in the septal number, which is the commonest cause of a falsely thick septum."
},
{
"id": "Q247.2",
"q": "Describe the apical variant of HCM and why it is easy to miss on a standard study.",
"a": "Apical HCM concentrates the hypertrophy in the distal third of the ventricle, so the cavity takes on a spade shape in the apical four-chamber view at end-diastole while the basal septum can look normal. Foreshortened apical views and near-field dropout hide the thick apex, and the wall may be mistaken for trabeculation or thrombus. Ultrasound enhancing agent is indicated when the apex is not well seen, and it also unmasks the apical aneurysm that develops in a minority of these patients. The ECG usually shows giant negative T waves in the precordial leads, which should prompt a careful apical look."
},
{
"id": "Q247.3",
"q": "Explain the mechanism of systolic anterior motion of the mitral valve in obstructive HCM.",
"a": "The thick basal septum narrows the outflow tract, so blood accelerates through it in early systole. Elongated, anteriorly displaced leaflets and papillary muscles place the mitral apparatus in that high-velocity stream, and drag forces plus a Venturi effect pull the anterior leaflet (or chordae) toward the septum. Leaflet-septal contact creates a dynamic gradient that peaks in mid-to-late systole, producing the dagger-shaped CW envelope. Because the leaflets are pulled apart, coaptation fails and a posteriorly directed MR jet appears in mid-late systole; an anteriorly directed jet should make you suspect intrinsic leaflet disease instead."
}
],
"numbers": [
{
"label": "HCM wall thickness, sporadic",
"value": "≥ 15",
"unit": "mm"
},
{
"label": "HCM wall thickness, family history or genotype positive",
"value": "≥ 13",
"unit": "mm"
},
{
"label": "Septal-to-posterior wall ratio suggesting asymmetric hypertrophy",
"value": "≥ 1.3",
"unit": "ratio"
},
{
"label": "Normal LV wall thickness",
"value": "0.6–1.0",
"unit": "cm"
}
],
"delta": null,
"pearl": "Fifteen for anyone, thirteen for family; a septum 1.3 times the posterior wall says asymmetric, and a spade-shaped apex says apical variant.",
"lookalike": {
"vs": "Hypertensive concentric LVH",
"discriminator": "Hypertensive hypertrophy is symmetric (ratio <1.3), rarely exceeds 15 mm, has no SAM, and comes with a blood pressure history; HCM is asymmetric, often >15 mm, and may show SAM with a dynamic LVOT gradient."
},
"related": [
"Q134",
"Q135",
"Q138",
"Q139",
"Q372",
"Q374"
],
"reviewed": "2026-08-26"
},
{
"id": "Q248",
"orig": 248,
"title": "Mimics of hypertrophic cardiomyopathy",
"lesions": [
"HCM",
"RCM",
"HTN"
],
"lens": "pitfall",
"items": [
{
"id": "Q248.1",
"q": "How do you separate athlete's heart from HCM when wall thickness falls in the gray zone?",
"a": "Endurance training produces balanced remodeling: the walls thicken modestly, usually no more than 13 mm, and the cavity enlarges in proportion, with an LVIDd often above 55 mm. HCM thickens the wall without enlarging the cavity, so a small ventricle with a thick wall is the key discriminator. Diastolic function is normal or supranormal in the athlete (brisk e', low E/e') and impaired in HCM, and the athlete's hypertrophy regresses after several weeks of detraining while HCM does not. Family history, an abnormal ECG beyond voltage criteria, and LA enlargement all tilt the answer toward HCM."
},
{
"id": "Q248.2",
"q": "What features distinguish hypertensive LVH and a sigmoid septum from true HCM?",
"a": "Hypertensive hypertrophy is concentric and symmetric, so the septal-to-posterior ratio stays below 1.3 and the increased relative wall thickness (>0.42) is accompanied by a clear pressure history. The sigmoid septum is an age-related angulation of the basal septum that bulges into the outflow tract; the rest of the septum and free wall are normal thickness, and while it can generate a small provoked gradient, there is no SAM at rest and no family history. Both entities lack the myocardial disarray that gives HCM its patchy, bright texture and its reduced longitudinal strain despite a normal EF."
},
{
"id": "Q248.3",
"q": "Why is cardiac amyloidosis a dangerous mimic of HCM, and what tells them apart?",
"a": "Amyloid infiltration thickens the LV walls and can produce asymmetric patterns and even outflow obstruction, so it fulfills the 15 mm rule. The giveaways are that the thickening is biventricular with thickened valves and interatrial septum, a small pericardial effusion is common, and strain shows an apical-sparing pattern rather than the septal strain drop of HCM. The ECG is the biggest clue: HCM shows high voltage and often deep T-wave inversion, whereas amyloid gives low or normal voltage despite a thick wall, the so-called voltage-mass mismatch. Restrictive filling with a very low e' in an older patient with a thick heart should always raise amyloid before labeling it HCM."
}
],
"numbers": [
{
"label": "Athlete's heart wall thickness, usual ceiling",
"value": "≤ 13",
"unit": "mm"
},
{
"label": "Gray zone between athlete and HCM",
"value": "13–15",
"unit": "mm"
},
{
"label": "Concentric remodeling relative wall thickness",
"value": "> 0.42",
"unit": "ratio"
},
{
"label": "Septal-to-posterior ratio favoring HCM",
"value": "≥ 1.3",
"unit": "ratio"
}
],
"delta": null,
"pearl": "Big cavity with a thick wall is the athlete; small cavity with a thick wall is HCM; thick wall with low voltage is amyloid.",
"lookalike": {
"vs": "Cardiac amyloidosis",
"discriminator": "Amyloid gives biventricular and valvular thickening, low ECG voltage, apical-sparing strain, and restrictive filling; HCM gives high voltage, asymmetric septal thickening, and reduced septal strain."
},
"related": [
"Q5",
"Q7",
"Q149",
"Q150",
"Q364",
"Q372"
],
"reviewed": "2026-08-26"
},
{
"id": "Q249",
"orig": 249,
"title": "Bedside findings in dilated cardiomyopathy",
"lesions": [
"DCM",
"MR"
],
"lens": "physical-exam",
"items": [
{
"id": "Q249.1",
"q": "What does the physical examination show in a patient with dilated cardiomyopathy, and why does each sign occur?",
"a": "The apical impulse is displaced laterally and downward and feels diffuse, because the enlarged ventricle rotates the apex toward the axilla. A third heart sound is heard at the apex; it is generated when early diastolic inflow abruptly decelerates against a stiff, volume-loaded ventricle, and its presence tracks elevated filling pressure. A holosystolic apical murmur of functional MR arises because annular dilation and papillary displacement prevent leaflet coaptation, and the murmur softens as the ventricle is unloaded with therapy. Elevated JVP, pulmonary rales, and peripheral edema appear when the failure becomes biventricular."
},
{
"id": "Q249.2",
"q": "How can the exam and the echo together suggest that the cardiomyopathy is not primary DCM?",
"a": "A blood pressure history and concentric rather than eccentric geometry point to hypertensive heart disease; a prior infarct produces regional thinning and akinesis rather than global hypokinesis. Ask about alcohol intake, chemotherapy, recent pregnancy, and a family history of heart failure or sudden death, since these define the reversible and heritable forms. A rapid, irregular pulse for months before the symptoms raises tachycardia-mediated cardiomyopathy, which recovers once rate control is achieved."
}
],
"numbers": [],
"delta": null,
"pearl": "Displaced diffuse apex, S3, and a soft holosystolic murmur: the ventricle is big, stiff, and leaking.",
"lookalike": {
"vs": "Primary severe MR with secondary LV dilation",
"discriminator": "In primary MR the leaflets are structurally abnormal (prolapse, flail) and the murmur is loud with a hyperdynamic ventricle early on; in DCM the leaflets are normal, tethered, and the ventricle is globally hypokinetic."
},
"related": [
"Q142",
"Q145",
"Q146"
],
"reviewed": "2026-08-26"
},
{
"id": "Q250",
"orig": 250,
"title": "Doppler assessment in dilated cardiomyopathy",
"lesions": [
"DCM",
"MR",
"DIASTOLIC"
],
"lens": "doppler",
"items": [
{
"id": "Q250.1",
"q": "Why does functional MR develop in DCM, and what Doppler features characterize it?",
"a": "Ventricular dilation pulls the papillary muscles apically and laterally, tethering the leaflets so they coapt below the annular plane in a tented configuration, and the annulus itself dilates. The result is a central jet, often with a low-velocity and rather blunt CW envelope because LV systolic pressure is low. Quantify with vena contracta and PISA, but remember that secondary MR is graded on the same thresholds as primary MR (EROA ≥0.4 cm², RVol ≥60 mL) and that even moderate EROA carries prognostic weight when the ventricle is failing."
},
{
"id": "Q250.2",
"q": "How does the mitral inflow pattern describe filling pressure in DCM, and what is the significance of a restrictive pattern?",
"a": "A dilated failing ventricle usually progresses from impaired relaxation (E/A ≤0.8) through pseudonormal to restrictive filling, where E/A is 2 or greater, deceleration time is short (under 160 ms), and E/e' exceeds 14. The restrictive pattern means LA pressure is high enough to overwhelm the slow relaxation, so the E wave is tall and decelerates fast against a non-compliant chamber. A restrictive pattern that persists after diuresis identifies the highest-risk group; one that reverts toward pseudonormal with treatment indicates reversible congestion."
},
{
"id": "Q250.3",
"q": "How do you derive LV dP/dt from the MR jet and estimate stroke volume from the LVOT?",
"a": "On the CW MR envelope, measure the time between the 1 m/s and 3 m/s points on the upstroke. Those velocities correspond to LV-LA gradients of 4 and 36 mmHg, so the 32 mmHg pressure rise divided by the interval in seconds gives dP/dt; a normal ventricle exceeds 1200 mmHg/s and a value under 600 indicates severely depressed contractility. Stroke volume comes from the LVOT: measure the diameter in PLAX, compute the area (π r²), and multiply by the LVOT VTI from PW Doppler in the apical five-chamber view. Indexing to body surface area below 35 mL/m² defines low flow, which matters when reading concurrent aortic stenosis."
}
],
"numbers": [
{
"label": "Restrictive filling E/A",
"value": "≥ 2",
"unit": "ratio"
},
{
"label": "Restrictive filling deceleration time",
"value": "< 160",
"unit": "ms"
},
{
"label": "Elevated filling pressure E/e' average",
"value": "> 14",
"unit": "ratio"
},
{
"label": "dP/dt pressure interval (1 to 3 m/s)",
"value": "32",
"unit": "mmHg"
},
{
"label": "Normal dP/dt",
"value": "> 1200",
"unit": "mmHg/s"
},
{
"label": "Severely reduced dP/dt",
"value": "< 600",
"unit": "mmHg/s"
},
{
"label": "Low-flow stroke volume index",
"value": "< 35",
"unit": "mL/m²"
},
{
"label": "Severe MR EROA",
"value": "≥ 0.4",
"unit": "cm²"
}
],
"delta": null,
"pearl": "dP/dt = 32 mmHg divided by the 1-to-3 m/s rise time; under 600 mmHg/s means a badly failing pump.",
"lookalike": null,
"related": [
"Q144",
"Q145",
"Q152",
"Q369"
],
"widgets": [
{
"id": "calc",
"opts": {
"k": "dpdt"
}
}
],
"reviewed": "2026-08-26"
},
{
"id": "Q251",
"orig": 251,
"title": "Pitfalls when imaging the dilated ventricle",
"lesions": [
"DCM",
"LV_FUNCTION",
"ARRHYTHMIA"
],
"lens": "pitfall",
"items": [
{
"id": "Q251.1",
"q": "How does foreshortening corrupt the assessment of a dilated cardiomyopathy?",
"a": "If the transducer is not at the true apex, the imaging plane cuts obliquely through the ventricle, so the chamber looks shorter and rounder, the apex appears thick and vigorous, and Simpson's volumes are underestimated. A dilated ventricle is spherical to begin with, so a foreshortened view can make it look nearly normal and can overestimate EF. Check that the long axis is maximal, that the apex is thin and stationary, and that the mitral annulus lies at the widest part of the sector; moving one intercostal space lower and more lateral usually fixes it."
},
{
"id": "Q251.2",
"q": "What distinguishes tachycardia-mediated cardiomyopathy and LV non-compaction from idiopathic DCM?",
"a": "Tachycardia-mediated cardiomyopathy looks identical to DCM on a single study, so the clue is the history: a persistent tachyarrhythmia (atrial fibrillation, atrial tachycardia, frequent PVCs) preceding the decline, followed by recovery of EF within weeks to months of rate or rhythm control. Non-compaction is suggested by a two-layer myocardium with a prominent trabeculated inner layer and deep intertrabecular recesses that fill with color, most often at the apex and lateral wall; a non-compacted to compacted ratio above 2 at end-systole is the classic criterion. Ultrasound enhancing agent helps outline the recesses, and it should be considered before calling an apical thrombus in these patients."
}
],
"numbers": [
{
"label": "Non-compacted to compacted ratio (end-systole)",
"value": "> 2",
"unit": "ratio"
}
],
"delta": null,
"pearl": "If the apex looks thick and moves well in a supposedly dilated heart, you are probably foreshortened.",
"lookalike": {
"vs": "LV non-compaction",
"discriminator": "Non-compaction shows a spongy two-layer wall with color-filled recesses and a non-compacted/compacted ratio >2; ordinary DCM has smooth thin walls."
},
"related": [
"Q163",
"Q145",
"Q375"
],
"reviewed": "2026-08-26"
},
{
"id": "Q252",
"orig": 252,
"title": "Key numbers in dilated cardiomyopathy",
"lesions": [
"DCM",
"LV_FUNCTION",
"CHAMBER_QUANT"
],
"lens": "numbers",
"items": [
{
"id": "Q252.1",
"q": "List the quantitative thresholds that define reduced systolic function and LV dilation in DCM.",
"a": "Ejection fraction by biplane Simpson's is normal at 52% or above in men and 54% in women, mildly reduced at 41–51% (41–53% in women), and reduced at 40% or below; DCM typically presents with EF under 40% and often under 30%. LVIDd above 5.8 cm in men or 5.2 cm in women is dilated, and indexing to BSA (roughly >3.1 cm/m²) corrects for body size. Global longitudinal strain less negative than −16% is abnormal and can precede the EF fall in early or chemotherapy-related cardiomyopathy."
},
{
"id": "Q252.2",
"q": "What M-mode and Doppler numbers support the diagnosis?",
"a": "E-point septal separation greater than 7 mm indicates a low EF, because a poorly ejecting ventricle produces a small stroke volume and therefore a small mitral opening while the cavity is large. A dP/dt below 600 mmHg/s from the MR jet indicates severely reduced contractility, with 800–1200 borderline and above 1200 normal. A restrictive inflow pattern (E/A ≥2, DT <160 ms) marks high filling pressure, and an LVOT VTI under about 15 cm signals a low stroke volume."
}
],
"numbers": [
{
"label": "Normal EF, men",
"value": "≥ 52",
"unit": "%"
},
{
"label": "Normal EF, women",
"value": "≥ 54",
"unit": "%"
},
{
"label": "Reduced EF",
"value": "≤ 40",
"unit": "%"
},
{
"label": "LVIDd upper normal, men",
"value": "5.8",
"unit": "cm"
},
{
"label": "LVIDd upper normal, women",
"value": "5.2",
"unit": "cm"
},
{
"label": "EPSS abnormal",
"value": "> 7",
"unit": "mm"
},
{
"label": "dP/dt severely reduced",
"value": "< 600",
"unit": "mmHg/s"
},
{
"label": "GLS abnormal",
"value": "> −16",
"unit": "%"
},
{
"label": "Restrictive E/A",
"value": "≥ 2",
"unit": "ratio"
}
],
"delta": null,
"pearl": "Forty, seven, six hundred: EF ≤40%, EPSS >7 mm, dP/dt <600 mmHg/s.",
"lookalike": null,
"related": [
"Q6",
"Q144",
"Q146"
],
"reviewed": "2026-08-26"
},
{
"id": "Q253",
"orig": 253,
"title": "Peripartum cardiomyopathy vignette",
"lesions": [
"DCM",
"MR"
],
"lens": "vignette",
"items": [
{
"id": "Q253.1",
"q": "A 31-year-old woman, three weeks after delivering twins, presents with orthopnea and ankle swelling. The echo shows a globally hypokinetic LV with EF 30%, LVIDd 6.0 cm, moderate central MR, and a small pericardial effusion. What is the diagnosis and what defines it?",
"a": "This is peripartum cardiomyopathy: heart failure with EF under 45% appearing in the last month of pregnancy or within five months of delivery, with no other identifiable cause. Twin pregnancy, multiparity, advanced maternal age, preeclampsia, and African ancestry increase the risk. The echo looks like any dilated cardiomyopathy, with a spherical ventricle, tethered mitral leaflets producing functional MR, and often a small effusion; the mechanism is thought to involve a cleaved prolactin fragment with anti-angiogenic effects on the myocardium."
},
{
"id": "Q253.2",
"q": "What should the sonographer look for on this study beyond EF, and what is the expected course?",
"a": "Search the apex carefully for thrombus, because a dilated, poorly contracting ventricle in the hypercoagulable postpartum state is a high-risk setting, and use an enhancing agent if the apex is unclear. Assess the RV with TAPSE and S', since RV involvement predicts a worse outcome, and estimate RVSP from the TR jet. Roughly half of patients recover to a normal EF within six months on standard heart-failure therapy; an initial EF below 30% or LVIDd above 6 cm predicts incomplete recovery, and a subsequent pregnancy carries a real risk of relapse."
}
],
"numbers": [
{
"label": "Peripartum cardiomyopathy EF threshold",
"value": "< 45",
"unit": "%"
},
{
"label": "Onset window after delivery",
"value": "≤ 5",
"unit": "months"
},
{
"label": "Poor-recovery marker LVIDd",
"value": "> 6.0",
"unit": "cm"
},
{
"label": "Poor-recovery marker EF",
"value": "< 30",
"unit": "%"
}
],
"delta": null,
"pearl": "New heart failure in the last month of pregnancy or first five months postpartum, with nothing else to blame, is peripartum cardiomyopathy; hunt for apical thrombus.",
"lookalike": {
"vs": "Preeclampsia with pulmonary edema",
"discriminator": "Preeclamptic pulmonary edema comes with hypertension and a preserved or hyperdynamic EF with diastolic dysfunction; peripartum cardiomyopathy shows a dilated ventricle with EF <45%."
},
"related": [
"Q142",
"Q146"
],
"reviewed": "2026-08-26"
},
{
"id": "Q254",
"orig": 254,
"title": "Bedside findings in restrictive cardiomyopathy",
"lesions": [
"RCM",
"HEMODYNAMICS"
],
"lens": "physical-exam",
"items": [
{
"id": "Q254.1",
"q": "What physical findings characterize restrictive cardiomyopathy, and how do they arise?",
"a": "The dominant picture is right-sided congestion out of proportion to left-sided symptoms: markedly elevated JVP with prominent x and y descents, hepatomegaly, ascites, and edema. The stiff ventricles fill only at high pressure, so the atria dilate massively and the jugular waveform shows a rapid y descent as blood drops into the ventricle in early diastole and then stops abruptly. A Kussmaul sign (JVP rising with inspiration) may be present because the RV cannot accept the inspiratory venous return. An S3 or S4 may be heard, the apex is usually not displaced, and the pulse pressure is narrow because stroke volume is small despite a preserved EF."
},
{
"id": "Q254.2",
"q": "Which bedside clues distinguish RCM from constrictive pericarditis, which produces a nearly identical congestive picture?",
"a": "A pericardial knock, an early diastolic sound higher-pitched than an S3, favors constriction, while a true S3 or S4 with a regurgitant murmur favors myocardial disease. A history of prior cardiac surgery, chest radiation, or tuberculosis points toward constriction; systemic features such as macroglossia, periorbital purpura, carpal tunnel syndrome, or peripheral neuropathy point toward amyloid. Low ECG voltage with a thick heart on echo favors infiltrative RCM, and conduction disease or atrial fibrillation is more common in RCM than in constriction."
}
],
"numbers": [],
"delta": null,
"pearl": "Ascites and a huge JVP with a normal-sized, normally contracting LV: think restriction or constriction, and let the echo choose.",
"lookalike": {
"vs": "Constrictive pericarditis",
"discriminator": "Both give elevated JVP with rapid y descent and ascites; a knock, surgical or radiation history, and normal e' favor constriction, while low voltage, systemic amyloid features, and low e' favor RCM."
},
"related": [
"Q3",
"Q28",
"Q125",
"Q148"
],
"reviewed": "2026-08-26"
},
{
"id": "Q255",
"orig": 255,
"title": "M-mode in restrictive cardiomyopathy",
"lesions": [
"RCM",
"DIASTOLIC"
],
"lens": "m-mode",
"items": [
{
"id": "Q255.1",
"q": "What does M-mode show in restrictive cardiomyopathy?",
"a": "Through the ventricle, M-mode records normal or small cavity dimensions with normal or increased wall thickness and preserved systolic excursion in early disease, which is what separates RCM from DCM on a single sweep. The LV posterior wall reaches its end-diastolic position early and then flattens, because filling is complete in early diastole and the stiff chamber cannot expand further; this early plateau is the M-mode counterpart of the dip-and-plateau pressure tracing. Through the mitral valve, the E-F slope is steep and the A-wave is diminutive, reflecting rapid early filling followed by an atrium too weak or too pressure-loaded to contribute. The left atrium is markedly enlarged on the aortic-root sweep, and a small posterior echo-free space is common in amyloid."
},
{
"id": "Q255.2",
"q": "Why is the septal motion pattern useful in separating RCM from constriction on M-mode?",
"a": "In constriction, the fixed total pericardial volume forces the septum to shift with respiration: it moves toward the LV on inspiration and back toward the RV on expiration, and an abrupt early-diastolic septal notch (bounce) is common. In RCM the pericardium is normal, so the septal position does not change with respiration and there is no bounce. Record an M-mode through the septum with the respirometer running; a stable septum with a flat posterior wall in a thick-walled ventricle favors restriction."
}
],
"numbers": [],
"delta": null,
"pearl": "Flat posterior wall in diastole, steep E-F slope, tiny A wave, and a septum that ignores respiration: restriction, not constriction.",
"lookalike": {
"vs": "Constrictive pericarditis M-mode",
"discriminator": "Constriction shows respirophasic septal shift and an early-diastolic septal bounce with a normal-thickness wall; RCM shows a stable septum, thick walls, and an early diastolic posterior-wall plateau."
},
"related": [
"Q149",
"Q151",
"Q152",
"Q259"
],
"reviewed": "2026-08-26"
},
{
"id": "Q256",
"orig": 256,
"title": "Best method to unmask cardiac amyloid",
"lesions": [
"RCM",
"LV_FUNCTION"
],
"lens": "best-method",
"items": [
{
"id": "Q256.1",
"q": "What is the single most specific echocardiographic finding for cardiac amyloidosis, and how is it obtained?",
"a": "Speckle-tracking longitudinal strain with a bull's-eye display is the most specific tool. In amyloid the basal and mid segments lose strain badly while the apical segments are relatively preserved, producing a bright apical center on the polar map, the so-called cherry-on-top or apical-sparing pattern. Amyloid deposits preferentially in the base, and the apex has less wall tension and thinner walls, so it keeps contracting. A relative apical longitudinal strain ratio (apical strain divided by the sum of basal plus mid strain) above 1 has high sensitivity and specificity against other causes of wall thickening. Acquire all three apical views at a good frame rate (50–80 fps) with clean endocardial tracking, because dropout in one basal segment can fabricate the pattern."
},
{
"id": "Q256.2",
"q": "What other findings, on echo and beyond, strengthen the diagnosis?",
"a": "Thick walls with a normal or small cavity, a sparkling granular myocardium, thickened valves and interatrial septum, biatrial enlargement, RV free-wall thickening above 5 mm, and a small pericardial effusion are the supporting 2D features. Restrictive filling with septal e' under 7 cm/s and E/e' over 14 shows the stiff physiology. The decisive non-echo clue is the voltage-mass mismatch: low QRS voltage on ECG despite echocardiographic LVH, because amyloid is electrically inert. Technetium pyrophosphate scintigraphy identifies transthyretin amyloid without biopsy once a plasma-cell dyscrasia has been excluded with serum free light chains and immunofixation."
}
],
"numbers": [
{
"label": "Relative apical strain ratio suggesting amyloid",
"value": "> 1.0",
"unit": "ratio"
},
{
"label": "Strain acquisition frame rate",
"value": "50–80",
"unit": "fps"
},
{
"label": "RV free-wall hypertrophy",
"value": "> 5",
"unit": "mm"
},
{
"label": "Septal e' abnormal",
"value": "< 7",
"unit": "cm/s"
},
{
"label": "Average E/e' abnormal",
"value": "> 14",
"unit": "ratio"
}
],
"delta": null,
"pearl": "Thick heart plus low voltage plus a cherry-on-top strain map equals amyloid until proven otherwise.",
"lookalike": {
"vs": "Hypertrophic cardiomyopathy strain",
"discriminator": "HCM shows the worst strain in the thickest (usually septal) segments with no apical sparing; amyloid shows a basal-to-apical gradient with a preserved apex."
},
"related": [
"Q7",
"Q148",
"Q150",
"Q151",
"Q364",
"Q378"
],
"reviewed": "2026-08-26"
},
{
"id": "Q257",
"orig": 257,
"title": "Key numbers in restrictive cardiomyopathy",
"lesions": [
"RCM",
"DIASTOLIC",
"CONSTRICTION"
],
"lens": "numbers",
"items": [
{
"id": "Q257.1",
"q": "List the Doppler and 2D numbers that define restrictive physiology and separate it from constriction.",
"a": "Restrictive filling is an E/A of 2 or more with a deceleration time under 160 ms and an IVRT under 70 ms, reflecting a high LA pressure driving rapid early filling into a chamber that fills to its limit almost immediately. Tissue Doppler is the discriminator: medial e' below 7 cm/s (often 3–5) and E/e' above 14 mean the myocardium itself is sick, whereas constriction preserves or exaggerates medial e' above 7 cm/s (above 8 favors constriction) with the lateral e' lower than the medial (annulus reversus). Mitral E variation with respiration is under 25% in RCM but 25% or more in constriction, and hepatic vein diastolic flow reversal occurs in inspiration in RCM but in expiration in constriction. Wall thickness above 12 mm, LAVi above 34 mL/m², and RV free wall above 5 mm favor infiltration."
}
],
"numbers": [
{
"label": "Restrictive E/A",
"value": "≥ 2",
"unit": "ratio"
},
{
"label": "Restrictive deceleration time",
"value": "< 160",
"unit": "ms"
},
{
"label": "Restrictive IVRT",
"value": "< 70",
"unit": "ms"
},
{
"label": "Medial e' in RCM",
"value": "< 7",
"unit": "cm/s"
},
{
"label": "Medial e' in constriction",
"value": "> 7 (> 8 favors)",
"unit": "cm/s"
},
{
"label": "E/e' elevated",
"value": "> 14",
"unit": "ratio"
},
{
"label": "Mitral E respiratory variation in RCM",
"value": "< 25",
"unit": "%"
},
{
"label": "LAVi enlarged",
"value": "> 34",
"unit": "mL/m²"
},
{
"label": "RV free wall thickened",
"value": "> 5",
"unit": "mm"
}
],
"delta": {
"was": "2011 card and the Mayo criteria (ASE 2013) set the constriction medial e' cut-off at ≥ 9 cm/s.",
"now": "ASE 2025 lowers the constriction medial e' cut-off to > 7 cm/s, with > 8 cm/s strongly favoring constriction; it pairs with respirophasic septal shift for about 80% sensitivity and 96% specificity.",
"source": "ASE 2025 diastolic function guideline"
},
"pearl": "Same inflow, different annulus: e' under 7 is restriction, e' above 7 (especially above 8) with annulus reversus is constriction.",
"lookalike": {
"vs": "Constrictive pericarditis",
"discriminator": "Identical restrictive inflow, but constriction shows medial e' > 7 cm/s (> 8 favors), ≥25% mitral E variation, expiratory hepatic reversal, and septal shift; RCM has e' <7, minimal respiratory variation, and inspiratory hepatic reversal."
},
"related": [
"Q126",
"Q149",
"Q152",
"Q262",
"Q379"
],
"reviewed": "2026-08-26"
},
{
"id": "Q258",
"orig": 258,
"title": "Defining constrictive pericarditis",
"lesions": [
"CONSTRICTION",
"HEMODYNAMICS"
],
"lens": "definition",
"items": [
{
"id": "Q258.1",
"q": "Define constrictive pericarditis and explain the two hemodynamic principles that produce its findings.",
"a": "Constriction is a condition in which a thickened, fibrotic, often calcified pericardium loses its compliance and encases the heart in a fixed-volume shell, so diastolic filling stops abruptly once that volume is reached. Two consequences follow. First, dissociation of intrathoracic and intracardiac pressures: the rigid pericardium shields the heart from the inspiratory fall in intrathoracic pressure, so pulmonary venous pressure drops on inspiration but LV pressure does not, and the LV filling gradient falls while RV filling rises. Second, enhanced ventricular interdependence: because total volume is fixed, whatever the RV gains on inspiration the LV must lose, and the septum shifts leftward, reversing on expiration. Myocardial relaxation itself is normal, which is why tissue Doppler e' is preserved and why the disease is curable by pericardiectomy."
},
{
"id": "Q258.2",
"q": "What are the main causes of constriction today, and what is the effusive-constrictive variant?",
"a": "In developed countries the leading causes are prior cardiac surgery, mediastinal radiation, and idiopathic or viral pericarditis, with tuberculosis dominating where it is endemic; connective tissue disease, uremia, and malignancy account for the rest. Effusive-constrictive pericarditis is the combination of a pericardial effusion under tension with a constricting visceral layer, so that draining the effusion fails to normalize RA pressure, which remains elevated with a constrictive waveform. Transient constriction can occur during the healing phase of acute pericarditis and may resolve with anti-inflammatory therapy, so an early follow-up echo is warranted before recommending surgery."
}
],
"numbers": [],
"delta": null,
"pearl": "A rigid shell means fixed volume: the ventricles compete for space (interdependence) and the heart cannot feel the breath (dissociation).",
"lookalike": {
"vs": "Restrictive cardiomyopathy",
"discriminator": "Constriction is a pericardial problem with normal myocardial relaxation (e' preserved) and respirophasic interdependence; RCM is myocardial with low e' and no respiratory variation."
},
"related": [
"Q124",
"Q125",
"Q126",
"Q134",
"Q261",
"Q263",
"Q380"
],
"reviewed": "2026-08-26"
},
{
"id": "Q259",
"orig": 259,
"title": "M-mode signs of constriction",
"lesions": [
"CONSTRICTION"
],
"lens": "m-mode",
"items": [
{
"id": "Q259.1",
"q": "Which M-mode findings support constrictive pericarditis, and what does each represent?",
"a": "The most useful is abnormal septal motion: an abrupt early-diastolic anterior notch (septal bounce) as the RV fills first and momentarily pushes the septum, and a respirophasic shift of the whole septum toward the LV on inspiration and toward the RV on expiration when recorded with a respirometer. The LV posterior wall flattens in mid-to-late diastole, because the pericardial shell halts filling early; a posterior wall that fails to move more than about 1 mm in diastole is a classic sign. Thickened, dense parallel pericardial echoes behind the posterior wall that move together with it suggest a thickened pericardium, though M-mode overestimates thickness and TEE or CT is more reliable. Premature pulmonic valve opening and a dilated non-collapsing IVC on subcostal M-mode reflect high RV diastolic and RA pressures."
}
],
"numbers": [
{
"label": "Posterior wall diastolic excursion in constriction",
"value": "< 1",
"unit": "mm"
}
],
"delta": null,
"pearl": "Septum that bounces and breathes, posterior wall that stops moving: M-mode constriction.",
"lookalike": {
"vs": "Left bundle branch block septal motion",
"discriminator": "LBBB produces an early systolic septal beak that is fixed with respiration; constriction produces an early diastolic bounce that shifts with respiration."
},
"related": [
"Q121",
"Q126",
"Q255"
],
"reviewed": "2026-08-26"
},
{
"id": "Q260",
"orig": 260,
"title": "2D findings in constrictive pericarditis",
"lesions": [
"CONSTRICTION",
"TEE"
],
"lens": "2d",
"items": [
{
"id": "Q260.1",
"q": "What 2D findings should raise the suspicion of constriction, and how reliable is each?",
"a": "Pericardial thickening appears as a bright, sometimes calcified band adherent to the epicardium, but transthoracic imaging cannot measure it accurately; TEE (thickness above 3 mm) or CT is the reference, and about one in five surgically proven cases has a normal-thickness pericardium, so a normal-looking pericardium does not exclude the diagnosis. The septal bounce, a brisk early-diastolic shudder of the septum toward the LV, is the most sensitive real-time sign and is best appreciated in the apical four-chamber and short-axis views. Look for a plethoric IVC (over 2.1 cm with less than 50% inspiratory collapse), dilated hepatic veins, and biatrial enlargement with normal-sized, normally contracting ventricles. Tethering is the finding of a ventricle whose free wall appears stuck to the pericardium, so that the epicardium and pericardium slide together without the normal separation, and it is often accompanied by a flattened or tubular LV shape."
},
{
"id": "Q260.2",
"q": "How do you image the respiratory septal shift on 2D, and what does it look like?",
"a": "Record a slow-sweep apical four-chamber or PSAX clip over at least two respiratory cycles with the respirometer on, asking the patient to breathe normally rather than deeply. On inspiration the septum moves toward the LV as the RV takes on the extra venous return within a fixed pericardial volume; on expiration it swings back toward the RV. Frame-by-frame review shows the shift is a gradual whole-septum displacement, distinct from the abrupt early-diastolic bounce that occurs on every beat. The finding is absent in RCM and reduced in patients on mechanical ventilation or with severe COPD, where the intrathoracic pressure swings behave differently."
}
],
"numbers": [
{
"label": "Pericardial thickness abnormal on TEE",
"value": "> 3",
"unit": "mm"
},
{
"label": "Constriction with normal-thickness pericardium",
"value": "≈ 20",
"unit": "%"
},
{
"label": "IVC plethora diameter",
"value": "> 2.1",
"unit": "cm"
},
{
"label": "IVC plethora inspiratory collapse",
"value": "< 50",
"unit": "%"
}
],
"delta": null,
"pearl": "Normal-sized ventricles that contract well, big atria, a fat IVC, and a septum that bounces: constriction until proven otherwise.",
"lookalike": {
"vs": "Epicardial fat pad",
"discriminator": "Fat is hypoechoic, anterior, and moves with the heart without restricting it; constrictive pericardium is bright, adherent, and comes with septal bounce and IVC plethora."
},
"related": [
"Q120",
"Q121",
"Q126"
],
"reviewed": "2026-08-26"
},
{
"id": "Q261",
"orig": 261,
"title": "Chamber effects of constriction",
"lesions": [
"CONSTRICTION",
"HEMODYNAMICS"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q261.1",
"q": "How does constriction affect each chamber, and why do the atria enlarge while the ventricles do not?",
"a": "The ventricles are confined by the rigid shell, so their end-diastolic volumes are normal or small and their walls are normal in thickness with preserved systolic function; the LV often takes an elongated tubular shape. Filling pressures equalize in diastole across all four chambers, typically within 5 mmHg of one another, and the pressure the ventricles cannot accommodate is transmitted back to the atria, which are outside the tightest part of the shell and dilate. The systemic and hepatic veins bear the highest load, giving the plethoric IVC, hepatomegaly, and ascites. Because the ventricles are small and stiff with an early halt to filling, stroke volume is fixed and cardiac output depends on heart rate, which is why tachycardia is the rule and beta-blockers are poorly tolerated."
},
{
"id": "Q261.2",
"q": "What happens to the mitral and tricuspid inflows and to pulmonary and hepatic venous flows with respiration?",
"a": "On inspiration LV filling falls because the pulmonary venous to LV gradient shrinks (intrathoracic pressure drops, LV pressure does not), so mitral E decreases by 25% or more and pulmonary venous diastolic flow also falls. The RV, in contrast, gets more of the fixed volume, so tricuspid E rises by 40% or more and hepatic vein forward flow increases. On expiration the pattern reverses: LV filling rises, RV filling falls, and the RV cannot empty its venous return, so the hepatic veins show prominent expiratory diastolic flow reversal. These reciprocal changes are the Doppler fingerprint of ventricular interdependence."
}
],
"numbers": [
{
"label": "Diastolic pressure equalization across chambers",
"value": "≤ 5",
"unit": "mmHg"
},
{
"label": "Mitral E inspiratory decrease in constriction",
"value": "≥ 25",
"unit": "%"
},
{
"label": "Tricuspid E inspiratory increase in constriction",
"value": "≥ 40",
"unit": "%"
}
],
"delta": null,
"pearl": "Small stiff ventricles, huge atria, fat veins: everything upstream of the shell dilates, everything inside it cannot.",
"lookalike": {
"vs": "Severe tricuspid regurgitation",
"discriminator": "Severe TR also dilates the RA and IVC, but the RV is enlarged, the hepatic vein shows systolic reversal, and there is no respirophasic septal shift."
},
"related": [
"Q126",
"Q149",
"Q258"
],
"reviewed": "2026-08-26"
},
{
"id": "Q262",
"orig": 262,
"title": "Mayo criteria for constriction",
"lesions": [
"CONSTRICTION",
"RCM"
],
"lens": "numbers",
"items": [
{
"id": "Q262.1",
"q": "State the Mayo Clinic echocardiographic criteria for constrictive pericarditis and their diagnostic performance.",
"a": "The Mayo criteria combine three findings. First, respiration-related ventricular septal shift, which is the required anchor because it encodes interdependence. Second, preserved medial mitral annular e' above 7 cm/s (above 8 cm/s strongly favors constriction, ASE 2025), often with annulus reversus (medial e' exceeding lateral e'), because the myocardium relaxes normally while the tethered lateral wall is restricted. Third, an expiratory hepatic vein diastolic reversal ratio of 0.79 or higher, calculated as the reversal velocity divided by forward diastolic velocity in expiration. Septal shift combined with either the medial e' criterion or a hepatic reversal ratio of 0.79 or more gave sensitivity around 87% and specificity around 91%; all three together are highly specific (about 97%) at the cost of lower sensitivity (about 64%)."
},
{
"id": "Q262.2",
"q": "Which supporting numbers are commonly added, and where does each fail?",
"a": "Mitral E respiratory variation of 25% or more and tricuspid E variation of 40% or more support the diagnosis but disappear in atrial fibrillation, tachycardia, and high LA pressure, and they are mimicked by COPD and obesity. In COPD the SVC flow varies markedly with respiration whereas in constriction it barely changes, which is a useful tiebreaker. E/e' is paradoxically low or normal in constriction despite very high filling pressures (annulus paradoxus), so a low E/e' with clinical congestion should raise constriction, not lower it. Effusive-constrictive disease and mixed constriction-restriction after radiation can blunt every criterion, so cardiac catheterization with simultaneous LV and RV pressures remains the arbiter."
}
],
"numbers": [
{
"label": "Medial e' criterion",
"value": "> 7 (> 8 favors)",
"unit": "cm/s"
},
{
"label": "Hepatic vein expiratory diastolic reversal ratio",
"value": "≥ 0.79",
"unit": "ratio"
},
{
"label": "Sensitivity, septal shift plus one other criterion",
"value": "≈ 87",
"unit": "%"
},
{
"label": "Specificity, septal shift plus one other criterion",
"value": "≈ 91",
"unit": "%"
},
{
"label": "Specificity, all three criteria",
"value": "≈ 97",
"unit": "%"
},
{
"label": "Mitral E respiratory variation supporting constriction",
"value": "≥ 25",
"unit": "%"
},
{
"label": "Tricuspid E respiratory variation supporting constriction",
"value": "≥ 40",
"unit": "%"
}
],
"delta": {
"was": "The original Mayo series (Welch 2014, ASE 2013) set the medial e' criterion at ≥ 9 cm/s; its 87%/91% performance figures were derived at that cut-off.",
"now": "ASE 2025 lowers the constriction medial e' cut-off to > 7 cm/s, with > 8 cm/s strongly favoring constriction; it pairs with respirophasic septal shift for about 80% sensitivity and 96% specificity.",
"source": "ASE 2025 diastolic function guideline"
},
"pearl": "Shift, seven, seventy-nine: septal shift plus medial e' > 7 (> 8 favors) or hepatic reversal ratio ≥0.79.",
"lookalike": {
"vs": "COPD respiratory variation",
"discriminator": "COPD exaggerates SVC flow variation and lacks septal shift and annulus reversus; constriction has a nearly fixed SVC flow with septal shift."
},
"related": [
"Q126",
"Q149",
"Q152",
"Q257",
"Q263",
"Q379"
],
"reviewed": "2026-08-26"
},
{
"id": "Q263",
"orig": 263,
"title": "Constriction after radiation and surgery",
"lesions": [
"CONSTRICTION",
"RCM",
"AS"
],
"lens": "vignette",
"items": [
{
"id": "Q263.1",
"q": "A 58-year-old man treated with mantle radiation for Hodgkin lymphoma 25 years ago presents with ascites and a JVP that rises on inspiration. Echo shows normal LV size and EF, a septal bounce, medial e' 6 cm/s, lateral e' 5 cm/s, plethoric IVC, and mild aortic and mitral leaflet thickening. What is the diagnosis and why is this case harder than typical constriction?",
"a": "This is radiation-induced pericardial constriction with coexistent radiation myocardial injury, a mixed constrictive-restrictive picture. Radiation fibroses the pericardium, but it also damages the microvasculature and myocardium, so the annular velocities are low on both sides rather than preserved medially, and the Mayo e' criterion fails. The septal bounce, respirophasic shift, IVC plethora, and Kussmaul sign still reflect the pericardial component. Radiation also thickens and calcifies the valves, especially the aortic and mitral, and accelerates coronary disease, so a full valve and ischemic assessment belongs in the report. Because myocardial fibrosis limits the benefit of pericardiectomy, cardiac MRI or catheterization to quantify the restrictive component is needed before surgery."
},
{
"id": "Q263.2",
"q": "A 66-year-old woman is readmitted with edema and fatigue six months after coronary bypass surgery. Echo shows a small localized posterolateral effusion, septal bounce, and mitral E variation of 35% with inspiration. What should you suspect and what should you do differently in the exam?",
"a": "Post-surgical constriction, which often develops within the first year after cardiac surgery and may be regional rather than circumferential, sometimes with a loculated effusion that produces effusive-constrictive physiology. Because the constriction can be focal, the classic global findings may be blunted, so scan all windows including off-axis and subcostal views to find the thickened or adherent segment and any localized collection compressing a chamber. Record the respirometer with every Doppler tracing and pay attention to hepatic vein expiratory reversal, which remains reliable when mitral variation is confounded by postoperative atrial fibrillation. Post-pericardiotomy constriction can be transient and inflammatory, so a course of anti-inflammatory therapy with repeat imaging in a few weeks is reasonable before pericardiectomy."
}
],
"numbers": [
{
"label": "Mitral E inspiratory fall supporting constriction",
"value": "≥ 25",
"unit": "%"
},
{
"label": "Medial e' expected in pure constriction",
"value": "> 7 (> 8 favors)",
"unit": "cm/s"
}
],
"delta": {
"was": "2011 card and the Mayo criteria (ASE 2013) set the constriction medial e' cut-off at ≥ 9 cm/s.",
"now": "ASE 2025 lowers the constriction medial e' cut-off to > 7 cm/s, with > 8 cm/s strongly favoring constriction; it pairs with respirophasic septal shift for about 80% sensitivity and 96% specificity.",
"source": "ASE 2025 diastolic function guideline"
},
"pearl": "Radiation constricts the pericardium and stiffens the muscle at the same time, so low e' does not exclude constriction in an irradiated chest.",
"lookalike": {
"vs": "Pure restrictive cardiomyopathy",
"discriminator": "Pure RCM lacks septal bounce and respirophasic shift; mixed radiation disease has both the bounce and the low e'."
},
"related": [
"Q124",
"Q125",
"Q258",
"Q262",
"Q379"
],
"reviewed": "2026-08-26"
},
{
"id": "Q264",
"orig": 264,
"title": "M-mode signs of pericardial effusion",
"lesions": [
"EFFUSION",
"HEMODYNAMICS"
],
"lens": "m-mode",
"items": [
{
"id": "Q264.1",
"q": "How does a pericardial effusion appear on M-mode, and how do you tell it from other posterior echo-free spaces?",
"a": "An effusion is an echo-free space that separates the epicardium of the LV posterior wall from the bright parietal pericardium and persists throughout the cardiac cycle; a space present only in systole is normal physiologic fluid. Anteriorly, an echo-free band between the chest wall and the RV free wall that is also present posteriorly confirms fluid, while an isolated anterior space is usually epicardial fat. On the sweep from apex toward the base, a pericardial effusion tapers and ends at the AV groove behind the LA because the pericardial reflection stops there, whereas a left pleural effusion continues posterior to the descending aorta and the LA. The parietal pericardium remains a flat, immobile line in effusion, while in a pleural effusion the pericardium moves with the heart."
},
{
"id": "Q264.2",
"q": "What do the swinging heart and early-diastolic RV collapse look like on M-mode, and what is the significance of the collapse timing?",
"a": "In a large effusion the heart swings freely within the fluid, so M-mode shows the entire cardiac silhouette oscillating anteriorly and posteriorly, often with a period of two beats, which produces electrical alternans on the ECG as the QRS axis rotates. RV early-diastolic collapse appears as an inward, posterior indentation of the RV anterior wall that begins just after the aortic valve closes and coincides with mitral valve opening on the same tracing, then resolves as RV pressure climbs later in diastole. The timing is the key: collapse occurs when intrapericardial pressure exceeds RV diastolic pressure, which happens at the moment RV pressure is lowest, in early diastole. Collapse that lasts longer into diastole indicates a higher intrapericardial pressure and more severe tamponade, and its absence in a patient with pulmonary hypertension or RV hypertrophy does not exclude tamponade because the stiff RV resists compression."
}
],
"numbers": [
{
"label": "Swinging heart oscillation period",
"value": "2",
"unit": "beats"
}
],
"delta": null,
"pearl": "Fluid behind the LV that stops at the AV groove is pericardial; fluid that runs past the descending aorta is pleural.",
"lookalike": {
"vs": "Left pleural effusion",
"discriminator": "Pleural fluid extends posterior to the descending aorta and behind the LA; pericardial fluid lies anterior to the descending aorta and tapers at the AV groove."
},
"related": [
"Q15",
"Q114",
"Q119",
"Q380"
],
"reviewed": "2026-08-26"
},
{
"id": "Q265",
"orig": 265,
"title": "Effusion size grading and collapse sequence",
"lesions": [
"EFFUSION",
"HEMODYNAMICS"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q265.1",
"q": "How is a pericardial effusion graded by size, and why is size alone a poor guide to hemodynamic significance?",
"a": "Measure the largest end-diastolic echo-free space perpendicular to the wall, usually posterior in PLAX or circumferentially in PSAX: under 1 cm is small (roughly under 100 mL), 1 to 2 cm is moderate (about 100–500 mL), and over 2 cm is large (over 500 mL). Distribution matters, so note whether the fluid is circumferential, posterior only, or loculated. The pericardium stretches slowly, so a chronic effusion of 1.5 L may cause no compromise while a rapid 200 mL bleed after a procedure can produce tamponade, because the pressure-volume curve of the pericardium is steep once its reserve volume is exhausted. Tamponade is therefore a clinical and physiologic diagnosis, not a size category."
},
{
"id": "Q265.2",
"q": "Describe the sequence in which chambers collapse as intrapericardial pressure rises, and explain the order.",
"a": "The chambers give way in order of their diastolic pressure and wall thickness, lowest and thinnest first. The right atrium collapses first, at end-diastole and into early systole when its pressure is lowest; a brief indentation is sensitive but nonspecific, and collapse persisting for more than one third of systole becomes specific for tamponade. The RV free wall collapses next in early diastole, which is more specific but less sensitive and is delayed by RV hypertrophy or pulmonary hypertension. LA collapse follows in late diastole in about a quarter of cases and is highly specific, while LV collapse is rare and generally seen only with regional posterior effusions or a very hypovolemic patient. Alongside the collapse sequence, IVC plethora and the exaggerated respiratory inflow variation (mitral over 30%, tricuspid over 60%) confirm the physiology."
}
],
"numbers": [
{
"label": "Small effusion",
"value": "< 1",
"unit": "cm"
},
{
"label": "Moderate effusion",
"value": "1–2",
"unit": "cm"
},
{
"label": "Large effusion",
"value": "> 2",
"unit": "cm"
},
{
"label": "Approximate volume, small",
"value": "< 100",
"unit": "mL"
},
{
"label": "Approximate volume, large",
"value": "> 500",
"unit": "mL"
},
{
"label": "RA collapse duration specific for tamponade",
"value": "> 1/3",
"unit": "of systole"
},
{
"label": "Mitral E respiratory variation in tamponade",
"value": "> 30",
"unit": "%"
},
{
"label": "Tricuspid E respiratory variation in tamponade",
"value": "> 60",
"unit": "%"
}
],
"delta": null,
"pearl": "Collapse follows pressure: RA first, then RV, then LA, and the LV almost never.",
"lookalike": {
"vs": "Large chronic effusion without tamponade",
"discriminator": "A big chronic effusion can lack any chamber collapse and show a normally collapsing IVC; tamponade requires collapse, IVC plethora, and inflow variation regardless of size."
},
"related": [
"Q118",
"Q119",
"Q122",
"Q266",
"Q380"
],
"reviewed": "2026-08-26"
},
{
"id": "Q266",
"orig": 266,
"title": "Key numbers in pericardial effusion",
"lesions": [
"EFFUSION",
"HEMODYNAMICS"
],
"lens": "numbers",
"items": [
{
"id": "Q266.1",
"q": "List the numbers a sonographer should know when reporting a pericardial effusion and evaluating for tamponade.",
"a": "Size grading uses the largest end-diastolic separation: under 1 cm small, 1–2 cm moderate, over 2 cm large, and the normal pericardial space holds only 15–50 mL of fluid, which may show as a systolic-only separation. Tamponade physiology is supported by RA collapse lasting more than one third of systole, any RV early-diastolic collapse, an IVC over 2.1 cm with less than 50% inspiratory collapse (implying RA pressure around 15 mmHg), mitral E variation above 30%, tricuspid E variation above 60%, and expiratory diastolic reversal in the hepatic veins. The clinical counterpart is a pulsus paradoxus over 10 mmHg, which mirrors the Doppler inflow variation. Older texts used 25% and 50% for the mitral and tricuspid thresholds; the 2013 ASE pericardial document raised them to 30% and 60% to improve specificity."
}
],
"numbers": [
{
"label": "Normal pericardial fluid volume",
"value": "15–50",
"unit": "mL"
},
{
"label": "Small effusion",
"value": "< 1",
"unit": "cm"
},
{
"label": "Moderate effusion",
"value": "1–2",
"unit": "cm"
},
{
"label": "Large effusion",
"value": "> 2",
"unit": "cm"
},
{
"label": "RA collapse duration for tamponade",
"value": "> 1/3",
"unit": "of systole"
},
{
"label": "IVC plethora diameter",
"value": "> 2.1",
"unit": "cm"
},
{
"label": "IVC inspiratory collapse in plethora",
"value": "< 50",
"unit": "%"
},
{
"label": "Estimated RA pressure with plethoric IVC",
"value": "15",
"unit": "mmHg"
},
{
"label": "Mitral E respiratory variation, tamponade",
"value": "> 30",
"unit": "%"
},
{
"label": "Tricuspid E respiratory variation, tamponade",
"value": "> 60",
"unit": "%"
},
{
"label": "Pulsus paradoxus",
"value": "> 10",
"unit": "mmHg"
}
],
"delta": {
"was": "Older teaching used mitral inflow variation >25% and tricuspid >50% as the Doppler thresholds for tamponade.",
"now": "Current ASE pericardial guideline uses mitral E variation >30% and tricuspid >60%, with RA collapse >1/3 of systole and IVC plethora as companion criteria.",
"source": "ASE 2013 pericardial disease guideline"
},
"pearl": "One, two, thirty, sixty: effusion grades in centimeters, then mitral and tricuspid variation in percent for tamponade.",
"lookalike": null,
"related": [
"Q118",
"Q119",
"Q122",
"Q265"
],
"reviewed": "2026-08-26"
},
{
"id": "Q267",
"orig": 267,
"title": "Bedside signs of pulmonary hypertension",
"lesions": [
"PH",
"TR"
],
"lens": "physical-exam",
"items": [
{
"id": "Q267.1",
"q": "Which auscultatory finding most directly reflects elevated pulmonary artery pressure, and why does it occur?",
"a": "A loud, sometimes palpable pulmonic component of the second heart sound (P2) is the most direct sign. The pulmonic valve closes when PA pressure exceeds RV pressure at end-systole; when PA diastolic pressure is high, the leaflets snap shut with more force and the closure sound carries farther, so P2 becomes audible at the apex rather than only at the left upper sternal border. In advanced disease P2 may fuse with A2 into a single loud S2 because RV ejection is no longer prolonged relative to the LV."
},
{
"id": "Q267.2",
"q": "What palpable and venous findings accompany chronic PH, and what do they tell you about the right heart?",
"a": "A sustained left parasternal (RV) heave means the RV has hypertrophied and dilated enough to lift the chest wall against the sternum during systole. Elevated jugular venous pressure with a prominent a wave indicates a stiff, pressure-loaded RV that resists atrial emptying; once functional TR develops the a wave gives way to a large v wave. A holosystolic murmur at the left lower sternal border that increases with inspiration (Carvallo sign) is TR from annular dilation, and a right-sided S4 may be heard early while a right-sided S3 marks decompensation."
}
],
"numbers": [],
"delta": null,
"pearl": "Loud P2 heard at the apex is abnormal; a normal P2 stays confined to the pulmonic area.",
"lookalike": {
"vs": "mitral regurgitation murmur",
"discriminator": "TR murmur is loudest at the left lower sternal border and gets louder with inspiration; MR is loudest at the apex, radiates to the axilla, and does not change with respiration."
},
"related": [
"Q130",
"Q82",
"Q359"
],
"reviewed": "2026-08-26"
},
{
"id": "Q268",
"orig": 268,
"title": "2D findings of pressure-loaded RV",
"lesions": [
"PH",
"RV_FUNCTION"
],
"lens": "2d",
"items": [
{
"id": "Q268.1",
"q": "Describe the 2D changes in the right heart and pulmonary artery that accompany chronic pulmonary hypertension.",
"a": "The RV first hypertrophies because pressure overload thickens the free wall; an end-diastolic free-wall thickness above 5 mm measured in the subcostal view is abnormal. As the ventricle fails it dilates, so the RV basal diameter exceeds 41 mm and the RV shares or takes over the apex in the apical four-chamber view, and the RA enlarges from elevated filling pressure and TR. The main pulmonary artery dilates beyond 25 mm as it accommodates chronically high pressure, and the IVC becomes plethoric with blunted inspiratory collapse."
},
{
"id": "Q268.2",
"q": "What is the D-shaped LV, when in the cardiac cycle does it appear in PH, and how is it quantified?",
"a": "In the parasternal short axis the interventricular septum normally bows toward the RV so the LV is circular. When RV pressure approaches or exceeds LV pressure the septum flattens and the LV cavity becomes D-shaped. In pressure overload the flattening is maximal at end-systole, when the RV-LV pressure difference is greatest; in pure RV volume overload it is maximal at end-diastole. The eccentricity index quantifies this as the ratio of the LV anteroposterior dimension to the septal-lateral dimension; a value above 1.1 is abnormal, and higher values track more severe RV pressure loading."
}
],
"numbers": [
{
"label": "RV free wall hypertrophy",
"value": "> 5",
"unit": "mm"
},
{
"label": "RV basal diameter dilated",
"value": "> 41",
"unit": "mm"
},
{
"label": "Main PA diameter dilated",
"value": "> 25",
"unit": "mm"
},
{
"label": "LV eccentricity index abnormal",
"value": "> 1.1",
"unit": "ratio"
}
],
"delta": null,
"pearl": "Systolic D = pressure, diastolic D = volume; the timing of septal flattening tells you which overload you are looking at.",
"lookalike": {
"vs": "RV volume overload from ASD or severe TR",
"discriminator": "Volume overload flattens the septum in diastole with normal RV wall thickness; pressure overload flattens it in systole with a thickened free wall."
},
"related": [
"Q131",
"Q132",
"Q381",
"Q382"
],
"reviewed": "2026-08-26"
},
{
"id": "Q269",
"orig": 269,
"title": "Doppler estimates of PA pressures",
"lesions": [
"PH",
"TR",
"PR"
],
"lens": "doppler",
"items": [
{
"id": "Q269.1",
"q": "How does the pulmonic regurgitation signal give you both mean and diastolic PA pressure?",
"a": "PR flows from the PA into the RV throughout diastole, so its velocity at each moment reflects the PA-to-RV pressure difference. The peak early-diastolic PR velocity, when RV pressure is close to RA pressure, approximates mean PAP: 4 × (peak PR velocity)² + RAP. The end-diastolic PR velocity, just before the pulmonic valve opens, gives PA diastolic pressure: 4 × (end-diastolic velocity)² + RAP. Both require a well-aligned CW signal through the RVOT in the parasternal short axis, and both use the same IVC-derived RAP as the TR method."
},
{
"id": "Q269.2",
"q": "What does the RVOT pulsed-wave profile look like in pulmonary hypertension?",
"a": "Normal RVOT flow is a rounded, symmetric envelope that peaks near mid-systole. With high PA pressure and PVR the pulmonary bed is stiff, so flow accelerates rapidly and peaks early; an acceleration time under 105 ms suggests PH, and under 80 ms usually means mean PAP above roughly 40 mmHg. Reflected pressure waves returning early from a stiff vascular bed can produce a mid-systolic notch in the envelope, which is a specific marker of elevated pulmonary vascular resistance rather than just high flow. Acceleration time is heart-rate dependent, so interpret it cautiously above about 100 beats per minute."
}
],
"numbers": [
{
"label": "Mean PAP from PR",
"value": "4 × peak PR v² + RAP",
"unit": "mmHg"
},
{
"label": "PADP from PR",
"value": "4 × end-diastolic PR v² + RAP",
"unit": "mmHg"
},
{
"label": "TR Vmax high probability of PH",
"value": "> 3.4",
"unit": "m/s"
},
{
"label": "PA acceleration time suggests PH",
"value": "< 105",
"unit": "ms"
},
{
"label": "PA acceleration time mPAP > ~40",
"value": "< 80",
"unit": "ms"
}
],
"delta": null,
"pearl": "Peak PR gives mean, end PR gives diastolic, TR gives systolic; all three add the same RAP.",
"lookalike": {
"vs": "notched RVOT flow from pulmonic stenosis",
"discriminator": "PS produces a high-velocity late-peaking jet with a gradient across the valve; the PH notch sits in a normal-velocity envelope with an early peak."
},
"related": [
"Q87",
"Q133",
"Q4"
],
"reviewed": "2026-08-26"
},
{
"id": "Q270",
"orig": 270,
"title": "ESC/ERS echo probability of PH",
"lesions": [
"PH",
"RV_FUNCTION"
],
"lens": "best-method",
"items": [
{
"id": "Q270.1",
"q": "How does the ESC/ERS 2022 guideline ask you to grade the echocardiographic probability of pulmonary hypertension rather than simply reporting an RVSP?",
"a": "Because TR-derived pressure can be under- or overestimated, the guideline combines the peak TR velocity with supporting signs from three categories: the ventricles (RV/LV basal diameter ratio above 1.0, systolic septal flattening or eccentricity index above 1.1, TAPSE/PASP ratio below 0.55 mm/mmHg), the pulmonary artery (acceleration time under 105 ms or mid-systolic notching, early-diastolic PR velocity above 2.2 m/s, PA diameter above the aortic root or above 25 mm), and the venous side (IVC over 21 mm with poor collapse, RA area over 18 cm²). Probability is low when TR Vmax is 2.8 m/s or less with no other signs, intermediate when TR Vmax is 2.8 or less with signs from at least two categories or 2.9 to 3.4 m/s without them, and high when TR Vmax exceeds 3.4 m/s or is 2.9 to 3.4 m/s with signs from at least two categories. The hemodynamic definition itself is a resting mean PAP above 20 mmHg with PVR above 2 Wood units for precapillary disease, confirmed by right heart catheterization."
}
],
"numbers": [
{
"label": "TR Vmax low probability",
"value": "≤ 2.8",
"unit": "m/s"
},
{
"label": "TR Vmax intermediate",
"value": "2.9–3.4",
"unit": "m/s"
},
{
"label": "TR Vmax high probability",
"value": "> 3.4",
"unit": "m/s"
},
{
"label": "Hemodynamic PH definition",
"value": "mPAP > 20",
"unit": "mmHg"
},
{
"label": "Precapillary PVR",
"value": "> 2",
"unit": "WU"
},
{
"label": "TAPSE/PASP abnormal",
"value": "< 0.55",
"unit": "mm/mmHg"
},
{
"label": "RA area abnormal",
"value": "> 18",
"unit": "cm²"
}
],
"delta": null,
"pearl": "Signs from two different categories (ventricle, PA, venous) upgrade the probability one step; two signs from the same category do not.",
"lookalike": null,
"related": [
"Q130",
"Q133",
"Q87",
"Q271",
"Q384"
],
"reviewed": "2026-08-26"
},
{
"id": "Q271",
"orig": 271,
"title": "Dyspneic woman with loud P2",
"lesions": [
"PH",
"TR"
],
"lens": "vignette",
"items": [
{
"id": "Q271.1",
"q": "A 47-year-old woman with limited scleroderma reports six months of exertional dyspnea and two syncopal episodes while climbing stairs. Examination shows a loud P2, a parasternal heave, and elevated jugular pressure. Echo shows an RV larger than the LV, systolic septal flattening, TR Vmax 4.1 m/s, an IVC of 2.4 cm with less than 50% collapse, and a normal-sized LA with E/A 0.7. What is the likely diagnosis and what should the report emphasize?",
"a": "This is high-probability pulmonary hypertension, most likely precapillary pulmonary arterial hypertension associated with connective tissue disease. The TR velocity of 4.1 m/s alone places her in the high-probability category, and the RV dilation and systolic septal flattening are supporting ventricular signs. The RAP is estimated at 15 mmHg because the IVC is both dilated and non-collapsing, so RVSP is roughly 4 × 4.1² + 15, about 82 mmHg. The small LA and low E/A argue against left heart disease as the cause, which is the key discrimination because group 2 (postcapillary) PH is managed very differently. Exertional syncope reflects a fixed RV output that cannot rise with demand and marks her as high risk, so the report should state the probability category, the estimated pressures, RV size and function (TAPSE, FAC, S'), the absence of left-sided disease, and recommend right heart catheterization for confirmation."
}
],
"numbers": [
{
"label": "RAP with dilated non-collapsing IVC",
"value": "15",
"unit": "mmHg"
},
{
"label": "Estimated RVSP in vignette",
"value": "≈ 82",
"unit": "mmHg"
},
{
"label": "TR Vmax high probability",
"value": "> 3.4",
"unit": "m/s"
}
],
"delta": null,
"pearl": "Always comment on the left atrium in a PH report: a small LA with low E/A points away from group 2 disease.",
"lookalike": {
"vs": "PH from left heart disease (group 2)",
"discriminator": "Group 2 PH shows a dilated LA, elevated E/e' or E/A ≥ 2, and often mitral disease; precapillary PH has a normal or small LA and normal LV filling pattern."
},
"related": [
"Q270",
"Q87",
"Q132"
],
"reviewed": "2026-08-26"
},
{
"id": "Q272",
"orig": 272,
"title": "Primary versus secondary hypertension",
"lesions": [
"HTN",
"COARCT"
],
"lens": "etiology",
"items": [
{
"id": "Q272.1",
"q": "What is the difference between primary and secondary hypertension, and roughly how common is each?",
"a": "Primary (essential) hypertension has no single identifiable cause and accounts for about 90 to 95 percent of adult cases; it emerges from the interaction of genetics, salt sensitivity, obesity, sympathetic tone, and vascular stiffening with age. Secondary hypertension, the remaining 5 to 10 percent, results from a specific and often treatable condition. Suspect it when hypertension begins before age 30 or after 55, is resistant to three drugs, is abruptly worse, or comes with a telltale clue such as hypokalemia."
},
{
"id": "Q272.2",
"q": "Which secondary causes should an echocardiographer be able to recognize or suggest?",
"a": "Coarctation of the aorta is the one the echo lab can diagnose directly: upper-limb hypertension with a suprasternal Doppler gradient that persists into diastole, and often a bicuspid aortic valve. Renal artery stenosis and intrinsic renal disease are the commonest secondary causes overall, followed by primary aldosteronism, which is the most common endocrine cause; pheochromocytoma, Cushing syndrome, thyroid disease, and obstructive sleep apnea round out the list. Disproportionate LVH for the measured blood pressure, or an abdominal bruit noted in the history, should prompt you to flag a secondary cause in the report."
}
],
"numbers": [
{
"label": "Primary hypertension share of cases",
"value": "90–95",
"unit": "%"
},
{
"label": "Secondary hypertension share of cases",
"value": "5–10",
"unit": "%"
}
],
"delta": null,
"pearl": "Young patient, hypertension, bicuspid valve: sweep the suprasternal notch before you finish the study.",
"lookalike": null,
"related": [
"Q127",
"Q189"
],
"reviewed": "2026-08-26"
},
{
"id": "Q273",
"orig": 273,
"title": "Examining the hypertensive heart",
"lesions": [
"HTN",
"DIASTOLIC"
],
"lens": "physical-exam",
"items": [
{
"id": "Q273.1",
"q": "What cardiac examination findings develop in long-standing systemic hypertension, and what is the mechanism of each?",
"a": "The earliest finding is a fourth heart sound, produced when the atrium contracts forcefully into a stiff, hypertrophied LV; it is low-pitched, best heard at the apex with the bell in the left lateral position. The apical impulse becomes sustained and forceful but, unlike in volume overload, is not displaced until the ventricle finally dilates. A2 is loud because the aortic valve closes against high diastolic pressure, and an aortic ejection sound or soft systolic murmur can arise from a dilated, stiff root. Late in the course, an S3 and a displaced apex signal transition to systolic failure, and an AR murmur may appear when root dilation pulls the leaflets apart."
},
{
"id": "Q273.2",
"q": "How should blood pressure be measured for the diagnosis of hypertension, and how does that matter to the echo lab?",
"a": "The ACC/AHA 2017 guideline requires an average of at least two readings on two or more occasions, with the patient seated, back supported, feet flat, arm at heart level, correct cuff size, and no caffeine or exercise for 30 minutes. Out-of-office confirmation with home or ambulatory monitoring is recommended to exclude white-coat and masked hypertension. For the sonographer this matters because the blood pressure recorded at the time of the study contextualizes the LV wall thickness and diastolic indices you measure; note it on the worksheet."
}
],
"numbers": [
{
"label": "Rest before BP measurement",
"value": "≥ 5",
"unit": "min"
},
{
"label": "No caffeine or exercise before BP",
"value": "30",
"unit": "min"
}
],
"delta": null,
"pearl": "S4 = stiff ventricle (hypertension, HCM, ischemia); S3 = volume-loaded failing ventricle.",
"lookalike": {
"vs": "aortic stenosis",
"discriminator": "AS has a harsh crescendo-decrescendo murmur radiating to the carotids with a delayed carotid upstroke and a soft A2; hypertension has a loud A2 and at most a soft flow murmur."
},
"related": [
"Q129",
"Q128",
"Q274"
],
"reviewed": "2026-08-26"
},
{
"id": "Q274",
"orig": 274,
"title": "Diastolic Doppler in hypertension",
"lesions": [
"HTN",
"DIASTOLIC"
],
"lens": "doppler",
"items": [
{
"id": "Q274.1",
"q": "What Doppler pattern of LV filling is typical of early hypertensive heart disease, and why does it occur?",
"a": "Chronic pressure overload thickens the ventricle and slows the energy-dependent process of active relaxation, so early diastolic suction is weakened. The mitral E velocity falls, the deceleration time lengthens beyond 240 ms, and the isovolumic relaxation time exceeds 90 ms because the ventricle takes longer to drop its pressure below LA pressure. Atrial contraction then does more of the filling work, so the A wave grows and E/A falls to 0.8 or less with E at or below 50 cm/s. This is grade I diastolic dysfunction (impaired relaxation), and at this stage LA pressure is still normal."
},
{
"id": "Q274.2",
"q": "What does tissue Doppler add, and how does the pattern evolve as hypertensive disease progresses?",
"a": "Annular e' velocity measures the speed of myocardial lengthening in early diastole and is largely independent of preload, so it drops early in hypertension: septal e' below 7 cm/s or lateral e' below 10 cm/s confirms that a low E/A is due to impaired relaxation rather than low volume status. As the stiff ventricle raises LA pressure, E rises again and the inflow looks pseudonormal (E/A 0.8 to 2), but e' stays low, so E/e' above 14 unmasks the elevated filling pressure; LA volume index above 34 mL/m² and TR velocity above 2.8 m/s are the other supporting variables. In a hypertensive with a normal-looking E/A, the e' is the number that tells you the truth."
}
],
"numbers": [
{
"label": "Grade I E/A",
"value": "≤ 0.8",
"unit": "ratio"
},
{
"label": "Grade I E velocity",
"value": "≤ 50",
"unit": "cm/s"
},
{
"label": "Prolonged deceleration time",
"value": "> 240",
"unit": "ms"
},
{
"label": "Prolonged IVRT",
"value": "> 90",
"unit": "ms"
},
{
"label": "Septal e' abnormal",
"value": "< 7",
"unit": "cm/s"
},
{
"label": "Lateral e' abnormal",
"value": "< 10",
"unit": "cm/s"
},
{
"label": "Average E/e' elevated",
"value": "> 14",
"unit": "ratio"
},
{
"label": "LAVi abnormal",
"value": "> 34",
"unit": "mL/m²"
}
],
"delta": null,
"pearl": "A low e' cannot be pseudonormalized; when E/A looks normal, look at the annulus.",
"lookalike": {
"vs": "healthy older adult",
"discriminator": "Normal aging also lowers E/A and e', but LAVi stays ≤ 34 mL/m², E/e' stays ≤ 14, and LV mass is normal; hypertensive disease adds LVH and LA enlargement."
},
"related": [
"Q129",
"Q273",
"Q278"
],
"reviewed": "2026-08-26"
},
{
"id": "Q275",
"orig": 275,
"title": "LV geometry by mass and RWT",
"lesions": [
"HTN",
"CHAMBER_QUANT",
"LV_FUNCTION"
],
"lens": "best-method",
"items": [
{
"id": "Q275.1",
"q": "What is the recommended way to classify LV geometry in a hypertensive patient, and what are the four categories?",
"a": "ASE 2015 classifies geometry with two measurements: LV mass indexed to body surface area and relative wall thickness (RWT), calculated as 2 × posterior wall thickness divided by LV internal diameter at end-diastole. Mass is derived from the linear method (the cube formula 0.8 × 1.04 × [(IVSd + LVIDd + PWd)³ − LVIDd³] + 0.6 g) using leading-edge measurements from the parasternal long axis, or from 2D area-length when the ventricle is asymmetric. Normal geometry is normal mass with RWT 0.42 or less; concentric remodeling is normal mass with RWT above 0.42; concentric hypertrophy is increased mass with RWT above 0.42; and eccentric hypertrophy is increased mass with RWT 0.42 or less."
},
{
"id": "Q275.2",
"q": "Why does the geometric pattern matter clinically in hypertension?",
"a": "Pressure overload adds sarcomeres in parallel, thickening the walls without enlarging the cavity, which is why hypertension usually produces concentric remodeling first and then concentric hypertrophy. Eccentric hypertrophy in a hypertensive patient implies added volume load or transition toward a failing, dilating ventricle and carries a worse prognosis. Concentric hypertrophy is the pattern most strongly linked to diastolic dysfunction, atrial fibrillation, and cardiovascular events, and regression of mass with treatment is itself an outcome marker, so the classification belongs in every hypertensive report."
}
],
"numbers": [
{
"label": "RWT formula",
"value": "2 × PWd / LVIDd",
"unit": "ratio"
},
{
"label": "RWT concentric threshold",
"value": "> 0.42",
"unit": "ratio"
},
{
"label": "LV mass index LVH men",
"value": "> 115",
"unit": "g/m²"
},
{
"label": "LV mass index LVH women",
"value": "> 95",
"unit": "g/m²"
}
],
"delta": null,
"pearl": "Thick walls with a small cavity is concentric; thick walls with a big cavity is eccentric. RWT sorts them, mass index decides if it is hypertrophy at all.",
"lookalike": {
"vs": "concentric remodeling",
"discriminator": "Remodeling has RWT > 0.42 but a normal indexed mass; concentric hypertrophy needs both RWT > 0.42 and mass above the sex-specific cutoff."
},
"related": [
"Q129",
"Q276",
"Q277",
"Q278"
],
"widgets": [
{
"id": "calc",
"opts": {
"k": "mass"
}
}
],
"reviewed": "2026-08-26"
},
{
"id": "Q276",
"orig": 276,
"title": "Hypertensive LVH versus HCM",
"lesions": [
"HTN",
"HCM"
],
"lens": "pitfall",
"items": [
{
"id": "Q276.1",
"q": "A hypertensive patient has a 16 mm septum. What features help you decide whether this is hypertensive hypertrophy or hypertrophic cardiomyopathy?",
"a": "Hypertensive hypertrophy is usually symmetric, rarely exceeds 15 to 16 mm, and comes with a history and blood pressure that explain it; HCM tends to be asymmetric (septal-to-posterior wall ratio above 1.3), often exceeds 15 mm without an adequate cause, and may show systolic anterior motion, LVOT obstruction, a small hyperdynamic cavity, and abnormal mitral apparatus such as elongated leaflets or displaced papillary muscles. Strain helps: HCM shows patchy regional reductions in longitudinal strain matching the hypertrophied segments, whereas hypertensive disease reduces strain more uniformly. Wall thickness above 15 mm in a patient whose hypertension is mild or controlled should be labeled unexplained and referred for genetic and cardiac MRI evaluation rather than attributed to blood pressure."
},
{
"id": "Q276.2",
"q": "How do you separate athlete's heart from pathologic hypertrophy?",
"a": "Endurance training produces balanced, mild enlargement: wall thickness rarely exceeds 12 mm, the LV cavity is enlarged rather than small (LVIDd often above 55 mm), diastolic function and e' are normal or supranormal, and strain is normal. Pathologic hypertrophy has a small or normal cavity, reduced e', an enlarged LA, and abnormal strain. Wall thickness of 13 to 15 mm is the gray zone; a period of detraining that shrinks the walls confirms a physiologic cause, whereas HCM does not regress."
}
],
"numbers": [
{
"label": "Septal/posterior wall ratio suggesting HCM",
"value": "> 1.3",
"unit": "ratio"
},
{
"label": "Wall thickness unexplained by hypertension",
"value": "> 15",
"unit": "mm"
},
{
"label": "Athlete's heart wall thickness upper limit",
"value": "≤ 12",
"unit": "mm"
},
{
"label": "Athlete gray zone",
"value": "13–15",
"unit": "mm"
}
],
"delta": null,
"pearl": "Big cavity with normal e' is an athlete; small cavity with low e' is disease.",
"lookalike": {
"vs": "cardiac amyloidosis",
"discriminator": "Amyloid gives concentric thickening with a low-voltage ECG, thickened RV and valves, a sparkling texture, and apical-sparing strain; hypertensive LVH has high ECG voltage and no apical sparing."
},
"related": [
"Q275",
"Q140",
"Q129",
"Q278"
],
"reviewed": "2026-08-26"
},
{
"id": "Q277",
"orig": 277,
"title": "Hypertension numbers to memorize",
"lesions": [
"HTN",
"CHAMBER_QUANT"
],
"lens": "numbers",
"items": [
{
"id": "Q277.1",
"q": "List the ACC/AHA 2017 blood pressure categories.",
"a": "Normal is below 120 systolic and below 80 diastolic. Elevated is 120 to 129 systolic with diastolic still below 80. Stage 1 hypertension is 130 to 139 systolic or 80 to 89 diastolic, and stage 2 is 140 or higher systolic or 90 or higher diastolic. The category is set by whichever number is higher, so a reading of 128/85 is stage 1. The 2017 guideline lowered the diagnostic threshold from the older 140/90 so that treatment could begin earlier in high-risk patients."
},
{
"id": "Q277.2",
"q": "What echo cutoffs define hypertrophy and abnormal geometry?",
"a": "LV mass index above 115 g/m² in men or 95 g/m² in women defines hypertrophy by the linear method; relative wall thickness above 0.42 defines a concentric pattern. Normal end-diastolic septal and posterior wall thickness is 0.6 to 1.0 cm, so 1.1 cm or more is thickened. Normal LVIDd is 4.2 to 5.8 cm in men and 3.8 to 5.2 cm in women. Left atrial volume index above 34 mL/m² marks the chronic elevation of filling pressure that follows hypertensive hypertrophy."
}
],
"numbers": [
{
"label": "Normal BP",
"value": "< 120/80",
"unit": "mmHg"
},
{
"label": "Elevated BP",
"value": "120–129 / < 80",
"unit": "mmHg"
},
{
"label": "Stage 1 hypertension",
"value": "130–139 / 80–89",
"unit": "mmHg"
},
{
"label": "Stage 2 hypertension",
"value": "≥ 140/90",
"unit": "mmHg"
},
{
"label": "LV mass index LVH men",
"value": "> 115",
"unit": "g/m²"
},
{
"label": "LV mass index LVH women",
"value": "> 95",
"unit": "g/m²"
},
{
"label": "RWT concentric",
"value": "> 0.42",
"unit": "ratio"
},
{
"label": "Normal wall thickness",
"value": "0.6–1.0",
"unit": "cm"
},
{
"label": "LAVi abnormal",
"value": "> 34",
"unit": "mL/m²"
}
],
"delta": null,
"pearl": "130/80 starts stage 1; 140/90 starts stage 2; 115/95 (men/women) starts LVH; 0.42 starts concentric.",
"lookalike": null,
"related": [
"Q127",
"Q275"
],
"reviewed": "2026-08-26"
},
{
"id": "Q278",
"orig": 278,
"title": "Headache and a thick septum",
"lesions": [
"HTN",
"DIASTOLIC"
],
"lens": "vignette",
"items": [
{
"id": "Q278.1",
"q": "A 58-year-old man with untreated blood pressure averaging 162/98 mmHg is referred for echo because of exertional dyspnea. You measure IVSd 1.3 cm, PWd 1.3 cm, LVIDd 4.6 cm, LV mass index 128 g/m², EF 62%, E/A 0.7 with E 45 cm/s, septal e' 5 cm/s, average E/e' 12, and LAVi 30 mL/m². How do you classify his ventricle and his diastolic function?",
"a": "RWT is 2 × 1.3 / 4.6, about 0.57, and mass index is above the male cutoff of 115 g/m², so this is concentric LV hypertrophy, the expected response to chronic pressure overload. Filling shows a low E/A with E under 50 cm/s and a reduced e', which is grade I diastolic dysfunction with impaired relaxation; the E/e' of 12 and LAVi of 30 mL/m² indicate that LA pressure is still within normal limits. The preserved EF with symptoms, hypertrophy, and abnormal relaxation is the substrate for heart failure with preserved ejection fraction, and his exertional dyspnea is likely the first manifestation. The report should state the geometry category, the diastolic grade with normal estimated filling pressure, and recommend blood pressure control, which can regress both mass and the relaxation abnormality."
}
],
"numbers": [
{
"label": "RWT in vignette",
"value": "≈ 0.57",
"unit": "ratio"
},
{
"label": "LV mass index LVH men",
"value": "> 115",
"unit": "g/m²"
},
{
"label": "Grade I E/A",
"value": "≤ 0.8",
"unit": "ratio"
},
{
"label": "Average E/e' normal",
"value": "≤ 14",
"unit": "ratio"
}
],
"delta": null,
"pearl": "Grade I plus normal E/e' and LAVi means impaired relaxation with normal filling pressure; do not call it elevated LA pressure.",
"lookalike": {
"vs": "hypertrophic cardiomyopathy",
"discriminator": "This septum and posterior wall are equally thick, under 15 mm, and explained by a 162/98 blood pressure; HCM is typically asymmetric or unexplained by the hemodynamic load."
},
"related": [
"Q274",
"Q275",
"Q276"
],
"reviewed": "2026-08-26"
},
{
"id": "Q279",
"orig": 279,
"title": "Auscultating the infarcted heart",
"lesions": [
"CAD",
"MR",
"VSD"
],
"lens": "physical-exam",
"items": [
{
"id": "Q279.1",
"q": "What heart sounds and murmurs should you expect during and after an acute myocardial infarction, and what do they mean?",
"a": "An S4 is almost universal during acute ischemia because the injured myocardium becomes stiff and the atrium contracts into a noncompliant ventricle; it is heard at the apex in the left lateral position and disappears if the patient goes into atrial fibrillation. An S3 signals a large infarct with elevated filling pressure and predicts a worse outcome. A pericardial friction rub in the first few days indicates transmural infarction reaching the epicardium, and a rub appearing weeks later suggests Dressler syndrome. Any new murmur after an infarct is a mechanical complication until proven otherwise and is an indication for urgent echo."
},
{
"id": "Q279.2",
"q": "How do you distinguish the two life-threatening new holosystolic murmurs after infarction at the bedside, and what does echo show for each?",
"a": "A new apical holosystolic murmur radiating to the axilla, often with pulmonary edema out of proportion to the infarct size, suggests acute MR from papillary muscle rupture or ischemic dysfunction; because the LA is small and noncompliant the murmur can be surprisingly soft or short. A new harsh holosystolic murmur at the left lower sternal border, frequently with a palpable thrill, suggests a ventricular septal rupture, and it is typically loud. Posteromedial papillary muscle rupture accompanies inferior infarcts because that muscle has a single blood supply from the RCA, whereas septal rupture follows anterior or inferior infarcts depending on the septal segment involved. Echo shows a flail leaflet with an eccentric MR jet in the first case and color flow crossing the septum with a systolic left-to-right CW signal in the second."
}
],
"numbers": [],
"delta": null,
"pearl": "Thrill at the sternal border is a hole in the septum; soft apical murmur with flash pulmonary edema is a torn papillary muscle.",
"lookalike": {
"vs": "post-MI VSD versus acute MR",
"discriminator": "VSD murmur is loud, parasternal, with a thrill and a step-up in RV oxygen saturation; acute MR is apical, may be soft, and shows a flail leaflet on echo."
},
"related": [
"Q155",
"Q160",
"Q51"
],
"reviewed": "2026-08-26"
},
{
"id": "Q280",
"orig": 280,
"title": "M-mode signs of infarction",
"lesions": [
"CAD",
"LV_FUNCTION"
],
"lens": "m-mode",
"items": [
{
"id": "Q280.1",
"q": "What does M-mode show in a healed myocardial infarction, and why?",
"a": "M-mode samples the septum and posterior wall with very high temporal resolution, so it can document both thickness and the amount and timing of systolic thickening along a single line. A scarred segment is thinned at end-diastole, often to 6 mm or less, and shows bright, dense echoes because fibrous tissue reflects more strongly than muscle. During systole the scar thickens less than 30 percent or not at all, and it may move passively with the neighboring normal myocardium, which is why thickening rather than endocardial motion is the better M-mode marker of viable muscle. Compensatory hyperkinesis of the opposite wall can exaggerate the difference between the two walls on the same tracing."
},
{
"id": "Q280.2",
"q": "A patient one week after coronary bypass surgery has a septum that moves toward the RV in systole. Is this an infarct?",
"a": "Usually not. Paradoxical septal motion after cardiac surgery is common and generally benign; the septum still thickens normally in systole, which distinguishes it from ischemic akinesis, where thickening is lost. The mechanism is thought to involve pericardial disruption and altered constraint with exaggerated translational motion of the whole heart, so the septum appears to move anteriorly while it is actually contracting. The same paradoxical pattern with normal thickening is seen in RV volume overload and left bundle branch block, so always assess thickening before calling a septum ischemic in a postoperative patient."
}
],
"numbers": [
{
"label": "Scar wall thickness",
"value": "< 6",
"unit": "mm"
},
{
"label": "Reduced systolic thickening",
"value": "< 30",
"unit": "%"
}
],
"delta": null,
"pearl": "Motion can be borrowed from a neighbor; thickening cannot. Judge the wall by how much it thickens.",
"lookalike": {
"vs": "left bundle branch block septum",
"discriminator": "LBBB produces an early septal beak and delayed posterior wall contraction with preserved thickening; infarct scar is thin, bright, and fails to thicken."
},
"related": [
"Q158",
"Q153",
"Q207"
],
"reviewed": "2026-08-26"
},
{
"id": "Q281",
"orig": 281,
"title": "Doppler in ischemic heart disease",
"lesions": [
"CAD",
"STRESS",
"MR"
],
"lens": "doppler",
"items": [
{
"id": "Q281.1",
"q": "Outline the standard stress echo protocols and the response that indicates ischemia.",
"a": "Treadmill stress uses the Bruce protocol with images at rest and immediately after peak exercise, within 60 to 90 seconds, because wall motion abnormalities resolve quickly; supine bicycle allows imaging during exercise at each stage. Dobutamine is infused at 5, 10, 20, 30, and 40 mcg/kg/min in three-minute stages with atropine added if heart rate falls short, and imaging at low dose (5 to 10) is used for viability, where a hibernating segment improves and then worsens again at high dose, the biphasic response. The target is 85 percent of age-predicted maximum heart rate. A normal response is uniform hyperkinesis with a smaller end-systolic cavity; a new or worsening wall motion abnormality, or a ventricle that dilates with a falling EF, indicates ischemia."
},
{
"id": "Q281.2",
"q": "How do you use Doppler to characterize ischemic MR and a post-infarction VSD?",
"a": "Ischemic MR results from apical and posterior displacement of the papillary muscles tethering the leaflets, so the jet is often posteriorly directed, and it is graded with the same measures as any MR: vena contracta at or above 0.7 cm, EROA at or above 0.4 cm², regurgitant volume at or above 60 mL, and systolic pulmonary vein reversal for severe; note that ischemic MR can be dynamic and worsen with exercise. For a post-infarct VSD, CW across the defect gives the peak LV-to-RV gradient, and RVSP equals systolic blood pressure minus that gradient, so a low gradient means a high RV pressure and a poor prognosis. The LVOT VTI, from PW at the outflow tract, indexes stroke volume and cardiac output (SV = LVOT area × VTI); a VTI under about 15 to 18 cm signals a low-output state after infarction."
}
],
"numbers": [
{
"label": "Dobutamine stages",
"value": "5, 10, 20, 30, 40",
"unit": "mcg/kg/min"
},
{
"label": "Target heart rate",
"value": "85",
"unit": "% of age-predicted max"
},
{
"label": "Post-exercise imaging window",
"value": "≤ 60–90",
"unit": "s"
},
{
"label": "Severe MR vena contracta",
"value": "≥ 0.7",
"unit": "cm"
},
{
"label": "Severe MR EROA",
"value": "≥ 0.4",
"unit": "cm²"
},
{
"label": "RVSP from VSD",
"value": "SBP − 4v²",
"unit": "mmHg"
},
{
"label": "Low-output LVOT VTI",
"value": "< 15–18",
"unit": "cm"
}
],
"delta": null,
"pearl": "Low-dose dobutamine finds the sleeping muscle; high-dose finds the starving muscle.",
"lookalike": {
"vs": "primary (degenerative) MR",
"discriminator": "Degenerative MR has prolapse or flail with an excursion above the annulus; ischemic MR has restricted, tethered leaflets with a tenting height that increases as the ventricle remodels."
},
"related": [
"Q164",
"Q205",
"Q155"
],
"reviewed": "2026-08-26"
},
{
"id": "Q282",
"orig": 282,
"title": "Infarct numbers worth knowing",
"lesions": [
"CAD",
"LV_FUNCTION"
],
"lens": "numbers",
"items": [
{
"id": "Q282.1",
"q": "How is the wall motion score index calculated and interpreted?",
"a": "Each of the 17 segments is scored 1 for normal, 2 hypokinetic, 3 akinetic, and 4 dyskinetic (an aneurysmal segment is often scored 5 in older schemes), and the index is the sum of scores divided by the number of segments visualized. A completely normal ventricle scores 1.0. An index above 1.7 indicates a large infarct involving roughly 20 percent or more of the myocardium and predicts heart failure and mortality; values of 1.1 to 1.7 denote smaller regional damage. Because unscored segments are excluded from the denominator, poor image quality can falsely lower the index, which is one indication for contrast."
},
{
"id": "Q282.2",
"q": "What thickness and thickening cutoffs identify scar versus viable myocardium?",
"a": "Normal myocardium thickens by 40 percent or more during systole; thickening under 30 percent defines hypokinesis and under 10 percent, akinesis. An end-diastolic wall thickness under 6 mm with increased echogenicity indicates transmural scar that will not recover with revascularization, whereas a thinned but not severely thinned segment that thickens with low-dose dobutamine is hibernating and may recover. Coronary anatomy maps onto the score: the LAD supplies the anterior wall, anterior septum, and apex, the RCA the inferior wall and inferior septum, and the circumflex the anterolateral and inferolateral walls."
}
],
"numbers": [
{
"label": "WMSI formula",
"value": "sum of scores / segments scored",
"unit": "index"
},
{
"label": "Normal WMSI",
"value": "1.0",
"unit": "index"
},
{
"label": "Large infarct WMSI",
"value": "> 1.7",
"unit": "index"
},
{
"label": "Hypokinesis thickening",
"value": "< 30",
"unit": "%"
},
{
"label": "Akinesis thickening",
"value": "< 10",
"unit": "%"
},
{
"label": "Normal thickening",
"value": "≥ 40",
"unit": "%"
},
{
"label": "Transmural scar thickness",
"value": "< 6",
"unit": "mm"
},
{
"label": "Segment count",
"value": "17",
"unit": "segments"
}
],
"delta": null,
"pearl": "WMSI 1.0 is perfect, 1.7 is the line for a big infarct; 6 mm is the wall too thin to save.",
"lookalike": null,
"related": [
"Q153",
"Q17",
"Q158"
],
"reviewed": "2026-08-26"
},
{
"id": "Q283",
"orig": 283,
"title": "Physical signs of aortic disease",
"lesions": [
"AORTA",
"AR"
],
"lens": "physical-exam",
"items": [
{
"id": "Q283.1",
"q": "What examination findings raise suspicion of acute aortic dissection, and why do they occur?",
"a": "A dissection flap can compress or occlude branch vessels, so a pulse deficit (absent or diminished carotid, brachial, or femoral pulse) or a systolic blood pressure difference above 20 mmHg between the arms is a high-risk feature; neither is sensitive, so a normal exam does not exclude dissection. A new diastolic decrescendo murmur of AR appears when a proximal (Stanford A) tear dilates the root, prolapses the intimal flap through the valve, or disrupts commissural support. Muffled heart sounds with hypotension and jugular distension mean rupture into the pericardium with tamponade, and neurologic deficits reflect carotid or spinal artery involvement. Pain described as tearing, abrupt, and maximal at onset is the classic history."
},
{
"id": "Q283.2",
"q": "Which body habitus features point to Marfan syndrome, and why does that change the echo you perform?",
"a": "Marfan patients are tall with long limbs and an arm span exceeding height, long fingers with positive wrist and thumb signs, pectus deformity, high-arched palate, scoliosis, joint laxity, and lens dislocation. The underlying fibrillin-1 defect weakens the aortic media, so the sinuses of Valsalva dilate before the ascending aorta, producing a pear-shaped root and eventually AR, and the mitral valve is myxomatous with prolapse. The echo therefore requires meticulous root measurement at the annulus, sinuses, sinotubular junction, and ascending aorta with z-scores, plus evaluation for MVP and MR, and serial studies to track growth; the surgical threshold is lower (5.0 cm, or less with risk factors) than in degenerative dilation."
}
],
"numbers": [
{
"label": "Interarm systolic BP difference",
"value": "> 20",
"unit": "mmHg"
},
{
"label": "Marfan root surgery threshold",
"value": "5.0",
"unit": "cm"
}
],
"delta": null,
"pearl": "Tearing pain plus a pulse deficit or a new AR murmur is dissection until CT or TEE says otherwise.",
"lookalike": {
"vs": "acute myocardial infarction",
"discriminator": "MI pain builds over minutes and has ECG and troponin changes; dissection pain is maximal at onset, migrates, and comes with pulse or BP asymmetry; note that a type A tear can occlude the RCA and cause both."
},
"related": [
"Q9",
"Q77",
"Q194",
"Q192"
],
"reviewed": "2026-08-26"
},
{
"id": "Q284",
"orig": 284,
"title": "Aortic root dimensions and thresholds",
"lesions": [
"AORTA",
"CHAMBER_QUANT"
],
"lens": "numbers",
"items": [
{
"id": "Q284.1",
"q": "What are the normal aortic root dimensions and how should they be measured and indexed?",
"a": "Measure in the parasternal long axis perpendicular to the long axis of the vessel at the annulus, sinuses of Valsalva, sinotubular junction, and proximal ascending aorta. ASE convention is leading-edge to leading-edge at end-diastole, while some newer guidance uses inner-edge to inner-edge; report which you used because the two differ by 2 to 4 mm. Normal sinus diameter is roughly up to 3.7 cm in men and 3.4 cm in women, and because size scales with body size an indexed diameter above 2.1 cm/m² is abnormal regardless of absolute value. In children and small or very tall adults a z-score, the number of standard deviations from the expected diameter for body surface area, is preferred, with z above 2 defining dilation."
},
{
"id": "Q284.2",
"q": "What diameters define dilation and trigger surgery?",
"a": "An ascending aorta or root above 4.0 cm is dilated and warrants surveillance imaging; 4.5 cm is the point at which concurrent replacement is recommended during surgery for another indication such as a bicuspid or regurgitant aortic valve. For degenerative disease, elective repair is indicated at 5.5 cm. Genetic aortopathy lowers the bar: Marfan syndrome is repaired at 5.0 cm, or 4.5 cm with a family history of dissection, rapid growth above 0.3 to 0.5 cm per year, severe AR, or planned pregnancy, and Loeys-Dietz or vascular Ehlers-Danlos can be operated even earlier. Growth rate matters as much as absolute size, which is why serial measurements must use the same technique and the same location."
}
],
"numbers": [
{
"label": "Normal sinus of Valsalva men",
"value": "≤ 3.7",
"unit": "cm"
},
{
"label": "Normal sinus of Valsalva women",
"value": "≤ 3.4",
"unit": "cm"
},
{
"label": "Indexed root diameter abnormal",
"value": "> 2.1",
"unit": "cm/m²"
},
{
"label": "Z-score dilation",
"value": "> 2",
"unit": "SD"
},
{
"label": "Dilated root, begin surveillance",
"value": "> 4.0",
"unit": "cm"
},
{
"label": "Replace at concurrent valve surgery",
"value": "≥ 4.5",
"unit": "cm"
},
{
"label": "Marfan elective repair",
"value": "≥ 5.0",
"unit": "cm"
},
{
"label": "Degenerative elective repair",
"value": "≥ 5.5",
"unit": "cm"
},
{
"label": "Rapid growth",
"value": "> 0.3–0.5",
"unit": "cm/year"
}
],
"delta": null,
"pearl": "4.0 watch, 4.5 fix if already operating, 5.0 fix if Marfan, 5.5 fix if degenerative.",
"lookalike": {
"vs": "oblique measurement of a normal root",
"discriminator": "An off-axis parasternal cut overestimates diameter; confirm the vessel is measured perpendicular to its long axis and at the same level on serial studies before calling growth."
},
"related": [
"Q77",
"Q195",
"Q193",
"Q362",
"Q363",
"Q370"
],
"reviewed": "2026-08-26"
},
{
"id": "Q285",
"orig": 285,
"title": "Embryology of the atrial septum",
"lesions": [
"ASD",
"ANATOMY"
],
"lens": "etiology",
"items": [
{
"id": "Q285.1",
"q": "How do the septum primum and septum secundum form the atrial septum, and where does each ASD type come from?",
"a": "The septum primum grows down from the roof of the common atrium toward the endocardial cushions, closing the ostium primum; before it fuses, fenestrations in its upper part coalesce into the ostium secundum. A thicker septum secundum then descends to the right of it, leaving a flap-covered opening, the fossa ovalis. A secundum ASD is a true deficiency of septum primum tissue in the fossa ovalis region. A primum ASD arises when the septum primum fails to fuse with the endocardial cushions, so it sits low, next to the AV valves, and is part of the AV septal defect spectrum. Sinus venosus defects are not septal at all: they result from abnormal incorporation of the sinus venosus, so the SVC or IVC overrides the septum, usually with anomalous pulmonary venous return."
},
{
"id": "Q285.2",
"q": "What is the difference between a patent foramen ovale and a secundum ASD?",
"a": "A PFO is the persistence of the normal fetal flap valve: the septum primum and septum secundum overlap but have not fused, so a tunnel opens when right atrial pressure exceeds left. There is no missing tissue, and flow is usually only transient right-to-left with Valsalva or cough. A secundum ASD is an actual hole in the septum primum with continuous left-to-right flow throughout the cardiac cycle. On imaging, a PFO shows a tunnel between two overlapping layers, whereas an ASD shows a discrete gap with a color jet that persists across the cycle."
}
],
"numbers": [],
"delta": null,
"pearl": "Primum = low and next to the AV valves (cushion problem); secundum = center of the fossa (septum primum hole); sinus venosus = high, where the cavae enter (not a septal problem).",
"lookalike": {
"vs": "PFO",
"discriminator": "PFO is overlapping flaps with a tunnel and mostly transient right-to-left flow; secundum ASD is a true tissue defect with continuous left-to-right color flow"
},
"related": [
"Q289",
"Q290"
],
"reviewed": "2026-08-26"
},
{
"id": "Q286",
"orig": 286,
"title": "Auscultation of an atrial septal defect",
"lesions": [
"ASD"
],
"lens": "physical-exam",
"items": [
{
"id": "Q286.1",
"q": "Why does an ASD produce a wide, fixed split of the second heart sound?",
"a": "Normally the split widens on inspiration because increased venous return delays pulmonic closure. In an ASD, the two atria are in free communication, so inspiratory changes in venous return are shared between the two sides and the relative timing of the two ventricles no longer varies with breathing. The RV is also chronically volume loaded, which prolongs its ejection and pushes P2 later at all times. The result is a split that is both wide and does not change with respiration, which is the classic auscultatory clue."
},
{
"id": "Q286.2",
"q": "Where does the murmur of an ASD come from, given that flow across the defect itself is silent?",
"a": "The interatrial pressure gradient is only a few mmHg, so flow across the hole generates no audible turbulence. The murmur is a soft, crescendo-decrescendo systolic ejection murmur at the upper left sternal border produced by the doubled or tripled stroke volume crossing a normal pulmonic valve. With large shunts, a mid-diastolic rumble at the lower left sternal border may be heard from increased flow across the tricuspid valve. A primum defect adds an apical holosystolic murmur from the associated cleft mitral leaflet."
}
],
"numbers": [],
"delta": null,
"pearl": "The ASD murmur is a relative pulmonic flow murmur; the hole itself is silent. Fixed split S2 is the finding that separates it from an innocent flow murmur.",
"lookalike": {
"vs": "innocent pulmonic flow murmur",
"discriminator": "innocent murmur has a normally moving S2 split; ASD gives a wide, fixed split and often a tricuspid diastolic rumble"
},
"related": [
"Q290"
],
"reviewed": "2026-08-26"
},
{
"id": "Q287",
"orig": 287,
"title": "2D imaging of atrial septal defects",
"lesions": [
"ASD",
"VIEWS"
],
"lens": "2d",
"items": [
{
"id": "Q287.1",
"q": "Which transthoracic view is best for demonstrating a secundum ASD, and why?",
"a": "The subcostal four-chamber and sagittal (bicaval) views are best because the ultrasound beam strikes the atrial septum nearly perpendicular. A perpendicular beam gives a strong specular reflection, so a real defect appears as a clean gap with bright echoes at its edges, and color Doppler is well aligned with the shunt flow. In the apical four-chamber view the beam runs parallel to the thin septum, producing dropout that mimics a defect."
},
{
"id": "Q287.2",
"q": "What rim measurements are needed before device closure of a secundum ASD?",
"a": "A device needs tissue to grip, so the septal rim around the defect is measured toward the aorta (anterosuperior), the SVC (superior), the IVC (inferior), the AV valves (inferoposterior), and the posterior wall. A rim of at least about 5 mm in most directions is desirable; a deficient aortic rim is common and often tolerated, but deficient inferior or posterior rims raise the risk of embolization or erosion. Maximum defect diameter, total septal length, and the number of defects (fenestrated septum) are also reported, usually by TEE or 3D imaging."
},
{
"id": "Q287.3",
"q": "Why is transthoracic echo often inadequate for a sinus venosus defect?",
"a": "The superior sinus venosus defect sits high at the junction of the SVC and the right atrium, an area that is far from the transthoracic transducer and poorly seen except in some subcostal bicaval windows. It is frequently accompanied by anomalous drainage of the right upper pulmonary vein into the SVC, which also lies out of the transthoracic field. When the RV is dilated without an obvious secundum defect, TEE with bicaval imaging is the next step to look for a sinus venosus defect and the anomalous vein."
}
],
"numbers": [
{
"label": "Desirable septal rim for device closure",
"value": "≥ 5",
"unit": "mm"
}
],
"delta": null,
"pearl": "Dilated RV with no visible ASD on transthoracic study means look higher: sinus venosus defect on TEE bicaval view.",
"lookalike": {
"vs": "apical four-chamber septal dropout",
"discriminator": "true defect shows bright T-sign edges and color flow crossing in subcostal views; dropout has no edge echoes and disappears with a perpendicular beam"
},
"related": [
"Q288",
"Q289",
"Q387"
],
"reviewed": "2026-08-26"
},
{
"id": "Q288",
"orig": 288,
"title": "Quantifying and sizing an ASD",
"lesions": [
"ASD",
"TEE"
],
"lens": "best-method",
"items": [
{
"id": "Q288.1",
"q": "How is the shunt ratio Qp:Qs calculated by Doppler in an ASD?",
"a": "Stroke volume equals cross-sectional area times VTI. Pulmonary flow (Qp) is measured at the RVOT: RVOT diameter in the parasternal short axis gives area (π × (d/2)²), multiplied by the pulsed Doppler VTI in the RVOT. Systemic flow (Qs) is measured the same way at the LVOT. Qp:Qs is the ratio of the two stroke volumes, since heart rate cancels. The main error is the squared diameter, so measure the RVOT carefully at the level where the sample volume is placed."
},
{
"id": "Q288.2",
"q": "When is TEE the preferred test in ASD evaluation?",
"a": "TEE is preferred when the transthoracic study cannot define the defect, particularly for a suspected sinus venosus defect, for anomalous pulmonary venous return, and before device closure. For closure, TEE measures the defect in multiple planes, defines all rims, and identifies additional fenestrations that transthoracic imaging can miss. Intraprocedural TEE or intracardiac echo also guides device deployment and confirms no residual shunt or impingement on the mitral valve, aorta, or caval veins. 3D TEE shows the true shape of the defect en face, which is often oval rather than round."
}
],
"numbers": [
{
"label": "Qp:Qs clinically significant shunt",
"value": "≥ 1.5",
"unit": "ratio"
}
],
"delta": null,
"pearl": "Qp at the RVOT, Qs at the LVOT; the pulmonary side is bigger in a left-to-right shunt.",
"lookalike": null,
"related": [
"Q287",
"Q290"
],
"reviewed": "2026-08-26"
},
{
"id": "Q289",
"orig": 289,
"title": "False positives in ASD imaging",
"lesions": [
"ASD",
"INSTRUMENTATION"
],
"lens": "pitfall",
"items": [
{
"id": "Q289.1",
"q": "Why does the apical four-chamber view frequently show a false atrial septal defect?",
"a": "In the apical window, the thin fossa ovalis lies parallel to the beam, so little energy returns and the septum appears to vanish, an artifact called dropout. Dropout has fuzzy edges and no color crossing, while a true defect shows a bright terminal echo at each edge (the T-sign) and a color jet that crosses the septum. Confirm from a subcostal view where the beam is perpendicular, and lower the color scale to catch low-velocity shunt flow."
},
{
"id": "Q289.2",
"q": "How do you avoid mistaking a PFO for a small ASD, and vice versa?",
"a": "A PFO shows the two septal layers overlapping with a tunnel between them, and flow is intermittent and often right-to-left only during release of Valsalva. A small ASD shows a single layer with a fixed gap and continuous left-to-right flow by color. Agitated saline helps: PFO bubbles cross only with provocation, while an ASD can show bubbles crossing at rest and a negative contrast jet of unopacified blood entering the right atrium. Do not call an ASD on bubbles alone without a corresponding 2D and color finding."
},
{
"id": "Q289.3",
"q": "Which normal right atrial structures can be misread as a defect or a mass in this setting?",
"a": "The Eustachian valve is a crescent of tissue at the IVC orifice that directs caval flow toward the fossa ovalis; a prominent one can look like a septal flap or a cor triatriatum dexter membrane. The Chiari network is a fenestrated remnant of the sinus venosus valves that moves freely in the right atrium and can mimic a thrombus, vegetation, or a flail septal edge. Both attach near the IVC and coronary sinus rather than to the fossa, and neither shows flow crossing to the left atrium. They also deflect saline bubbles toward the septum, which can make a PFO study look more positive."
}
],
"numbers": [],
"delta": null,
"pearl": "Edges tell the truth: a real defect has a bright T-sign at each margin; dropout fades away with nothing at the edge.",
"lookalike": {
"vs": "Chiari network or Eustachian valve",
"discriminator": "these attach at the IVC orifice, move freely, and show no transseptal color flow; an ASD is a fixed gap in the fossa with color crossing"
},
"related": [
"Q285",
"Q287",
"Q290",
"Q388"
],
"reviewed": "2026-08-26"
},
{
"id": "Q290",
"orig": 290,
"title": "Key numbers in interatrial shunting",
"lesions": [
"ASD",
"CONTRAST"
],
"lens": "numbers",
"items": [
{
"id": "Q290.1",
"q": "What shunt ratio makes an ASD hemodynamically significant?",
"a": "A Qp:Qs of 1.5 or more indicates a significant left-to-right shunt, meaning pulmonary flow is at least one and a half times systemic flow. Closure is generally considered at this level when the right heart is enlarged, provided pulmonary vascular resistance is not prohibitively high. Below 1.5 without RV enlargement, the defect is usually followed rather than closed."
},
{
"id": "Q290.2",
"q": "How common is a PFO in adults, and how does bubble timing separate an intracardiac shunt from an intrapulmonary one?",
"a": "Autopsy series find a probe-patent foramen ovale in roughly a quarter of adults, so a positive bubble study is not by itself a disease. With agitated saline, bubbles that appear in the left atrium within about three cardiac cycles after right atrial opacification indicate an intracardiac shunt such as a PFO or ASD. Bubbles that arrive late, after five or more beats, and enter via the pulmonary veins rather than across the septum suggest an intrapulmonary shunt such as pulmonary arteriovenous malformations or hepatopulmonary syndrome. The timing works because transit through the lungs takes longer than crossing a hole in the septum."
},
{
"id": "Q290.3",
"q": "What are the relative frequencies of the ASD types?",
"a": "Secundum defects account for about 75 percent, primum defects 15 to 20 percent, sinus venosus defects 5 to 10 percent, and coronary sinus defects under 1 percent. Knowing the distribution matters because the common secundum type is the one amenable to device closure, while the others require surgery."
}
],
"numbers": [
{
"label": "Qp:Qs significant shunt",
"value": "≥ 1.5",
"unit": "ratio"
},
{
"label": "PFO prevalence in adults",
"value": "≈ 25",
"unit": "%"
},
{
"label": "Intracardiac shunt bubble arrival",
"value": "≤ 3",
"unit": "beats"
},
{
"label": "Intrapulmonary shunt bubble arrival",
"value": "> 5",
"unit": "beats"
},
{
"label": "Secundum ASD share",
"value": "≈ 75",
"unit": "%"
},
{
"label": "Primum ASD share",
"value": "15–20",
"unit": "%"
},
{
"label": "Sinus venosus ASD share",
"value": "5–10",
"unit": "%"
},
{
"label": "Coronary sinus ASD share",
"value": "< 1",
"unit": "%"
}
],
"delta": null,
"pearl": "Early bubbles (within 3 beats) cross the septum; late bubbles (after 5 beats) come through the lungs.",
"lookalike": {
"vs": "pulmonary AVM",
"discriminator": "bubbles arrive late and emerge from the pulmonary veins rather than across the atrial septum"
},
"related": [
"Q288",
"Q289",
"Q285",
"Q286",
"Q388"
],
"reviewed": "2026-08-26"
},
{
"id": "Q291",
"orig": 291,
"title": "Auscultation of a ventricular septal defect",
"lesions": [
"VSD"
],
"lens": "physical-exam",
"items": [
{
"id": "Q291.1",
"q": "Describe the murmur of a VSD and explain why a smaller defect is louder.",
"a": "The classic finding is a harsh, high-pitched holosystolic murmur at the lower left sternal border, often with a palpable thrill. It is holosystolic because the LV-to-RV pressure difference exists from the moment the mitral valve closes until the aortic valve closes. A small restrictive defect maintains the full LV-RV gradient, so blood jets through at high velocity with intense turbulence, producing a loud murmur. A large non-restrictive defect equalizes the pressures, velocity falls, and the murmur softens or disappears even though the shunt volume is larger."
},
{
"id": "Q291.2",
"q": "What additional exam findings suggest that a VSD is large?",
"a": "A large shunt returns extra blood to the left heart, so there may be a displaced, hyperdynamic apex and a mid-diastolic rumble at the apex from increased mitral inflow. As pulmonary pressure rises, P2 becomes loud and the murmur shortens. When Eisenmenger physiology develops, the systolic murmur may vanish entirely, replaced by cyanosis, an RV heave, and a loud single S2."
}
],
"numbers": [],
"delta": null,
"pearl": "Loud VSD is a small VSD; a large defect can be almost silent because there is no gradient to make noise.",
"lookalike": {
"vs": "tricuspid regurgitation",
"discriminator": "TR murmur increases with inspiration and is usually softer; the VSD murmur is harsh, often with a thrill, and does not change with breathing"
},
"related": [
"Q293"
],
"reviewed": "2026-08-26"
},
{
"id": "Q292",
"orig": 292,
"title": "Locating a VSD by echo view",
"lesions": [
"VSD",
"VIEWS"
],
"lens": "2d",
"items": [
{
"id": "Q292.1",
"q": "In the parasternal short axis at the aortic valve level, how do you tell a perimembranous from a supracristal VSD?",
"a": "Picture the aortic valve as a clock face with the tricuspid valve on the left of the screen and the pulmonic valve at the top right. A perimembranous defect sits adjacent to the septal leaflet of the tricuspid valve, roughly at the 9 to 12 o'clock position, just below the aortic valve. A supracristal (outlet, subpulmonic) defect lies above the crista supraventricularis, immediately beneath the pulmonic valve, at about 12 to 3 o'clock. The supracristal location matters because the right coronary cusp can prolapse into it and cause progressive aortic regurgitation."
},
{
"id": "Q292.2",
"q": "Where do muscular and inlet VSDs appear, and which views show them?",
"a": "Muscular defects are entirely surrounded by muscle and are commonly in the trabecular apical septum; they are best seen in the apical four-chamber view and the parasternal short axis at the mid and apical levels, where color Doppler is essential because the defects are often multiple and serpiginous. An inlet defect lies posteriorly beneath the AV valves and is best seen in the apical four-chamber view near the septal tricuspid leaflet, often with an associated AV septal defect. Perimembranous defects also show well in the parasternal long axis just below the aortic valve and in the apical five-chamber view."
}
],
"numbers": [
{
"label": "Perimembranous share of VSDs",
"value": "≈ 80",
"unit": "%"
},
{
"label": "Perimembranous position in PSAX",
"value": "9–12",
"unit": "o'clock"
},
{
"label": "Supracristal position in PSAX",
"value": "12–3",
"unit": "o'clock"
}
],
"delta": null,
"pearl": "PSAX clock: 9 to 12 hugs the tricuspid (perimembranous), 12 to 3 hugs the pulmonic (supracristal). Watch the right coronary cusp in the supracristal type.",
"lookalike": null,
"related": [
"Q293",
"Q294",
"Q370"
],
"reviewed": "2026-08-26"
},
{
"id": "Q293",
"orig": 293,
"title": "Doppler assessment of a VSD",
"lesions": [
"VSD",
"HEMODYNAMICS"
],
"lens": "doppler",
"items": [
{
"id": "Q293.1",
"q": "How do you derive RV systolic pressure from the VSD jet?",
"a": "Continuous-wave Doppler across the defect gives the peak systolic velocity, and 4v² converts it to the peak LV-to-RV pressure difference. Because LV systolic pressure equals cuff systolic pressure in the absence of LVOT obstruction, RVSP equals systolic blood pressure minus the VSD gradient. A high gradient means a low RV pressure and a restrictive defect; a low gradient means the RV pressure approaches systemic. Cross-check with the TR jet-derived RVSP, since the two should agree."
},
{
"id": "Q293.2",
"q": "What distinguishes a restrictive from a non-restrictive VSD on Doppler?",
"a": "A restrictive defect is small enough to limit flow and maintain a large pressure difference: the jet is high velocity, typically above 4 m/s, giving a gradient above about 64 mmHg and near-normal RV pressure. A non-restrictive defect is large enough that the ventricles behave as a common chamber; the velocity is low, the gradient is small, and RV pressure is systemic, with shunt direction determined by the relative vascular resistances rather than by the hole. The color jet in a restrictive defect is narrow and turbulent with aliasing; in a non-restrictive defect it is broad and laminar."
}
],
"numbers": [
{
"label": "RVSP from VSD",
"value": "SBP − 4v²",
"unit": "mmHg"
},
{
"label": "Restrictive VSD jet velocity",
"value": "> 4",
"unit": "m/s"
},
{
"label": "Restrictive VSD gradient",
"value": "> 64",
"unit": "mmHg"
}
],
"delta": null,
"pearl": "A fast VSD jet is good news: the higher the gradient, the lower the RV pressure.",
"lookalike": null,
"related": [
"Q291",
"Q294",
"Q292",
"Q299",
"Q389"
],
"reviewed": "2026-08-26"
},
{
"id": "Q294",
"orig": 294,
"title": "Pitfalls in VSD interpretation",
"lesions": [
"VSD",
"CAD",
"INSTRUMENTATION"
],
"lens": "pitfall",
"items": [
{
"id": "Q294.1",
"q": "Why can a VSD be missed or mismeasured because of aliasing, and how do you fix it?",
"a": "A restrictive VSD jet exceeds the Nyquist limit of both color and pulsed Doppler, so color shows a mosaic and pulsed-wave wraps around the baseline, giving no usable peak. Use continuous-wave Doppler aligned with the jet, which has no velocity ceiling, and shift the baseline if needed. Conversely, with the color scale set too high, a low-velocity jet in a large non-restrictive defect can be invisible; lower the scale when the defect is large."
},
{
"id": "Q294.2",
"q": "How is a VSD jet confused with tricuspid regurgitation, and how do you separate them?",
"a": "Both are high-velocity systolic jets entering the right ventricle or right atrium region near the septal tricuspid leaflet, and a perimembranous VSD jet often streams directly into the RA through or alongside the tricuspid valve. Trace the origin: a VSD jet begins at the septum in the LV outflow region, whereas TR begins at the tricuspid coaptation point. The VSD signal starts with mitral closure, before the TR jet, and the VSD gradient is usually much larger than the TR gradient in the same patient. Confusing them overestimates RV pressure if the VSD jet is read as TR."
},
{
"id": "Q294.3",
"q": "After a myocardial infarction, how do you distinguish a ventricular septal rupture from papillary muscle rupture?",
"a": "Both present with a new murmur and shock a few days after infarction, but the anatomy differs. A septal rupture shows a color jet crossing the septum from LV to RV, usually in the inferobasal septum after inferior MI or the apical septum after anterior MI, with a step-up in oxygen saturation at the RV level if catheterized. Papillary muscle rupture shows a flail mitral leaflet with a mobile mass attached to the chordae and torrential eccentric MR, often with a surprisingly soft murmur because LA pressure rises so quickly. The septum is intact in papillary rupture, and the LV is typically hyperdynamic."
}
],
"numbers": [],
"delta": null,
"pearl": "Trace the jet to its origin: septal origin equals VSD, coaptation-point origin equals TR.",
"lookalike": {
"vs": "papillary muscle rupture",
"discriminator": "flail mitral leaflet with severe eccentric MR and intact septum; septal rupture shows transseptal color flow into the RV"
},
"related": [
"Q292",
"Q293",
"Q295"
],
"reviewed": "2026-08-26"
},
{
"id": "Q295",
"orig": 295,
"title": "Post-infarction septal rupture vignette",
"lesions": [
"VSD",
"CAD"
],
"lens": "vignette",
"items": [
{
"id": "Q295.1",
"q": "A 71-year-old woman had a late-presenting inferior STEMI four days ago. She now has hypotension, a new harsh holosystolic murmur at the left sternal border with a thrill, and elevated neck veins. What is the likely diagnosis, and what should the echo show?",
"a": "The timing, the harsh murmur with thrill, and the sudden hemodynamic collapse point to post-infarction ventricular septal rupture, which typically occurs three to five days after infarction as the necrotic septum liquefies. Risk is higher in older patients, women, first infarctions, and those without collateral flow or delayed reperfusion. Echo should show a defect in the inferobasal septum, often serpiginous, with left-to-right color flow into the RV; inferior infarcts produce basal septal ruptures, anterior infarcts produce apical ones. Continuous-wave Doppler gives the LV-RV gradient, and the RV is usually dilated with acute volume load. The treatment is urgent mechanical support and surgical or percutaneous closure; medical therapy alone carries very high mortality."
},
{
"id": "Q295.2",
"q": "What findings on the same study would have argued instead for papillary muscle rupture?",
"a": "Papillary muscle rupture would show a flail posterior mitral leaflet with a mobile ruptured head prolapsing into the left atrium, severe eccentric MR, and an intact septum with no transseptal flow. The murmur is often soft or absent because of rapid LA pressure equalization, and pulmonary edema dominates rather than right heart overload. Both complications cluster in the same post-infarction window, so the septum and the mitral apparatus must each be examined deliberately."
}
],
"numbers": [
{
"label": "Typical timing of post-MI septal rupture",
"value": "3–5",
"unit": "days"
}
],
"delta": null,
"pearl": "Harsh murmur with thrill and right heart strain days after MI means septal rupture; soft murmur with flash pulmonary edema means papillary rupture.",
"lookalike": {
"vs": "papillary muscle rupture",
"discriminator": "flail mitral leaflet and severe MR with an intact septum versus a transseptal color jet with RV volume load"
},
"related": [
"Q294",
"Q376"
],
"reviewed": "2026-08-26"
},
{
"id": "Q296",
"orig": 296,
"title": "What a patent ductus is",
"lesions": [
"PDA",
"CONGENITAL"
],
"lens": "definition",
"items": [
{
"id": "Q296.1",
"q": "What is a patent ductus arteriosus, and what is its normal function before birth?",
"a": "The ductus arteriosus is a fetal vessel connecting the main pulmonary artery, near the origin of the left pulmonary artery, to the descending aorta just beyond the left subclavian artery. In the fetus, the lungs are fluid-filled with high vascular resistance, so most RV output bypasses them through the ductus into the aorta. After birth, rising oxygen tension and falling prostaglandin levels constrict the ductal smooth muscle and the vessel closes, eventually becoming the ligamentum arteriosum. A PDA is persistence of this channel, which after birth carries flow from the higher-pressure aorta into the pulmonary artery."
},
{
"id": "Q296.2",
"q": "What conditions predispose to a persistent ductus?",
"a": "Prematurity is the most important factor because the immature ductal muscle is less responsive to oxygen and more sensitive to circulating prostaglandins. Maternal rubella infection in the first trimester damages the ductal wall and is a classic cause, often with pulmonary artery branch stenosis. Birth at high altitude raises the incidence because the relatively low oxygen tension weakens the closure stimulus. Hypoxia and respiratory distress in the newborn act the same way, and there is a female predominance."
}
],
"numbers": [],
"delta": null,
"pearl": "Oxygen closes the duct; anything that lowers oxygen or raises prostaglandin, such as prematurity, altitude, or lung disease, keeps it open.",
"lookalike": null,
"related": [
"Q297",
"Q299",
"Q301"
],
"reviewed": "2026-08-26"
},
{
"id": "Q297",
"orig": 297,
"title": "Bedside signs of a patent ductus",
"lesions": [
"PDA"
],
"lens": "physical-exam",
"items": [
{
"id": "Q297.1",
"q": "Why is the PDA murmur continuous, and where is it best heard?",
"a": "Aortic pressure exceeds pulmonary pressure in both systole and diastole, so flow through the ductus never stops and the murmur runs through S2 without a gap. It peaks around the second heart sound, giving the rough, rolling quality described as a machinery murmur, and it is loudest in the left infraclavicular area or upper left sternal border, often with a thrill. When pulmonary pressure rises, the diastolic component shortens first, so a purely systolic murmur in a known PDA is a warning sign of pulmonary hypertension."
},
{
"id": "Q297.2",
"q": "What peripheral findings accompany a large PDA, and what causes them?",
"a": "Diastolic runoff from the aorta into the pulmonary circulation lowers aortic diastolic pressure, while the augmented LV stroke volume raises systolic pressure. The result is a wide pulse pressure with bounding, collapsing peripheral pulses similar to those of aortic regurgitation. The apex is displaced and hyperdynamic from LV volume loading, and a mid-diastolic apical rumble may appear from increased mitral inflow."
}
],
"numbers": [],
"delta": null,
"pearl": "A continuous murmur under the left clavicle with bounding pulses is a PDA until proven otherwise; loss of the diastolic component means pulmonary pressure is climbing.",
"lookalike": {
"vs": "venous hum",
"discriminator": "venous hum is heard at the right supraclavicular area, disappears with jugular compression or lying flat; PDA murmur is left infraclavicular and fixed"
},
"related": [
"Q296",
"Q299",
"Q302"
],
"reviewed": "2026-08-26"
},
{
"id": "Q298",
"orig": 298,
"title": "2D imaging of the ductus",
"lesions": [
"PDA",
"VIEWS"
],
"lens": "2d",
"items": [
{
"id": "Q298.1",
"q": "Which views show the ductus arteriosus directly?",
"a": "The parasternal short axis at the high aortic level, tilted superiorly to open the pulmonary artery bifurcation, shows the ductus as a channel entering the main pulmonary artery near the origin of the left branch. A dedicated ductal view is obtained from a high left parasternal or suprasternal position with the transducer rotated to lay out the main PA, the ductus, and the descending aorta in one plane, sometimes called the ductal arch. In adults the ductus is hard to see on 2D, and the diagnosis rests on color Doppler flow entering the PA."
},
{
"id": "Q298.2",
"q": "Which chambers enlarge with a PDA, and why is this pattern the opposite of an ASD?",
"a": "Shunted blood enters the pulmonary artery, traverses the lungs, and returns to the left atrium and left ventricle, which then eject the extra volume into the aorta again. The left atrium and left ventricle therefore dilate, and the main pulmonary artery is enlarged, while the right ventricle remains normal size unless pulmonary hypertension develops. An ASD loads the right heart because the shunt enters before the RV; a PDA loads the left heart because it enters after the RV."
}
],
"numbers": [],
"delta": null,
"pearl": "PDA loads the left heart, ASD loads the right; the shunt site relative to the RV decides which side dilates.",
"lookalike": null,
"related": [
"Q299",
"Q300"
],
"reviewed": "2026-08-26"
},
{
"id": "Q299",
"orig": 299,
"title": "Doppler signature of a PDA",
"lesions": [
"PDA",
"HEMODYNAMICS"
],
"lens": "doppler",
"items": [
{
"id": "Q299.1",
"q": "What does color and spectral Doppler show in the main pulmonary artery with a PDA?",
"a": "Color shows a jet entering the main pulmonary artery from its distal end near the left branch, coursing retrograde toward the pulmonic valve, and the flow persists through systole and diastole. Pulsed or continuous-wave Doppler in the PA shows a continuous signal above the baseline, peaking in late systole and declining through diastole but never reaching zero as long as aortic pressure exceeds pulmonary pressure throughout the cycle. The velocity is high in a restrictive ductus and low in a large one."
},
{
"id": "Q299.2",
"q": "What is seen in the descending aorta, and how is pulmonary systolic pressure estimated from the ductus?",
"a": "Because blood leaves the aorta through the ductus in diastole, pulsed Doppler in the descending aorta below the ductus shows holodiastolic flow reversal, the same runoff pattern seen with aortic regurgitation. Pulmonary artery systolic pressure is estimated by applying 4v² to the peak systolic ductal velocity to get the aorta-to-PA gradient and subtracting it from systolic cuff pressure. A high ductal velocity means a large gradient and near-normal pulmonary pressure; a low velocity means pulmonary pressure is close to systemic."
}
],
"numbers": [
{
"label": "PASP from ductal jet",
"value": "SBP − 4v²",
"unit": "mmHg"
}
],
"delta": null,
"pearl": "Retrograde continuous flow in the PA plus diastolic reversal in the descending aorta equals a PDA; the ductal gradient gives PA pressure the same way a VSD gradient gives RV pressure.",
"lookalike": {
"vs": "pulmonic regurgitation",
"discriminator": "PR is diastolic only and originates at the pulmonic valve moving toward the RV; PDA flow is continuous and enters the PA from its distal end"
},
"related": [
"Q293",
"Q298",
"Q301",
"Q296",
"Q297",
"Q300",
"Q302"
],
"reviewed": "2026-08-26"
},
{
"id": "Q300",
"orig": 300,
"title": "Hemodynamic consequences of a PDA",
"lesions": [
"PDA",
"PH"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q300.1",
"q": "Trace the path of the shunted blood in a PDA and the chamber changes it produces.",
"a": "Blood passes from the aorta into the pulmonary artery, through the pulmonary vascular bed, into the pulmonary veins, and then to the left atrium and left ventricle, which must pump both the systemic output and the recirculated shunt volume. This produces LA enlargement, LV dilation with preserved or increased ejection fraction in the compensated phase, and a dilated main pulmonary artery from the extra flow. Over time, the volume-loaded LV may develop eccentric hypertrophy and eventual systolic dysfunction. The right ventricle is spared until pulmonary vascular disease develops."
},
{
"id": "Q300.2",
"q": "What happens to the chambers and the shunt when pulmonary hypertension supervenes?",
"a": "Prolonged high-flow, high-pressure exposure of the pulmonary arterioles causes medial hypertrophy and intimal fibrosis, raising pulmonary vascular resistance. The RV then hypertrophies and dilates, the ductal gradient shrinks, and the diastolic component of the shunt disappears first. When pulmonary pressure exceeds aortic pressure, the shunt reverses to right-to-left across the ductus, delivering desaturated blood to the descending aorta distal to the left subclavian artery. This produces differential cyanosis, with blue toes but pink fingers, a finding specific to Eisenmenger PDA."
}
],
"numbers": [],
"delta": null,
"pearl": "Blue feet, pink hands: reversed ductal flow enters the aorta beyond the arm vessels, so only the lower body is cyanosed.",
"lookalike": null,
"related": [
"Q298",
"Q299",
"Q302"
],
"reviewed": "2026-08-26"
},
{
"id": "Q301",
"orig": 301,
"title": "Neonatal ductal numbers",
"lesions": [
"PDA",
"CHAMBER_QUANT"
],
"lens": "numbers",
"items": [
{
"id": "Q301.1",
"q": "When does the ductus normally close after birth?",
"a": "Functional closure by smooth muscle constriction usually occurs within the first 24 to 72 hours of life in a term infant, triggered by the rise in arterial oxygen and the withdrawal of placental prostaglandins. Anatomic closure with fibrosis into the ligamentum arteriosum follows over the next several weeks. A ductus that remains open beyond this window in a term infant is unlikely to close spontaneously, whereas in a premature infant delayed closure is common and often responds to indomethacin or ibuprofen."
},
{
"id": "Q301.2",
"q": "How is the LA-to-aortic root ratio used to judge ductal significance in a neonate?",
"a": "In the parasternal long axis, M-mode or 2D measures the LA diameter and the aortic root diameter at the same level, and the ratio serves as a body-size-independent index of left atrial volume load. A ratio above about 1.4 suggests a hemodynamically significant ductus with enough pulmonary recirculation to dilate the left atrium; a normal ratio is roughly 1.0 or less. It is used together with ductal diameter, the continuous ductal flow pattern, and descending aortic diastolic reversal to decide on treatment."
}
],
"numbers": [
{
"label": "Normal functional ductal closure",
"value": "24–72",
"unit": "hours"
},
{
"label": "LA:Ao ratio suggesting significant PDA",
"value": "> 1.4",
"unit": "ratio"
}
],
"delta": null,
"pearl": "LA:Ao above 1.4 in a neonate means the ductus is stealing enough flow to stretch the left atrium.",
"lookalike": null,
"related": [
"Q296",
"Q299"
],
"reviewed": "2026-08-26"
},
{
"id": "Q302",
"orig": 302,
"title": "Adult patent ductus vignette",
"lesions": [
"PDA"
],
"lens": "vignette",
"items": [
{
"id": "Q302.1",
"q": "A 34-year-old woman is referred for a murmur found at a pre-employment physical. She has a continuous murmur under the left clavicle, a blood pressure of 138/54 mmHg, and bounding radial pulses. The echo shows a dilated left atrium and left ventricle with normal ejection fraction and a normal right ventricle. What is the diagnosis, and what should you look for to confirm it?",
"a": "A continuous infraclavicular murmur, a wide pulse pressure from diastolic runoff, and isolated left-sided chamber enlargement point to a patent ductus arteriosus. Confirm with color Doppler in the high parasternal short axis, where a continuous jet enters the main pulmonary artery from the left pulmonary artery region and runs retrograde toward the pulmonic valve. Pulsed Doppler in the descending aorta should show holodiastolic flow reversal. Measure the peak ductal velocity and subtract 4v² from her systolic pressure to estimate pulmonary artery systolic pressure, and confirm with the TR jet. A ductus with left heart enlargement and normal pulmonary pressure is closed, usually by a transcatheter device, to prevent progressive LV dilation, pulmonary hypertension, and endarteritis."
},
{
"id": "Q302.2",
"q": "How would the presentation differ if she had developed Eisenmenger physiology?",
"a": "The murmur would have lost its diastolic component or become inaudible, the pulse pressure would narrow, and she would have a loud single S2 and an RV heave. Echo would show RV hypertrophy and dilation, a low-velocity or bidirectional ductal jet, and no diastolic reversal in the descending aorta. Oxygen saturation would be lower in the toes than in the fingers because deoxygenated blood enters the aorta distal to the left subclavian artery. At that stage the ductus is no longer closable, because it acts as a pressure relief valve for the right ventricle."
}
],
"numbers": [],
"delta": null,
"pearl": "In an adult with a continuous murmur, big left heart and a normal RV, search the pulmonary artery for retrograde continuous flow before looking anywhere else.",
"lookalike": {
"vs": "ruptured sinus of Valsalva aneurysm",
"discriminator": "also continuous but usually of abrupt onset with chest pain and a jet entering the RV or RA from the aortic root, not the pulmonary artery"
},
"related": [
"Q297",
"Q299",
"Q300"
],
"reviewed": "2026-08-26"
},
{
"id": "Q303",
"orig": 303,
"title": "Coarctation of the aorta defined",
"lesions": [
"COARCT",
"AORTA",
"CONGENITAL"
],
"lens": "definition",
"items": [
{
"id": "Q303.1",
"q": "What is coarctation of the aorta, and where is the narrowing usually found?",
"a": "Coarctation is a discrete, shelf-like narrowing of the aorta caused by an infolding of the posterolateral aortic wall, most often at the isthmus just distal to the left subclavian artery and opposite the ductal insertion. Ductal tissue extending into the aortic wall is the favored mechanism, which is why the lesion sits at the ductus and why it can tighten after the ductus closes. Less commonly a longer segment of hypoplastic arch accompanies the shelf, which changes surgical planning."
},
{
"id": "Q303.2",
"q": "Which associated lesions should you actively look for when coarctation is found?",
"a": "A bicuspid aortic valve coexists in roughly 50 to 75 percent of patients, so interrogate the aortic valve in short axis in every coarctation study. Turner syndrome (45,X) carries a high rate of coarctation and bicuspid valve, and Shone complex bundles coarctation with left-sided inflow obstruction: supravalvar mitral ring, parachute mitral valve, and subaortic stenosis. Ventricular septal defects, PDA, and intracranial berry aneurysms also travel with coarctation, and a bicuspid valve raises the risk of ascending aortopathy that must be tracked over time."
}
],
"numbers": [
{
"label": "Bicuspid aortic valve with coarctation",
"value": "50–75",
"unit": "%"
}
],
"delta": null,
"pearl": "Coarctation is a left-heart obstruction series in disguise: look above (bicuspid valve), inside (Shone lesions), and at the karyotype (Turner).",
"lookalike": {
"vs": "interrupted aortic arch",
"discriminator": "In coarctation there is luminal continuity with a shelf and a gradient; in interruption there is no lumen between arch segments and distal flow depends entirely on the ductus."
},
"related": [
"Q178",
"Q189",
"Q309",
"Q310",
"Q361",
"Q362"
],
"reviewed": "2026-08-26"
},
{
"id": "Q304",
"orig": 304,
"title": "Bedside clues to coarctation",
"lesions": [
"COARCT",
"HTN"
],
"lens": "physical-exam",
"items": [
{
"id": "Q304.1",
"q": "Which physical findings should prompt an echo request for coarctation in a hypertensive patient?",
"a": "The signature finding is a blood pressure that is higher in the arms than in the legs, with an arm-to-leg systolic difference greater than 20 mmHg considered significant; in a normal person leg pressure equals or exceeds arm pressure. The femoral pulses are diminished and arrive later than the radial pulse (radiofemoral delay) because the pulse wave has to pass through the obstruction and collaterals. An interscapular systolic murmur that may spill into diastole comes from turbulent flow across the shelf, and continuous murmurs over the back or chest wall mark enlarged intercostal collaterals."
},
{
"id": "Q304.2",
"q": "What does the chest radiograph add?",
"a": "Bilateral inferior rib notching, usually ribs three through eight, is produced by dilated, pulsatile intercostal arteries eroding the rib undersurface as they carry collateral flow around the coarctation. A figure-3 contour of the aortic knob reflects pre- and post-stenotic dilation on either side of the indented isthmus. These signs take years to develop, so their absence in a child does not exclude the diagnosis."
}
],
"numbers": [
{
"label": "Significant arm-leg systolic BP gradient",
"value": "> 20",
"unit": "mmHg"
},
{
"label": "Ribs typically notched",
"value": "3–8",
"unit": "rib number"
}
],
"delta": null,
"pearl": "Check a leg pressure on every young hypertensive; if legs are lower than arms by more than 20 mmHg, the aorta is the problem.",
"lookalike": {
"vs": "subclavian steal or peripheral arterial disease",
"discriminator": "Coarctation lowers both leg pressures symmetrically with a delayed femoral pulse; peripheral disease is usually asymmetric and lacks the interscapular murmur and rib notching."
},
"related": [
"Q189",
"Q310"
],
"reviewed": "2026-08-26"
},
{
"id": "Q305",
"orig": 305,
"title": "Imaging the isthmus shelf",
"lesions": [
"COARCT",
"VIEWS",
"AORTA"
],
"lens": "2d",
"items": [
{
"id": "Q305.1",
"q": "Which echo view shows coarctation, and what does the 2D image look like?",
"a": "The suprasternal long-axis view of the arch is the working window: the patient's neck is extended, the transducer sits in the notch, and you sweep to open the ascending aorta, transverse arch, left subclavian origin, and proximal descending aorta in one plane. Coarctation appears as a posterior shelf or focal indentation at the isthmus just beyond the left subclavian artery, often with a bright, thickened wall and a dilated post-stenotic segment. Measure the arch segments so that a hypoplastic transverse arch is not overlooked, and use color to confirm that the aliasing begins exactly at the shelf."
},
{
"id": "Q305.2",
"q": "How does the ductus relate to the coarctation, and why does it matter?",
"a": "The shelf sits opposite the ductal insertion, and classifying the lesion as preductal, juxtaductal, or postductal by its relationship to the ductus predicts physiology. A neonate with a preductal coarctation depends on right-to-left ductal flow to perfuse the lower body and can collapse when the ductus closes, so a widely patent ductus can mask the gradient entirely. In an adult the ductus is closed and the lesion is nearly always juxtaductal, so what you see is the mature shelf with collaterals."
}
],
"numbers": [],
"delta": null,
"pearl": "If you cannot see beyond the left subclavian in the suprasternal view, you have not excluded coarctation.",
"lookalike": {
"vs": "pseudo-coarctation (kinked, elongated arch)",
"discriminator": "A kinked arch shows tortuosity without a discrete shelf, no gradient on CW, and a normal pulsatile abdominal aortic Doppler."
},
"related": [
"Q189",
"Q188"
],
"reviewed": "2026-08-26"
},
{
"id": "Q306",
"orig": 306,
"title": "What coarctation does to the ventricle",
"lesions": [
"COARCT",
"HTN",
"LV_FUNCTION"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q306.1",
"q": "What are the upstream cardiac consequences of untreated coarctation?",
"a": "The fixed aortic obstruction plus proximal hypertension raises LV afterload, so the ventricle develops concentric hypertrophy, often out of proportion to the measured cuff pressure. Over years this progresses to diastolic dysfunction and eventually reduced systolic function; in a neonate with a preductal lesion, LV failure can appear within days of ductal closure. Because a bicuspid aortic valve so often coexists, stenosis or regurgitation of that valve can add to the load, and the ascending aorta should be measured for aortopathy."
},
{
"id": "Q306.2",
"q": "What role do collaterals play, and how do they affect the echo findings?",
"a": "Intercostal, internal mammary, and scapular arteries enlarge to bypass the obstruction and deliver blood to the descending aorta below the shelf. The better the collateral network, the smaller the pressure drop across the coarctation and the lower the CW gradient, which means a well-collateralized severe lesion can produce a modest velocity. Collaterals therefore make the echo gradient unreliable as a sole marker of severity; use the abdominal aortic flow pattern, the diastolic tail, and CT or MRI to judge anatomic extent."
}
],
"numbers": [],
"delta": null,
"pearl": "Big collaterals, small gradient: a low velocity in coarctation can mean good bypass, not mild disease.",
"lookalike": null,
"related": [
"Q189",
"Q361"
],
"reviewed": "2026-08-26"
},
{
"id": "Q307",
"orig": 307,
"title": "Measuring the coarctation gradient",
"lesions": [
"COARCT",
"DOPPLER_PHYSICS",
"AORTA"
],
"lens": "best-method",
"items": [
{
"id": "Q307.1",
"q": "How should the coarctation gradient be measured by Doppler?",
"a": "Continuous-wave Doppler from the suprasternal notch, aligned parallel to descending aortic flow, gives the peak velocity through the shelf. Because the proximal arch is frequently dilated or has accelerated flow, the simplified Bernoulli equation overestimates the gradient; when the pre-coarctation velocity exceeds 1 m/s use the expanded form, gradient = 4(V2² − V1²), with V1 sampled by pulsed Doppler just proximal to the shelf. Report both the peak gradient and the presence of persistent forward flow in diastole."
},
{
"id": "Q307.2",
"q": "What is the significance of the diastolic runoff tail?",
"a": "In a hemodynamically important coarctation the pressure difference persists after aortic valve closure, so forward flow continues throughout diastole and the CW envelope shows a sawtooth profile with a slow decay rather than returning to baseline. This diastolic tail is a better marker of severity than the peak velocity alone, because it persists even when collaterals blunt the peak. A trivial or absent tail with a modest peak generally indicates a mild lesion."
},
{
"id": "Q307.3",
"q": "When is echo not enough?",
"a": "Echo cannot reliably define the length of the narrowed segment, arch hypoplasia, aneurysm formation, or collateral anatomy, and the suprasternal window deteriorates in adults. CT angiography or MRI defines the full extent of the lesion and is standard before any intervention and for surveillance after repair; MRI phase-contrast flow can also quantify collateral flow."
}
],
"numbers": [
{
"label": "Expanded Bernoulli",
"value": "4(V2² − V1²)",
"unit": "mmHg"
},
{
"label": "Proximal velocity requiring expanded Bernoulli",
"value": "> 1",
"unit": "m/s"
}
],
"delta": null,
"pearl": "Peak velocity tells you turbulence; the diastolic tail tells you obstruction.",
"lookalike": {
"vs": "PDA jet in the descending aorta",
"discriminator": "PDA flow is continuous but directed into the pulmonary artery and best seen in the PSAX; coarctation flow stays in the aortic lumen with a systolic peak and decaying diastolic tail."
},
"related": [
"Q189",
"Q188"
],
"reviewed": "2026-08-26"
},
{
"id": "Q308",
"orig": 308,
"title": "Coarctation traps and screening",
"lesions": [
"COARCT",
"DOPPLER_PHYSICS"
],
"lens": "pitfall",
"items": [
{
"id": "Q308.1",
"q": "How can the abdominal aorta be used to screen for coarctation when the arch is hard to image?",
"a": "Place a pulsed Doppler sample in the abdominal aorta from the subcostal window. Normal flow is briskly pulsatile with a sharp systolic upstroke and little or no diastolic flow. Downstream from a significant coarctation the profile is blunted and delayed, with a slow upstroke, low peak velocity, and continuous forward flow into diastole, because the obstruction and collaterals damp the pressure pulse. A normal, crisp abdominal signal makes significant coarctation unlikely; a damped continuous one demands an arch study or cross-sectional imaging."
},
{
"id": "Q308.2",
"q": "What mimics coarctation and what confounds the post-repair study?",
"a": "Pseudo-coarctation is an elongated, kinked arch that looks alarming on 2D and radiographs but produces no gradient, no diastolic tail, and a normal abdominal Doppler, so it needs no intervention. After surgical or balloon repair, a residual velocity of 2 to 3 m/s with a normal abdominal pattern often reflects a mild step-down rather than recoarctation, whereas a renewed diastolic tail and damped abdominal flow point to true restenosis. The other post-repair concern is aneurysm at the patch or dilation site, which echo may miss; that is a reason for routine CT or MRI surveillance rather than echo alone."
}
],
"numbers": [
{
"label": "Post-repair velocity often benign if no tail",
"value": "2–3",
"unit": "m/s"
}
],
"delta": null,
"pearl": "Subcostal abdominal aorta is the coarctation screen: crisp equals reassuring, damped and continuous equals go find the shelf.",
"lookalike": {
"vs": "pseudo-coarctation",
"discriminator": "Pseudo-coarctation has no gradient, no diastolic runoff, and normal abdominal pulsatility despite a kinked arch."
},
"related": [
"Q189"
],
"reviewed": "2026-08-26"
},
{
"id": "Q309",
"orig": 309,
"title": "Coarctation by the numbers",
"lesions": [
"COARCT",
"HTN"
],
"lens": "numbers",
"items": [
{
"id": "Q309.1",
"q": "List the testable numbers for coarctation of the aorta.",
"a": "Coarctation accounts for roughly 5 to 8 percent of congenital heart disease with a male predominance of about 2 to 1. A bicuspid aortic valve accompanies it in 50 to 75 percent of cases, and about 10 percent of women with Turner syndrome have coarctation. An arm-leg systolic gradient above 20 mmHg is significant clinically, and after repair a resting Doppler gradient of 20 mmHg or more with anatomic narrowing, or a lower gradient with a diastolic tail and hypertension, raises concern for recoarctation. The expanded Bernoulli equation is required when proximal velocity exceeds 1 m/s, and rib notching typically involves ribs 3 to 8."
}
],
"numbers": [
{
"label": "Coarctation share of congenital heart disease",
"value": "5–8",
"unit": "%"
},
{
"label": "Male to female ratio",
"value": "2:1",
"unit": "ratio"
},
{
"label": "Bicuspid aortic valve coexistence",
"value": "50–75",
"unit": "%"
},
{
"label": "Turner syndrome with coarctation",
"value": "~10",
"unit": "%"
},
{
"label": "Arm-leg BP gradient significant",
"value": "> 20",
"unit": "mmHg"
},
{
"label": "Recoarctation concern, resting gradient",
"value": "≥ 20",
"unit": "mmHg"
},
{
"label": "Proximal velocity requiring expanded Bernoulli",
"value": "> 1",
"unit": "m/s"
}
],
"delta": null,
"pearl": "Twenty is the coarctation number: 20 mmHg arm-leg gap, 20 mmHg post-repair gradient.",
"lookalike": null,
"related": [
"Q189",
"Q303",
"Q362"
],
"reviewed": "2026-08-26"
},
{
"id": "Q310",
"orig": 310,
"title": "Young hypertensive with a click",
"lesions": [
"COARCT",
"HTN",
"AS"
],
"lens": "vignette",
"items": [
{
"id": "Q310.1",
"q": "A 24-year-old man is referred for hypertension of 162/94 in the right arm found at a pre-employment physical. He has an early systolic ejection click at the apex and a soft systolic murmur heard best between the scapulae. Femoral pulses are faint and lag behind the radial pulse. What is the likely diagnosis and what should the echo protocol include?",
"a": "Hypertension in a young adult with a radiofemoral delay and an interscapular murmur is coarctation until proven otherwise, and the ejection click points to the bicuspid aortic valve that accompanies it in most cases. The echo should begin with a PSAX of the aortic valve to define leaflet number, raphe, and any stenosis or regurgitation, then measure the sinuses and ascending aorta for aortopathy. Go to the suprasternal notch for 2D of the arch and isthmus, CW through the shelf with a pulsed sample proximal to it for the expanded Bernoulli, and document a diastolic tail; finish with subcostal pulsed Doppler of the abdominal aorta and LV mass for hypertensive remodeling. Recommend CT or MR angiography to define arch anatomy before any intervention."
}
],
"numbers": [
{
"label": "Bicuspid aortic valve with coarctation",
"value": "50–75",
"unit": "%"
}
],
"delta": null,
"pearl": "Young, hypertensive, ejection click: image the valve, then the arch, then the abdominal aorta.",
"lookalike": {
"vs": "essential hypertension with a flow murmur",
"discriminator": "Essential hypertension has equal or higher leg pressures, synchronous femoral pulses, and no diastolic runoff in the descending aorta."
},
"related": [
"Q189",
"Q303",
"Q304",
"Q361"
],
"reviewed": "2026-08-26"
},
{
"id": "Q311",
"orig": 311,
"title": "Why Ebstein anomaly happens",
"lesions": [
"EBSTEIN",
"CONGENITAL"
],
"lens": "etiology",
"items": [
{
"id": "Q311.1",
"q": "What causes Ebstein anomaly, and which exposures or genetic factors are associated with it?",
"a": "Ebstein anomaly results from failed delamination of the septal and posterior tricuspid leaflets from the RV myocardium during development, so those leaflets remain plastered to the wall and their functional hinge point is displaced toward the apex. Most cases are sporadic, but first-trimester lithium exposure is the classic teratogenic association; the absolute risk is small and lower than older reports suggested, yet it remains a board-favorite link. Familial clustering and mutations in the sarcomeric gene MYH7, sometimes with LV non-compaction, plus associations with trisomy 21 and 22q11 deletion, indicate a genetic contribution in a minority."
}
],
"numbers": [],
"delta": null,
"pearl": "Lithium in the first trimester is the exam link to Ebstein, but the anomaly is a leaflet delamination failure, not a valve that moved.",
"lookalike": null,
"related": [
"Q190",
"Q10"
],
"reviewed": "2026-08-26"
},
{
"id": "Q312",
"orig": 312,
"title": "Auscultating Ebstein anomaly",
"lesions": [
"EBSTEIN",
"TR",
"ASD"
],
"lens": "physical-exam",
"items": [
{
"id": "Q312.1",
"q": "What are the characteristic physical findings in Ebstein anomaly?",
"a": "The hallmark is a widely split first heart sound because the large, sail-like anterior leaflet closes late and loudly, producing the so-called sail sound; the second sound is also widely split from delayed pulmonic closure with right bundle branch block. A holosystolic murmur of tricuspid regurgitation is heard at the lower left sternal border but often does not rise with inspiration, because the small functional RV cannot augment its stroke volume. Multiple extra sounds, including a third and fourth heart sound and clicks, give the classic polyrhythmic or triple-cadence auscultation."
},
{
"id": "Q312.2",
"q": "Why can a patient with Ebstein anomaly be cyanotic?",
"a": "Severe tricuspid regurgitation and a small functional RV raise right atrial pressure, and since 80 to 90 percent of patients have an ASD or patent foramen ovale, blood shunts right to left across the atrial septum and desaturates the systemic circulation. Cyanosis therefore tracks the degree of TR and RV dysfunction and may worsen with exercise or pregnancy, and the same shunt is the route for paradoxical embolism."
}
],
"numbers": [
{
"label": "ASD or PFO in Ebstein",
"value": "80–90",
"unit": "%"
}
],
"delta": null,
"pearl": "Widely split S1 with a sail sound plus cyanosis in an adult: think Ebstein with a right-to-left atrial shunt.",
"lookalike": {
"vs": "isolated tricuspid regurgitation",
"discriminator": "Ordinary TR murmurs increase with inspiration and lack the sail sound and cyanosis; Ebstein TR is often fixed and comes with a widely split S1."
},
"related": [
"Q190",
"Q10"
],
"reviewed": "2026-08-26"
},
{
"id": "Q313",
"orig": 313,
"title": "Doppler in Ebstein anomaly",
"lesions": [
"EBSTEIN",
"TR",
"PH"
],
"lens": "doppler",
"items": [
{
"id": "Q313.1",
"q": "How is tricuspid regurgitation evaluated in Ebstein anomaly?",
"a": "TR is nearly universal and often severe because the displaced septal and posterior leaflets cannot coapt with the tethered anterior leaflet. Grade it with standard ASE 2017 tools: vena contracta of 0.7 cm or more, dense triangular early-peaking CW signal, systolic flow reversal in the hepatic veins, and a dilated annulus, remembering that the regurgitant origin is displaced into the RV body so the color jet must be sought below the true annulus. Multiple jets from a fenestrated anterior leaflet are common."
},
{
"id": "Q313.2",
"q": "Why is the TR-derived RV systolic pressure unreliable here?",
"a": "The TR jet velocity is usually low, often under 2.5 m/s, because the functional RV is small and weak and cannot generate a high pressure, and the massive regurgitant orifice with near-equalization of RA and RV pressure produces a low-velocity, early-peaking jet. A low velocity therefore does not exclude pulmonary hypertension, and a truly high pressure would be unusual; when pulmonary pressure matters, use the pulmonic acceleration time or catheterization."
},
{
"id": "Q313.3",
"q": "How do you establish shunt direction across the atrial septum?",
"a": "Color and pulsed Doppler at the septum from subcostal or A4C views show the direction, and an agitated saline study confirms right-to-left passage when bubbles appear in the left atrium within three beats. Shunting is usually right to left or bidirectional because RA pressure is high, and its magnitude explains the patient's saturation."
}
],
"numbers": [
{
"label": "Severe TR vena contracta",
"value": "≥ 0.7",
"unit": "cm"
},
{
"label": "Typical Ebstein TR jet velocity",
"value": "< 2.5",
"unit": "m/s"
},
{
"label": "Bubble arrival for intracardiac shunt",
"value": "≤ 3",
"unit": "beats"
}
],
"delta": null,
"pearl": "In Ebstein a low TR velocity means a weak RV, not a normal pulmonary pressure.",
"lookalike": null,
"related": [
"Q190",
"Q191",
"Q10",
"Q386"
],
"reviewed": "2026-08-26"
},
{
"id": "Q314",
"orig": 314,
"title": "Chambers in Ebstein anomaly",
"lesions": [
"EBSTEIN",
"RV_FUNCTION",
"TR"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q314.1",
"q": "Describe the chamber changes produced by Ebstein anomaly.",
"a": "Displacement of the tricuspid hinge point splits the RV into an atrialized portion above the functional valve, which is thin-walled and contracts with the ventricle but fills like an atrium, and a small functional RV below it that is often only the outflow and trabecular portions. The true right atrium plus the atrialized RV forms an enormous right-sided chamber that can occupy most of the cardiac silhouette, and chronic severe TR enlarges it further. The functional RV is reduced in size and contractility, the interventricular septum bows leftward and moves paradoxically, and LV filling and function can be impaired by septal shift and by the associated LV non-compaction."
},
{
"id": "Q314.2",
"q": "Why does the atrialized RV matter clinically?",
"a": "The atrialized segment contracts out of phase with the atrium, so during atrial systole it pushes blood backward and during ventricular systole its wall is regurgitant chamber rather than pump. Its size relative to the functional RV governs prognosis: when the functional RV is less than about a third of the total RV area, surgical outcomes are worse. Accessory pathways run across the malformed annulus, which is why pre-excitation is so common."
}
],
"numbers": [
{
"label": "Functional RV area predicting worse outcome",
"value": "< ~1/3",
"unit": "of total RV"
}
],
"delta": null,
"pearl": "Giant right heart, tiny working RV: the bigger the atrialized segment, the worse the pump.",
"lookalike": {
"vs": "dilated RA and RV from severe primary TR",
"discriminator": "Primary TR keeps the tricuspid hinge at the annulus; Ebstein shows the septal leaflet hinge displaced apically with a thin-walled atrialized segment between annulus and leaflet."
},
"related": [
"Q190",
"Q191",
"Q386"
],
"reviewed": "2026-08-26"
},
{
"id": "Q315",
"orig": 315,
"title": "Quantifying tricuspid displacement",
"lesions": [
"EBSTEIN",
"VIEWS"
],
"lens": "best-method",
"items": [
{
"id": "Q315.1",
"q": "What is the best echo method to confirm and grade Ebstein anomaly?",
"a": "In the apical four-chamber view measure the distance between the mitral septal leaflet hinge and the tricuspid septal leaflet hinge, index it to body surface area, and diagnose Ebstein when the apical offset is 8 mm/m² or more, or roughly 20 mm or more in an adult. The A4C view is required because it lines up both atrioventricular valves along the septum; the RV inflow view can show the displacement but cannot provide the mitral reference. Add the severity assessment of the Great Ormond Street (Celermajer) ratio: the combined area of the RA and atrialized RV divided by the area of the functional RV plus LA plus LV in end-diastole, with grades 1 (< 0.5) through 4 (> 1.5), higher ratios predicting worse outcomes."
},
{
"id": "Q315.2",
"q": "How does the Carpentier classification guide treatment?",
"a": "Carpentier types A through D describe increasing leaflet tethering and RV atrialization: type A has a mobile anterior leaflet and a small atrialized chamber, type B a large atrialized chamber with a mobile leaflet, type C a restricted anterior leaflet that limits the outflow, and type D almost complete atrialization with the leaflet forming a sac. Echo should therefore describe the anterior leaflet's mobility, attachments, and any fenestrations, because a mobile anterior leaflet is what the cone repair depends on."
}
],
"numbers": [
{
"label": "Diagnostic apical displacement, indexed",
"value": "≥ 8",
"unit": "mm/m²"
},
{
"label": "Diagnostic apical displacement, adult",
"value": "≥ 20",
"unit": "mm"
},
{
"label": "GOSE grade 1",
"value": "< 0.5",
"unit": "ratio"
},
{
"label": "GOSE grade 4",
"value": "> 1.5",
"unit": "ratio"
}
],
"delta": null,
"pearl": "Measure hinge to hinge in A4C, index to BSA, and call it Ebstein at 8 mm/m²; then describe the anterior leaflet, because repair depends on it.",
"lookalike": null,
"related": [
"Q190",
"Q191",
"Q10",
"Q317"
],
"reviewed": "2026-08-26"
},
{
"id": "Q316",
"orig": 316,
"title": "Ebstein overcalls and mimics",
"lesions": [
"EBSTEIN",
"TR",
"CONGENITAL"
],
"lens": "pitfall",
"items": [
{
"id": "Q316.1",
"q": "What normal finding is most often mistaken for Ebstein anomaly?",
"a": "The tricuspid septal leaflet normally inserts slightly closer to the apex than the mitral septal leaflet, giving an offset of a few millimeters in every heart. That physiologic offset can reach up to about 8 mm/m² and is often exaggerated by foreshortened or off-axis apical views, so a modest displacement in a patient with a normal-sized RV and a normal, well-formed leaflet is not Ebstein. Reserve the diagnosis for displacement of 8 mm/m² or more accompanied by tethered septal and posterior leaflets and an atrialized segment."
},
{
"id": "Q316.2",
"q": "Which congenital conditions mimic Ebstein but are distinct?",
"a": "Tricuspid valve dysplasia has thickened, redundant, poorly coapting leaflets with severe TR but the leaflet hinge stays at the annulus, so there is no atrialized RV. Uhl anomaly is a parchment-thin RV free wall with near-absent myocardium; the tricuspid valve is normally positioned and the problem is the ventricular wall, not the valve. Both share a giant right heart and severe TR with Ebstein, so the discriminator is always the position of the septal leaflet hinge relative to the mitral annulus."
}
],
"numbers": [
{
"label": "Upper limit of normal apical offset",
"value": "up to 8",
"unit": "mm/m²"
}
],
"delta": null,
"pearl": "Every heart has a small tricuspid offset; the diagnosis needs 8 mm/m² and a tethered leaflet, not just a gap.",
"lookalike": {
"vs": "tricuspid dysplasia",
"discriminator": "Dysplasia has thick redundant leaflets hinged at the true annulus with no atrialized RV; Ebstein hinges apically with an atrialized segment."
},
"related": [
"Q190",
"Q191"
],
"reviewed": "2026-08-26"
},
{
"id": "Q317",
"orig": 317,
"title": "Ebstein anomaly by the numbers",
"lesions": [
"EBSTEIN",
"ASD",
"ARRHYTHMIA"
],
"lens": "numbers",
"items": [
{
"id": "Q317.1",
"q": "List the testable numbers for Ebstein anomaly.",
"a": "The diagnostic apical displacement of the septal tricuspid leaflet is 8 mm/m² or more indexed to body surface area, or 20 mm or more in an adult. An atrial communication, either ASD or PFO, is present in 80 to 90 percent and provides the route for right-to-left shunting and cyanosis. About 20 percent have Wolff-Parkinson-White pre-excitation from accessory pathways along the malformed annulus, often right-sided and sometimes multiple. Ebstein accounts for well under 1 percent of congenital heart disease, and the GOSE ratio grades severity from 1 (< 0.5) to 4 (> 1.5)."
}
],
"numbers": [
{
"label": "Septal leaflet displacement, indexed",
"value": "≥ 8",
"unit": "mm/m²"
},
{
"label": "Septal leaflet displacement, adult",
"value": "≥ 20",
"unit": "mm"
},
{
"label": "ASD or PFO coexistence",
"value": "80–90",
"unit": "%"
},
{
"label": "Wolff-Parkinson-White",
"value": "~20",
"unit": "%"
},
{
"label": "Ebstein share of congenital heart disease",
"value": "< 1",
"unit": "%"
},
{
"label": "GOSE ratio grade range",
"value": "1 (< 0.5) to 4 (> 1.5)",
"unit": "ratio"
}
],
"delta": null,
"pearl": "Eight, twenty, twenty, ninety: 8 mm/m², 20 mm, 20 percent WPW, up to 90 percent atrial shunt.",
"lookalike": null,
"related": [
"Q190",
"Q191",
"Q10",
"Q315",
"Q386"
],
"reviewed": "2026-08-26"
},
{
"id": "Q318",
"orig": 318,
"title": "Doppler signatures of endocarditis destruction",
"lesions": [
"ENDOCARDITIS",
"MR",
"AR"
],
"lens": "doppler",
"items": [
{
"id": "Q318.1",
"q": "A patient with suspected endocarditis has a vegetation on the anterior mitral leaflet. What Doppler findings tell you the infection is destroying tissue rather than just sitting on it?",
"a": "Look for regurgitation that is new compared with any prior study, because infection erodes leaflet tissue and chordae so that coaptation fails. A leaflet perforation produces a distinct eccentric color jet that originates from the body of the leaflet, away from the coaptation line, and on CW Doppler it is holosystolic and often high velocity. Chordal rupture yields a flail segment with a very eccentric, wall-hugging jet directed opposite to the affected leaflet. A new regurgitant jet in a febrile patient is a major Duke echo criterion, so document it carefully with color and CW."
},
{
"id": "Q318.2",
"q": "How do you recognize an abscess or fistula with Doppler, and why does color flow matter for a paravalvular echolucent space?",
"a": "An abscess begins as a thickened, heterogeneous or echolucent region in the annulus or root, most often at the aortic-mitral intervalvular fibrosa. If color Doppler shows flow entering that space, the abscess has ruptured into a cavity and become a pseudoaneurysm; flow crossing between two chambers, such as from the aortic root into the right atrium or from LVOT into the left atrium, defines a fistula. A fistula shows continuous or biphasic high-velocity flow because the pressure difference persists through much of the cycle. Any flow in a periannular space, or a new paravalvular leak around a prosthesis, marks a complicated infection that usually needs surgery."
}
],
"numbers": [],
"delta": null,
"pearl": "A jet that starts in the middle of a leaflet, not at the coaptation line, is a perforation until proven otherwise.",
"lookalike": {
"vs": "degenerative MR with flail from chordal rupture",
"discriminator": "Perforation jet arises from the leaflet body with the coaptation line intact; a flail jet arises from coaptation and points away from the flail leaflet, and fever plus a vegetation favors infection"
},
"related": [
"Q76",
"Q99",
"Q50",
"Q370",
"Q391"
],
"reviewed": "2026-08-26"
},
{
"id": "Q319",
"orig": 319,
"title": "Choosing TTE versus TEE for endocarditis",
"lesions": [
"ENDOCARDITIS",
"TEE"
],
"lens": "best-method",
"items": [
{
"id": "Q319.1",
"q": "What is the recommended imaging sequence when endocarditis is suspected, and why is TTE still done first?",
"a": "Transthoracic echo is the first study because it is fast, noninvasive, and gives the baseline LV function, valve regurgitation severity, and pericardial assessment that management depends on. Its sensitivity for vegetations is only around 60 percent because vegetations under 2 to 3 mm, posterior structures, and prosthetic valves are hard to resolve from the chest wall. TEE places a high-frequency probe a few centimeters from the mitral and aortic valves, which raises sensitivity to roughly 90 percent and greatly improves detection of abscess, perforation, and prosthetic involvement. So TTE first, then TEE whenever TTE is negative or nondiagnostic with moderate to high clinical suspicion, whenever a prosthetic valve or device lead is present, and whenever TTE is positive but you need to define complications before surgery."
},
{
"id": "Q319.2",
"q": "Which echo findings count as major criteria in the modified Duke classification, and when should the study be repeated?",
"a": "The major echo findings are an oscillating intracardiac mass on a valve or supporting structure, in the path of a regurgitant jet, or on implanted material; an abscess; new partial dehiscence of a prosthetic valve; and new valvular regurgitation. Repeat imaging is indicated when the first study is negative but suspicion stays high, typically after 5 to 7 days, because vegetations grow and early infection may be too small to see. Repeat also for any clinical change such as a new murmur, heart failure, persistent bacteremia, new conduction block, or embolic event, since these suggest progression to abscess or destruction. A completion study at the end of therapy documents residual valve dysfunction and vegetation size as the new baseline."
}
],
"numbers": [
{
"label": "TTE vegetation sensitivity",
"value": "~60",
"unit": "%"
},
{
"label": "TEE vegetation sensitivity",
"value": "~90",
"unit": "%"
},
{
"label": "Repeat interval if initial study negative with high suspicion",
"value": "5–7",
"unit": "days"
}
],
"delta": null,
"pearl": "A negative TTE does not exclude endocarditis; a negative TEE nearly does, and a repeat TEE in a week closes the gap.",
"lookalike": null,
"related": [
"Q2",
"Q98",
"Q99",
"Q391"
],
"reviewed": "2026-08-26"
},
{
"id": "Q320",
"orig": 320,
"title": "Vegetation mimics on valves",
"lesions": [
"ENDOCARDITIS",
"MASS",
"PROSTHETIC"
],
"lens": "pitfall",
"items": [
{
"id": "Q320.1",
"q": "What benign or noninfectious structures are mistaken for vegetations on native valves, and how do you separate them?",
"a": "Lambl's excrescences are thin, filamentous strands on the closure line of the aortic or mitral leaflets, usually under 1 mm wide and up to 10 mm long, found in many older adults and unrelated to infection. A papillary fibroelastoma is a small, frond-like, well-circumscribed mass with a stalk that typically sits on the downstream side of the aortic valve or the atrial side of the mitral leaflets and shimmers at the edges; it has no fever or bacteremia and does not cause leaflet destruction. Libman-Sacks lesions in lupus and antiphospholipid syndrome, and marantic (nonbacterial thrombotic) vegetations in cancer, are small, sessile, broad-based verrucous masses near the leaflet edges that seldom oscillate and often produce regurgitation without positive cultures. The core discriminators are clinical context, the mobility and attachment site, and whether tissue is actually being destroyed."
},
{
"id": "Q320.2",
"q": "Why are prosthetic valves and previously treated patients especially prone to false-positive calls?",
"a": "Fibrin strands are common on mechanical and bioprosthetic valves, appearing as thin, mobile, highly reflective threads that are a normal finding and not infection. Sutures, the sewing ring, pledgets, and residual chordae after mitral repair are all echogenic and can look like masses in certain views, so sweep through multiple planes and use TEE. A healed vegetation from a prior episode may persist for years as a dense, calcified, less mobile mass; without a prior study for comparison it cannot be distinguished from active infection by echo alone. Always ask for the surgical and infectious history and compare with previous images before labeling a prosthesis as infected."
}
],
"numbers": [
{
"label": "Lambl's excrescence width",
"value": "< 1",
"unit": "mm"
},
{
"label": "Lambl's excrescence length",
"value": "up to 10",
"unit": "mm"
}
],
"delta": null,
"pearl": "Echo sees a mass, not an organism: fever, blood cultures, and tissue destruction make the diagnosis, not the blob alone.",
"lookalike": {
"vs": "papillary fibroelastoma",
"discriminator": "Fibroelastoma is a stalked, frond-like mass with a shimmering edge on the downstream valve surface without fever, bacteremia, or leaflet destruction; a vegetation sits on the upstream (regurgitant-jet) surface and is accompanied by new regurgitation"
},
"related": [
"Q98",
"Q99",
"Q170",
"Q392"
],
"reviewed": "2026-08-26"
},
{
"id": "Q321",
"orig": 321,
"title": "Endocarditis numbers to memorize",
"lesions": [
"ENDOCARDITIS"
],
"lens": "numbers",
"items": [
{
"id": "Q321.1",
"q": "Which vegetation size thresholds and organism factors drive embolic risk and the decision for early surgery?",
"a": "Emboli occur in roughly 20 to 40 percent of left-sided endocarditis, most in the first two weeks, and the risk falls sharply once effective antibiotics begin. Vegetation length above 10 mm roughly doubles embolic risk, and mobile mitral vegetations are the highest-risk group because they are exposed to a large regurgitant jet. Length above 15 mm, or above 10 mm with a prior embolus despite therapy, is an indication to consider early surgery; heart failure, abscess, fistula, and persistent bacteremia are the other surgical triggers. Staphylococcus aureus is the most common organism in developed countries and carries the highest rates of embolism, abscess, and mortality, which is why S. aureus bacteremia alone justifies TEE."
},
{
"id": "Q321.2",
"q": "What sensitivity figures for TTE and TEE should you quote, and how do they differ for prosthetic valves?",
"a": "For native-valve vegetations TTE detects about 60 percent and TEE about 90 percent, with specificity for both above 90 percent. For prosthetic valves TTE sensitivity drops further, often below 50 percent, because acoustic shadowing and reverberation hide the sewing ring and the atrial side of a mitral prosthesis. TEE for abscess is roughly 80 to 90 percent sensitive versus under 50 percent for TTE. These gaps explain why guidelines route every prosthetic-valve or device-lead suspicion straight to TEE after the initial TTE."
}
],
"numbers": [
{
"label": "Vegetation size raising embolic risk",
"value": "> 10",
"unit": "mm"
},
{
"label": "Vegetation size where surgery is considered",
"value": "> 15",
"unit": "mm"
},
{
"label": "Embolic events in left-sided endocarditis",
"value": "~20–40",
"unit": "%"
},
{
"label": "TTE sensitivity native valves",
"value": "~60",
"unit": "%"
},
{
"label": "TEE sensitivity native valves",
"value": "~90",
"unit": "%"
},
{
"label": "TTE sensitivity prosthetic valves",
"value": "< 50",
"unit": "%"
},
{
"label": "TEE sensitivity for abscess",
"value": "~80–90",
"unit": "%"
}
],
"delta": null,
"pearl": "10 mm worries you, 15 mm operates you, and S. aureus makes every number worse.",
"lookalike": null,
"related": [
"Q100",
"Q101",
"Q2",
"Q369",
"Q391",
"Q392"
],
"reviewed": "2026-08-26"
},
{
"id": "Q322",
"orig": 322,
"title": "Auscultating a prosthetic valve",
"lesions": [
"PROSTHETIC"
],
"lens": "physical-exam",
"items": [
{
"id": "Q322.1",
"q": "What should a normally functioning mechanical valve sound like, and what does a change in the clicks imply?",
"a": "A mechanical prosthesis produces crisp, high-pitched metallic opening and closing clicks that are often audible without a stethoscope; the closing click is louder, so a mechanical aortic valve gives a loud crisp S2 and a mechanical mitral valve gives a loud crisp S1. A soft systolic ejection murmur across a mechanical aortic valve and short washing-jet sounds are expected. Muffled, diminished, or absent clicks are a red flag because thrombus or pannus restricting the occluder damps the impact of the disc against the housing; a beat-to-beat variation in click intensity suggests intermittent sticking. Bioprosthetic valves have no clicks and sound like a soft native valve, so the exam finding for their failure is a new murmur rather than a change in clicks."
},
{
"id": "Q322.2",
"q": "Which new murmur should prompt an urgent echo in a patient with a prosthesis?",
"a": "A new diastolic murmur after aortic valve replacement, or a new holosystolic murmur after mitral replacement, points to a regurgitant leak, which is either paravalvular from dehiscence or infection, or transvalvular from a stuck occluder or a degenerated bioprosthetic cusp. A new or louder diastolic rumble across a mitral prosthesis, or a harsher, longer systolic murmur across an aortic prosthesis, suggests obstruction. Any new murmur plus fever, embolic symptoms, or heart failure needs TTE promptly and usually TEE, because prosthetic dysfunction can progress quickly and the physical exam is the earliest clue."
}
],
"numbers": [],
"delta": null,
"pearl": "Loud clicks are reassuring; a quiet mechanical valve is a valve that is not moving freely.",
"lookalike": {
"vs": "normal physiologic regurgitant washing jets",
"discriminator": "Washing jets are brief, low-volume, and symmetric on echo and produce no audible murmur; a pathologic leak gives an audible new murmur with a broad, eccentric, or paravalvular color jet"
},
"related": [
"Q102",
"Q111",
"Q112"
],
"reviewed": "2026-08-26"
},
{
"id": "Q323",
"orig": 323,
"title": "M-mode of prosthetic occluder motion",
"lesions": [
"PROSTHETIC"
],
"lens": "m-mode",
"items": [
{
"id": "Q323.1",
"q": "What does M-mode add when assessing a mechanical prosthesis, and what does restricted excursion look like?",
"a": "M-mode samples the occluder at a very high rate, so it captures the abrupt opening and closing of a disc or leaflet that 2D at 30 to 60 frames per second can blur. A normal tilting disc or bileaflet leaflet shows a sharp, box-like excursion with rapid opening at the start of the flow period and a full plateau. Restricted excursion appears as reduced amplitude, delayed or rounded opening, or an occluder that opens on some beats and not others, which is characteristic of thrombus or pannus interfering with the hinge. Because the housing shadows the far-field occluder, M-mode is most reliable for aortic prostheses from the parasternal window and for mitral prostheses on TEE, where the leaflets face the probe."
},
{
"id": "Q323.2",
"q": "How is prosthetic dehiscence recognized on M-mode and 2D?",
"a": "A well-seated sewing ring moves with the annulus as a unit, so its M-mode trace runs parallel to the annular motion. Dehiscence tears sutures over part of the circumference, and the ring then rocks independently, producing an exaggerated, rotational excursion of the ring relative to the annulus that is obvious in real time and appears as a large, out-of-phase ring motion on M-mode. Rocking of 15 degrees or more indicates dehiscence involving a large portion of the circumference and is nearly always accompanied by a significant paravalvular jet on color Doppler. Infection is the leading cause, so a rocking prosthesis should prompt a search for abscess and blood cultures."
}
],
"numbers": [
{
"label": "Sewing ring rocking suggesting major dehiscence",
"value": "≥ 15",
"unit": "degrees"
}
],
"delta": null,
"pearl": "Discs should snap and rings should sit still; a lazy disc means obstruction and a rocking ring means dehiscence.",
"lookalike": null,
"related": [
"Q108",
"Q105",
"Q111"
],
"reviewed": "2026-08-26"
},
{
"id": "Q324",
"orig": 324,
"title": "Doppler assessment of prosthetic valves",
"lesions": [
"PROSTHETIC",
"DOPPLER_PHYSICS"
],
"lens": "doppler",
"items": [
{
"id": "Q324.1",
"q": "Why is a baseline echo obtained after valve replacement, and which Doppler parameters are used for a prosthetic aortic valve?",
"a": "Every prosthesis is mildly obstructive and every patient has a different annulus size and flow state, so a baseline study 6 weeks to 3 months after surgery, once the anemia and hyperdynamic state have settled, defines what normal looks like for that specific valve and patient. Later gradients are then judged against the baseline rather than against a population table. For an aortic prosthesis you record peak velocity, mean gradient, the Doppler velocity index (LVOT VTI divided by prosthetic jet VTI), the effective orifice area by the continuity equation, and the acceleration time from onset of flow to peak velocity. A DVI below 0.25 or an acceleration time above 100 ms with a rounded jet contour points to true obstruction, whereas a high gradient with a normal DVI and short acceleration time reflects high flow or patient-prosthesis mismatch."
},
{
"id": "Q324.2",
"q": "How is a mitral prosthesis assessed, and which small regurgitant jets are normal?",
"a": "For a mitral prosthesis measure the peak E velocity, the mean gradient at a documented heart rate, the pressure half-time, and the ratio of prosthetic VTI to LVOT VTI. A mean gradient above 10 mmHg or a PHT above 200 ms is suspicious for obstruction, but PHT-derived area is not valid for prostheses and you should not apply the 220 constant. Mechanical valves normally show small closing-volume and washing jets inside the sewing ring: bileaflet valves have two to four brief, narrow, low-momentum jets that converge, and a tilting disc has one or two jets around the disc edge. These are physiologic and are distinguished from pathologic regurgitation by their small size, short duration, symmetric origin within the ring, and lack of proximal flow convergence."
}
],
"numbers": [
{
"label": "Baseline prosthetic study timing",
"value": "6 weeks – 3 months",
"unit": "post-op"
},
{
"label": "Prosthetic aortic DVI suggesting obstruction",
"value": "< 0.25",
"unit": ""
},
{
"label": "Prosthetic aortic acceleration time suggesting obstruction",
"value": "> 100",
"unit": "ms"
},
{
"label": "Mitral prosthesis mean gradient suspicious",
"value": "> 10",
"unit": "mmHg"
},
{
"label": "Mitral prosthesis PHT suspicious",
"value": "> 200",
"unit": "ms"
}
],
"delta": null,
"pearl": "High gradient with normal DVI and a short acceleration time is flow or mismatch; high gradient with low DVI and a long, rounded upstroke is a stuck valve.",
"lookalike": {
"vs": "high-flow state after surgery",
"discriminator": "Anemia or sepsis raises the gradient but keeps DVI normal and acceleration time short; obstruction lowers DVI and prolongs acceleration time"
},
"related": [
"Q112",
"Q110",
"Q107",
"Q325",
"Q326"
],
"reviewed": "2026-08-26"
},
{
"id": "Q325",
"orig": 325,
"title": "Patient-prosthesis mismatch and LV remodeling",
"lesions": [
"PROSTHETIC",
"AS",
"LV_FUNCTION"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q325.1",
"q": "What is patient-prosthesis mismatch and how is it quantified?",
"a": "Mismatch means the prosthesis functions normally but its effective orifice is too small for the patient's body size, so the resting gradient stays high and the LV continues to face an outflow obstruction after surgery. It is quantified by indexing the Doppler-derived effective orifice area to body surface area. For an aortic prosthesis an indexed EOA of 0.85 cm² per m² or less is moderate mismatch and 0.65 or less is severe; for a mitral prosthesis 1.2 cm² per m² or less is moderate and 0.9 or less is severe. The indexed EOA is compared with the published normal reference EOA for that valve model and size, which is what separates mismatch from acquired obstruction: in mismatch the measured EOA matches the expected value for the valve, whereas in obstruction it is well below it."
},
{
"id": "Q325.2",
"q": "What chamber changes are expected after a successful aortic valve replacement, and how does mismatch alter them?",
"a": "Relief of afterload allows LV mass to regress, with much of the reduction in the first year and continued regression over several years; wall thickness and mass index move toward normal and diastolic filling improves. Symptoms and exercise capacity track this regression. With significant mismatch the gradient remains elevated, LV hypertrophy regresses incompletely or not at all, and diastolic dysfunction and pulmonary pressures tend to persist, which translates into worse symptoms and higher late mortality, particularly in patients with reduced EF who cannot generate the extra pressure. For a mitral prosthesis, mismatch shows up as persistent LA enlargement and pulmonary hypertension rather than LV changes."
}
],
"numbers": [
{
"label": "Aortic PPM moderate iEOA",
"value": "≤ 0.85",
"unit": "cm²/m²"
},
{
"label": "Aortic PPM severe iEOA",
"value": "≤ 0.65",
"unit": "cm²/m²"
},
{
"label": "Mitral PPM moderate iEOA",
"value": "≤ 1.2",
"unit": "cm²/m²"
},
{
"label": "Mitral PPM severe iEOA",
"value": "≤ 0.9",
"unit": "cm²/m²"
}
],
"delta": null,
"pearl": "Mismatch is a size problem, not a valve problem: the measured EOA equals the expected EOA for the model but is too small for the body attached to it.",
"lookalike": {
"vs": "prosthetic valve obstruction",
"discriminator": "Both raise the gradient, but mismatch has a measured EOA equal to the reference value for that valve size with normal occluder motion, while obstruction has EOA well below reference with restricted occluder motion"
},
"related": [
"Q112",
"Q324"
],
"reviewed": "2026-08-26"
},
{
"id": "Q326",
"orig": 326,
"title": "Rising mitral prosthetic gradient after INR lapse",
"lesions": [
"PROSTHETIC",
"MS"
],
"lens": "vignette",
"items": [
{
"id": "Q326.1",
"q": "A 58-year-old woman with a bileaflet mechanical mitral valve placed 6 years ago presents with two weeks of worsening dyspnea. Her INR has been subtherapeutic for a month after a medication change. The mean transmitral gradient is 12 mmHg at 80 bpm compared with 4 mmHg at baseline, PHT is 260 ms, and the closing clicks sound muffled. What is the likely diagnosis and how do you confirm it?",
"a": "This is prosthetic valve thrombosis until proven otherwise: a mechanical valve in the low-flow mitral position, inadequate anticoagulation, and a new obstruction signature of tripled mean gradient, prolonged PHT, and damped clicks. TTE establishes the hemodynamics but usually cannot see the atrial side of a mitral prosthesis because of shadowing, so TEE is the confirmatory test; it shows a soft, mobile, low-echogenicity mass on the atrial side of the ring or leaflets and a leaflet that opens incompletely or not at all. Fluoroscopy or gated CT of the leaflet opening angles is a useful adjunct when TEE is equivocal. Pannus is the main alternative, but pannus develops slowly over years, is echodense and fixed, and is not tied to an anticoagulation lapse."
},
{
"id": "Q326.2",
"q": "What determines whether she receives thrombolysis or surgery?",
"a": "Treatment is guided by symptom severity, thrombus size, and surgical risk. A small thrombus under about 10 mm with mild symptoms may respond to intensified anticoagulation or low-dose slow-infusion thrombolysis, with serial TEE to document resolution. A large or highly mobile thrombus, obstructive symptoms with heart failure, or a prior embolus favors urgent surgery when the patient is a reasonable operative candidate, since thrombolysis of a large left-sided thrombus carries a meaningful risk of stroke. Whichever path is chosen, repeat Doppler gradients and TEE are the measures of success, and the baseline post-op study is the reference target."
}
],
"numbers": [
{
"label": "Mitral prosthesis mean gradient suspicious",
"value": "> 10",
"unit": "mmHg"
},
{
"label": "Mitral prosthesis PHT suspicious",
"value": "> 200",
"unit": "ms"
},
{
"label": "Small thrombus manageable medically (approx.)",
"value": "< 10",
"unit": "mm"
}
],
"delta": null,
"pearl": "Mechanical mitral plus low INR plus a gradient that has tripled: order TEE, not another TTE.",
"lookalike": {
"vs": "pannus ingrowth",
"discriminator": "Pannus is dense, fixed, develops over years, and is unrelated to INR; thrombus is soft, mobile, recent, and follows an anticoagulation gap"
},
"related": [
"Q111",
"Q112",
"Q324"
],
"reviewed": "2026-08-26"
},
{
"id": "Q327",
"orig": 327,
"title": "M-mode of a prolapsing atrial myxoma",
"lesions": [
"MASS",
"MS"
],
"lens": "m-mode",
"items": [
{
"id": "Q327.1",
"q": "What does M-mode through the mitral valve show when a large left atrial myxoma prolapses into the orifice, and how does it differ from rheumatic mitral stenosis?",
"a": "A pedunculated myxoma attached to the fossa ovalis swings toward the mitral orifice as the atrium empties, so in diastole the M-mode trace shows a dense cloud of echoes appearing behind the anterior leaflet shortly after the leaflet opens. The key detail is a brief echo-free gap between the leaflet opening at the E point and the arrival of the mass, because the tumor lags behind the leaflet as it travels from the atrium. The anterior leaflet EF slope is flattened, mimicking mitral stenosis, since the mass physically obstructs inflow. In rheumatic stenosis the leaflets themselves are thickened with a reduced EF slope and anterior motion of the posterior leaflet, but there is no separate mass and no gap behind a thin, freely opening leaflet."
},
{
"id": "Q327.2",
"q": "Why can this obstruction change from day to day or with position?",
"a": "Because the mass is tethered by a stalk, its position depends on gravity and atrial flow, so a patient may have a diastolic rumble and a tumor plop when upright that disappear when supine, and the Doppler gradient can vary between studies. The tumor plop is a low-pitched early diastolic sound produced when the mass reaches the end of its stalk against the valve. This positional variability is a clue that separates a myxoma from a fixed stenosis and explains the classic history of intermittent syncope and postural dyspnea."
}
],
"numbers": [],
"delta": null,
"pearl": "Echoes behind the leaflet that arrive a beat later than the leaflet opens are a mass on a stalk, not a thick valve.",
"lookalike": {
"vs": "rheumatic mitral stenosis on M-mode",
"discriminator": "Rheumatic MS thickens the leaflets themselves with no separate diastolic echo mass and no gap after the E point; a myxoma fills the space behind a thin leaflet after a short delay"
},
"related": [
"Q167",
"Q168"
],
"reviewed": "2026-08-26"
},
{
"id": "Q328",
"orig": 328,
"title": "2D features separating cardiac masses",
"lesions": [
"MASS",
"CAD",
"ENDOCARDITIS"
],
"lens": "2d",
"items": [
{
"id": "Q328.1",
"q": "Using location, attachment, mobility, and texture, how do you tell an LV thrombus, a myxoma, a vegetation, and a papillary fibroelastoma apart on 2D?",
"a": "Thrombus forms where blood stagnates: the LV apex or an aneurysm overlying an akinetic segment, the left atrial appendage in atrial fibrillation, or on a catheter or lead. It has a broad base, is usually laminar or sessile with a texture distinct from myocardium, moves with the wall rather than independently, and appears in a chamber with a reason for stasis. A myxoma is a mobile, often gelatinous-looking mass with a narrow stalk attached to the fossa ovalis of the interatrial septum, prolapsing toward the mitral valve. A vegetation is an irregular, shaggy mass on the upstream side of a valve leaflet that oscillates independently of leaflet motion and sits in the path of a regurgitant jet. A fibroelastoma is small, stalked, and frond-like with a shimmering border, on the aortic valve or the atrial side of the mitral leaflets, in a patient without fever."
},
{
"id": "Q328.2",
"q": "Why is TEE required to evaluate the left atrial appendage, and what does thrombus there look like?",
"a": "The appendage is a multilobed, trabeculated pouch behind the aorta that is far from the transthoracic transducer and rarely visualized well from the chest. TEE views it from a few centimeters away in the mid-esophageal position at 0 to 135 degrees, allowing you to sweep every lobe. Thrombus appears as a well-defined echodense mass, often with a texture different from the surrounding wall, located in the body or tip of the appendage, frequently within dense spontaneous echo contrast. Pectinate muscles are the main mimic; they are linear ridges continuous with the wall, seen in multiple planes with the same relationship to the wall, whereas thrombus is discrete and can be shown to be separate from the wall in at least two planes."
}
],
"numbers": [],
"delta": null,
"pearl": "Location answers most of the question: apex means thrombus, septum means myxoma, upstream valve surface means vegetation, downstream valve surface means fibroelastoma.",
"lookalike": {
"vs": "pectinate muscle in the appendage",
"discriminator": "Pectinate muscles are continuous with the wall, linear, and identical in every plane; thrombus is a discrete mass separable from the wall in two or more planes and usually surrounded by smoke"
},
"related": [
"Q32",
"Q170",
"Q161",
"Q99",
"Q329",
"Q331",
"Q333"
],
"reviewed": "2026-08-26"
},
{
"id": "Q329",
"orig": 329,
"title": "Doppler clues to mass obstruction and stasis",
"lesions": [
"MASS",
"ARRHYTHMIA",
"TEE"
],
"lens": "doppler",
"items": [
{
"id": "Q329.1",
"q": "How do you quantify obstruction from an intracardiac mass with Doppler?",
"a": "When a mass sits in a valve orifice or outflow tract it narrows the effective area, so CW Doppler across the mass records an increased velocity and gradient just like a stenotic valve, and for a mitral position a prolonged pressure half-time. The gradient depends on where the mass is at that moment and on heart rate, so record it in the position and at the rate in which symptoms occur and note both. Because the obstruction is caused by a mobile object rather than a fixed valve, the Doppler signal may vary beat to beat and between studies, which is itself a diagnostic clue. Color Doppler shows flow diverted around the mass and helps define whether the obstruction is central or eccentric."
},
{
"id": "Q329.2",
"q": "How is left atrial appendage emptying velocity measured, and what do spontaneous echo contrast and a low velocity mean?",
"a": "On TEE, place the pulsed-wave sample volume about 1 cm inside the appendage orifice and record the emptying and filling waves over several beats; in atrial fibrillation average multiple cycles. A normal appendage in sinus rhythm empties at 50 cm/s or more, and a velocity below 20 cm/s identifies severe stasis with a high risk of existing or future thrombus. Spontaneous echo contrast, or smoke, is swirling low-velocity blood that aggregates red cells enough to scatter ultrasound; its density grades stasis, with dense smoke and sludge sitting just short of solid thrombus. Low emptying velocity and dense smoke together mark a patient in whom cardioversion or appendage instrumentation should be approached with caution and in whom you must search every lobe for clot."
}
],
"numbers": [
{
"label": "LAA emptying velocity high thrombus risk",
"value": "< 20",
"unit": "cm/s"
},
{
"label": "Normal LAA emptying velocity (sinus rhythm)",
"value": "≥ 50",
"unit": "cm/s"
},
{
"label": "LAA PW sample position from orifice",
"value": "~1",
"unit": "cm"
}
],
"delta": null,
"pearl": "Under 20 cm/s in the appendage means the blood is barely moving; treat smoke there as thrombus in the making.",
"lookalike": {
"vs": "spontaneous echo contrast versus thrombus",
"discriminator": "Smoke swirls, changes with each frame, and has no defined border; thrombus is a discrete mass with fixed borders that persists across frames and planes"
},
"related": [
"Q328",
"Q161",
"Q332",
"Q371",
"Q393"
],
"reviewed": "2026-08-26"
},
{
"id": "Q330",
"orig": 330,
"title": "How masses alter the chambers",
"lesions": [
"MASS",
"HEMODYNAMICS"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q330.1",
"q": "What downstream chamber effects does an obstructing left atrial mass produce, and how do they reverse after removal?",
"a": "A large LA myxoma acts as a functional mitral stenosis, so the left atrium enlarges from the elevated pressure, pulmonary venous pressure rises, and pulmonary hypertension with RV enlargement and TR can follow if the obstruction is long-standing. The LV is typically underfilled and normal or small in size, which is a helpful distinction from primary MR or cardiomyopathy. Right atrial masses obstruct tricuspid inflow and cause systemic venous congestion, IVC dilation, and hepatomegaly. Because the obstruction is mechanical and the leaflets are intact, LA size and pulmonary pressure usually regress after surgical removal, and the follow-up echo is also the surveillance study for recurrence, which occurs in a small minority, more often in familial or Carney-complex disease."
},
{
"id": "Q330.2",
"q": "How do intramural and infiltrating tumors change the heart differently from intracavitary masses?",
"a": "Intramural tumors such as rhabdomyoma, fibroma, and metastases thicken and stiffen the wall they invade, so they can present as a regional bulge that mimics hypertrophic cardiomyopathy, cause conduction block or ventricular arrhythmia, or restrict filling. Infiltrating malignancy, most often angiosarcoma in the right atrium or direct extension from lung and breast cancer, distorts chamber borders, invades the pericardium, and produces a hemorrhagic effusion that may progress to tamponade. Renal cell carcinoma and hepatocellular carcinoma extend up the IVC into the right atrium as a tongue of tumor that can obstruct tricuspid inflow. With these lesions the chamber effect is dictated by the wall or pericardium being replaced, not by an orifice being blocked."
}
],
"numbers": [],
"delta": null,
"pearl": "Big LA, small LV, high PA pressure, and a normal mitral valve: look for something sitting in the orifice.",
"lookalike": {
"vs": "rheumatic mitral stenosis",
"discriminator": "Both enlarge the LA and raise PA pressure, but MS has thickened doming leaflets with commissural fusion; a myxoma leaves the leaflets normal and the obstruction is a separate mobile mass"
},
"related": [
"Q168",
"Q169",
"Q171",
"Q208"
],
"reviewed": "2026-08-26"
},
{
"id": "Q331",
"orig": 331,
"title": "Best imaging tools for cardiac masses",
"lesions": [
"MASS",
"CONTRAST",
"TEE"
],
"lens": "best-method",
"items": [
{
"id": "Q331.1",
"q": "How does an ultrasound enhancing agent help distinguish thrombus from tumor, and how is the study performed?",
"a": "Thrombus has no blood supply, so after intravenous microbubble injection it remains a dark filling defect while the surrounding cavity opacifies; a tumor is vascular and takes up bubbles, with malignant and highly vascular lesions enhancing as much as or more than adjacent myocardium and benign stromal tumors such as myxoma enhancing less. Image with low mechanical index below about 0.3 using a perfusion setting so bubbles survive in the tissue, then apply a brief high-MI flash to destroy them and watch whether the mass refills. This perfusion approach, and simple LV opacification to sharpen the apical border, are the main reasons an enhancing agent is indicated whenever two or more contiguous segments are poorly seen or an apical mass is suspected."
},
{
"id": "Q331.2",
"q": "When should you move to TEE or cardiac MRI rather than relying on TTE?",
"a": "TEE is the method for the left atrial appendage, the interatrial septum, prosthetic valves, and small valvular masses, because it resolves millimeter structures that TTE cannot, and it is the standard before cardioversion or appendage closure. Cardiac MRI is the tissue-characterization tool: T1 and T2 signal, first-pass perfusion, and late gadolinium enhancement separate thrombus (no enhancement on any sequence) from vascular tumor, and identify fat in a lipoma or lipomatous septal hypertrophy and the infiltrative pattern of malignancy. CT is preferred when MRI is contraindicated, for calcified masses, and for staging extracardiac spread. In practice TTE finds the mass, enhancing agent or TEE refines it, and MRI names it."
}
],
"numbers": [
{
"label": "Low-MI perfusion imaging",
"value": "< 0.3",
"unit": "MI"
},
{
"label": "Contrast indication: poorly seen contiguous LV segments",
"value": "≥ 2",
"unit": "segments"
}
],
"delta": null,
"pearl": "No blood supply, no bubbles: a mass that stays black after contrast is thrombus.",
"lookalike": {
"vs": "hypervascular tumor",
"discriminator": "Tumor enhances with microbubbles or gadolinium; thrombus never does on any modality"
},
"related": [
"Q32",
"Q170",
"Q328",
"Q333",
"Q393"
],
"reviewed": "2026-08-26"
},
{
"id": "Q332",
"orig": 332,
"title": "Cardiac mass numbers to memorize",
"lesions": [
"MASS",
"CAD"
],
"lens": "numbers",
"items": [
{
"id": "Q332.1",
"q": "Which frequency and timing figures for myxoma and LV thrombus are commonly tested?",
"a": "Myxoma is the most common primary cardiac tumor in adults, and about 75 percent arise in the left atrium, almost always on a stalk from the fossa ovalis region of the septum; roughly 15 to 20 percent are in the right atrium and the remainder ventricular or multiple, the latter more common in familial disease. LV thrombus after myocardial infarction typically forms within the first one to two weeks, most often at 6 to 10 days, when the akinetic apex is fresh and the endocardium is inflamed. Historically about 40 percent of anterior infarctions developed apical thrombus, whereas with modern reperfusion and antithrombotic therapy the rate is below 5 percent overall, though it remains higher in large anterior infarcts with EF under 40 percent or an apical aneurysm."
},
{
"id": "Q332.2",
"q": "What Doppler numbers define stasis in the left atrial appendage?",
"a": "An appendage emptying velocity below 20 cm/s on TEE indicates severe stasis and is associated with thrombus formation and future stroke; normal sinus rhythm values are 50 cm/s or higher. Dense spontaneous echo contrast frequently accompanies velocities in this range. These values are why a pulsed-wave trace of the appendage is part of every pre-cardioversion TEE."
}
],
"numbers": [
{
"label": "Myxoma in left atrium",
"value": "~75",
"unit": "%"
},
{
"label": "Myxoma in right atrium",
"value": "~15–20",
"unit": "%"
},
{
"label": "Typical timing of LV thrombus after MI",
"value": "6–10",
"unit": "days"
},
{
"label": "Historical apical thrombus after anterior MI",
"value": "~40",
"unit": "%"
},
{
"label": "Apical thrombus with reperfusion era",
"value": "< 5",
"unit": "%"
},
{
"label": "LAA emptying velocity high thrombus risk",
"value": "< 20",
"unit": "cm/s"
}
],
"delta": null,
"pearl": "Three-quarters of myxomas hang from the left side of the fossa ovalis, and a fresh anterior infarct grows its clot in the second week.",
"lookalike": null,
"related": [
"Q167",
"Q161",
"Q329"
],
"reviewed": "2026-08-26"
},
{
"id": "Q333",
"orig": 333,
"title": "Stroke workup for a cardiac source",
"lesions": [
"MASS",
"CAD",
"ARRHYTHMIA"
],
"lens": "vignette",
"items": [
{
"id": "Q333.1",
"q": "A 71-year-old man with paroxysmal atrial fibrillation who stopped his anticoagulant presents with an embolic stroke. TTE shows a mildly dilated LA, normal LV, and no mass. What is the next imaging step and what are you looking for?",
"a": "TTE almost never visualizes the left atrial appendage, and the appendage is the site of more than 90 percent of atrial thrombi in nonvalvular atrial fibrillation, so TEE is the appropriate next study. Image the appendage in several angles from the mid-esophageal position, measure the emptying velocity, and grade spontaneous echo contrast; a discrete echodense mass separable from the wall in two planes is thrombus. At the same time interrogate the interatrial septum with color and agitated saline for a patent foramen ovale or septal aneurysm, examine the aortic arch for mobile atheroma 4 mm or thicker, and look at the valves for vegetations or fibroelastoma. These findings change management from empiric anticoagulation to a defined source with a plan for closure, anticoagulation intensity, or surgery."
},
{
"id": "Q333.2",
"q": "A 63-year-old woman had a large anterior infarction 3 weeks ago and now presents with a transient ischemic attack. Her apex is thin and dyskinetic. What are you looking for and how do you make the study definitive?",
"a": "A dyskinetic or aneurysmal apex is the classic site for LV thrombus, which appears as a mass with a texture distinct from myocardium, a defined border, and location within the aneurysm rather than in normally contracting wall. Foreshortened apical views and near-field clutter frequently hide or mimic thrombus, so image from several apical positions with the focus zone at the apex, use a higher-frequency setting, and give an ultrasound enhancing agent; thrombus stays as a dark filling defect against the opacified cavity. Cardiac MRI with late gadolinium enhancement is the reference standard when echo is still uncertain. A confirmed thrombus mandates anticoagulation with follow-up imaging in about 3 months to document resolution."
}
],
"numbers": [
{
"label": "Nonvalvular AF thrombi located in LAA",
"value": "> 90",
"unit": "%"
},
{
"label": "Aortic arch atheroma considered high risk",
"value": "≥ 4",
"unit": "mm"
},
{
"label": "Follow-up imaging after LV thrombus treatment",
"value": "~3",
"unit": "months"
}
],
"delta": null,
"pearl": "Embolic stroke with a clean TTE is not a clean workup: the appendage, the septum, and the arch all live on the TEE.",
"lookalike": {
"vs": "apical near-field artifact",
"discriminator": "Artifact changes with transducer angle and frequency and vanishes with contrast; thrombus persists in multiple views and remains a filling defect after enhancing agent"
},
"related": [
"Q32",
"Q161",
"Q328",
"Q331",
"Q371",
"Q375",
"Q388",
"Q393"
],
"reviewed": "2026-08-26"
},
{
"id": "Q334",
"orig": 334,
"title": "What diastole is and what echo measures",
"lesions": [
"DIASTOLIC",
"HEMODYNAMICS"
],
"lens": "definition",
"items": [
{
"id": "Q334.1",
"q": "Name the phases of diastole and the Doppler measurement that reflects each.",
"a": "Diastole begins when the aortic valve closes. Isovolumic relaxation — pressure falling with both valves shut — is measured as IVRT (aortic closure click to mitral opening, 70–90 ms normally). Early rapid filling is the mitral E wave, driven by the LV's suction and the LA-to-LV gradient; its deceleration time reflects how quickly the gradient collapses. Diastasis is the mid-diastolic pause when pressures equalise. Atrial contraction is the A wave. Tissue Doppler adds e′ (early annular recoil, the most direct index of relaxation) and a′. The 2025 guideline treats these as answers to two separate questions — is relaxation impaired, and is left atrial pressure elevated — and asks you to report both."
},
{
"id": "Q334.2",
"q": "Why is e′ the first variable in the 2025 algorithms?",
"a": "Because e′ tracks relaxation and is least affected by preload when relaxation is normal, whereas E rises with LA pressure. A ventricle that relaxes poorly has a low e′ regardless of pressure, so a normal-looking E over a low e′ (high E/e′) reveals pressure-driven filling. The 2025 cut-offs are septal ≤ 6, lateral ≤ 7 or average ≤ 6.5 cm/s, with optional age-adjusted limits (20–39 y < 7/< 10/< 9; 40–65 y < 6/< 8/< 7; > 65 y < 6/< 7/< 6.5)."
}
],
"numbers": [
{
"label": "Normal IVRT",
"value": "70–90",
"unit": "ms"
},
{
"label": "Reduced e′ septal / lateral / average (2025)",
"value": "≤ 6 / ≤ 7 / ≤ 6.5",
"unit": "cm/s"
},
{
"label": "Normal E/A",
"value": "1–2",
"unit": "ratio"
},
{
"label": "Normal DT",
"value": "160–240",
"unit": "ms"
}
],
"delta": {
"was": "2016 used septal e′ < 7 and lateral e′ < 10 cm/s for all ages as the abnormal thresholds.",
"now": "2025: septal ≤ 6, lateral ≤ 7, average ≤ 6.5 cm/s, or age-adjusted values from Table 6; e′ is the first step of both the dysfunction (Figure 2) and LAP (Figure 3) algorithms.",
"source": "ASE 2025 (Nagueh et al., JASE 2025;38:7) — supersedes ASE/EACVI 2016"
},
"pearl": "Two questions, reported separately: is relaxation impaired (e′), and is LAP high (E/e′, TR, then the second stage)?",
"lookalike": null,
"related": [
"Q335",
"Q336"
],
"reviewed": "2026-08-27"
},
{
"id": "Q335",
"orig": 335,
"title": "The 2025 ASE algorithm for LA pressure and grade",
"lesions": [
"DIASTOLIC"
],
"lens": "doppler",
"items": [
{
"id": "Q335.1",
"q": "In sinus rhythm, which three primary variables does the 2025 ASE algorithm use, and how are they combined?",
"a": "Reduced e′ (septal ≤ 6, lateral ≤ 7 or average ≤ 6.5 cm/s), increased E/e′ (septal ≥ 15, lateral ≥ 13 or average ≥ 14), and TR velocity ≥ 2.8 m/s or PASP ≥ 35 mmHg when RAP can be estimated. All three normal means normal LAP and normal diastolic function; all three abnormal means elevated LAP. Reduced e′ alone with E/A ≤ 0.8 is grade 1 with normal LAP. Any other mixture — e′ reduced with E/A > 0.8, only E/e′ or only TR abnormal, or any two — goes to a second stage: pulmonary-vein S/D ≤ 0.67, LA reservoir strain ≤ 18%, LAVi > 34 mL/m², or alternatively IVRT ≤ 70 ms. One positive second-stage marker means elevated LAP; none means normal. Supplemental markers (PR end-diastolic velocity ≥ 2 m/s, PA diastolic pressure ≥ 16 mmHg, mitral L-wave ≥ 50 cm/s, Ar − A > 30 ms, an E/A fall ≥ 50% with Valsalva) are used only when none of those is available or reliable."
},
{
"id": "Q335.2",
"q": "How are grades 1, 2 and 3 assigned once LAP is known?",
"a": "Normal LAP with impaired relaxation is grade 1. Elevated LAP is graded by E/A: below 2 is grade 2 (mild-to-moderate elevation, the pseudonormal pattern) and 2 or more is grade 3 (marked elevation, restrictive). Grade 3 can be split into 3a when the E/A ratio falls by ≥ 50% with Valsalva (reversible) and 3b when it does not. Diastolic dysfunction itself is diagnosed separately (Figure 2): reduced e′ plus one marker, or preserved e′ plus two markers among average E/e′ > 14, LARS ≤ 18%, E/A ≤ 0.8 or ≥ 2, LAVi > 34, and increased LV mass index — which is what separates normal function from grade 1 when LAP is normal."
},
{
"id": "Q335.3",
"q": "Which patients must not be put through the general algorithm?",
"a": "Atrial fibrillation, moderate or severe mitral annular calcification, any mitral stenosis, severe primary MR, heart transplant, non-cardiac pulmonary hypertension, pericardial constriction, LV assist devices, and patients after mitral repair, replacement or transcatheter edge-to-edge repair. Each has a dedicated pathway; AF uses E ≥ 100 cm/s, septal E/e′ > 11, TR > 2.8 m/s and DT ≤ 160 ms (three or more elevated, one or none normal, two → LARS < 18%, PV S/D < 1, BMI > 30)."
}
],
"numbers": [
{
"label": "Increased E/e′ septal / lateral / average",
"value": "≥ 15 / ≥ 13 / ≥ 14",
"unit": "ratio"
},
{
"label": "TR velocity / PASP threshold",
"value": "≥ 2.8 / ≥ 35",
"unit": "m/s / mmHg"
},
{
"label": "Second stage: PV S/D",
"value": "≤ 0.67",
"unit": "ratio"
},
{
"label": "Second stage: LA reservoir strain",
"value": "≤ 18",
"unit": "%"
},
{
"label": "Second stage: LAVi",
"value": "> 34",
"unit": "mL/m²"
},
{
"label": "Alternative second stage: IVRT",
"value": "≤ 70",
"unit": "ms"
},
{
"label": "Grade 3 E/A",
"value": "≥ 2",
"unit": "ratio"
},
{
"label": "Grade 1 E/A (with reduced e′)",
"value": "≤ 0.8",
"unit": "ratio"
}
],
"delta": {
"was": "2016: four variables (average E/e′ > 14, septal e′ < 7 or lateral < 10, TR > 2.8, LAVi > 34); > 50% positive = dysfunction, 50% = indeterminate; grade 1 required E/A ≤ 0.8 with E ≤ 50 cm/s.",
"now": "2025: three primary variables (e′, E/e′, TR/PASP) with a defined second stage (PV S/D ≤ 0.67, LARS ≤ 18%, LAVi > 34, or IVRT ≤ 70 ms); no indeterminate outcome in sinus rhythm; grade 1 = reduced e′ with E/A ≤ 0.8; LAP and grade reported separately.",
"source": "ASE 2025 (Nagueh et al., JASE 2025;38:7) — supersedes ASE/EACVI 2016"
},
"pearl": "All normal → normal. All abnormal → up. Anything mixed → second stage (S/D, LARS, LAVi, or IVRT). Then E/A splits grade 2 from 3.",
"lookalike": {
"vs": "Pseudonormal (grade II) vs truly normal inflow",
"discriminator": "Both have E/A 0.8–2; pseudonormal has low e', E/e' >14, dilated LA, and E/A falls below 0.8 with Valsalva."
},
"related": [
"Q334",
"Q336",
"Q337",
"Q338"
],
"reviewed": "2026-08-27"
},
{
"id": "Q336",
"orig": 336,
"title": "Diastolic numbers to know (2025)",
"lesions": [
"DIASTOLIC"
],
"lens": "numbers",
"items": [
{
"id": "Q336.1",
"q": "List the 2025 cut-offs for e′, E/e′, TR, LAVi and LARS, and the normal ranges for E/A, DT and IVRT.",
"a": "Reduced e′: septal ≤ 6, lateral ≤ 7, average ≤ 6.5 cm/s (age-adjusted: 20–39 y < 7/< 10/< 9; 40–65 y < 6/< 8/< 7; > 65 y < 6/< 7/< 6.5). Increased E/e′: septal ≥ 15, lateral ≥ 13, average ≥ 14. TR ≥ 2.8 m/s or PASP ≥ 35 mmHg. LAVi > 34 mL/m². LA reservoir strain ≤ 18% is the decision threshold; ≥ 23% is within normal and healthy adults average about 39%. Pulmonary-vein S/D ≤ 0.67; IVRT ≤ 70 ms; Ar − A > 30 ms. Normal E/A is 1–2 (E/A ≤ 0.8 impaired relaxation, ≥ 2 restrictive), DT 160–240 ms (< 160 restrictive, > 240 impaired relaxation), IVRT 70–90 ms."
}
],
"numbers": [
{
"label": "LARS decision threshold",
"value": "≤ 18",
"unit": "%"
},
{
"label": "LARS lower limit of normal",
"value": "23",
"unit": "%"
},
{
"label": "Ar − A duration abnormal",
"value": "> 30",
"unit": "ms"
},
{
"label": "Restrictive DT",
"value": "< 160",
"unit": "ms"
},
{
"label": "Impaired-relaxation DT",
"value": "> 240",
"unit": "ms"
},
{
"label": "Age-adjusted average e′ (20–39 / 40–65 / > 65 y)",
"value": "< 9 / < 7 / < 6.5",
"unit": "cm/s"
}
],
"delta": {
"was": "2016 thresholds: septal e′ < 7, lateral < 10; four-variable vote; no LA strain.",
"now": "2025 thresholds above, with LA reservoir strain ≤ 18% and pulmonary-vein S/D ≤ 0.67 added, and age-adjusted e′ limits.",
"source": "ASE 2025 (Nagueh et al., JASE 2025;38:7) — supersedes ASE/EACVI 2016"
},
"pearl": "6 / 7 / 6.5 for e′; 15 / 13 / 14 for E/e′; 2.8 / 35 for TR / PASP; 0.67 / 18 / 34 / 70 for the second stage.",
"lookalike": null,
"related": [
"Q335",
"Q347",
"Q334",
"Q337",
"Q338"
],
"reviewed": "2026-08-27"
},
{
"id": "Q337",
"orig": 337,
"title": "Diastolic traps and special pathways",
"lesions": [
"DIASTOLIC",
"ARRHYTHMIA",
"MS"
],
"lens": "pitfall",
"items": [
{
"id": "Q337.1",
"q": "Name the situations where inflow and annular Doppler mislead, and what the 2025 guideline uses instead.",
"a": "Atrial fibrillation: no A wave and beat-to-beat variation — average five beats and use E ≥ 100 cm/s, septal E/e′ > 11, TR > 2.8, DT ≤ 160 ms, with LARS, PV S/D and BMI as the tie-breakers; never LAVi or E/A. Moderate–severe MAC: e′ and E/e′ are falsely high — E/A < 0.8 normal, > 1.8 elevated, in between IVRT < 80 ms means elevated. Significant primary MR: use IVRT < 60 ms, Ar − A ≥ 30 ms, IVRT/T(E−e′) < 5.6; E/e′ only if EF is reduced; LARS is unreliable. Mitral stenosis: IVRT < 60 ms, A > 1.5 m/s, IVRT/T(E−e′) < 4.2. Non-cardiac pulmonary hypertension: use the lateral annulus only — E/A ≤ 0.8 with E ≤ 50 is normal LAP, E/A ≥ 2 elevated, in between LARS ≤ 18% elevated. Heart transplant: average E/e′ < 7 normal, > 14 elevated, otherwise E/SR-IVR > 200 cm. LBBB or RV pacing: the septal annulus is dyssynchronous — use lateral E/e′, TR and LA size and strain. Tachycardia or first-degree block fuse E and A; athletes and the young have E/A ≥ 2 with high e′ and normal LAVi, which is supernormal filling, not grade 3."
},
{
"id": "Q337.2",
"q": "How do you tell constriction from restriction with Doppler?",
"a": "Both produce a restrictive inflow. Constriction shows respirophasic septal shift, medial e′ > 7 cm/s (> 8 strongly favours it) with medial ≥ lateral (annulus reversus), mitral inflow variation > 25% (tricuspid > 40%), and expiratory hepatic-vein diastolic reversal with a reversal-to-forward ratio ≥ 0.8; longitudinal strain is preserved. Restrictive cardiomyopathy shows e′ < 5 cm/s, minimal respiratory variation, inspiratory hepatic-vein reversal, reduced global strain and often thick bright walls. Septal shift plus medial e′ together give about 80% sensitivity and 96% specificity. Normal pericardial thickness never excludes constriction."
}
],
"numbers": [
{
"label": "AF: E threshold",
"value": "≥ 100",
"unit": "cm/s"
},
{
"label": "AF: septal E/e′",
"value": "> 11",
"unit": "ratio"
},
{
"label": "MAC: IVRT deciding elevated LAP",
"value": "< 80",
"unit": "ms"
},
{
"label": "Constriction: medial e′",
"value": "> 7 (> 8 favors)",
"unit": "cm/s"
},
{
"label": "Constriction: HV expiratory reversal ratio",
"value": "≥ 0.8",
"unit": "ratio"
},
{
"label": "Constriction: mitral / tricuspid inflow variation",
"value": "> 25 / > 40",
"unit": "%"
},
{
"label": "Restriction: e′",
"value": "< 5",
"unit": "cm/s"
}
],
"delta": {
"was": "2016 AF criteria: septal E/e′ > 11, IVRT ≤ 65 ms, DT ≤ 160 ms, TR > 2.8; constriction medial e′ ≥ 9 with hepatic-vein ratio ≥ 0.79.",
"now": "2025 AF pathway (E ≥ 100, septal E/e′ > 11, TR > 2.8, DT ≤ 160; LARS/PV S/D/BMI tier) and dedicated MAC, MR, MS, PH, transplant and pacing rules; constriction medial e′ > 7 and reversal ratio ≥ 0.8.",
"source": "ASE 2025 (Nagueh et al., JASE 2025;38:7) — supersedes ASE/EACVI 2016"
},
"pearl": "If the annulus is calcified, paced, transplanted or under RV pressure, stop trusting e′ and switch pathways.",
"lookalike": {
"vs": "Athlete's E/A >2 vs restrictive filling",
"discriminator": "The athlete has high e' (often >12 cm/s) and normal E/e'; restriction has low e' and E/e' >14 with a short DT."
},
"related": [
"Q335",
"Q336",
"Q338",
"Q368",
"Q379"
],
"reviewed": "2026-08-27"
},
{
"id": "Q338",
"orig": 338,
"title": "HFpEF workup with the 2025 pathway",
"lesions": [
"DIASTOLIC",
"HTN"
],
"lens": "vignette",
"items": [
{
"id": "Q338.1",
"q": "A 68-year-old with exertional dyspnea, EF 62%, septal e′ 5 cm/s, lateral e′ 6 cm/s, E 82 cm/s, A 60 cm/s, TR 2.6 m/s and LAVi 40 mL/m². Work through the 2025 algorithm.",
"a": "Primary variables: e′ is reduced (both below the cut-offs); average E/e′ is 82 ÷ 5.5 ≈ 15, so E/e′ is increased; TR 2.6 m/s is normal. Two of three abnormal sends the case to the second stage, where LAVi 40 mL/m² exceeds 34 — one positive marker, so mean LAP is elevated. E/A is 1.37, below 2, so this is grade 2 diastolic dysfunction with mildly to moderately elevated LAP. In a symptomatic patient with a normal EF, elevated resting LAP is enough to make the diagnosis of HFpEF; no exercise test is needed."
},
{
"id": "Q338.2",
"q": "What if the same patient had a normal resting study?",
"a": "With a normal resting LAP and persisting exertional symptoms the guideline recommends diastolic exercise echocardiography, because filling pressure may rise only with effort. The test is positive when the average E/e′ reaches 14 (or septal 15) and TR velocity reaches 3.2 m/s or more — both, since E/e′ alone rises with exercise in normal people. A positive test makes the HFpEF diagnosis; a negative one argues for a non-cardiac cause. LA reservoir strain and LV global longitudinal strain belong in the resting study because HFpEF patients often show abnormal LA function and subtle systolic impairment despite a normal EF."
}
],
"numbers": [
{
"label": "Diastolic exercise echo positive: average E/e′ (septal)",
"value": "≥ 14 (≥ 15)",
"unit": "ratio"
},
{
"label": "Diastolic exercise echo positive: TR velocity",
"value": "≥ 3.2",
"unit": "m/s"
}
],
"delta": {
"was": "2016 offered no HFpEF pathway; exercise E/e′ > 14 with TR > 2.8 m/s was the suggested positive result.",
"now": "2025: symptomatic + elevated resting LAP = HFpEF; if resting LAP is normal, diastolic exercise echo is positive when average E/e′ ≥ 14 (septal ≥ 15) and TR ≥ 3.2 m/s.",
"source": "ASE 2025 (Nagueh et al., JASE 2025;38:7) — supersedes ASE/EACVI 2016"
},
"pearl": "Elevated LAP at rest in a breathless patient with a normal EF is HFpEF; a normal resting study earns a treadmill, not a discharge.",
"lookalike": {
"vs": "Constrictive pericarditis",
"discriminator": "Constriction has a preserved or supernormal medial e' (annulus reversus) with septal shift and expiratory hepatic reversal; HFpEF has a uniformly low e'."
},
"related": [
"Q335",
"Q336",
"Q337"
],
"reviewed": "2026-08-27"
},
{
"id": "Q339",
"orig": 339,
"title": "Preferred methods for ejection fraction",
"lesions": [
"LV_FUNCTION",
"CONTRAST"
],
"lens": "best-method",
"items": [
{
"id": "Q339.1",
"q": "Which 2D method does the ASE recommend for LVEF, and why is Teichholz or a single-plane linear estimate discouraged?",
"a": "Biplane method of disks (modified Simpson's) is the recommended 2D technique. You trace the endocardial border at end-diastole and end-systole in the apical 4- and 2-chamber views, and the software slices the cavity into about 20 disks, summing their volumes. Because it samples the ventricle along its length in two orthogonal planes, it tolerates regional wall motion abnormalities and irregular shapes. Teichholz and cube-formula methods derive volume from a single minor-axis diameter measured at the base, which assumes a symmetric ellipsoid; a basal segment that contracts normally over an akinetic apex produces a normal-looking EF that is simply wrong. Any single linear dimension should be reported only as a dimension, not converted to EF, in patients with regional disease."
},
{
"id": "Q339.2",
"q": "When is 3D echo preferred, and when should an ultrasound enhancing agent be added?",
"a": "Three-dimensional full-volume acquisition is preferred whenever image quality permits and the lab has the expertise, because it needs no geometric assumption and cannot foreshorten the apex; its volumes track cardiac MRI more closely and vary less between readers. An enhancing agent is indicated when two or more contiguous LV segments cannot be seen in the apical views. Opacifying the cavity defines the true endocardial border, excludes trabeculae from the traced volume, and brings interobserver agreement close to that of MRI, which matters most in serial studies such as chemotherapy surveillance where a change of a few EF points alters management."
}
],
"numbers": [
{
"label": "Segments unseen prompting enhancing agent",
"value": "≥ 2 contiguous",
"unit": "segments"
},
{
"label": "Disks in Simpson's method (typical)",
"value": "≈ 20",
"unit": ""
}
],
"delta": null,
"pearl": "Trace, don't estimate; two planes, not one; and if you cannot see two neighboring segments, add contrast before you guess.",
"lookalike": null,
"related": [
"Q340",
"Q342",
"Q343",
"Q350",
"Q341",
"Q351"
],
"widgets": [
{
"id": "calc",
"opts": {
"k": "ef"
}
}
],
"reviewed": "2026-08-26"
},
{
"id": "Q340",
"orig": 340,
"title": "Left ventricular size and function cutoffs",
"lesions": [
"LV_FUNCTION",
"CHAMBER_QUANT"
],
"lens": "numbers",
"items": [
{
"id": "Q340.1",
"q": "State the ASE 2015 ejection fraction categories by sex, and the normal ranges for LV internal diameter and wall thickness.",
"a": "Normal EF is 52% or more in men and 54% or more in women. Mildly reduced EF is 41–51% in men and 41–53% in women; 30–40% is moderately reduced and below 30% severely reduced in both sexes. The sex difference exists because women have slightly smaller ventricles and higher normal EF in reference populations. LV end-diastolic diameter measured in the parasternal long axis is normally 4.2–5.8 cm in men and 3.8–5.2 cm in women, and septal or posterior wall thickness at end-diastole is 0.6–1.0 cm. A wall over 1.0 cm is hypertrophied, though mass index rather than a single thickness is the better descriptor."
},
{
"id": "Q340.2",
"q": "What thresholds define LV hypertrophy by mass index and relative wall thickness, and what is a normal global longitudinal strain?",
"a": "LV mass indexed to body surface area is abnormal above 115 g/m² in men and 95 g/m² in women when derived from linear measurements. Relative wall thickness is twice the posterior wall thickness divided by the LV diastolic diameter; a value above 0.42 means the wall is thick relative to the cavity. Combining the two yields four geometries: normal, concentric remodeling (RWT high, mass normal), concentric hypertrophy (both high), and eccentric hypertrophy (mass high, RWT normal). Global longitudinal strain in a healthy adult is about −18 to −22%; values less negative than −16% are clearly abnormal, with a gray zone between."
}
],
"numbers": [
{
"label": "Normal EF men",
"value": "≥ 52",
"unit": "%"
},
{
"label": "Normal EF women",
"value": "≥ 54",
"unit": "%"
},
{
"label": "Mildly reduced EF men",
"value": "41–51",
"unit": "%"
},
{
"label": "Mildly reduced EF women",
"value": "41–53",
"unit": "%"
},
{
"label": "Moderately reduced EF",
"value": "30–40",
"unit": "%"
},
{
"label": "Severely reduced EF",
"value": "< 30",
"unit": "%"
},
{
"label": "LVIDd men",
"value": "4.2–5.8",
"unit": "cm"
},
{
"label": "LVIDd women",
"value": "3.8–5.2",
"unit": "cm"
},
{
"label": "Wall thickness normal",
"value": "0.6–1.0",
"unit": "cm"
},
{
"label": "LV mass index LVH men",
"value": "> 115",
"unit": "g/m²"
},
{
"label": "LV mass index LVH women",
"value": "> 95",
"unit": "g/m²"
},
{
"label": "RWT concentric",
"value": "> 0.42",
"unit": ""
},
{
"label": "GLS normal",
"value": "−18 to −22",
"unit": "%"
},
{
"label": "GLS abnormal",
"value": "> −16",
"unit": "%"
}
],
"delta": null,
"pearl": "52/54 for EF, 115/95 for mass, 0.42 for RWT: men first, women second, except EF where women are higher.",
"lookalike": null,
"related": [
"Q339",
"Q341",
"Q347"
],
"reviewed": "2026-08-26"
},
{
"id": "Q341",
"orig": 341,
"title": "Global longitudinal strain basics",
"lesions": [
"LV_FUNCTION",
"RCM"
],
"lens": "doppler",
"items": [
{
"id": "Q341.1",
"q": "What is global longitudinal strain, how is it measured by speckle tracking, and what is the normal range?",
"a": "Strain is the percentage change in length of a myocardial segment between end-diastole and end-systole. Longitudinal strain is negative because the ventricle shortens from base to apex in systole; a more negative number means more shortening and better function. Speckle-tracking software follows the natural acoustic pattern of the myocardium frame by frame in the three apical views (4-, 2-, and 3-chamber), computes segmental strain for each of the 17 segments, and averages them into a global value displayed as a bull's-eye. Unlike tissue Doppler strain it is angle-independent, but it requires good endocardial definition and a frame rate of roughly 50–80 frames per second. Normal GLS is about −18 to −22%, and a value less negative than −16% is abnormal."
},
{
"id": "Q341.2",
"q": "How is GLS used in cardio-oncology, and what does the apical sparing pattern indicate?",
"a": "GLS falls before EF does because subendocardial longitudinal fibers are the first casualties of most myocardial injury. In patients receiving anthracyclines or trastuzumab, a relative drop in GLS of more than 15% from baseline (for example from −20% to −16.5%) flags subclinical cardiotoxicity, whereas a change under 8% is within measurement noise. Detecting the change early allows cardioprotective therapy before EF declines. Apical sparing describes a bull's-eye in which the basal and mid segments have severely reduced strain while the apex is preserved, giving a cherry-on-top appearance; it is strongly suggestive of cardiac amyloidosis and helps separate it from hypertensive or hypertrophic thickening, in which the strain loss is more diffuse or septal."
}
],
"numbers": [
{
"label": "GLS normal",
"value": "−18 to −22",
"unit": "%"
},
{
"label": "GLS abnormal",
"value": "> −16",
"unit": "%"
},
{
"label": "Cardiotoxicity relative GLS drop",
"value": "> 15",
"unit": "% relative"
},
{
"label": "GLS change within noise",
"value": "< 8",
"unit": "% relative"
},
{
"label": "Speckle tracking frame rate",
"value": "50–80",
"unit": "fps"
}
],
"delta": null,
"pearl": "For strain, more negative is better; a relative 15% fall from the patient's own baseline is the cardio-oncology trigger.",
"lookalike": {
"vs": "Amyloid apical sparing vs HCM",
"discriminator": "Amyloid spares the apex with basal loss in all walls; HCM strain loss concentrates in the hypertrophied septum and the apex is not selectively preserved."
},
"related": [
"Q339",
"Q340",
"Q359",
"Q360"
],
"reviewed": "2026-08-26"
},
{
"id": "Q342",
"orig": 342,
"title": "Three-dimensional LV volumes",
"lesions": [
"LV_FUNCTION",
"INSTRUMENTATION"
],
"lens": "2d",
"items": [
{
"id": "Q342.1",
"q": "Why does 3D echo produce more accurate LV volumes than 2D, and how is the dataset acquired?",
"a": "Every 2D volume method fills in the unseen ventricle with an assumed shape, such as stacked disks in Simpson's method, and depends on the operator hitting the true apex. A 3D full-volume dataset contains the whole ventricle, so the software traces the endocardium in three dimensions and counts the voxels inside without assuming any shape, and there is no apex to foreshorten because the true long axis is chosen after acquisition. The result is that 3D volumes are systematically larger than 2D volumes and much closer to MRI, with better reproducibility. Acquisition uses a matrix-array transducer from the apical window; a full volume is usually built from several ECG-gated sub-volumes captured over 2–6 consecutive beats during a breath hold, then stitched."
},
{
"id": "Q342.2",
"q": "What are the principal artifacts and limitations of 3D LV acquisition?",
"a": "Stitching artifacts arise when the sub-volumes do not align, seen as step-like discontinuities across the dataset, and they come from patient breathing, translation of the probe, or an irregular rhythm such as atrial fibrillation or frequent ectopy that changes cavity size between beats. Single-beat acquisition avoids stitching but at a lower volume rate. Temporal resolution is the other trade-off: full-volume rates of about 20–30 volumes per second are far below 2D frame rates, so end-systole may be missed at fast heart rates and volumes are slightly underestimated. Spatial resolution, especially in the elevation plane, is poorer than 2D, so dropout of the lateral wall and the anterior apex is common and enhancing agents or a good acoustic window are prerequisites. Finally, the endocardial border in 3D is often traced outside the trabeculae, which is part of why 3D volumes run larger."
}
],
"numbers": [
{
"label": "Beats for multi-beat full volume",
"value": "2–6",
"unit": "beats"
},
{
"label": "Typical 3D volume rate",
"value": "20–30",
"unit": "volumes/s"
}
],
"delta": null,
"pearl": "3D trades time for space: no shape assumption and no foreshortening, but stitching and low volume rate are the price.",
"lookalike": {
"vs": "Stitching artifact vs true regional wall motion abnormality",
"discriminator": "A stitch is a straight, geometric seam that runs through all structures regardless of anatomy and disappears with single-beat acquisition."
},
"related": [
"Q339",
"Q343"
],
"reviewed": "2026-08-26"
},
{
"id": "Q343",
"orig": 343,
"title": "Errors in ejection fraction measurement",
"lesions": [
"LV_FUNCTION",
"MR"
],
"lens": "pitfall",
"items": [
{
"id": "Q343.1",
"q": "How do foreshortening, trabeculae, and off-axis imaging corrupt volume and EF measurements?",
"a": "Foreshortening occurs when the imaging plane cuts through the ventricle short of the true apex, typically because the transducer sits one interspace too high or too medial. The traced cavity is shorter and rounder, end-diastolic volume is underestimated, and the apical segments you are scoring are really mid-ventricular, so an apical infarct can be missed. The fix is to move down and lateral until the ventricle appears longest with the apex thinnest and least mobile. Trabeculae and papillary muscles should be included in the cavity, tracing the compacted-myocardium border; tracing inside them shrinks the volume and inflates EF. Off-axis parasternal images cut the ventricle obliquely, so linear diameters are overestimated and wall thickness looks greater than it is."
},
{
"id": "Q343.2",
"q": "Why is EF load-dependent, and how does mitral regurgitation produce a misleadingly high EF?",
"a": "Ejection fraction is a ratio of stroke volume to end-diastolic volume, and stroke volume is governed by preload, afterload, and contractility together. Dehydration lowers preload and can drop EF; vasodilation lowers afterload and raises it; a hypertensive crisis does the opposite, all without any change in intrinsic contractility. Significant mitral regurgitation adds a low-resistance exit for the ventricle: a large part of the total stroke volume goes backward into the atrium, so the ventricle empties well and EF looks normal or even supernormal while the forward output is reduced. This is why an EF that is only 'normal' in severe MR is already a sign of myocardial impairment, and why guidelines use an EF threshold of 60% rather than 50% to time surgery in primary MR."
}
],
"numbers": [
{
"label": "EF threshold for intervention in primary MR",
"value": "≤ 60",
"unit": "%"
}
],
"delta": null,
"pearl": "In severe MR a normal EF is a bad EF: the ventricle is unloading into the atrium, so the number flatters a failing pump.",
"lookalike": {
"vs": "Foreshortened apex vs apical hypertrophy",
"discriminator": "In a foreshortened view the 'thick apex' thins out and the cavity lengthens as you slide the probe down and lateral; true apical HCM persists with a spade-shaped cavity from every window."
},
"related": [
"Q339",
"Q342"
],
"reviewed": "2026-08-26"
},
{
"id": "Q344",
"orig": 344,
"title": "Right ventricular function thresholds",
"lesions": [
"RV_FUNCTION",
"PH"
],
"lens": "numbers",
"items": [
{
"id": "Q344.1",
"q": "Give the ASE 2015 abnormal thresholds for TAPSE, tricuspid annular S', and fractional area change, and explain what each one captures.",
"a": "TAPSE, measured by M-mode through the lateral tricuspid annulus in the apical 4-chamber view, is the distance the annulus travels toward the apex in systole; less than 17 mm is abnormal. It works because most RV ejection comes from longitudinal shortening rather than circumferential squeeze. S' is the tissue Doppler velocity of the same annulus, an abnormal value being under 9.5 cm/s; it is quicker to obtain and less dependent on frame rate than TAPSE. Fractional area change is the percentage change in RV cavity area between diastole and systole traced in an RV-focused 4-chamber view; below 35% is abnormal, and it is the only one of the three that also reflects the radial and outflow components of contraction."
},
{
"id": "Q344.2",
"q": "What values define RV dilation, RV hypertrophy, and abnormal RV free-wall strain?",
"a": "The basal RV diameter measured at end-diastole in the RV-focused apical view is dilated above 41 mm; the mid-cavity diameter is dilated above 35 mm. RV free-wall thickness measured in the subcostal view at end-diastole is normally under 5 mm, and greater than that indicates hypertrophy, which is the response to chronic pressure overload. RV free-wall longitudinal strain is abnormal when less negative than −20%; it is measured over the three free-wall segments only, excluding the septum, because septal strain is dominated by the left ventricle and would dilute the RV signal."
}
],
"numbers": [
{
"label": "TAPSE abnormal",
"value": "< 17",
"unit": "mm"
},
{
"label": "S' abnormal",
"value": "< 9.5",
"unit": "cm/s"
},
{
"label": "FAC abnormal",
"value": "< 35",
"unit": "%"
},
{
"label": "RV basal diameter dilated",
"value": "> 41",
"unit": "mm"
},
{
"label": "RV mid diameter dilated",
"value": "> 35",
"unit": "mm"
},
{
"label": "RV free-wall thickness hypertrophy",
"value": "> 5",
"unit": "mm"
},
{
"label": "RV free-wall strain abnormal",
"value": "> −20",
"unit": "%"
}
],
"delta": null,
"pearl": "17-9.5-35-41: TAPSE mm, S' cm/s, FAC %, basal diameter mm.",
"lookalike": null,
"related": [
"Q345",
"Q346",
"Q359",
"Q381",
"Q382"
],
"widgets": [
{
"id": "calc",
"opts": {
"k": "fac"
}
}
],
"reviewed": "2026-08-26"
},
{
"id": "Q345",
"orig": 345,
"title": "Imaging the right ventricle",
"lesions": [
"RV_FUNCTION",
"VIEWS",
"ANATOMY"
],
"lens": "2d",
"items": [
{
"id": "Q345.1",
"q": "Describe the RV-focused apical 4-chamber view and the other views needed to assess RV size and function.",
"a": "From the standard apical 4-chamber position you slide the transducer laterally and rotate slightly so that the RV free wall sits in the center of the sector and the RV appears at its maximum diameter, with the interventricular septum still fully visualized. This is the view for basal and mid diameters, FAC, TAPSE, S', and free-wall strain, and it is essential because the crescentic ventricle wraps around the LV and a standard 4-chamber cut frequently underestimates its width. The RV inflow view from the parasternal long axis shows the tricuspid valve and inferior wall; the parasternal short axis at the aortic level and the parasternal long axis of the RVOT show the outflow tract, where you measure the proximal RVOT diameter and PA. The subcostal view is best for RV wall thickness because the free wall lies perpendicular to the beam there."
},
{
"id": "Q345.2",
"q": "What anatomic features identify the right ventricle on echo, and what RV-to-LV size ratio indicates dilation?",
"a": "The morphologic right ventricle has a moderator band crossing the apical third of the cavity, coarser apical trabeculations, a tricuspid valve whose septal leaflet inserts more apically than the mitral, and no fibrous continuity between its inflow and outflow valves because the infundibulum separates them. In a properly obtained 4-chamber view a normal RV basal diameter is less than two-thirds of the LV, the RV does not share the apex, and the apex is formed by the LV. An RV:LV basal diameter ratio above 0.6 suggests dilation, above 1.0 marks severe dilation, and when the RV forms the apex in a non-foreshortened view it is dilated regardless of the ratio."
}
],
"numbers": [
{
"label": "RV:LV basal ratio normal",
"value": "< 0.6",
"unit": ""
},
{
"label": "RV:LV basal ratio severe dilation",
"value": "> 1.0",
"unit": ""
}
],
"delta": null,
"pearl": "The RV owns the moderator band and the apical tricuspid hinge; if it also owns the apex, it is dilated.",
"lookalike": {
"vs": "Prominent moderator band vs RV thrombus or tumor",
"discriminator": "The moderator band is a fixed, linear structure running from septum to free wall with the same echogenicity as myocardium and is present in every view; a mass is mobile, spherical, and attaches at one point."
},
"related": [
"Q344",
"Q346",
"Q383"
],
"reviewed": "2026-08-26"
},
{
"id": "Q346",
"orig": 346,
"title": "Traps in RV assessment",
"lesions": [
"RV_FUNCTION",
"PH",
"PROSTHETIC"
],
"lens": "pitfall",
"items": [
{
"id": "Q346.1",
"q": "Why are TAPSE and S' unreliable after cardiac surgery, and how does angle dependence affect them?",
"a": "TAPSE and S' are both one-dimensional measures of how far or how fast the lateral tricuspid annulus moves along the ultrasound beam, so they are strictly angle-dependent: if the annulus travels obliquely to the M-mode cursor or Doppler sample, the excursion and velocity are underestimated in proportion to the cosine of the angle. After pericardiotomy, coronary bypass, or valve surgery the RV loses longitudinal motion almost immediately, and TAPSE and S' fall by 30–40% and may never recover, even though global RV function is preserved. The mechanism appears to be loss of pericardial constraint and altered septal motion, with the RV switching to a more radial pattern of contraction. Fractional area change, 3D RV EF, and free-wall strain remain valid in these patients, so they should be the primary metrics after surgery."
},
{
"id": "Q346.2",
"q": "What is McConnell's sign, and why does foreshortening matter for the right ventricle?",
"a": "McConnell's sign is akinesis or severe hypokinesis of the RV mid free wall with preserved or hyperdynamic motion of the apex, classically described in acute pulmonary embolism. The apex likely appears to move because it is tethered to a vigorously contracting LV apex, while the free wall, suddenly loaded by acute pressure rise, fails. It is specific but not sensitive, and the same regional pattern appears in RV infarction, so it should prompt a search for thrombus, pulmonary pressure, and clinical context rather than settle the diagnosis. Foreshortening affects the RV even more than the LV: a standard 4-chamber view that is not RV-focused cuts the crescent obliquely and shrinks the basal diameter, so a dilated RV can be reported as normal, while an over-rotated view exaggerates it. Always confirm size from the RV-focused view and cross-check with the subcostal and short-axis appearance."
}
],
"numbers": [
{
"label": "Post-cardiac-surgery TAPSE/S' fall",
"value": "30–40",
"unit": "%"
}
],
"delta": null,
"pearl": "After the sternum has been opened, ignore a low TAPSE unless FAC and strain agree.",
"lookalike": {
"vs": "McConnell's sign in PE vs RV infarction",
"discriminator": "RV infarction usually shows inferior LV wall involvement on the same study and normal pulmonary pressures; PE shows a normal inferior wall, a raised TR velocity, and often a dilated RVOT with a short acceleration time."
},
"related": [
"Q344",
"Q345",
"Q382",
"Q383"
],
"reviewed": "2026-08-26"
},
{
"id": "Q347",
"orig": 347,
"title": "Normal chamber and vessel dimensions",
"lesions": [
"CHAMBER_QUANT",
"AORTA"
],
"lens": "numbers",
"items": [
{
"id": "Q347.1",
"q": "State the normal upper limits for left atrial volume index, LA anteroposterior diameter, and right atrial area.",
"a": "The left atrial volume indexed to body surface area is normal at 34 mL/m² or less, with 35–41 mildly, 42–48 moderately, and above 48 severely enlarged. Volume is preferred because the atrium enlarges asymmetrically and a single anteroposterior diameter from the parasternal long axis, roughly normal below 4.0 cm in men and 3.8 cm in women, underestimates remodeling that occurs in the superior-inferior and medial-lateral directions. Right atrial area traced at end-systole in the apical 4-chamber view is normal below 18 cm²; RA volume index is also reported, with sex-specific upper limits of about 32 mL/m² in men and 27 mL/m² in women."
},
{
"id": "Q347.2",
"q": "Give normal values for LV internal diameters, the aortic root, and the inferior vena cava.",
"a": "In the parasternal long axis the LV end-diastolic diameter is 4.2–5.8 cm in men and 3.8–5.2 cm in women, and the end-systolic diameter is roughly 2.5–4.0 cm in men and 2.2–3.5 cm in women. The aortic sinuses of Valsalva measured at end-diastole are normally 3.7 cm or less in men and 3.4 cm or less in women, or about 2.1 cm/m² when indexed, and the ascending aorta is generally under 3.5 cm. The inferior vena cava measured 1–2 cm from the RA junction in the subcostal view is normal at 2.1 cm or less with more than 50% collapse on a sniff, which corresponds to a right atrial pressure of about 3 mmHg."
}
],
"numbers": [
{
"label": "LAVi normal",
"value": "≤ 34",
"unit": "mL/m²"
},
{
"label": "LAVi mild / moderate / severe",
"value": "35–41 / 42–48 / > 48",
"unit": "mL/m²"
},
{
"label": "LA AP diameter men / women",
"value": "< 4.0 / < 3.8",
"unit": "cm"
},
{
"label": "RA area normal",
"value": "< 18",
"unit": "cm²"
},
{
"label": "RA volume index men / women",
"value": "≤ 32 / ≤ 27",
"unit": "mL/m²"
},
{
"label": "LVIDd men / women",
"value": "4.2–5.8 / 3.8–5.2",
"unit": "cm"
},
{
"label": "LVIDs men / women",
"value": "2.5–4.0 / 2.2–3.5",
"unit": "cm"
},
{
"label": "Sinuses of Valsalva men / women",
"value": "≤ 3.7 / ≤ 3.4",
"unit": "cm"
},
{
"label": "Aortic root indexed",
"value": "≈ 2.1",
"unit": "cm/m²"
},
{
"label": "IVC normal",
"value": "≤ 2.1",
"unit": "cm"
},
{
"label": "IVC collapse normal",
"value": "> 50",
"unit": "%"
}
],
"delta": null,
"pearl": "34 for the LA, 18 for the RA, 21 for the IVC in millimeters: three numbers that decide most chamber reports.",
"lookalike": null,
"related": [
"Q340",
"Q348",
"Q349",
"Q336",
"Q362",
"Q367",
"Q368",
"Q371",
"Q384"
],
"reviewed": "2026-08-26"
},
{
"id": "Q348",
"orig": 348,
"title": "How to measure the chambers correctly",
"lesions": [
"CHAMBER_QUANT",
"AORTA"
],
"lens": "best-method",
"items": [
{
"id": "Q348.1",
"q": "Why are chamber dimensions indexed to body surface area, and how should left atrial volume be measured?",
"a": "Heart size scales with body size, so a 5.6 cm ventricle is normal in a large man and dilated in a small woman. Dividing by body surface area removes most of that variation and lets a single cutoff serve everyone, which is why LA volume, LV volumes, aortic root, and RA volume are all reported indexed. LA volume should be measured at ventricular end-systole, the frame just before mitral opening when the atrium is largest, using either the biplane area-length method or biplane Simpson's method from dedicated apical 4- and 2-chamber views in which the atrium is not foreshortened. Trace the blood-tissue interface, exclude the pulmonary vein confluences and the appendage, and draw a straight line across the mitral annulus as the inferior border."
},
{
"id": "Q348.2",
"q": "What are the leading-edge conventions and timing rules for linear measurements of the LV and aorta?",
"a": "LV linear dimensions are taken in the parasternal long axis, perpendicular to the long axis at the level of the mitral leaflet tips, at end-diastole (the frame after mitral closure or the onset of the QRS) and at end-systole (the smallest cavity or the frame before mitral opening). Current ASE practice measures the LV cavity from the inner edge of the septum to the inner edge of the posterior wall, and wall thickness inner edge to inner edge, avoiding the older leading-edge-to-leading-edge method that folded a bit of endocardium into each measurement. For the aortic root the ASE 2015 document retains leading edge to leading edge at end-diastole, perpendicular to the long axis of the vessel, at the sinuses, sinotubular junction, and proximal ascending aorta, while some newer aortic guidance prefers inner edge to inner edge; report which convention you used so serial studies stay comparable."
}
],
"numbers": [
{
"label": "LA volume timing",
"value": "ventricular end-systole",
"unit": ""
},
{
"label": "Aortic root timing",
"value": "end-diastole",
"unit": ""
}
],
"delta": null,
"pearl": "Atrium biggest when ventricle smallest: measure LA volume at end-systole, LV cavity at end-diastole, and the aorta at end-diastole.",
"lookalike": null,
"related": [
"Q347",
"Q349"
],
"reviewed": "2026-08-26"
},
{
"id": "Q349",
"orig": 349,
"title": "Chamber measurement errors",
"lesions": [
"CHAMBER_QUANT"
],
"lens": "pitfall",
"items": [
{
"id": "Q349.1",
"q": "How does left atrial foreshortening arise, and what should and should not be included in the traced LA volume?",
"a": "The apical views are optimized for the ventricle, and the plane that shows the longest LV rarely shows the longest LA; the atrium sits behind and slightly to the right, so it is cut obliquely and its long axis is underestimated. Because volume calculations use the atrial length as a key term, even a small foreshortening reduces the reported LAVi and can move a patient from enlarged to normal. Acquire dedicated LA-focused clips in which the atrium appears longest, and check that the LA lengths in the 4- and 2-chamber views differ by no more than about 5 mm. The pulmonary vein confluences and the LA appendage are outpouchings rather than chamber, so they are excluded from the tracing; including them adds spurious volume, which is one reason older single-plane values ran inconsistently."
},
{
"id": "Q349.2",
"q": "How do incorrect timing and body surface area in obesity distort chamber quantification?",
"a": "Measuring the LA a few frames too early or too late misses its maximum volume, since the atrium is only at its largest for a brief window before mitral opening; using the ECG alone as a guide is unreliable, so identify the frame from the mitral leaflets. Similarly, LV end-diastolic diameter measured a frame after the onset of contraction is smaller than the true value and shifts EF upward. Indexing to body surface area assumes that cardiac size scales with total body mass, but adipose tissue adds body surface area without adding metabolic demand, so in severe obesity indexing divides the chamber by an inflated denominator and can hide true enlargement. Some labs index to height or lean mass in such patients, and at minimum the absolute values should be reported alongside the indexed ones."
}
],
"numbers": [
{
"label": "Acceptable LA length difference between apical views",
"value": "≤ 5",
"unit": "mm"
}
],
"delta": null,
"pearl": "A normal LAVi in a very obese patient may be a big atrium divided by a bigger body; look at the absolute volume too.",
"lookalike": {
"vs": "Pulmonary vein confluence vs atrial cavity",
"discriminator": "The vein enters as a tubular channel with Doppler flow directed into the atrium; the cavity has no such inflow signal and is bounded by a continuous curved wall."
},
"related": [
"Q347",
"Q348"
],
"reviewed": "2026-08-26"
},
{
"id": "Q350",
"orig": 350,
"title": "Microbubbles versus agitated saline",
"lesions": [
"CONTRAST",
"ASD"
],
"lens": "definition",
"items": [
{
"id": "Q350.1",
"q": "What is an ultrasound enhancing agent, and how does it differ physically from agitated saline?",
"a": "Commercial ultrasound enhancing agents such as Definity, Optison, and Lumason are suspensions of gas-filled microbubbles, typically perfluorocarbon or sulfur hexafluoride encapsulated in a lipid or albumin shell, with diameters of roughly 1–4 micrometers, smaller than a red cell. Because they are that small and their shell keeps the gas from dissolving, they pass through the pulmonary capillaries intact and reach the left heart, where they oscillate and emit harmonic signals that the scanner detects. Agitated saline is created at the bedside by pushing saline back and forth between two syringes, producing air bubbles tens of micrometers across with no shell. Those bubbles are filtered by the pulmonary capillaries and dissolve within a few beats, so in a normal circulation they opacify only the right heart."
},
{
"id": "Q350.2",
"q": "What does each agent demonstrate clinically?",
"a": "Because enhancing agents fill the LV cavity, they are used to delineate the endocardial border for volumes and wall motion, to expose an apical thrombus or non-compaction, and to characterize masses by their perfusion; with dedicated software they can also image myocardial perfusion. Agitated saline is a right-heart tracer used to test for shunts: bubbles appearing in the left atrium within three beats of RA opacification indicate an intracardiac communication such as a patent foramen ovale or ASD, whereas bubbles arriving after about five beats via the pulmonary veins indicate a pulmonary arteriovenous connection. It also confirms a persistent left SVC when injected in the left arm and the coronary sinus opacifies first. The essential difference is transit: agitated saline is only useful because it does not cross the lungs, whereas the commercial agents are only useful because they do."
}
],
"numbers": [
{
"label": "Enhancing agent microbubble size",
"value": "1–4",
"unit": "µm"
},
{
"label": "Intracardiac shunt: LA bubbles within",
"value": "≤ 3",
"unit": "beats"
},
{
"label": "Pulmonary AVM: LA bubbles after",
"value": "≥ 5",
"unit": "beats"
}
],
"delta": null,
"pearl": "Saline stays right, contrast goes left: pick the agent by whether you want the lungs to filter it.",
"lookalike": {
"vs": "Intracardiac shunt vs pulmonary AV malformation on bubble study",
"discriminator": "Intracardiac shunts deliver bubbles to the LA within three beats and often across a visible septal defect; pulmonary AVMs deliver them late, from the pulmonary veins, with a clean septum."
},
"related": [
"Q339",
"Q351"
],
"reviewed": "2026-08-26"
},
{
"id": "Q351",
"orig": 351,
"title": "Using ultrasound enhancing agents",
"lesions": [
"CONTRAST",
"PROCEDURE"
],
"lens": "procedure",
"items": [
{
"id": "Q351.1",
"q": "What are the ASE 2018 indications for an ultrasound enhancing agent, and how are the imaging settings adjusted?",
"a": "The principal indication is inadequate endocardial definition, defined as two or more contiguous LV segments not visualized in the apical views, since that degrades EF, regional wall motion, and stress echo interpretation. Additional indications are suspected apical thrombus or apical HCM, characterization of an intracardiac mass, suspected non-compaction, Doppler signal enhancement, and improving accuracy of LV volumes in serial studies. The scanner is switched to a contrast-specific mode with a low mechanical index, generally below 0.3, because higher energy destroys the bubbles; the transmit frequency and focus are set so that the agent resonates while tissue is suppressed. Inject slowly, roughly 0.5 mL boluses or a dilute infusion, and wait for attenuation in the near field to clear; too much agent shadows the basal segments. If the cavity is over-filled or you want a perfusion assessment, a brief high-MI flash destroys the bubbles and lets you watch replenishment."
},
{
"id": "Q351.2",
"q": "What are the safety considerations and contraindications, and how have they changed?",
"a": "Serious reactions are rare, on the order of 1 in 10,000, mostly anaphylactoid responses within minutes of injection, so the patient is observed for 30 minutes and resuscitation equipment must be available. The only firm contraindication is prior hypersensitivity to the agent or its components, including polyethylene glycol for Definity and Lumason. Following large registry data, the FDA in 2017 removed the earlier contraindications for right-to-left, bidirectional, or transient right-to-left shunts and for pulmonary hypertension, and the agents are now considered safe in critically ill patients, in pregnancy when needed, and in those with prosthetic valves. Agents should not be injected intra-arterially, and a high mechanical index should be avoided during the injection to limit microvascular bioeffects."
}
],
"numbers": [
{
"label": "Mechanical index for contrast imaging",
"value": "< 0.3",
"unit": ""
},
{
"label": "Segments unseen triggering use",
"value": "≥ 2 contiguous",
"unit": "segments"
},
{
"label": "Serious reaction rate",
"value": "≈ 1 in 10,000",
"unit": ""
},
{
"label": "Post-injection observation",
"value": "30",
"unit": "min"
}
],
"delta": null,
"pearl": "Low MI to see the bubbles, high MI flash to pop them; the shunt and PH warnings are gone, hypersensitivity is what remains.",
"lookalike": {
"vs": "Near-field attenuation from too much agent vs basal akinesis",
"discriminator": "Attenuation shadows the entire basal region including the septum and lateral wall together and clears as the bolus washes out; a true wall motion abnormality persists at the same segment in every injection."
},
"related": [
"Q339",
"Q350"
],
"reviewed": "2026-08-26"
},
{
"id": "Q352",
"orig": 352,
"title": "Performing a transesophageal echo",
"lesions": [
"TEE",
"PROCEDURE"
],
"lens": "procedure",
"items": [
{
"id": "Q352.1",
"q": "How is a patient prepared for TEE, and what are the contraindications?",
"a": "The patient fasts for 4–6 hours for solids and at least 2 hours for clear liquids to lower aspiration risk, and a focused history covers dysphagia, odynophagia, hematemesis, known esophageal disease, prior esophageal or gastric surgery, and cervical spine instability. Absolute contraindications are esophageal stricture, tumor, perforation, active varices with recent bleeding, and a perforated viscus; relative ones include a large hiatal hernia, Zenker's diverticulum, esophageal varices, recent upper GI surgery, severe coagulopathy, and prior chest radiation. Any unexplained dysphagia warrants evaluation before the study. Dentures come out, IV access is established, and continuous ECG, pulse oximetry, and blood pressure monitoring are applied. Topical pharyngeal anesthesia is followed by moderate sedation, usually midazolam with or without fentanyl, or propofol when an anesthesia provider is present."
},
{
"id": "Q352.2",
"q": "Describe positioning, probe handling, and the complications you counsel patients about.",
"a": "The patient lies in the left lateral decubitus position with the neck slightly flexed, which drops the tongue forward, keeps saliva draining out of the mouth, and lines up the esophagus for passage. The probe is inspected before every case for bite marks or insulation breaks, checked for electrical leakage as scheduled, and inserted with a bite block in place, advancing gently with the patient swallowing rather than pushing against resistance. Probe temperature is monitored and imaging pauses automatically if the tip exceeds about 41–42 °C, because sustained heat can injure the mucosa. After the study the probe undergoes high-level disinfection according to the manufacturer. Major complications occur in under 0.2% of studies and include esophageal perforation, bleeding, aspiration, arrhythmia, and oversedation; minor ones are sore throat, transient hoarseness, and lip or dental trauma. Patients are observed until sedation wears off and instructed not to eat until the pharyngeal anesthesia has resolved and not to drive that day."
}
],
"numbers": [
{
"label": "NPO solids",
"value": "4–6",
"unit": "h"
},
{
"label": "NPO clear liquids",
"value": "≥ 2",
"unit": "h"
},
{
"label": "Probe temperature limit",
"value": "≈ 41–42",
"unit": "°C"
},
{
"label": "Major complication rate",
"value": "< 0.2",
"unit": "%"
}
],
"delta": null,
"pearl": "Ask about swallowing before you ask about the valve: unexplained dysphagia is a stop sign for TEE.",
"lookalike": null,
"related": [
"Q353"
],
"reviewed": "2026-08-26"
},
{
"id": "Q353",
"orig": 353,
"title": "When TEE beats TTE and vice versa",
"lesions": [
"TEE",
"PROSTHETIC",
"ENDOCARDITIS"
],
"lens": "best-method",
"items": [
{
"id": "Q353.1",
"q": "For which questions is TEE clearly superior to transthoracic echo, and why?",
"a": "The esophagus sits directly behind the left atrium, so a high-frequency probe there images posterior structures without lung or rib interference and at far better resolution. That makes TEE the standard for the left atrial appendage and its thrombus before cardioversion or ablation, for mitral prosthetic regurgitation, where the transthoracic view is blocked by acoustic shadowing of the sewing ring and the regurgitant jet lies on the atrial side, and for endocarditis, where small vegetations, leaflet perforation, and aortic root abscess are seen with sensitivity above 90% versus roughly 50–60% by TTE. TEE visualizes the thoracic aorta from root to descending segment for dissection with sensitivity near 98% and shows the intimal flap and entry tear. The interatrial septum is imaged in profile, so PFO and secundum ASD are sized with rims measured for device closure, and the sinus venosus defect and anomalous pulmonary venous return, which are near the SVC and invisible transthoracically, are identified in the bicaval view."
},
{
"id": "Q353.2",
"q": "Where does transthoracic echo remain the better test?",
"a": "The LV apex is the region farthest from the esophagus and closest to the chest wall, so an apical thrombus, apical aneurysm, or apical HCM is better seen transthoracically, especially with an enhancing agent, and can be missed on TEE where the apex is in the far field and often foreshortened. Doppler alignment is the other advantage: the apical windows line the beam up with LVOT and aortic outflow, so peak gradients across a stenotic aortic valve or prosthesis and LVOT VTI for stroke volume are reliably obtained from the chest, whereas TEE views the outflow tract at an angle from the deep transgastric position and tends to underestimate velocities. TTE also provides the subcostal IVC for RA pressure, is non-invasive and repeatable for serial follow-up, and is the appropriate first test in nearly every scenario, with TEE reserved for the specific questions it answers better."
}
],
"numbers": [
{
"label": "TEE sensitivity for vegetations",
"value": "> 90",
"unit": "%"
},
{
"label": "TTE sensitivity for vegetations",
"value": "≈ 50–60",
"unit": "%"
},
{
"label": "TEE sensitivity for aortic dissection",
"value": "≈ 98",
"unit": "%"
}
],
"delta": null,
"pearl": "TEE for what lies behind the heart (appendage, mitral prosthesis, septum, aorta); TTE for the apex and for any gradient you need aligned.",
"lookalike": {
"vs": "LAA thrombus vs pectinate muscles on TEE",
"discriminator": "Pectinate muscles are multiple, parallel ridges continuous with the appendage wall and present in every angle; a thrombus is a discrete, often mobile mass with different echogenicity, usually accompanied by dense spontaneous echo contrast and low appendage emptying velocity."
},
"related": [
"Q352",
"Q387",
"Q393"
],
"reviewed": "2026-08-26"
},
{
"id": "Q354",
"orig": 354,
"title": "Why low-flow low-gradient AS exists",
"lesions": [
"AS",
"HEMODYNAMICS"
],
"lens": "definition",
"items": [
{
"id": "Q354.1",
"q": "Explain how a truly severe aortic valve can produce a mean gradient below 40 mmHg.",
"a": "The gradient is generated by flow, not by the valve alone: ΔP = 4v², and velocity is stroke volume divided by orifice area over the ejection time. When the ventricle ejects a small stroke volume — because it is weak (reduced EF) or small and stiff (preserved EF with concentric remodeling) — even a fixed 0.8 cm² orifice passes blood slowly and the gradient falls into the 20–39 mmHg range. The area calculation still reports a small valve, so the measurements disagree: AVA says severe, gradient says moderate. Roughly a third of small-AVA patients are discordant like this, and the work-up exists to decide whether the valve or the flow explains it."
},
{
"id": "Q354.2",
"q": "Define the four flow–gradient categories of aortic stenosis.",
"a": "High-gradient AS: Vmax ≥ 4 m/s or mean ≥ 40 mmHg, with AVA usually ≤ 1.0 cm² — severe regardless of flow. Classical low-flow low-gradient: AVA ≤ 1.0 cm², mean < 40, SVi ≤ 35 mL/m², EF < 50% (ACC/AHA stage D2). Paradoxical low-flow low-gradient: the same valve numbers with SVi ≤ 35 and EF ≥ 50% (stage D3). Normal-flow low-gradient: AVA ≤ 1.0, mean < 40, SVi > 35, EF ≥ 50% — which by fluid dynamics is usually moderate AS or a measurement error and carries the outcome of moderate AS."
}
],
"numbers": [
{
"label": "Low flow",
"value": "≤ 35",
"unit": "mL/m² SVi"
},
{
"label": "Severe AVA / indexed",
"value": "≤ 1.0 / ≤ 0.6",
"unit": "cm² / cm²/m²"
},
{
"label": "High gradient",
"value": "≥ 4 / ≥ 40",
"unit": "m/s / mmHg"
},
{
"label": "High flow that inflates gradients",
"value": "> 58",
"unit": "mL/m² SVi"
},
{
"label": "Discordant grading prevalence",
"value": "~ 1/3",
"unit": "of small-AVA patients"
}
],
"delta": null,
"pearl": "Gradient needs flow. Small AVA + small gradient = ask how much blood was crossing the valve.",
"lookalike": null,
"related": [
"Q60",
"Q64",
"Q355",
"Q356",
"Q357",
"Q358",
"Q364"
],
"reviewed": "2026-08-27"
},
{
"id": "Q355",
"orig": 355,
"title": "Classical LFLG AS and dobutamine",
"lesions": [
"AS",
"STRESS",
"LV_FUNCTION"
],
"lens": "best-method",
"items": [
{
"id": "Q355.1",
"q": "How is low-dose dobutamine stress echo performed and read in low-flow low-gradient AS with reduced EF?",
"a": "Start at 2.5–5 µg/kg/min and increase every 3–5 minutes to 10–20 µg/kg/min, recording LVOT VTI, aortic velocity and mean gradient, stroke volume, AVA (same LVOT diameter throughout) and biplane EF at each stage. Stop when the result is positive, when heart rate rises more than 10–20 bpm over baseline or above 100, or with symptoms, hypotension or arrhythmia. Flow reserve means stroke volume rises by more than 20%. True severe AS: the AVA stays ≤ 1.0 cm² while Vmax reaches ≥ 4 m/s or mean gradient ≥ 30–40 mmHg at any flow. Pseudo-severe AS: the AVA rises above 1.0 cm² as flow increases, meaning a moderately diseased valve was under-opening at low flow. Without flow reserve the test cannot grade the valve, and the CT calcium score takes over."
},
{
"id": "Q355.2",
"q": "What is the projected AVA and why was it introduced?",
"a": "Because patients augment flow by different amounts, their peak-dose AVAs are not comparable. The projected AVA extrapolates each patient's AVA to a standard normal flow rate of 250 mL/s using the slope of AVA against flow between rest and peak (flow = stroke volume ÷ ejection time). A projected AVA ≤ 1.0 cm² indicates true severe AS; it reclassifies patients whose gradient never reached the severe range simply because flow rose too little."
}
],
"numbers": [
{
"label": "Dobutamine dose range",
"value": "2.5–5 → 20",
"unit": "µg/kg/min"
},
{
"label": "Flow reserve",
"value": "> 20",
"unit": "% SV increase"
},
{
"label": "True severe at any flow",
"value": "AVA ≤ 1.0 with Vmax ≥ 4 or mean ≥ 30–40",
"unit": ""
},
{
"label": "Projected AVA reference flow",
"value": "250",
"unit": "mL/s"
},
{
"label": "Stop when HR rises",
"value": "> 10–20 over baseline or > 100",
"unit": "bpm"
}
],
"delta": null,
"pearl": "Reserve tests the ventricle; the AVA at peak tests the valve. No reserve → CT calcium.",
"lookalike": null,
"related": [
"Q354",
"Q356",
"Q205",
"Q358"
],
"reviewed": "2026-08-27"
},
{
"id": "Q356",
"orig": 356,
"title": "Paradoxical LFLG AS: the integrated approach",
"lesions": [
"AS",
"HTN",
"LV_FUNCTION"
],
"lens": "best-method",
"items": [
{
"id": "Q356.1",
"q": "Describe the patient and the pitfalls of paradoxical low-flow low-gradient AS.",
"a": "The typical patient is elderly, often a woman, with long-standing hypertension: a small hypertrophied ventricle with impaired longitudinal function and a small stroke volume despite a normal EF. Before accepting the label, hunt for measurement error, because this is where LVOT under-measurement does the most harm: re-measure the LVOT in a zoomed mid-systolic PLAX, confirm it with 3D TEE or CT if available, check that the PW sample sits where the diameter was measured, repeat the aortic velocity from every window, and measure when the patient is normotensive. Dobutamine helps less in a small hyperdynamic ventricle."
},
{
"id": "Q356.2",
"q": "Which findings raise the likelihood of true severe AS when AVA < 1.0 cm² and mean gradient < 40 mmHg with preserved EF?",
"a": "EACVI/ASE 2017 list: physical examination consistent with severe AS; typical symptoms without another explanation; age over 70; LVH (allowing for hypertension); reduced longitudinal LV function; mean gradient 30–40 mmHg; AVA ≤ 0.8 cm²; low flow confirmed by a technique other than standard Doppler (3D TEE or CT LVOT, CMR, invasive data); and a CT calcium score in the likely or very likely range — men ≥ 2000 / ≥ 3000, women ≥ 1200 / ≥ 1600 Agatston units, with < 1600 / < 800 making severe AS unlikely."
}
],
"numbers": [
{
"label": "Calcium score severe likely (men / women)",
"value": "≥ 2000 / ≥ 1200",
"unit": "AU"
},
{
"label": "Calcium score severe very likely",
"value": "≥ 3000 / ≥ 1600",
"unit": "AU"
},
{
"label": "Calcium score severe unlikely",
"value": "< 1600 / < 800",
"unit": "AU"
},
{
"label": "AVA that favours true severe",
"value": "≤ 0.8",
"unit": "cm²"
},
{
"label": "Mean gradient grey zone",
"value": "30–40",
"unit": "mmHg"
}
],
"delta": null,
"pearl": "Small thick ventricle, small stroke volume, normal EF: measure the LVOT twice, then let the CT calcium score decide.",
"lookalike": {
"vs": "normal-flow low-gradient AS",
"discriminator": "SVi ≤ 35 mL/m² (with EF ≥ 50%) is paradoxical LFLG; SVi > 35 with a small AVA is normal-flow low-gradient, which behaves like moderate AS and usually reflects measurement error."
},
"related": [
"Q354",
"Q355",
"Q358"
],
"reviewed": "2026-08-27"
},
{
"id": "Q357",
"orig": 357,
"title": "Measurement errors behind discordant AS grading",
"lesions": [
"AS",
"INSTRUMENTATION"
],
"lens": "pitfall",
"items": [
{
"id": "Q357.1",
"q": "List the technical errors that create a falsely small AVA or falsely low gradient.",
"a": "LVOT diameter: measured in diastole, off-axis, or at a different level from the PW sample — the diameter is squared, so 1 mm changes AVA by about 10%, and the elliptical LVOT makes 2D underestimate area. LVOT VTI: sample volume too far from the valve (under-reads) or in the valve (over-reads with a closing click). Aortic velocity: only one window used, angle error, or gain too low, giving a low Vmax and gradient. Mean gradient: traced inside the envelope. Physiology: hypertension at the time of the study lowers the gradient; a small ascending aorta produces pressure recovery so Doppler overstates the gradient the ventricle sees; AF and post-PVC beats need averaging and exclusion. DVI (LVOT VTI ÷ AV VTI, severe < 0.25) sidesteps the LVOT diameter and is the quickest cross-check."
}
],
"numbers": [
{
"label": "AVA change per 1 mm LVOT error",
"value": "~ 10",
"unit": "%"
},
{
"label": "DVI severe",
"value": "< 0.25",
"unit": "ratio"
},
{
"label": "Pressure recovery matters when ascending aorta",
"value": "< 30",
"unit": "mm"
},
{
"label": "Beats to average in AF",
"value": "≥ 5",
"unit": ""
}
],
"delta": null,
"pearl": "Before you call the flow low, prove the LVOT right.",
"lookalike": null,
"related": [
"Q63",
"Q64",
"Q201",
"Q354"
],
"reviewed": "2026-08-27"
},
{
"id": "Q358",
"orig": 358,
"title": "Intervention recommendations in LFLG AS",
"lesions": [
"AS",
"PROCEDURE"
],
"lens": "numbers",
"items": [
{
"id": "Q358.1",
"q": "What do the guidelines recommend for symptomatic low-flow low-gradient AS once severity is confirmed?",
"a": "Classical LFLG with reduced EF: intervention is a class I recommendation — ACC/AHA 2020 for stage D2 when AVA stays ≤ 1.0 cm² at any dobutamine dose, ESC/EACTS 2021 when flow reserve is present (IIa without reserve), and ESC 2025 recommends intervention after confirmation of severity irrespective of flow reserve, because outcomes improve even without reserve. Paradoxical LFLG with preserved EF: class IIa in both systems — intervention should be considered after careful confirmation that the stenosis is severe and is the likely cause of symptoms. For work-up, ESC 2025 gives a class I to dobutamine stress echo and/or CT calcium scoring when EF is 50% or less, and the calcium score is the key adjunct when EF is preserved."
},
{
"id": "Q358.2",
"q": "What else changed for aortic stenosis in the 2025 ESC/EACTS guideline?",
"a": "New trial evidence supports intervening in severe AS irrespective of symptoms, EF and flow reserve, so asymptomatic severe AS moves toward earlier intervention; moderate AS with LV dysfunction is recognised as an active research area; the choice between TAVI and SAVR is framed around age, anatomy and Heart Team judgement rather than surgical-risk scores alone; and the document emphasises sex differences — paradoxical LFLG is a major cause of under-recognised severe AS in women."
}
],
"numbers": [
{
"label": "Classical LFLG, symptomatic, confirmed severe",
"value": "Class I",
"unit": "intervention"
},
{
"label": "Paradoxical LFLG, symptomatic, confirmed",
"value": "Class IIa",
"unit": "intervention"
},
{
"label": "DSE and/or CT calcium when EF ≤ 50% (ESC 2025)",
"value": "Class I",
"unit": "work-up"
}
],
"delta": {
"was": "2011-era teaching: low gradient with reduced EF meant 'pseudo-stenosis unless dobutamine proves otherwise', and absent contractile reserve was treated as a reason not to operate.",
"now": "ESC 2025: intervene in confirmed severe LFLG AS irrespective of flow reserve; DSE and/or CT calcium score class I for work-up with EF ≤ 50%; paradoxical LFLG recognised and treated (IIa).",
"source": "EACVI/ASE 2017 AS focused update · ESC/EACTS 2021 & 2025 VHD · ACC/AHA 2020 VHD"
},
"pearl": "Confirm, then treat: reserve changes risk, not the indication.",
"lookalike": null,
"related": [
"Q354",
"Q355",
"Q356"
],
"reviewed": "2026-08-27"
},
{
"id": "Q359",
"orig": 359,
"title": "Strain, prosthetic and right-heart standards at a glance",
"lesions": [
"LV_FUNCTION",
"PROSTHETIC",
"RV_FUNCTION"
],
"lens": "numbers",
"items": [
{
"id": "Q359.1",
"q": "Give the headline numbers from the 2025 strain, 2024 prosthetic valve and 2025 right-heart guidelines.",
"a": "Strain (ASE/EACVI 2025): LV GLS normal more negative than −18%, borderline −16 to −18%, abnormal less negative than −16%; a relative change of 10–15% is significant; RV free-wall strain lower limit −20% men / −21% women; LA reservoir strain normal 23–60%, < 18% suggests raised LAP; amyloid apical sparing when apical strain exceeds twice the rest. Prosthetic valves (ASE 2024): aortic prosthesis significant stenosis when Vmax ≥ 4 m/s, mean ≥ 35 mmHg, DVI < 0.25, acceleration time > 100 ms with a rounded contour; aortic PPM severe at indexed EOA ≤ 0.65 cm²/m² (≤ 0.55 if BMI ≥ 30), mitral severe ≤ 0.90 (≤ 0.75 obese); grade change from the 1–3-month baseline. Right heart (ASE 2025): TAPSE > 17 mm, S′ > 9.5 cm/s, FAC > 35%, RV strain more negative than −20%, RV wall < 5 mm, RA area < 19 cm², RAP 3/8/15 mmHg around a 2.1 cm IVC, PH suggested by TR ≥ 2.9 m/s or ≥ 2.8 with two adjunctive signs, RVOT acceleration time > 105 ms normal, TAPSE/PASP 0.3–0.4 mm/mmHg = RV–PA uncoupling."
}
],
"numbers": [
{
"label": "LV GLS abnormal",
"value": "less negative than −16",
"unit": "%"
},
{
"label": "RV free-wall strain LLN (m / f)",
"value": "−20 / −21",
"unit": "%"
},
{
"label": "LARS raised LAP",
"value": "< 18",
"unit": "%"
},
{
"label": "Prosthetic AV significant stenosis DVI / AT",
"value": "< 0.25 / > 100",
"unit": "ratio / ms"
},
{
"label": "Aortic PPM severe iEOA (BMI < 30 / ≥ 30)",
"value": "≤ 0.65 / ≤ 0.55",
"unit": "cm²/m²"
},
{
"label": "Mitral PPM severe iEOA",
"value": "≤ 0.9",
"unit": "cm²/m²"
},
{
"label": "PH suggested by TR",
"value": "≥ 2.9 (or ≥ 2.8 + 2 signs)",
"unit": "m/s"
},
{
"label": "RV–PA uncoupling TAPSE/PASP",
"value": "0.3–0.4",
"unit": "mm/mmHg"
}
],
"delta": null,
"pearl": "−16, −20, 18: GLS, RV strain, LARS. 0.25 and 100: prosthetic DVI and acceleration time.",
"lookalike": null,
"related": [
"Q102",
"Q112",
"Q267",
"Q341",
"Q344"
],
"reviewed": "2026-08-27"
},
{
"id": "Q360",
"orig": 360,
"title": "Cardio-oncology and amyloid red flags",
"lesions": [
"LV_FUNCTION",
"RCM"
],
"lens": "definition",
"items": [
{
"id": "Q360.1",
"q": "Define cancer-therapy-related cardiac dysfunction and the echo surveillance that detects it.",
"a": "ESC 2022 cardio-oncology: asymptomatic mild CTRCD is EF ≥ 50% with a relative GLS decline of more than 15% and/or a new troponin or natriuretic peptide rise; moderate is EF 40–49% (a new drop of ≥ 10 points, or a smaller drop with GLS or biomarker change); severe is EF below 40%. Surveillance means a baseline 3D or biplane EF and GLS before anthracyclines, HER2-targeted therapy or chest radiotherapy, repeated on a risk-based schedule with the same vendor, and the 2025 strain consensus treats a relative GLS fall of 12–15% as the trigger to consider cardioprotection."
},
{
"id": "Q360.2",
"q": "Which echo findings should make you suspect cardiac amyloidosis?",
"a": "Increased wall thickness (≥ 12 mm, concentric, RWT > 0.42) that is out of proportion to ECG voltage and hypertension history; thick RV free wall, valves and interatrial septum; biatrial enlargement; small pericardial effusion; grade II–III diastolic dysfunction with e′ < 5 cm/s and E/e′ > 15 while EF is low-normal; and a global longitudinal strain that is impaired basally with relative apical sparing — apical strain more than twice the rest of the ventricle. Echo raises the suspicion; bone-tracer scintigraphy and light-chain testing make the diagnosis (ASE 2023 multimodality guideline)."
}
],
"numbers": [
{
"label": "Mild CTRCD GLS relative decline",
"value": "> 15",
"unit": "%"
},
{
"label": "Moderate CTRCD EF",
"value": "40–49",
"unit": "%"
},
{
"label": "Severe CTRCD EF",
"value": "< 40",
"unit": "%"
},
{
"label": "Amyloid wall thickness",
"value": "≥ 12",
"unit": "mm"
},
{
"label": "Apical sparing ratio",
"value": "> 2",
"unit": "× rest of LV"
}
],
"delta": null,
"pearl": "Thick walls with small voltages and a cherry-on-top bull's-eye: think amyloid before 'hypertensive heart'.",
"lookalike": null,
"related": [
"Q148",
"Q150",
"Q341",
"Q364",
"Q378"
],
"reviewed": "2026-08-27"
},
{
"id": "Q361",
"orig": 361,
"title": "Bicuspid valve and its aortopathy",
"lesions": [
"AS",
"AORTA",
"COARCT"
],
"lens": "etiology",
"items": [
{
"id": "Q361.1",
"q": "You count two cusps and a raphe in the short axis of a 26-year-old. Why does the study not end at the valve?",
"a": "Both are left-heart obstructive lesions arising from shared abnormal embryologic development and altered fetal flow patterns; they cluster together far more often than chance. A majority of patients with coarctation also have a bicuspid aortic valve. Whenever you see a bicuspid valve, sweep to the suprasternal notch to interrogate the aortic isthmus for coarctation — and vice versa. Record the peak velocity through the isthmus and watch for forward flow that persists into diastole, then confirm from the subcostal window that the abdominal aortic waveform is still crisply pulsatile."
},
{
"id": "Q361.2",
"q": "The bicuspid valve opens widely with a peak velocity of 1.4 m/s. Does a normal gradient let you skip the aortic measurements?",
"a": "Bicuspid valve disease includes an intrinsic aortopathy (medial wall abnormality) plus eccentric jet flow, both of which dilate the ascending aorta independent of stenosis severity. Aortic dilation develops in a large fraction of bicuspid-valve patients over time, so a normal gradient predicts nothing about the wall. Always measure the ascending aorta when you identify a bicuspid valve, even if the valve works well. Report the sinuses of Valsalva, the sinotubular junction and the tubular ascending aorta as three separate end-diastolic numbers from a zoomed parasternal long axis, and move to a high right parasternal window when the widest segment sits above the standard image."
},
{
"id": "Q361.3",
"q": "A 46-year-old presents with heavily calcified aortic stenosis. What substrate does the age point to?",
"a": "The abnormal two-cusp geometry generates turbulent flow and accelerated calcific degeneration, so bicuspid valves tend to stenose decades earlier than tricuspid valves. In an adult with calcific AS who is younger than expected, look closely at cusp number. Heavy calcium buries the original architecture, so pull up any earlier study, where a less calcified valve often shows the two-cusp opening plainly. Then measure the ascending aorta in the same sitting, because the aortopathy travels with the valve whatever the gradient turns out to be."
},
{
"id": "Q361.4",
"q": "A 22-year-old is referred for concentric hypertrophy with no history of hypertension. What must you exclude before calling it hypertensive heart disease?",
"a": "The fixed obstruction creates chronic LV pressure overload and upper-body hypertension, driving compensatory hypertrophy. Unexplained LVH in a young patient warrants excluding coarctation. Take septal and posterior wall thickness in the parasternal long axis and calculate LV mass index, then go to the suprasternal notch for the isthmus rather than accepting essential hypertension at that age. Ask for a simultaneous arm and leg cuff pressure, because a systolic gradient above 20 mmHg settles the question faster than a poor suprasternal window will."
}
],
"numbers": [],
"pearl": "A bicuspid valve is never only a valve finding: measure the aorta above it and interrogate the isthmus beyond it.",
"related": [
"Q62",
"Q65",
"Q178",
"Q303",
"Q306",
"Q310"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "degenerative calcific aortic stenosis in an older patient",
"discriminator": "Bicuspid disease stenoses one to two decades earlier, domes in systole with two commissures and a raphe, and carries a dilated ascending aorta; degenerative disease calcifies the cusp bodies, leaves three commissures, and spares the aortic wall."
},
"delta": null
},
{
"id": "Q362",
"orig": 362,
"title": "Turner syndrome aortic surveillance",
"lesions": [
"COARCT",
"AORTA",
"CONGENITAL"
],
"lens": "vignette",
"items": [
{
"id": "Q362.1",
"q": "A 17-year-old girl, 145 cm tall, with primary amenorrhea and a webbed neck is sent for a screening echo. Which cardiac lesion are you most likely to find, and where do you look for it?",
"a": "45,X monosomy strongly predisposes to left-heart obstructive lesions; the bicuspid aortic valve is the most common cardiac finding in Turner syndrome. Bicuspid valve is seen in roughly a quarter to a third of Turner patients. Screen every Turner patient for a bicuspid valve and aortopathy. Zoom the parasternal short axis at the leaflet tips and step through systolic frames to establish cusp number and any raphe, then measure the sinuses and ascending aorta in the long axis. The valve is not an incidental note here, because it compounds the aortopathy that makes this syndrome dangerous."
},
{
"id": "Q362.2",
"q": "The valve is bicuspid. Which second left-heart obstruction do you now have to exclude, and how often is it there?",
"a": "The same predisposition to left-heart obstruction makes coarctation a classic Turner-associated lesion. It is less common than the bicuspid valve and is one of several contributors to the elevated aortic dissection risk, alongside the intrinsic Turner aortopathy, the bicuspid valve, and hypertension. Reported rates run from 7 to 30 percent depending on how the series was ascertained, an order of magnitude of spread around the commonly quoted 10 percent. Image the isthmus from the suprasternal notch, run continuous wave through the narrowing for the peak velocity and a diastolic tail, then sample the abdominal aorta subcostally for a damped waveform."
},
{
"id": "Q362.3",
"q": "Her ascending aorta measures 3.4 cm and the previous report called it normal. Why is that reassurance premature?",
"a": "Turner syndrome carries an intrinsic aortopathy (abnormal aortic wall elasticity/medial properties) compounded by frequent bicuspid aortic valve and coarctation, driving dilation of the ascending aorta and dissection at smaller absolute diameters than the general population. Risk is amplified by hypertension and pregnancy. Aortic dilation is already present in about 23 percent of these patients. Because patients are short, index the aorta to body size: an aortic size index (ASI) >2.5 cm/m2 (or >=2.0 with a risk factor) flags high dissection risk and is a pregnancy contraindication. Measure the sinuses and ascending aorta carefully (PLAX/suprasternal) and screen even with a normal absolute diameter. Note ASI has low sensitivity, so absolute diameter and TS-specific z-scores are complementary. TS there means Turner syndrome, not tricuspid stenosis. At 145 cm her body surface area is about 1.3 m², so 3.4 cm indexes to roughly 2.6 cm/m² and is already past the threshold the previous report never applied."
},
{
"id": "Q362.4",
"q": "The same patient, now 26 and 24 weeks pregnant, arrives with sudden interscapular pain; her aorta measured 3.6 cm three months ago. What is the working diagnosis?",
"a": "Intrinsic medial/elastic abnormality of the aortic wall plus high prevalence of bicuspid aortic valve, coarctation, and hypertension predisposes to type A dissection, often at smaller, 'normal-appearing' aortic diameters than in other aortopathies. Cumulative lifetime dissection risk runs about 1 to 2.5 percent, roughly a hundred times the general population, and it concentrates in young adults and in pregnancy. Maintain a low threshold for dissection in Turner patients with chest/back pain even when the aorta looks only mildly dilated; serial indexed measurements and pre-pregnancy aortic imaging (echo plus CT/MRI) are essential because catastrophic dissection can occur at modest diameters. Scan the root and ascending aorta in the long axis and the arch from the suprasternal notch for an intimal flap, look for new aortic regurgitation and pericardial fluid, and take her to TEE or CT if the transthoracic study is unrevealing."
}
],
"numbers": [
{
"label": "Turner aortic size index, high dissection risk",
"value": "> 2.5",
"unit": "cm/m²"
},
{
"label": "Bicuspid aortic valve in Turner syndrome",
"value": "25–33",
"unit": "%"
},
{
"label": "Turner dissection risk vs the general population",
"value": "~ 100",
"unit": "× higher"
}
],
"pearl": "In Turner syndrome the aorta dissects at diameters that would be called normal in anyone else, so index it rather than merely measuring it.",
"related": [
"Q284",
"Q303",
"Q309",
"Q347"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "Marfan syndrome",
"discriminator": "Marfan dilates the sinuses of Valsalva into a pear-shaped root in a tall patient; Turner dilates the tubular ascending aorta in a short one, which is why absolute diameter misleads and the aortic size index is required."
},
"delta": null
},
{
"id": "Q363",
"orig": 363,
"title": "Aortic root dilation and dissection",
"lesions": [
"AORTA",
"EFFUSION"
],
"lens": "numbers",
"items": [
{
"id": "Q363.1",
"q": "Where does the Marfan aorta enlarge first, and which measurement carries the surveillance?",
"a": "Defective fibrillin-1 weakens the aortic media, so the sinuses of Valsalva dilate progressively — the cardinal cardiovascular feature of Marfan syndrome. Measure at the sinuses of Valsalva and index to body size; root dilation drives prophylactic surgery thresholds. Take that diameter in a zoomed parasternal long axis, perpendicular to the long axis of the vessel and at end-diastole, and keep the sinus number separate from the tubular ascending aorta. A sinus diameter above 4.0 cm starts surveillance imaging and 5.0 cm is the elective repair threshold in Marfan, so the sinus measurement, not the widest number anywhere in the aorta, is the one the operation is timed from."
},
{
"id": "Q363.2",
"q": "A report reads 'dilated aorta, 4.6 cm.' What makes that sentence useless, and what should it have said?",
"a": "Aortopathy can involve the root, the tubular ascending aorta, or both; dilation at one level may accompany the other because of a shared medial/connective-tissue process — but the two are partly distinct phenotypes (a root-dominant Marfan pattern vs a tubular-ascending degenerative/bicuspid pattern) and do not always progress together. A single number with no level attached cannot be compared with the last study or matched to a surgical threshold. Report the annulus, sinuses of Valsalva, sinotubular junction and proximal ascending aorta as four separate end-diastolic measurements, and state whether you measured leading edge to leading edge or inner edge to inner edge, because the two conventions differ by 2 to 4 mm. Serial studies only mean something when the same level is measured the same way."
},
{
"id": "Q363.3",
"q": "A 31-year-old with Marfan syndrome has a root that has gone from 4.4 to 4.9 cm in a year. What does the growth rate tell you that the diameter does not?",
"a": "Fibrillin-1 deficiency causes cystic medial degeneration that weakens the aortic media, predisposing to progressive root/ascending aneurysm and ultimately type A dissection — the leading cause of death in Marfan syndrome. Risk scales with root diameter and growth rate. Measure the aortic root at the sinuses of Valsalva, indexed to body size, and track the growth rate across studies — not just the absolute number. An intimal flap, new AR, or pericardial effusion in a dilated root is a type A dissection emergency (Loeys-Dietz dissects at smaller calibers). Growth above 0.3 to 0.5 cm per year is itself an operative trigger and drops the Marfan repair threshold from 5.0 cm to 4.5 cm, so 0.5 cm in a year turns a 4.9 cm root into an operative conversation before it ever reaches the usual diameter."
},
{
"id": "Q363.4",
"q": "You find a flap in a dilated root and a new rim of pericardial fluid. What has happened, and what must not be done next?",
"a": "A Stanford type A dissection involving the ascending aorta can rupture or weep retrograde into the pericardial sac (the proximal ascending aorta lies within the pericardial reflection), producing acute hemopericardium. Because blood accumulates rapidly, even a modest volume causes acute tamponade. In any patient with a dilated aortic root, an intimal flap, or new aortic regurgitation, look immediately for pericardial fluid: a new effusion in suspected type A dissection signals impending or active tamponade and is a surgical emergency. Avoid aggressive full pericardiocentesis, which can re-expand the false lumen and accelerate fatal rupture; controlled drainage as a bridge to the OR is preferred. Sweep subcostally for the fluid, for right atrial and right ventricular diastolic collapse, and for a plethoric IVC, and call the surgeon while you finish the study, because this complicates roughly 15 to 20 percent of acute type A dissections."
}
],
"numbers": [
{
"label": "Pericardial effusion in acute type A dissection",
"value": "15–20",
"unit": "%"
}
],
"pearl": "Fluid around the heart in a dissected root is not a finding to grade: it is a phone call to the surgeon.",
"related": [
"Q77",
"Q118",
"Q194",
"Q195",
"Q284"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "degenerative or bicuspid ascending aortopathy",
"discriminator": "Marfan balloons the sinuses and effaces the sinotubular junction; degenerative and bicuspid disease widen the tubular ascending aorta above a relatively spared root, which is why the level of the measurement decides the diagnosis."
},
"delta": null
},
{
"id": "Q364",
"orig": 364,
"title": "Severe aortic stenosis beyond the gradient",
"lesions": [
"AS",
"RCM",
"LV_FUNCTION"
],
"lens": "pitfall",
"items": [
{
"id": "Q364.1",
"q": "Why does the ventricle in aortic stenosis grow thick rather than large, and how does that geometry set a trap for the gradient?",
"a": "Chronic outflow obstruction raises LV systolic pressure; the ventricle hypertrophies concentrically to normalize wall stress (Laplace's law). The wall thickens while the cavity stays small, so the stroke volume it ejects falls even while the ejection fraction reads normal. Calculate the stroke volume index from the LVOT diameter and velocity-time integral in every thick-walled stenotic valve, because a value at or below 35 mL/m² is what turns a genuinely severe valve into a sub-40 mmHg gradient. Read a thick wall and a small cavity as a warning that the gradient is about to under-report the disease."
},
{
"id": "Q364.2",
"q": "A 79-year-old has a calcified aortic valve, a mean gradient of 28 mmHg, walls of 15 mm and low ECG voltage. Which second diagnosis is hiding behind that low gradient?",
"a": "Amyloid (especially wild-type ATTR) and calcific aortic stenosis share an elderly population and frequently coexist. Amyloid infiltration produces a low-flow state that, superimposed on a calcified valve, yields the low-flow / low-gradient severe AS phenotype where gradients underestimate true severity. Conversely, paradoxical low-gradient AS with thick walls and low ECG voltage should trigger a search for occult amyloid. Severe AS with wall thickness > 14 mm, apical-sparing strain, a small effusion and low ECG voltage is probably low-flow/low-gradient AS on an amyloid substrate — use dobutamine or projected AVA and refer for bone scintigraphy rather than grading on resting gradients alone. The 14 mm figure is the higher bar used once a calcified valve is already in play; 12 mm is the threshold that starts an amyloid search when nothing else explains the wall. ATTR amyloid turns up in roughly 8 to 16 percent, about one in seven, of elderly patients with severe AS referred for TAVR."
},
{
"id": "Q364.3",
"q": "An 82-year-old with severe AS keeps returning with iron-deficiency anemia and no source found at endoscopy. What connects the valve to the bleeding?",
"a": "High shear stress across the stenotic aortic valve mechanically unfolds von Willebrand factor multimers, exposing the A2 domain (Tyr1605-Met1606 scissile bond) to cleavage by ADAMTS13. Loss of high-molecular-weight vWF multimers produces an acquired type 2A von Willebrand syndrome, impairing platelet adhesion and causing bleeding from GI angiodysplastic lesions. Aortic valve replacement (surgical or transcatheter) restores vWF multimers and is curative in roughly 80% of cases. In an older patient with severe AS and unexplained iron-deficiency anemia or recurrent GI (angiodysplasia) bleeding, think Heyde and quantify AS rigorously (peak velocity, mean gradient, AVA, dimensionless index). Documenting severe AS supports AVR, which often cures the bleeding by restoring vWF multimers. Subclinical von Willebrand abnormalities are common in severe AS; the full overt triad with gastrointestinal bleeding is not."
}
],
"numbers": [
{
"label": "Heyde bleeding resolved by aortic valve replacement",
"value": "~ 80",
"unit": "%"
}
],
"pearl": "When the aortic gradient is low it is the least reliable witness in the study: read the walls, the flow, and the hemoglobin.",
"related": [
"Q61",
"Q248",
"Q256",
"Q354",
"Q360"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "moderate aortic stenosis with a genuinely low gradient",
"discriminator": "Moderate AS has a valve area above 1.0 cm² and a dimensionless index above 0.25 with normal flow; severe low-flow low-gradient AS keeps the small area and index while the stroke volume index falls to 35 mL/m² or less."
},
"delta": null
},
{
"id": "Q365",
"orig": 365,
"title": "Myxomatous prolapse and flail leaflet",
"lesions": [
"MVP",
"MR",
"AORTA"
],
"lens": "2d",
"items": [
{
"id": "Q365.1",
"q": "A 24-year-old with dilated sinuses of Valsalva also has bileaflet prolapse. Why do the aorta and the mitral valve fail in the same patient?",
"a": "The same connective-tissue defect causes myxomatous, redundant mitral leaflets that prolapse. Fibrillin-1 builds the mitral leaflet as well as the aortic media, so a Marfan study that stops at the root has done half the job. Measure leaflet displacement beyond the annular plane in the parasternal long axis, record leaflet thickness, and grade the regurgitation at every visit. The two lesions run on separate clocks: a root repaired on time does nothing for a mitral valve heading toward its own operation, and in Marfan the mitral valve is the second surgical problem these patients bring."
},
{
"id": "Q365.2",
"q": "A previously well 58-year-old has flash pulmonary edema, a flail posterior scallop, and a left atrium and left ventricle that both measure normal. Why do the chamber sizes argue against you here?",
"a": "Myxomatous degeneration elongates and weakens the chordae; when a chord ruptures the leaflet loses its tethering and whips into the left atrium — the structural extreme of prolapse. A prolapsing leaflet bulges past the annular plane with its tip still toward the LV, whereas a flail leaflet has its tip pointing into the atrium, producing acute, usually severe, eccentric MR directed away from the affected leaflet. Scan frame-by-frame on PLAX / A4C / A3C for a leaflet TIP that points into the LA and for a mobile torn chord. The eccentric jet hugs the atrial wall (Coanda effect) and underestimates severity — grade with vena contracta and PISA, not jet area. Chronic severe MR dilates both chambers over years, so their size is the usual corroboration for a severe grade. An acute flail drives the same volume into an atrium that has had no time to stretch, so normal chamber sizes are the expected finding rather than reassurance."
}
],
"numbers": [],
"pearl": "Prolapse points its tip at the ventricle and flail points it at the atrium, and in an acute flail the normal-sized chambers are the disease, not the reassurance.",
"related": [
"Q1",
"Q44",
"Q51",
"Q215",
"Q217"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "chronic severe degenerative MR",
"discriminator": "Chronic MR has an enlarged left atrium and ventricle and a well-tolerated clinical course; acute flail MR has normal chamber sizes, a soft murmur, and pulmonary edema out of proportion to everything else on the study."
},
"delta": null
},
{
"id": "Q366",
"orig": 366,
"title": "Rheumatic disease across the valves",
"lesions": [
"MS",
"MR",
"AS"
],
"lens": "etiology",
"items": [
{
"id": "Q366.1",
"q": "The anterior mitral leaflet bows into the ventricle while its tip stays tethered. In which part of the cardiac cycle must you be looking to see that, and where do you set the planimetry plane?",
"a": "Rheumatic inflammation fuses the commissures and thickens the leaflet tips, producing the classic 'hockey-stick' diastolic doming and a fixed orifice. Rheumatic disease is the dominant cause of mitral stenosis worldwide. The doming is a diastolic finding, so scroll to mid-diastole in PLAX; in systole the same valve closes almost normally and gives nothing away. Planimeter in the PSAX view at the leaflet tips rather than at the annulus, sweeping from base to apex until the orifice is smallest, and drop the gain until the fish-mouth border just disappears, because excess gain shrinks the traced area."
},
{
"id": "Q366.2",
"q": "A rheumatic mitral valve is both narrowed and leaking. Is that a second diagnosis, and how should it change what you measure?",
"a": "It is one lesion, not two. Leaflet retraction and restricted motion from rheumatic scarring often produce mixed mitral disease — stenosis plus regurgitation. Quantify both in the same study: planimeter the orifice in the PSAX mitral view and take the mean gradient from CW inflow, then measure vena contracta and map jet direction in the apical four- and two-chamber views. A coexisting leak inflates the transmitral gradient and shortens the pressure half-time, so a PHT-derived valve area reads falsely large in exactly the valve where you most need it."
},
{
"id": "Q366.3",
"q": "You have confirmed rheumatic mitral stenosis. What else has to be on the report before you end the study, and why?",
"a": "Rheumatic disease can involve the aortic valve as well, typically when the mitral valve is already affected. When rheumatic mitral disease is present, interrogate the aortic valve too. Look in the PSAX aortic view for commissural fusion with triangular systolic doming rather than the lumpy cusp calcification of degenerative disease, then take peak velocity and mean gradient from the apical five-chamber view and compute valve area by continuity."
}
],
"numbers": [],
"pearl": "Rheumatic disease fuses the tips and retracts the leaflets, so it hands you stenosis and regurgitation in the same valve, and it rarely stops at the mitral.",
"related": [
"Q36",
"Q42",
"Q67",
"Q89",
"Q219"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "calcific mitral stenosis from annular calcification",
"discriminator": "Rheumatic disease fuses the commissures and thickens the tips while the leaflet bodies stay mobile and dome; annular calcification builds at the base with free commissures, so there is no fish-mouth orifice and nothing a balloon can split."
},
"delta": null
},
{
"id": "Q367",
"orig": 367,
"title": "Consequences of a stenotic mitral valve",
"lesions": [
"MS",
"PH",
"ARRHYTHMIA"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q367.1",
"q": "A study shows a strikingly dilated left atrium beside a normal-sized left ventricle. How does mitral stenosis create that mismatch, and how should you record the atrial size?",
"a": "The stenotic valve obstructs LA emptying, so chronically elevated LA pressure dilates the atrium. Record left atrial volume index from biplane tracings in the apical four- and two-chamber views at ventricular end-systole rather than from the PLAX diameter alone, because the atrium enlarges asymmetrically and a single linear dimension underestimates it. Above 34 mL/m² is abnormal. In long-standing mitral stenosis the atrium often outgrows the sector, so widen the sector and drop the transmit frequency to get the whole chamber in rather than truncating the trace at the screen edge."
},
{
"id": "Q367.2",
"q": "What does significant mitral stenosis predict about the right heart, and which measurement should never be missing from the report?",
"a": "Elevated LA pressure transmits backward into the pulmonary circulation, producing post-capillary (and later reactive) pulmonary hypertension. Estimate PASP from the TR jet in any significant mitral stenosis. Take peak TR velocity with CW from the apical four-chamber and RV inflow views, apply 4v², and add an RA pressure estimated from IVC size and collapse in the subcostal window. Report that pressure beside the mean gradient and valve area, because pulmonary pressure, not the valve area alone, is what pushes a symptomatic patient toward commissurotomy."
},
{
"id": "Q367.3",
"q": "Your patient with rheumatic mitral stenosis drops into an irregularly irregular rhythm during the study. What has changed about your measurements?",
"a": "The dilated, pressure-loaded left atrium of mitral stenosis is highly arrhythmogenic; atrial fibrillation is a common and clinically pivotal complication. Losing atrial contraction removes the A wave and shortens diastole at fast rates, so the mean gradient climbs even though the orifice has not changed. Average it over at least five consecutive beats and report the heart rate beside it, then interrogate the atrium and appendage for spontaneous echo contrast and thrombus, which is a TEE question, because mitral stenosis with atrial fibrillation carries one of the highest embolic risks in valvular heart disease."
}
],
"numbers": [],
"pearl": "The valve area tells you the lesion; the rhythm and the TR jet tell you what it has already cost.",
"related": [
"Q38",
"Q40",
"Q172",
"Q347"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "pulmonary hypertension from left ventricular disease",
"discriminator": "Mitral stenosis raises pulmonary pressure with a normal-sized, normally contracting left ventricle; left ventricular disease raising the same pressure comes with a dilated or stiff ventricle and an elevated E/e′."
},
"delta": null
},
{
"id": "Q368",
"orig": 368,
"title": "The calcified mitral annulus",
"lesions": [
"MS",
"MR",
"ARRHYTHMIA"
],
"lens": "pitfall",
"items": [
{
"id": "Q368.1",
"q": "An 84-year-old has a mean mitral gradient of 7 mmHg and a shelf of calcium along the posterior annulus. Why will your usual valve-area methods mislead you here?",
"a": "Calcium deposition in the fibrous annulus extends into the leaflet bases, displaces the mitral hinge points into the LV inlet, and encroaches on the orifice while restricting (especially anterior) leaflet excursion. The result is degenerative (calcific) mitral stenosis with a non-commissural mechanism, unlike rheumatic MS. This is an increasingly recognized cause of stenosis in older adults, accounting for about 60 percent of mitral stenosis over the age of 80, although clinically significant valve dysfunction occurs in only about 10 percent of patients with annular calcification. Unlike rheumatic MS, MAC-related MS spares the commissures (no fish-mouth), so planimetry and the Hatle pressure-half-time are unreliable; favor mean gradient and continuity-based methods, but note continuity is also corrupted when calcium invades the LVOT/aorto-mitral curtain. Acoustic shadowing degrades Doppler alignment, so use multiple windows."
},
{
"id": "Q368.2",
"q": "The posterior annulus is a rigid calcified bar and there is a 7 mmHg diastolic gradient. Which of the two lesions is the more likely one, and which one will the shadow hide?",
"a": "Annular calcification stiffens the mitral annulus and impairs its systolic sphincteric contraction, and calcium extending onto the leaflet bases tethers/restricts leaflet coaptation, producing degenerative mitral regurgitation. MR is actually more common than MS in MAC. When you see a rigid, calcified posterior annulus, interrogate carefully for both MR and MS in the same valve; shadowing can hide a regurgitant jet, so use off-axis and apical color Doppler with the annulus out of the acoustic shadow (or TEE). Among patients with significant valve dysfunction from annular calcification, regurgitation runs about 10 to 12 percent against 2 to 7 percent for stenosis. Note also that the same regurgitation invalidates a continuity-derived valve area, so on this valve the mean gradient is often the only number left standing."
},
{
"id": "Q368.3",
"q": "You are about to sign out mitral annular calcification as an incidental age-related finding. What does that finding actually predict?",
"a": "MAC is best understood as a marker of left atrial myopathy, systemic/valvular atherosclerosis, and shared risk factors (hypertension, age, LV hypertrophy, diastolic dysfunction). These promote atrial remodeling and elevated LA pressure, increasing AF risk. In prospective cohorts MAC independently predicts incident AF (MESA HR ~1.9), an effect only partially mediated by LA enlargement, so MAC is a robust risk marker rather than a proven direct mechanical cause. Treat MAC as more than an incidental finding: it independently predicts incident AF and stroke. Reporting MAC severity should prompt attention to LA size, diastolic function, and thromboembolic risk stratification. Measure the calcium's thickness and its circumferential extent in PLAX and PSAX, so the severity you report is a measurement rather than an adjective."
}
],
"numbers": [
{
"label": "MAC as the cause of mitral stenosis over age 80",
"value": "~ 60",
"unit": "%"
},
{
"label": "MR among MAC patients with significant valve dysfunction",
"value": "10–12",
"unit": "%"
},
{
"label": "MS among MAC patients with significant valve dysfunction",
"value": "2–7",
"unit": "%"
}
],
"pearl": "Calcium at the base leaks more often than it stenoses, shadows the very jet you need to see, and predicts the rhythm you will find on the next study.",
"related": [
"Q52",
"Q219",
"Q337",
"Q347"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "rheumatic mitral stenosis",
"discriminator": "Rheumatic disease fuses the commissures, so planimetry and pressure half-time work and a balloon can split it; annular calcification spares the commissures, so both methods fail and there is nothing to split."
},
"delta": null
},
{
"id": "Q369",
"orig": 369,
"title": "Mechanisms of severe mitral regurgitation",
"lesions": [
"MR",
"CAD",
"ENDOCARDITIS"
],
"lens": "etiology",
"items": [
{
"id": "Q369.1",
"q": "The jet direction has told you the anterior leaflet failed. The surgeon now wants a scallop. Which cuts give you one?",
"a": "Prolapsing or flail myxomatous leaflets fail to coapt, producing an eccentric MR jet directed away from the affected leaflet. Map jet direction — it points away from the prolapsing leaflet and helps localize the lesion. Direction narrows it to a leaflet; only a systematic sweep narrows it to a segment. The PLAX and apical three-chamber planes cut A2 and P2, and a slow apical four-chamber sweep moves from A3 and P3 medially, through A2 and P2, to A1 and P1 laterally as you tilt anteriorly. Name the segment in the impression, because a posterior P2 prolapse is a routine resection and an anterior A2 prolapse is a harder repair."
},
{
"id": "Q369.2",
"q": "An ejection fraction of 22 percent with a dilated spherical ventricle and moderate MR. Is the valve the problem, and what do you tell the team about how this leak may behave?",
"a": "LV dilation displaces the papillary muscles and dilates the mitral annulus, tethering the leaflets and producing secondary (functional) MR. Functional MR severity tracks with LV remodeling and may improve with guideline-directed therapy. Document the geometry that drives it, recording LV end-diastolic dimension, sphericity, and leaflet tenting height and area at mid-systole in the apical views. Then repeat the quantification after guideline-directed therapy rather than treating today's grade as the patient's fixed severity, because the same valve can drop a grade when the ventricle is unloaded."
},
{
"id": "Q369.3",
"q": "A febrile patient has mitral regurgitation that was absent on a study six months ago. Why does that one change carry so much weight?",
"a": "Vegetations destroy leaflet tissue and may cause perforation, producing new or worsening regurgitation. New regurgitation in the right clinical setting is itself a diagnostic criterion. Document the mass on the atrial side of the leaflets in the apical four-chamber and PLAX views, recording size, mobility and attachment site, and move to TEE when the transthoracic images cannot settle it."
},
{
"id": "Q369.4",
"q": "You already suspect papillary muscle rupture in a post-infarct patient who has collapsed. Which two findings on this study will falsely reassure you?",
"a": "Acute infarction can rupture a papillary muscle head, abruptly detaching chordae so the supported leaflet segment prolapses into the atrium and produces torrential acute MR. The posteromedial muscle is far more vulnerable because it has a single coronary supply, so rupture classically follows an inferior/posterior MI. Days after an inferior MI, sudden flash pulmonary edema and shock should trigger a hunt for a flail leaflet with a mobile mass swinging between LV and LA. The murmur may be soft because LA pressure equalizes fast — do not be reassured by auscultation; this is a surgical emergency. The soft murmur is the first, and the ejection fraction is the second: it is often preserved, so a vigorous-looking ventricle is no reassurance either. Rupture complicates roughly 1 percent of acute infarcts and ranks among the most lethal mechanical complications, so neither finding buys you time."
}
],
"numbers": [
{
"label": "Papillary muscle rupture after acute MI",
"value": "~ 1",
"unit": "%"
}
],
"pearl": "Ask what actually failed, the leaflet, the ventricle that holds it, or the cord that anchors it, because the mechanism and not the jet chooses the operation.",
"related": [
"Q51",
"Q99",
"Q160",
"Q215",
"Q250",
"Q321"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "post-infarction ventricular septal rupture",
"discriminator": "Both collapse days after an infarct; septal rupture gives a harsh murmur with a thrill and a mosaic transseptal jet with right heart overload, while papillary rupture gives a soft murmur, a flail leaflet with a mobile head, and an intact septum."
},
"delta": null
},
{
"id": "Q370",
"orig": 370,
"title": "Leaflet and root causes of AR",
"lesions": [
"AR",
"AORTA",
"VSD"
],
"lens": "etiology",
"items": [
{
"id": "Q370.1",
"q": "A 26-year-old with a bicuspid valve has a peak aortic velocity of only 1.8 m/s but moderate aortic regurgitation. Why can a bicuspid valve leak long before it ever stenoses?",
"a": "Asymmetric cusps and a raphe impair coaptation, allowing diastolic regurgitation; AR can dominate over stenosis especially in younger patients. Define the morphology in the PSAX aortic view in systole and count the commissures there rather than in diastole, because a closed raphe mimics a third one. An eccentric closure line predicts the eccentric jet you will meet on PLAX, and that is exactly the jet the jet-width-to-LVOT ratio overestimates, so quantify with vena contracta at the origin and holodiastolic reversal in the descending aorta from the suprasternal notch, adding pressure half-time from CW in the apical five-chamber view."
},
{
"id": "Q370.2",
"q": "The aortic cusps look thin, mobile and structurally normal, yet there is a central AR jet. Where does the lesion actually live?",
"a": "Dilation of the aortic root effaces the sinotubular junction and splays the commissures outward (with sinus enlargement), pulling the cusp free edges apart so they no longer coapt centrally — regurgitation despite structurally normal leaflets. Annular dilation can contribute, but the relatively fixed annulus is usually not the primary driver. When you see AR, assess the root: 'functional' AR from root dilation is repaired differently than leaflet disease. Measure the annulus, sinuses of Valsalva, sinotubular junction and proximal ascending aorta separately on PLAX, because a root-driven leak is fixed by remodeling the root while a cusp-driven leak is fixed at the cusp, and the four diameters are what tell the surgeon which operation this is."
},
{
"id": "Q370.3",
"q": "New aortic regurgitation appears in a patient being treated for endocarditis, and the PR interval has lengthened since admission. What should you suspect?",
"a": "Aortic vegetations can perforate or prevent coaptation, and may extend to a root abscess — a surgical red flag. Aortic IE with new AR and conduction disease suggests a perivalvular abscess. The conduction tissue runs immediately beneath the aortic root at the membranous septum, so treat a lengthening PR interval as an anatomic warning rather than an incidental rhythm change, and take the patient to TEE."
},
{
"id": "Q370.4",
"q": "You find a perimembranous VSD on PLAX. Which valve must you interrogate in the same view, and what decides the timing of surgery?",
"a": "In perimembranous and especially outlet/subarterial VSDs, the muscular support beneath the adjacent aortic cusp (typically the right coronary cusp) is deficient. The high-velocity left-to-right shunt jet generates a Venturi effect that, combined with the unsupported cusp, draws the cusp downward into the defect during diastole, producing progressive aortic cusp prolapse and regurgitation (Laubry-Pezzi syndrome). Whenever you see a perimembranous or subarterial VSD on PLAX, deliberately interrogate the aortic valve in the same view and A5C for cusp override, abnormal motion, and a diastolic AR jet. The right coronary cusp prolapsing into the LVOT/defect is the classic sign; AR often worsens even as the VSD partially closes, so the prolapse, not shunt size, drives surgery. Cusp prolapse and regurgitation complicate roughly 5 to 10 percent of perimembranous defects overall, and up to 50 percent of outlet or subarterial ones, particularly in Asian populations."
}
],
"numbers": [
{
"label": "Aortic cusp prolapse with a perimembranous VSD",
"value": "5–10",
"unit": "%"
},
{
"label": "Aortic cusp prolapse with an outlet or subarterial VSD",
"value": "up to 50",
"unit": "%"
}
],
"pearl": "Thin mobile cusps with a central jet mean the lesion is the root, and the root, not the valve, is what gets replaced.",
"related": [
"Q221",
"Q222",
"Q284",
"Q292",
"Q318"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "cusp disease from a bicuspid valve or endocarditis",
"discriminator": "Root dilation gives a central jet with structurally normal cusps and an effaced sinotubular junction; cusp disease gives an eccentric jet with a raphe, prolapse or a perforation away from the coaptation line."
},
"delta": null
},
{
"id": "Q371",
"orig": 371,
"title": "Atrial enlargement to appendage thrombus",
"lesions": [
"ARRHYTHMIA",
"MASS",
"DIASTOLIC"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q371.1",
"q": "A hypertensive man with a 14 mm septum has a left atrial volume index of 41 mL/m² and no mitral valve disease. What band does that number sit in, and why does the band matter more than the number?",
"a": "A stiff hypertrophied ventricle raises diastolic filling pressure; the left atrium enlarges as it works against that resistance — a marker of diastolic dysfunction. LA enlargement is the 'HbA1c' of diastolic dysfunction — it reflects chronically elevated filling pressure. Grade it rather than reporting it: 34 mL/m² or less is normal, 35 to 41 mildly enlarged, 42 to 48 moderately and above 48 severely. At 41 he is one point below moderate, so the next study either confirms a stable atrium or documents a tier change, and it is the tier change, not the raw figure, that the referring team can act on."
},
{
"id": "Q371.2",
"q": "The same man returns two years later in atrial fibrillation. What connects the atrium you measured then to the rhythm now, and why does the process accelerate once it starts?",
"a": "Atrial stretch and remodeling create the structural substrate for atrial fibrillation; the arrhythmia in turn enlarges the atrium — a self-reinforcing loop. Losing organized contraction removes the atrial kick and lets the chamber dilate further, so every year in fibrillation makes the next year of fibrillation easier to sustain. On this study the mitral inflow has no A wave and the velocities swing beat to beat, so average five or more consecutive cycles before you report any Doppler number, and re-measure the volume index in both apical views to document how far the chamber has moved."
},
{
"id": "Q371.3",
"q": "Cardiology wants this patient cardioverted this afternoon and the anticoagulation history is unclear. What must the study exclude first, and which window will actually show it?",
"a": "Loss of organized atrial contraction causes blood stasis in the left atrial appendage, where thrombus forms — the source of cardioembolic stroke. Before cardioversion, exclude appendage thrombus with TEE when anticoagulation is uncertain. Restoring sinus rhythm restores atrial contraction, which can eject a clot that has been sitting quietly for weeks. Transthoracic imaging does not see the appendage reliably, so sweep the mid-esophageal views through the full multiplane arc, since a clot hides easily in a second or third lobe that one angle never displays."
},
{
"id": "Q371.4",
"q": "You find a mobile echodensity in the appendage of a patient admitted with a middle cerebral artery stroke. Trace how that clot became this stroke.",
"a": "Stasis in the left atrium/appendage (atrial fibrillation, mitral stenosis) produces spontaneous echo contrast and organized thrombus, usually in the LAA. Dislodged thrombus enters the systemic circulation and embolizes preferentially to the brain, causing cardioembolic stroke; >90% of AF-related LA thrombi arise in the LAA. TTE poorly visualizes the LAA; TEE is the reference standard (sens 93-100%) and is guideline-indicated to exclude appendage thrombus before cardioversion or LAA closure when anticoagulation is inadequate. Grade spontaneous echo contrast ('smoke') and measure LAA emptying velocity (<20 cm/s denotes high stasis/thrombus risk). What you find depends on who you are scanning, running about 3 percent in unselected or anticoagulated atrial fibrillation and up to about 14 percent in non-anticoagulated patients presenting for cardioversion, and both thrombus and dense smoke are strongly associated with prior and future thromboembolism."
}
],
"numbers": [
{
"label": "TEE sensitivity for left atrial appendage thrombus",
"value": "93–100",
"unit": "%"
},
{
"label": "LAA thrombus before cardioversion without anticoagulation",
"value": "~ 14",
"unit": "%"
}
],
"pearl": "The stroke was forecast years earlier by a number you had already measured, and the last chance to act on it is the appendage velocity before you cardiovert.",
"related": [
"Q38",
"Q329",
"Q333",
"Q347"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "a pectinate muscle ridge in the appendage",
"discriminator": "A pectinate ridge is linear, continuous with the wall and seen in every plane; thrombus is separable from the wall in two planes and usually sits in dense spontaneous echo contrast with an emptying velocity under 20 cm/s."
},
"delta": null
},
{
"id": "Q372",
"orig": 372,
"title": "Hypertrophic cardiomyopathy and dynamic obstruction",
"lesions": [
"HCM",
"LV_FUNCTION"
],
"lens": "2d",
"items": [
{
"id": "Q372.1",
"q": "A normotensive 34-year-old man has a 19 mm septum and an 11 mm posterior wall. What does that ratio settle, and what does it leave open?",
"a": "HCM is defined by inappropriate hypertrophy, classically asymmetric septal thickening with a septal-to-posterior-wall ratio ≥1.3. This septum is 1.7 times the posterior wall in a young man with no pressure load, so the ratio settles that the hypertrophy is asymmetric and not explained by afterload. Distinguish from hypertensive LVH (usually concentric) and infiltrative mimics like amyloid. It does not settle athlete's heart, which is the mimic that matters at 34: training thickens the wall modestly while enlarging the cavity, so an LV end-diastolic diameter above 55 mm with normal diastolic function argues for the athlete no matter how the ratio reads."
},
{
"id": "Q372.2",
"q": "Classic teaching says Venturi suction pulls the anterior mitral leaflet into the outflow tract. Why is drag now considered the dominant force, and where on the study do you see it?",
"a": "A protruding septum — often with anteriorly displaced papillary muscles and elongated mitral leaflets — redirects early systolic flow so that drag, the pushing force of the flow, sweeps the anterior mitral leaflet into the outflow tract (SAM). Drag, not the classically-taught Venturi suction, is now considered the dominant force: SAM begins at low LVOT velocities, before significant Venturi forces develop. Look for SAM on PLAX and M-mode — it is the engine of dynamic obstruction. On the mitral M-mode the anterior leaflet steps forward in mid-systole and may touch the septum, while PLAX and the apical three-chamber show the leaflet tip and chordae entering the outflow tract, often with a bright contact plaque on the septum where they have struck it for years."
},
{
"id": "Q372.3",
"q": "The resting outflow gradient in a breathless HCM patient is 18 mmHg. Does that number exclude obstructive disease?",
"a": "Roughly a third of HCM patients have resting obstruction and many more become obstructive with provocation, defining obstructive HCM. A resting 18 mmHg rules out resting obstruction and nothing more, because the label depends on the highest gradient you can produce rather than the one the patient happens to have while lying still. Record the LVOT with continuous wave from the apical five- and three-chamber views at rest, then again during Valsalva strain and after the patient stands, and take the study to exercise if the symptoms are exertional and the bedside maneuvers stay quiet. Report the resting and provoked values separately, since 30 mmHg or more defines obstruction and 50 mmHg or more identifies the patient who may be offered septal reduction."
}
],
"numbers": [
{
"label": "HCM patients with resting LVOT obstruction",
"value": "~ 33",
"unit": "%"
}
],
"pearl": "The septum makes the diagnosis, the mitral leaflet makes the obstruction, and only provocation makes it visible.",
"related": [
"Q135",
"Q139",
"Q140",
"Q247",
"Q248"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "athlete's heart",
"discriminator": "The athlete has a large cavity with a wall usually at or under 13 mm, brisk e′, and regression on deconditioning; HCM keeps a small cavity behind the thick wall and impairs diastolic function."
},
"delta": null
},
{
"id": "Q373",
"orig": 373,
"title": "Systolic anterior motion and outflow gradients",
"lesions": [
"HCM",
"MR"
],
"lens": "doppler",
"items": [
{
"id": "Q373.1",
"q": "Describe the continuous-wave envelope that leaflet-septal contact produces, and explain why it peaks late in systole rather than in the middle.",
"a": "Mid-systolic leaflet–septal contact from SAM physically obstructs the LVOT, producing a late-peaking 'dagger' CW signal that intensifies with provocation. It peaks late because the obstruction builds as the ventricle empties: the cavity shrinks through systole, the leaflet is held against the septum, and the narrowest orifice arrives at the end of ejection rather than the start. Provoke with Valsalva or standing if the resting gradient is low but symptoms suggest obstruction. Record from the apical five- or three-chamber view and convert the peak velocity with the simplified Bernoulli equation, taking care not to trace the MR jet by mistake, which is faster, starts before ejection and runs past aortic closure."
},
{
"id": "Q373.2",
"q": "Color Doppler shows an MR jet hugging the posterior left atrial wall through the second half of systole. Why must you re-record it after a Valsalva strain?",
"a": "SAM distorts leaflet coaptation, opening a gap that yields a characteristically posteriorly-directed MR jet timed to mid-late systole. A posteriorly-directed MR jet with dynamic LVOT obstruction is the SAM signature. Its severity tracks the obstruction, so it waxes and wanes with the same maneuvers that move the gradient and a resting grade can understate it badly. Grade the jet at rest and again after provocation and state its timing, because the mid-to-late systolic onset separates SAM-related regurgitation from the holosystolic jet of primary mitral disease. An anteriorly or centrally directed jet does not fit SAM alone and points to intrinsic leaflet disease, which changes the surgical plan."
},
{
"id": "Q373.3",
"q": "A woman admitted with apical ballooning after a sudden bereavement becomes hypotensive, and the team reaches for dobutamine. What do you have to put on the screen before they start it?",
"a": "Hypercontractile basal segments narrow the outflow tract while the ballooning apex offloads, generating a Venturi effect that draws the anterior mitral leaflet toward the septum (SAM). This creates a dynamic, late-peaking LVOT gradient that worsens with hypovolemia and inotropes, the same physiology as obstructive HCM. If a Takotsubo patient is hypotensive, do NOT reflexively give inotropes: place CW Doppler through the LVOT to look for a dynamic, dagger-shaped late-peaking gradient and assess for SAM on PLAX. Inotropes and vasodilators worsen the obstruction; gentle volume and phenylephrine/beta-blockade are preferred. The physics is the same as in HCM, and so is the correction: drag starts the leaflet moving before Venturi forces are large enough to matter, whichever segment does the narrowing. Dynamic LVOT obstruction complicates roughly 10 to 20 percent of Takotsubo cases and is an important, treatable cause of acute hypotension."
}
],
"numbers": [
{
"label": "Dynamic LVOT obstruction complicating Takotsubo",
"value": "10–20",
"unit": "%"
}
],
"pearl": "A dagger in the outflow tract and a jet aimed at the back of the left atrium are one lesion seen twice.",
"related": [
"Q5",
"Q137",
"Q140",
"Q141"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "valvular aortic stenosis",
"discriminator": "Fixed valvular stenosis gives a symmetric mid-peaking envelope that barely moves with provocation; dynamic obstruction gives a late-peaking dagger that rises with Valsalva and standing and falls with volume."
},
"delta": null
},
{
"id": "Q374",
"orig": 374,
"title": "Causes of an apical aneurysm",
"lesions": [
"CAD",
"LV_FUNCTION",
"HCM"
],
"lens": "etiology",
"items": [
{
"id": "Q374.1",
"q": "Why is the apex the commonest site of a true left ventricular aneurysm after infarction, and what on the image separates it from a pseudoaneurysm?",
"a": "Occlusion of the LAD artery infarcts the anteroapical myocardium. Transmural necrosis is replaced by thin, non-contractile fibrous full-thickness scar that permanently bulges outward (in systole and diastole) with paradoxical systolic dyskinesis, producing a true aneurysm with a wide neck. The apex is the LAD's terminal territory and the thinnest part of the LV, making it the most common aneurysm site. On A4C and A2C, watch for a thin, akinetic/dyskinetic apex that bulges outward and fails to thicken; the aneurysm neck is as wide as the body (vs the narrow neck of a pseudoaneurysm). Foreshortening hides the true apex, so angle off-axis and use contrast (LVO) if the apex is poorly defined. Apical and anterior aneurysm is the classic late complication of large anterior STEMI, accounting for more than 80 percent of true LV aneurysms, and apical akinesis is the dominant substrate for post-MI thrombus."
},
{
"id": "Q374.2",
"q": "An apex balloons outward but the abnormal segments cross more than one coronary territory. What will the follow-up study show, and when should it be booked?",
"a": "Catecholamine surge stuns the apex (highest apical beta-receptor density, with a beta2-AR Gs-to-Gi switch under supraphysiologic epinephrine), producing transient mid-apical akinesis with basal hypercontraction and the pathognomonic apical 'ballooning' that mimics a true aneurysm but, unlike post-MI scar, recovers over days to weeks and crosses multiple coronary territories. On A4C/A2C, look for circumferential mid-to-apical akinesis with vigorous basal contraction in a pattern that does NOT respect a single coronary territory, classically in a postmenopausal woman after acute stress. Re-image in 1-4 weeks to confirm full functional recovery, the key feature distinguishing it from infarct aneurysm. Apical ballooning is the dominant variant, roughly 80 percent of Takotsubo cases, and the aneurysmal appearance is a transient functional mimic that typically reverses on follow-up, so the diagnosis is not finished until that second study proves the apex came back."
},
{
"id": "Q374.3",
"q": "The spade-shaped cavity and giant precordial T-wave inversions are already in the report. Why must you keep imaging distal to the mid-cavity gradient?",
"a": "Severe apical hypertrophy can produce mid-cavity obliteration and high apical afterload/wall stress with localized ischemia (demand-supply mismatch despite normal epicardial coronaries), leading over time to apical myocardial thinning, scarring, and a true apical aneurysm. In apical HCM, don't stop at the 'spade-shaped' cavity and giant precordial T-wave inversions: interrogate distal to any mid-cavity gradient for a thin-walled apical aneurysm, easily missed on foreshortened apical views. Use contrast (LVO) or CMR to delineate the apical pouch and screen it for thrombus; this phenotype carries increased SCD and thromboembolic risk. Apical aneurysm develops in about 2 percent of HCM overall and is concentrated in exactly this apical and mid-cavity-obstructive phenotype, and about 46 percent of those aneurysms hold mural thrombus, so finding the pouch commits you to looking inside it."
}
],
"numbers": [
{
"label": "True LV aneurysms that are anterior or apical",
"value": "> 80",
"unit": "%"
},
{
"label": "Apical aneurysm developing in HCM",
"value": "~ 2",
"unit": "%"
},
{
"label": "HCM apical aneurysms containing thrombus",
"value": "~ 46",
"unit": "%"
}
],
"pearl": "Three common roads reach a bulging apex, scar that will never move again, stunning that will, and hypertrophy that strangled its own blood supply; a fourth runs through Chagas.",
"related": [
"Q143",
"Q154",
"Q158",
"Q159",
"Q247"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "pseudoaneurysm from contained free-wall rupture",
"discriminator": "A true aneurysm has a wide mouth and a wall of thinned myocardial scar; a pseudoaneurysm has a narrow neck under half the sac diameter, no myocardium in its wall, and to-and-fro flow across the neck."
},
"delta": null
},
{
"id": "Q375",
"orig": 375,
"title": "Left ventricular thrombus and embolic stroke",
"lesions": [
"MASS",
"LV_FUNCTION",
"CAD"
],
"lens": "2d",
"items": [
{
"id": "Q375.1",
"q": "Which limb of Virchow's triad does an apical aneurysm supply, and how do you set the machine up so a mural clot cannot hide in it?",
"a": "The akinetic/dyskinetic aneurysm sac creates a low-flow stasis pocket where blood pools (Virchow's stasis). Combined with endocardial injury from the infarct and a post-MI hypercoagulable state, this completes Virchow's triad and seeds mural thrombus, typically layered against the apical endocardium. Interrogate the apex in multiple planes (A4C, A2C, off-axis apical) at high frequency with reduced depth; a true thrombus has a distinct border from underlying myocardium, is visible in 2 planes, and lacks intertrabecular flow. If the apex is suboptimal, use ultrasound contrast (LVO), which markedly improves sensitivity over non-contrast TTE. Thrombus complicates roughly 19 percent of anterior STEMIs with an ejection fraction under 50 percent, and an aneurysmal or akinetic apex is among the strongest morphologic predictors."
},
{
"id": "Q375.2",
"q": "A 28-year-old with heart failure has a heavily trabeculated apex and something dark sitting between the trabeculations. What is the underlying disease, and which Doppler finding decides whether that darkness is clot?",
"a": "Arrest of normal embryonic myocardial compaction leaves prominent trabeculations and deep intertrabecular recesses, mostly at the apex, mid-lateral, and mid-inferior walls. Sluggish blood flow within these recesses, plus frequent systolic dysfunction, promotes thrombus formation and systemic embolism. Suspect LVNC when the apex/lateral wall shows >3 trabeculations apical to the papillary muscles with a two-layered myocardium and a noncompacted:compacted ratio >2 at end-systole. Use color Doppler to show flow filling the deep recesses (distinguishing trabeculae from apical thrombus), and screen carefully for clot within them. Drop the color scale to a low Nyquist so the sluggish recess flow registers at all: color filling the recesses means trabeculation, while a defect that stays black in two planes at that setting is thrombus. Reported thromboembolism in adult non-compaction runs roughly 13 to 24 percent, so screen the recesses for clot in every study."
},
{
"id": "Q375.3",
"q": "You have confirmed an apical thrombus. Which of its features must appear in your report because they change embolic risk?",
"a": "Fragments of LV thrombus detach into the systemic arterial circulation, lodging in cerebral, mesenteric, renal, or peripheral arteries. Embolic risk rises with thrombus mobility, protrusion/pedunculation, larger size, and a freshly formed (vs organized/laminated) clot, typically at the akinetic/dyskinetic apex after anterior MI. Risk is highest in the first 3 months and is substantially reduced by adequate anticoagulation. When you find an LV thrombus, characterize embolic-risk morphology: mobility, protrusion/pedunculation, and visualization in multiple views all raise risk. A patient with stroke or acute limb/mesenteric ischemia plus an apical wall-motion abnormality should trigger a dedicated, contrast-enhanced apex hunt. Left alone, a documented thrombus embolizes in roughly 10 to 16 percent of patients, and the mobile protruding ones carry the highest risk of all."
}
],
"numbers": [
{
"label": "LV thrombus after anterior STEMI with reduced EF",
"value": "~ 19",
"unit": "%"
},
{
"label": "Thromboembolism in adult LV non-compaction",
"value": "13–24",
"unit": "%"
},
{
"label": "Embolization risk of untreated LV thrombus",
"value": "10–16",
"unit": "%"
}
],
"pearl": "Stasis has two addresses in the left ventricle: the aneurysm sac and the intertrabecular recess.",
"related": [
"Q32",
"Q161",
"Q251",
"Q333"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "near-field clutter or a prominent apical trabeculation",
"discriminator": "Artifact and trabeculae vanish when you change plane or frequency and take color into the recesses; thrombus persists in two planes, has a border distinct from myocardium, and stays a dark filling defect after contrast."
},
"delta": null
},
{
"id": "Q376",
"orig": 376,
"title": "Cardiac rupture after myocardial infarction",
"lesions": [
"CAD",
"VSD",
"EFFUSION"
],
"lens": "vignette",
"items": [
{
"id": "Q376.1",
"q": "A 68-year-old is four days out from a late-reperfused anterior STEMI and collapses into shock. There is no murmur, because the output is too low to make one. Where do you point color Doppler, and what confirms it?",
"a": "Transmural anteroseptal infarction necroses and weakens the septum; within days the friable, neutrophil-infiltrated wall ruptures at the junction of infarcted and viable myocardium, creating an acquired ventricular septal defect with left-to-right shunting and abrupt hemodynamic collapse. In a post-MI patient with a new harsh holosystolic murmur and shock, scan the septum (PSAX, A4C, off-axis) with color Doppler for a mosaic left-to-right jet at the infarct border ('hinge point'). Anterior MIs rupture the apical septum; distinguish from acute MR (clinically indistinguishable) and look for associated RV pressure/volume overload. Auscultation is the least reliable part of this diagnosis, so hunt the septum with color whether or not a murmur is audible, then confirm with continuous wave: an LV to RV systolic gradient with an acutely volume-loaded right ventricle settles it. Rupture now complicates about 0.2 percent of infarcts and is lethal enough to justify the search in every post-infarct collapse."
},
{
"id": "Q376.2",
"q": "Five days after a first inferior STEMI, a patient goes from talking to pulseless electrical activity in under a minute. You are at the bedside with the machine on. What window do you take?",
"a": "Transmural myocardial infarction (typically 2-7 days post-MI, more often with first/large transmural infarcts and delayed reperfusion) weakens and tears the necrotic free wall, allowing blood to escape into the pericardium. The resulting acute hemopericardium causes rapid tamponade and electromechanical dissociation. In a post-MI patient who suddenly becomes hypotensive, bradycardic, or develops PEA, scan for pericardial effusion immediately: a new effusion >15 mm with RV compression and intrapericardial echodensity (clot) suggests free-wall rupture. Contained ruptures form a pseudoaneurysm (narrow neck, to-and-fro flow) and can be diagnosed before frank tamponade. Call the surgeon now. Take the subcostal window first, because it needs no repositioning during compressions, and do not wait for a large effusion: an acute bleed tamponades at volumes a chronic effusion tolerates. Free-wall rupture complicates roughly 1 to 3 percent of infarcts and carries very high mortality."
}
],
"numbers": [
{
"label": "Post-infarction ventricular septal rupture incidence",
"value": "~ 0.2",
"unit": "%"
}
],
"pearl": "The septum announces its tear with a murmur; the free wall announces its with silence.",
"related": [
"Q119",
"Q154",
"Q155",
"Q295"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "acute mitral regurgitation from papillary muscle rupture",
"discriminator": "Both give shock days after an infarct; septal rupture shows a mosaic transseptal jet with a calculable LV to RV gradient and right heart overload, while papillary rupture shows a flail leaflet with an intact septum and no transseptal flow."
},
"delta": null
},
{
"id": "Q377",
"orig": 377,
"title": "Dilated cardiomyopathy and its sarcoid mimic",
"lesions": [
"DCM",
"ARRHYTHMIA",
"LV_FUNCTION"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q377.1",
"q": "A patient with known dilated cardiomyopathy returns a year later. The ejection fraction is unchanged at 28 percent, but the left atrial volume index has risen from 36 to 48 mL/m². What has changed?",
"a": "Chronically elevated LV filling pressure and functional MR raise LA pressure, enlarging the atrium. The ejection fraction has not moved, so the atrium is reporting something the ventricle is not: filling pressure has climbed enough to take him from mildly to moderately enlarged in a year. Grade it as a tier change rather than a number, and quantify the secondary mitral regurgitation in the same study, since its regurgitant volume is part of what stretched the chamber. Then flag the new size as fresh substrate for atrial fibrillation, which is the complication that will bring him back."
},
{
"id": "Q377.2",
"q": "A 47-year-old with a reduced ejection fraction has akinesis of the basal septum and the mid inferolateral wall with a normal apex, and the coronary angiogram is clean. Which infiltrative disease does that distribution point to?",
"a": "Patchy non-caseating granulomatous infiltration replaces myocardium and later scars, producing segmental akinesis/dyskinesis and characteristic basal interventricular septal thinning. The key feature is that wall-motion abnormalities do NOT follow a single coronary distribution, distinguishing infiltrative disease from ischemic CAD. On PLAX and A4C, look for focal thinning and hypokinesis of the BASAL septum out of proportion to other segments, plus aneurysms or defects that cross coronary territories. Echo is insensitive (abnormal in only ~25-55%), so a normal study does NOT exclude sarcoid; pair with PET/CMR and use strain to unmask subtle regional dysfunction. Basal septal thinning is roughly 99 percent specific but easy to overlook, so measure the segment rather than eyeballing it, and put a regional wall-motion score in the report even when you are calling the ventricle globally impaired."
},
{
"id": "Q377.3",
"q": "You are asked to scan a 44-year-old before a pacemaker is implanted for new complete heart block, and the chambers and ejection fraction look normal. What are you hunting for, and why does it change the plan?",
"a": "Granulomas and subsequent fibrosis have a predilection for the basal interventricular septum, which houses the AV node and proximal conduction system. Infiltration of this region interrupts AV conduction, producing PR prolongation, Mobitz II, or complete heart block. Conduction disease is frequently the earliest cardiac manifestation. Unexplained high-grade AV block in a patient under ~60 should trigger a hunt for cardiac sarcoidosis (and Lyme/Chagas/Lev-Lenegre). On echo, scrutinize the basal septum for focal thinning or wall-motion abnormality; a structurally near-normal heart with complete heart block is a red flag mandating CMR/FDG-PET before assuming idiopathic conduction disease. Conduction abnormalities occur in roughly 25 to 30 percent of cardiac sarcoidosis patients and are often the presenting feature, and sarcoid underlies 16 to 34 percent of unexplained AV block under 60. The answer can change the device from a pacemaker to a defibrillator, so the question has to be asked before the leads go in."
},
{
"id": "Q377.4",
"q": "What has to be looked at before a globally dilated, poorly contracting ventricle is signed out as idiopathic dilated cardiomyopathy?",
"a": "Progressive granulomatous destruction and replacement fibrosis of the myocardium can culminate in global chamber dilation and systolic dysfunction, producing a dilated-cardiomyopathy phenotype that mimics idiopathic DCM. When a 'DCM' shows regional thinning (especially basal septum), conduction disease, or RV involvement out of proportion to LV, reconsider sarcoid before labeling it idiopathic. CMR late-gadolinium enhancement and FDG-PET change management because immunosuppression can halt deterioration and reverse early disease (LVEF ~30-55%). Sweep the septum in PLAX and PSAX and measure basal septal thickness instead of reporting global hypokinesis alone, and add global longitudinal strain, which unmasks the regional pattern that eyeballing misses."
}
],
"numbers": [
{
"label": "Echo abnormal in clinically manifest cardiac sarcoidosis",
"value": "~ 25–55",
"unit": "%"
},
{
"label": "Basal septal thinning specificity for sarcoid",
"value": "~ 99",
"unit": "%"
},
{
"label": "AV conduction disease in cardiac sarcoidosis",
"value": "25–30",
"unit": "%"
},
{
"label": "Cardiac sarcoid among unexplained AV block under 60",
"value": "16–34",
"unit": "%"
}
],
"pearl": "Regional thinning and heart block in a dilated ventricle is sarcoid until PET says otherwise.",
"related": [
"Q142",
"Q146",
"Q148",
"Q163"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "ischemic cardiomyopathy",
"discriminator": "Ischemic scar is territorial, matching a coronary distribution with an occluded vessel to account for it; sarcoid thins the basal septum out of proportion to everything else and puts akinesis across territories with clean coronaries."
},
"delta": null
},
{
"id": "Q378",
"orig": 378,
"title": "Cardiac amyloid and restrictive filling",
"lesions": [
"RCM",
"DIASTOLIC",
"EFFUSION"
],
"lens": "2d",
"items": [
{
"id": "Q378.1",
"q": "The septum measures 15 mm and the posterior wall 14 mm. Where exactly do you put the calipers, and why does the plane matter more here than usual?",
"a": "Amyloid infiltration thickens the walls, mimicking hypertrophy — but the muscle is infiltrated, not hypertrophied, classically with low ECG voltage despite thick walls. Thick walls + low ECG voltage + apical-sparing strain pattern should raise amyloid over true LVH. Measure in PLAX at end-diastole on a true minor axis, just beyond the mitral leaflet tips and perpendicular to the septum, because an oblique cut through an already thick wall inflates it further and pushes a borderline heart over a threshold it never reached. Report septal and posterior thickness separately, since amyloid usually thickens them near-equally while pressure overload does not."
},
{
"id": "Q378.2",
"q": "You find a small circumferential pericardial effusion in a thick-walled ventricle with large atria. Does the fluid explain the patient's breathlessness?",
"a": "Infiltrative restrictive cardiomyopathies, including amyloid, are frequently accompanied by a (usually small) pericardial effusion. The fluid marks the disease rather than causing the symptoms: measure the echo-free space at end-diastole in PLAX and subcostal views and expect under 1 cm with no chamber collapse. The breathlessness belongs to the stiff ventricle and the high filling pressures, so document the restrictive inflow and the annular velocities before blaming the pericardium. If a thick-walled heart carries a moderate or large effusion or shows right-sided collapse, hunt for a second process such as malignancy, uremia, or inflammatory pericarditis, because amyloid on its own rarely tamponades."
},
{
"id": "Q378.3",
"q": "Which atrial measurements belong in the report when amyloid is on the differential, and what do they add to wall thickness?",
"a": "Restrictive physiology raises filling pressures, dilating the atria; biatrial enlargement is typical in advanced amyloid. Measure LA volume by biplane disk summation at ventricular end-systole and index it to body surface area, then add RA area from the apical four-chamber view, because it is both atria enlarging together that separates infiltration from hypertensive thickening. Hypertensive heart disease reaches the right side late and by way of postcapillary pulmonary hypertension; amyloid thickens and stiffens the RV directly, so biatrial enlargement appears early and out of proportion to the pressure history. Atrial reservoir strain falls before the volumes look abnormal, so record an atrial-focused four-chamber clip and report LARS alongside LAVi."
},
{
"id": "Q378.4",
"q": "A 71-year-old has normal-sized ventricles, an ejection fraction of 58 percent, and enormous atria. What must you record next, and in which order?",
"a": "Stiff, non-compliant ventricles have markedly impaired diastolic filling while cavity size and systolic function stay near-normal; the high filling pressures transmit upstream so both atria dilate massively — small/normal ventricles with severe biatrial enlargement. Huge atria but normal-sized, normally-squeezing ventricles means restrictive physiology: confirm with a restrictive mitral inflow and low tissue-Doppler e', then chase the cause (amyloid and others) rather than calling it isolated atrial disease. Take the mitral inflow at the leaflet tips and the septal and lateral annular velocities in the same apical four-chamber window, so the deceleration time and e′ come from the same beats and are not compared across different loading conditions."
}
],
"numbers": [],
"pearl": "Thick walls with small QRS complexes: amyloid is deposit, not muscle, so the voltage never follows the wall.",
"related": [
"Q7",
"Q151",
"Q256",
"Q360"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "hypertensive left ventricular hypertrophy",
"discriminator": "Hypertensive LVH gives high ECG voltage for the mass, a normal RV free wall and valves, and left atrial enlargement alone; amyloid gives low voltage, thickened RV free wall, valves and interatrial septum, biatrial enlargement, and apical-sparing strain."
},
"delta": null
},
{
"id": "Q379",
"orig": 379,
"title": "Constrictive pericarditis and its mimic",
"lesions": [
"CONSTRICTION",
"RCM"
],
"lens": "doppler",
"items": [
{
"id": "Q379.1",
"q": "The septum in constriction moves twice, once on every beat and once with every breath. Which movement is the bounce, and what do you do when the mitral inflow shows no respiratory variation at all?",
"a": "A rigid pericardium dissociates intrathoracic from intracardiac pressures and enhances ventricular interdependence. With respiration the fixed total cardiac volume forces the interventricular septum to shift abruptly toward the LV (inspiration, increased RV filling) and back toward the RV (expiration), producing a characteristic early-diastolic septal bounce. Look for the septal bounce in PLAX/PSAX and A4C M-mode timed to respiration (sensitivity ~60-80%, specificity ~90%). Pair it with the other constrictive Doppler markers (annulus reversus, hepatic vein expiratory diastolic reversal, >25% respirophasic mitral E variation); use a multiparametric approach since ~1/3 of constriction patients lack mitral inflow respiratory variation. The bounce is the beat-by-beat event, an early-diastolic notch timed to mitral opening; the shift is a slower whole-septum displacement tracking the breath. The one-in-three figure is an instruction: flat mitral inflow does not exclude constriction, so go to the hepatic vein and the annulus."
},
{
"id": "Q379.2",
"q": "Two patients in heart failure have identical restrictive mitral inflows and identically small ventricles. Which measurement decides which one belongs in an operating room?",
"a": "Both produce stiff-heart physiology with elevated filling pressures and small ventricles, but the mechanism differs: constriction is an extrinsic pericardial constraint with preserved myocardium, whereas restriction is intrinsic myocardial disease (infiltration/fibrosis) that impairs relaxation. This mechanistic split drives the opposite tissue-Doppler signatures used to tell them apart. The classic discriminator pair. Constriction: preserved/exaggerated medial e' (> 7 cm/s, > 8 strongly favors constriction) with annulus reversus, prominent respirophasic mitral inflow variation, septal bounce, expiratory hepatic vein diastolic flow reversal. Restriction: reduced e', high E/e', biatrial enlargement, little respiratory variation, pulmonary hypertension. High septal e' in a heart-failure patient means think constriction. Stakes are high: pericardiectomy can cure constriction. Biatrial enlargement is the weakest item on that list, because constriction enlarges both atria too; the annular velocities are what separate them."
},
{
"id": "Q379.3",
"q": "A young patient from a tuberculosis-endemic region has a moderate effusion with fibrin strands and a thickened pericardium. What are you predicting on the follow-up study?",
"a": "Mycobacterial pericardial infection provokes intense granulomatous inflammation, fibrinous exudate, and eventual dense fibrosis and calcification of the pericardium, which evolves into a rigid constrictive shell limiting diastolic filling. In endemic regions or immunocompromised patients with a pericardial effusion, fibrinous strands, and thickened pericardium, suspect TB and follow for constriction: TB pericarditis progresses to constriction in 20-30% of cases, often via an effusive-constrictive stage. Track pericardial thickness, calcification, and constrictive Doppler markers over serial studies. Record the same subcostal and apical windows at every visit with the respirometer running, so the first bounce or new expiratory hepatic vein reversal reads as a change in the patient rather than a change in technique."
}
],
"numbers": [
{
"label": "Septal bounce sensitivity for constriction",
"value": "~ 60–80",
"unit": "%"
},
{
"label": "TB pericarditis progressing to constriction",
"value": "20–30",
"unit": "%"
}
],
"pearl": "Bounce with a preserved medial e′ is the pericardium talking; bounce with a low e′ means the radiation reached the muscle too.",
"related": [
"Q126",
"Q257",
"Q262",
"Q263",
"Q337"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "restrictive cardiomyopathy",
"discriminator": "Constriction preserves the medial e′ and adds respirophasic septal shift, annulus reversus and expiratory hepatic vein diastolic reversal; restriction drops e′, raises E/e′, and shows little respiratory variation."
},
"delta": {
"was": "The Mayo criterion, quoted in the discriminator on this card, sets the constriction cut-off at a medial e′ of 9 cm/s or more.",
"now": "ASE 2025 lowers it to a medial e′ above 7 cm/s, with above 8 cm/s strongly favoring constriction, and pairs it with respirophasic septal shift for about 80 percent sensitivity and 96 percent specificity.",
"source": "ASE 2025 diastolic function"
}
},
{
"id": "Q380",
"orig": 380,
"title": "Pericardial effusion becoming tamponade",
"lesions": [
"EFFUSION",
"CONSTRICTION",
"HEMODYNAMICS"
],
"lens": "m-mode",
"items": [
{
"id": "Q380.1",
"q": "A patient on warfarin becomes hypotensive three days after a pacemaker implant, and the echo-free space measures only 0.8 cm. Why can an effusion this small be tamponading?",
"a": "When pericardial fluid accumulates faster than the parietal pericardium can stretch, intrapericardial pressure rises and equalizes with diastolic chamber pressures, compressing the lower-pressure right heart during diastole, impairing filling and dropping stroke volume. It is the rate of accumulation and the pericardial pressure-volume compliance curve, not the absolute fluid volume, that determines whether an effusion tamponades: a rapidly accumulating 150-200 mL hemorrhagic effusion can tamponade while a slow 1-2 L chronic effusion may not. Tamponade is a clinical and hemodynamic diagnosis: scan subcostal and apical 4-chamber, then prove it with Doppler. Earliest sign is systolic RA collapse (most sensitive when inversion lasts >1/3 of the cycle); diastolic RV free-wall collapse is most specific. Confirm with a plethoric IVC and exaggerated respirophasic inflow (mitral E drop >25-30%, tricuspid E rise >40-60%). Use 30 and 60 percent as the tamponade cut-offs; 25 and 40 percent belong to constriction."
},
{
"id": "Q380.2",
"q": "Six hundred milliliters came off yesterday and the pericardial space is nearly dry, but the neck veins are still distended and the septum still bounces. What has happened?",
"a": "An inflamed, thickened visceral pericardium constricts the heart while a tense effusion is simultaneously present. After the fluid is drained, the constrictive physiology of the stiff visceral layer persists, so right atrial pressure stays elevated despite normalization of intrapericardial pressure. Suspect effusive-constrictive disease when, after pericardiocentesis, RA pressure fails to fall by >50% or stays >10 mmHg, or when post-tap echo still shows septal bounce, annulus reversus, and respirophasic septal shift despite little residual fluid. Document constrictive Doppler features before and after drainage; TB is the classic cause worldwide. It is reported in roughly 5 to 15 percent of pericardiocenteses and is strongly associated with tuberculous and malignant effusions, so the post-drainage study is part of the procedure rather than a formality."
},
{
"id": "Q380.3",
"q": "Which single view argues hardest against tamponade in a patient with a large effusion, and what makes it convincing?",
"a": "Elevated and equalized intrapericardial/right atrial pressure obstructs systemic venous return, so the inferior vena cava and hepatic veins dilate and lose their normal inspiratory collapse, reflecting markedly elevated central venous pressure transmitted backward from the compressed right atrium. Always sweep to the subcostal IVC view in any effusion: a dilated IVC (>2.1 cm) with <50% inspiratory collapse is the most sensitive sign of tamponade (~92%), so a fully collapsing IVC makes tamponade very unlikely. Beware: IVC plethora is nonspecific (any high-RA-pressure state) and IVC respiratory dynamics are unreliable in positive-pressure-ventilated patients. Measure it in the subcostal long axis 1 to 2 cm from the cavo-atrial junction, perpendicular to the vessel, at quiet end-expiration and again on a sniff."
},
{
"id": "Q380.4",
"q": "The right atrium indents briefly on two of ten beats and the right ventricle never inverts. How do you report that?",
"a": "When intrapericardial pressure transiently exceeds the pressure inside a low-pressure chamber, that chamber wall inverts. The right atrium collapses in late diastole/systole (when RA pressure is lowest) and the right ventricle collapses in early diastole (when RV pressure is lowest). Left-sided or isolated chamber collapse occurs with loculated or post-surgical effusions. Confirm and time the collapse with M-mode through the chamber wall referenced to the ECG: RA inversion is sensitive (earliest) and becomes specific when it persists >1/3 of the cycle; RV diastolic collapse is the most specific 2D sign. In post-surgery patients, look for loculated posterior clot selectively compressing the LA or RV. Brief, intermittent right atrial indentation is a normal finding at low pericardial pressure, so report it as present but non-diagnostic and give the fraction of the cycle it occupies rather than the word 'collapse', which the referring team will read as tamponade."
}
],
"numbers": [
{
"label": "IVC plethora sensitivity for tamponade",
"value": "~ 92",
"unit": "%"
}
],
"pearl": "If the neck veins stay up after the tap, the visceral pericardium was constricting all along.",
"related": [
"Q118",
"Q119",
"Q258",
"Q264",
"Q265"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "a large chronic effusion without tamponade",
"discriminator": "A slowly grown effusion leaves a collapsing IVC, no sustained chamber inversion and normal respirophasic inflow however big it looks; tamponade adds a plethoric IVC, right atrial inversion beyond a third of the cycle, and exaggerated inflow variation."
},
"delta": {
"was": "Older teaching, quoted in the discriminator on this card, put the tamponade inflow thresholds at a mitral E fall above 25 to 30 percent and a tricuspid E rise above 40 to 60 percent.",
"now": "The 2013 ASE pericardial document raised them to a mitral E fall above 30 percent and a tricuspid E rise above 60 percent to improve specificity; 25 and 40 percent are the constriction figures and using them for tamponade blurs the two diagnoses.",
"source": "ASE 2013 pericardial disease"
}
},
{
"id": "Q381",
"orig": 381,
"title": "Cor pulmonale and RV hypertrophy",
"lesions": [
"PH",
"RV_FUNCTION"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q381.1",
"q": "A 68-year-old with advanced emphysema is referred for dyspnea, and the parasternal and apical windows are almost unusable. Why does chronic lung disease raise pulmonary pressure, and how do you still get the numbers?",
"a": "Chronic alveolar hypoxia triggers hypoxic pulmonary vasoconstriction and, with emphysematous destruction of the pulmonary capillary bed plus vascular remodeling, raises pulmonary vascular resistance. The resulting Group 3 pulmonary hypertension chronically pressure-loads the RV, producing cor pulmonale (RV hypertrophy then dilation/dysfunction). Hyperinflated lungs make parasternal/apical windows poor, so lean on the subcostal view in COPD patients. Estimate PASP from the TR jet (4v² + RA pressure) and look for RV free-wall hypertrophy (>5 mm) plus a dilated RV. Suspect cor pulmonale when RV changes appear without left-heart disease. COPD is the underlying cause in more than half of cor pulmonale cases, and mild-to-moderate pulmonary hypertension is common in advanced disease and predicts worse survival."
},
{
"id": "Q381.2",
"q": "The pulmonary pressure has been high for years and the free wall is already thick. Why does the RV go on to dilate, and which single comparison in the apical 4-chamber tells you the loading is serious?",
"a": "Chronic pressure overload from elevated PA pressure dilates and eventually fails the thin-walled right ventricle. Hypertrophy buys the RV time but not much: it is a thin-walled chamber built for volume, so once wall stress outruns what added sarcomeres can offset, the ventricle dilates and then fails. Compare RV to LV size in the apical 4-chamber; an RV larger than the LV signals serious right-heart loading. Take the basal diameter at end-diastole from an RV-focused apical view, where above 41 mm is dilated, and cross-check it subcostally before you call the RV normal, because a cut that is not RV-focused foreshortens the crescent."
},
{
"id": "Q381.3",
"q": "The RV is dilated and the TR velocity is 3.6 m/s. What does free-wall thickness add that the velocity cannot?",
"a": "Chronic pressure overload forces the RV to generate higher systolic pressures, triggering compensatory concentric hypertrophy of the free wall (Laplace's law). A free-wall thickness > 5 mm indicates the pulmonary hypertension is chronic rather than acute. Measure RV free-wall thickness in the subcostal 4-chamber view at end-diastole, away from trabeculations. A wall > 5 mm tells you the load is chronic — distinguishing cor pulmonale from the thin, dilated, akinetic RV of acute PE."
}
],
"numbers": [
{
"label": "COPD share of cor pulmonale cases",
"value": "> 50",
"unit": "%"
}
],
"pearl": "Hypertrophy takes months, so a free wall over 5 mm dates the pulmonary pressure as old.",
"related": [
"Q131",
"Q268",
"Q344"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "acute pulmonary embolism",
"discriminator": "Acute embolism dilates a thin RV free wall of 5 mm or less with no time to hypertrophy; cor pulmonale carries a free wall above 5 mm, which dates the load in months rather than hours."
},
"delta": null
},
{
"id": "Q382",
"orig": 382,
"title": "Septal flattening and falling TAPSE",
"lesions": [
"RV_FUNCTION",
"PH"
],
"lens": "numbers",
"items": [
{
"id": "Q382.1",
"q": "The left ventricle is a D rather than a circle in the parasternal short axis. What must you establish about that shape before you report it?",
"a": "RV pressure overload exceeds LV pressure in systole, flattening the septum and giving the LV a 'D' shape in short axis. Systolic septal flattening (D-shape) on PSAX points to RV pressure overload. Freeze at the papillary-muscle level and time the flattening across the loop, because a septum that is flat at end-diastole and round in systole is volume overload instead, and put a number on the deformity with the end-systolic eccentricity index."
},
{
"id": "Q382.2",
"q": "A patient with established pulmonary hypertension returns for surveillance. Which measurement marks the moment the right ventricle stops compensating?",
"a": "Sustained pressure overload eventually exhausts RV compensation and the dilated ventricle fails. Because the RV contracts mainly by longitudinal shortening, failure shows as reduced descent of the tricuspid annulus (low TAPSE) — marking the transition from compensated PH to RV failure, with strong prognostic weight. Run M-mode through the lateral tricuspid annulus in A4C: TAPSE < 17 mm (with S' < 9.5 cm/s) signals RV systolic dysfunction. Pair it with PASP for the TAPSE/PASP coupling ratio — never report PH without an RV function number. One caveat before you act on a low value: TAPSE is angle-dependent and falls by a third after any pericardiotomy, so in a post-surgical or severely regurgitant right heart confirm it against fractional area change or free-wall strain before calling the RV failed."
}
],
"numbers": [
{
"label": "TAPSE abnormal",
"value": "< 17",
"unit": "mm"
},
{
"label": "S' abnormal",
"value": "< 9.5",
"unit": "cm/s"
}
],
"pearl": "Septal flattening says the pressure is high; a falling TAPSE says the ventricle has stopped coping with it.",
"related": [
"Q132",
"Q268",
"Q344",
"Q346"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "RV volume overload from a shunt",
"discriminator": "Volume overload flattens the septum at end-diastole and lets it round out in systole; pressure overload flattens it through systole and raises the end-systolic eccentricity index."
},
"delta": null
},
{
"id": "Q383",
"orig": 383,
"title": "Acute pulmonary embolism and RV strain",
"lesions": [
"RV_FUNCTION",
"PH",
"HEMODYNAMICS"
],
"lens": "2d",
"items": [
{
"id": "Q383.1",
"q": "A hypotensive patient with pleuritic chest pain gets a bedside study. What does a dilated, hypokinetic right ventricle change about the next hour?",
"a": "A large embolus acutely raises RV afterload; the unprepared thin RV dilates and becomes hypokinetic, marking a high-risk PE. In suspected PE, a dilated hypokinetic RV identifies a patient who may need escalation. Judge size and function from the RV-focused apical 4-chamber with the subcostal view as backup, and remember the finding does not run backwards: a normal RV does not exclude pulmonary embolism, it only removes the high-risk label."
},
{
"id": "Q383.2",
"q": "The RV mid free wall is akinetic while the apex beats vigorously. What is this pattern called, and how much weight does it carry on its own?",
"a": "Acute RV pressure overload can produce a regional pattern of free-wall akinesis with preserved apical contraction (McConnell's sign). McConnell's sign supports acute RV strain but is not specific — interpret in context. Reported specificity is high and sensitivity low, and the same regional pattern appears in RV infarction, so a positive sign does not settle the diagnosis and a negative one does not exclude it. Compare free-wall with apical motion in the apical 4-chamber view and read it alongside RV size, TAPSE and the TR velocity."
},
{
"id": "Q383.3",
"q": "Acute embolism and long-standing pulmonary hypertension both flatten the septum in systole. What does the D shape prove here, and what separates the two?",
"a": "Acute RV pressure overload flattens the septum in systole, the same D-shape seen in chronic pulmonary hypertension. The shape therefore proves the RV is pressure-loaded but says nothing about how long it has been that way. What separates them is the wall behind it: in acute embolism the free wall is still thin at 5 mm or less, because hypertrophy takes months to build."
}
],
"numbers": [],
"pearl": "A thin RV that is dilated, D-shaped and hypokinetic failed today, not over years.",
"related": [
"Q162",
"Q345",
"Q346"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "right ventricular infarction",
"discriminator": "RV infarction reproduces the dilated hypokinetic RV and even McConnell's pattern, but comes with inferior ST elevation, inferior LV wall-motion abnormality and no pulmonary hypertension."
},
"delta": null
},
{
"id": "Q384",
"orig": 384,
"title": "Functional tricuspid regurgitation and venous congestion",
"lesions": [
"TR",
"RV_FUNCTION",
"PH"
],
"lens": "doppler",
"items": [
{
"id": "Q384.1",
"q": "The tricuspid leaflets look structurally normal, yet a broad central jet fills the right atrium. Name the lesion and explain how it sustains itself.",
"a": "RV and tricuspid annular dilation pull the leaflets apart, producing functional TR; the regurgitant volume further enlarges the RV. Each increment of dilation stretches the annulus a little further and widens the leak, so the lesion feeds itself. Measure the annular diameter at end-diastole in the RV-focused apical 4-chamber view, where 4 cm or more supports severe functional TR, and state in the report that the leaflets themselves are normal, because that one sentence is what tells the surgeon to ring the annulus rather than repair a cusp."
},
{
"id": "Q384.2",
"q": "Why is the tricuspid regurgitant jet both a consequence of pulmonary hypertension and the tool you use to measure it, and when does that tool fail?",
"a": "Two linked relationships travel together here. Causally, chronic pulmonary hypertension imposes RV pressure overload that dilates the RV and tricuspid annulus and tethers the leaflets, producing functional (secondary) TR. Diagnostically, the peak TR-jet velocity is the primary echo signal used to estimate pulmonary-artery systolic pressure (simplified Bernoulli plus estimated RA pressure) — a measurement relationship, not the cause. Capture a clean CW TR envelope from several windows and use the highest velocity for PASP; a TR Vmax > 2.8–2.9 m/s flags probable PH. Trap: in torrential TR the RA and RV pressures equalize fast, the envelope becomes a low-velocity 'V-cutoff' triangle, and PASP is badly underestimated. TR peak velocity is the cornerstone parameter for echocardiographic PH-probability assessment, but a single velocity is not a probability: 2.8 m/s or less with no other sign is low, 2.9 to 3.4 m/s without supporting signs is intermediate, and it takes signs from two categories to upgrade a step."
},
{
"id": "Q384.3",
"q": "Severe tricuspid regurgitation is confirmed. What do you expect in the subcostal window and the hepatic veins, and why does it happen?",
"a": "Severe TR transmits the RV pressure pulse directly into the right atrium and venae cavae during systole, producing a dilated, non-collapsing inferior vena cava and systolic flow reversal in the IVC and hepatic veins. The elevated mean right atrial pressure prevents the normal inspiratory IVC collapse. On the subcostal view, measure IVC diameter 1-2 cm from the RA junction and assess collapse with a sniff. IVC >=21 mm with <50% collapse = plethora (RA pressure ~15 mmHg). Confirm with pulsed-wave Doppler of a hepatic vein: systolic flow reversal is ~80% sensitive for severe TR and is a key supportive sign, though it is confounded by AF/pacing and must be integrated with vena contracta and EROA. Plethora on its own is nonspecific, because it reflects elevated right atrial pressure from any cause."
},
{
"id": "Q384.4",
"q": "In chronic tricuspid regurgitation, which chamber gives way first, and what do you measure to prove it?",
"a": "Chronic tricuspid regurgitant volume loads the right atrium throughout systole, causing progressive RA dilation and annular stretching. RA/annular dilation in turn worsens leaflet coaptation, creating an atrial functional TR feedback loop. Atrial enlargement typically precedes RV dilation in chronic TR. In the apical 4-chamber view, planimeter RA area at end-systole (abnormal >19 cm2, with lower sex-specific cutoffs) and watch for interatrial septal bowing toward the left atrium, signaling RA pressure exceeding LA pressure. A giant RA with severe TR is a hallmark of long-standing or atrial-functional TR. The 19 cm² figure is the one the TR literature quotes; the ASE chamber-quantitation cut-off used everywhere else is 18 cm², so report 18 as your threshold and treat anything above it as a dilated atrium."
}
],
"numbers": [
{
"label": "Hepatic vein systolic flow reversal sensitivity for severe TR",
"value": "≈ 80",
"unit": "%"
}
],
"pearl": "Functional TR is a failure of geometry, not of leaflets: grade the annulus, not the cusps.",
"related": [
"Q82",
"Q86",
"Q232",
"Q233",
"Q270",
"Q347"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "primary (organic) tricuspid regurgitation",
"discriminator": "Functional TR has normal leaflets and a dilated annulus of 4 cm or more; primary TR shows the lesion on the leaflet itself, a vegetation, a carcinoid plaque, a flail segment or a pacing lead through the orifice."
},
"delta": null
},
{
"id": "Q385",
"orig": 385,
"title": "Carcinoid plaque on right-sided valves",
"lesions": [
"PS",
"TR",
"PR"
],
"lens": "2d",
"items": [
{
"id": "Q385.1",
"q": "A tricuspid valve is thickened, retracted and fixed half open, with torrential low-velocity regurgitation. Three diseases do that. How do you tell which one you are looking at?",
"a": "Serotonin and other mediators from metastatic midgut neuroendocrine tumors deposit fibrous plaque on the right-sided valve endocardium, leaving the tricuspid leaflets thickened, retracted and fixed semi-open so they cannot coapt — producing severe TR (often with some stenosis). The lungs inactivate serotonin, which is why the left-sided valves are typically spared. With flushing and diarrhea, a thick, retracted, fixed-open tricuspid valve with torrential free-flowing TR is carcinoid until proven otherwise. The CW TR signal is often low-velocity and dagger-shaped from rapid RA/RV equalization. Carcinoid retracts both right-sided valves and spares the left, so check the pulmonary valve; rheumatic disease fuses the commissures and essentially never spares the mitral valve, so look left; and a pacing lead splints one leaflet open while the rest looks normal. Carcinoid heart disease develops in roughly half of carcinoid syndrome patients, series ranging 20 to 50 percent, and TR is present in essentially all cardiac cases."
},
{
"id": "Q385.2",
"q": "You have called the tricuspid valve carcinoid. Where does the probe go next, and what will make that valve hard to find?",
"a": "The same serotonin-driven plaque scars the pulmonary valve, leaving the cusps thickened and immobile — a mixed lesion of pulmonary regurgitation and stenosis, often with a diminutive, barely visible valve. Simultaneous tricuspid AND pulmonary involvement strongly points to carcinoid. Whenever the tricuspid valve looks carcinoid-thickened, sweep immediately to the RVOT / pulmonary valve — it may be so retracted it is nearly invisible. Combined TV + PV disease is the carcinoid fingerprint. The pulmonary valve is involved in roughly 40 to 50 percent of carcinoid heart disease, so interrogate it from the PSAX aortic level and the parasternal RVOT view with color and CW even when you can barely see leaflet tissue."
}
],
"numbers": [],
"pearl": "Serotonin dies in the lungs, so carcinoid ruins the two valves upstream of them and spares the two downstream.",
"related": [
"Q88",
"Q94",
"Q95",
"Q229"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "rheumatic tricuspid disease",
"discriminator": "Rheumatic disease fuses commissures and almost never spares the mitral valve; carcinoid retracts the leaflets into a fixed semi-open position, takes the pulmonary valve with it, and leaves the left heart untouched."
},
"delta": null
},
{
"id": "Q386",
"orig": 386,
"title": "Ebstein anomaly and the atrialized ventricle",
"lesions": [
"EBSTEIN",
"TR",
"ASD"
],
"lens": "anatomy",
"items": [
{
"id": "Q386.1",
"q": "A 24-year-old with cyanosis has an enormous right atrium, and the septal tricuspid leaflet hinges 26 mm below the mitral hinge. Where is the regurgitant orifice, and why does that change how you hunt for the jet?",
"a": "Apical displacement and tethering of the septal and posterior tricuspid leaflets — with a large, redundant 'sail-like' anterior leaflet — prevent coaptation, producing the characteristic regurgitation; the proximal inlet RV is 'atrialized'. The regurgitant orifice sits below the true annulus, inside the ventricle, so look for the color jet down in the RV body rather than at the annular plane, where a quick sweep will miss it entirely. Work from the apical 4-chamber view and describe the size of the atrialized segment alongside the severity of the regurgitation, because the functional RV that is left is what determines whether this valve can be repaired."
},
{
"id": "Q386.2",
"q": "What must you add to the protocol before an Ebstein patient leaves the lab, and why?",
"a": "An interatrial communication (ASD or patent foramen) commonly coexists with Ebstein anomaly and permits right-to-left shunting and cyanosis. The route opens because the massive regurgitant load and the small functional RV hold right atrial pressure above left atrial pressure through much of the cycle. Interrogate the septum with color and pulsed Doppler from the subcostal and apical 4-chamber views and run an agitated saline study, watching for bubbles crossing into the left atrium within three beats."
},
{
"id": "Q386.3",
"q": "Which electrical diagnosis travels with Ebstein anomaly, and what should the echo report say about it?",
"a": "In Ebstein anomaly the failure of delamination of the tricuspid leaflets is accompanied by disrupted formation of the tricuspid annulus and atrialization of the inflow RV. This abnormal AV junction predisposes to accessory atrioventricular pathways (usually right-sided/posteroseptal, often multiple) that bypass the AV node, creating ventricular pre-excitation and a propensity for atrioventricular reentrant tachycardia. When echo shows apical displacement of the septal tricuspid leaflet (>8 mm/m2) with an atrialized RV, flag the ECG for a delta wave and short PR. Pathways here are frequently right-sided and often multiple, and the associated SVT can be the presenting problem. Always co-read the ECG with the Ebstein echo. Ebstein is the congenital lesion most commonly associated with WPW, with pre-excitation in about 20 percent of patients and higher rates in some series."
}
],
"numbers": [],
"pearl": "The leaflets never delaminated, so the annulus never insulated: the same failure that makes the valve leak lays down the accessory pathway.",
"related": [
"Q190",
"Q191",
"Q313",
"Q314",
"Q317"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "severe functional TR with a normally sited valve",
"discriminator": "In Ebstein the septal leaflet hinge is displaced 8 mm/m² or more below the mitral hinge with an atrialized inlet RV; functional TR keeps both hinges at the same level and dilates the annulus instead."
},
"delta": null
},
{
"id": "Q387",
"orig": 387,
"title": "Atrial septal defect and its variants",
"lesions": [
"ASD",
"CONGENITAL",
"TEE"
],
"lens": "best-method",
"items": [
{
"id": "Q387.1",
"q": "A 44-year-old is scanned for palpitations. The RV looks as large as the LV and the septum flattens in diastole, while the left-sided chambers are normal. Why are the left chambers normal, and what does that oblige you to do?",
"a": "A chronic left-to-right shunt volume-loads the right heart, dilating the RA and RV; paradoxical septal motion accompanies the volume overload. Normal left-sided chambers are part of the signature, because the shunted blood bypasses the left ventricle entirely and returns to the right heart. Unexplained RV dilation should prompt a careful search for an ASD (agitated-saline study, subcostal views). Record the RV basal diameter and the RV:LV ratio from the apical four-chamber, then move subcostal, where the beam meets the septum perpendicularly. Size the defect and estimate Qp:Qs there before you sign it out."
},
{
"id": "Q387.2",
"q": "Why is a superior sinus venosus defect almost never an isolated lesion, and what does its companion add to the hemodynamics?",
"a": "Sinus venosus ASDs result from deficient infolding between the right pulmonary veins and the cardinal/caval system, so they are almost always accompanied by partial anomalous pulmonary venous return, typically the right upper (and sometimes right middle) pulmonary vein draining anomalously into the SVC or RA. The anomalous vein adds an additional left-to-right shunt, augmenting right heart volume overload beyond the interatrial shunt. When you find unexplained RV and RA dilation with no obvious secundum defect, think PAPVR and a superior sinus venosus defect near the SVC-RA junction, poorly seen on standard TTE. Track each pulmonary vein to its drainage site, look for the right upper vein entering the SVC, and use agitated saline; a negative TTE does not exclude it. Go to TEE or CMR/CT when RV size and shunt physiology do not match the visible septum. Anomalous venous return accompanies 80 to 90 percent of sinus venosus defects and is not a feature of the common secundum defect."
},
{
"id": "Q387.3",
"q": "The RV is dilated with diastolic septal flattening, but the fossa ovalis looks intact and no color crosses it. Where do you look next, and with which window?",
"a": "A sinus venosus defect at the SVC-RA (superior) or IVC-RA (inferior) junction permits a left-to-right interatrial shunt, and the near-universal accompanying anomalous pulmonary vein adds further left-to-right flow. The combined volume load is delivered to the right heart, producing chronic RA and RV dilation with diastolic septal flattening. Sinus venosus defects sit outside the true atrial septum near the SVC entry and are frequently missed on transthoracic windows, so when you see RV dilation with a paradoxically intact-looking septum, this is the lesion to chase. Sweep high on subcostal and use the bicaval TEE view. Unexplained RV dilation should never be signed out without excluding a sinus venosus ASD and PAPVR. Sinus venosus defects account for roughly 5 to 10 percent of atrial septal defects, and the superior SVC-type variant predominates."
},
{
"id": "Q387.4",
"q": "You find a defect at the very bottom of the atrial septum, sitting against the AV valves in the apical four-chamber. Which valve lesion is essentially guaranteed?",
"a": "An ostium primum ASD is a partial atrioventricular septal defect arising from failure of the atrioventricular (endocardial) cushions to fuse. The same developmental defect produces a cleft in the left AV valve (the zone of apposition of the trifoliate left AV valve, commonly termed a cleft of the anterior/septal mitral leaflet). The cleft points toward the interventricular septum and creates a fixed regurgitant orifice producing a characteristically posteriorly-directed MR jet; a significant atrial shunt plus MR causes LA and LV volume overload. Whenever you identify a primum ASD low in the atrial septum adjacent to the AV valves on A4C, immediately look en face at the mitral valve in PSAX: a triangular cleft in the anterior leaflet points toward the septum, and color Doppler shows a posteriorly-directed MR jet from the cleft. The AV valves insert at the same level (loss of normal apical offset), confirming the AVSD substrate. A cleft is essentially universal here, and primum defects are 15 to 20 percent of ASDs."
}
],
"numbers": [
{
"label": "PAPVR accompanying a sinus venosus ASD",
"value": "80–90",
"unit": "%"
}
],
"pearl": "Believe the right ventricle, not the septum: when the fossa looks intact, the defect is sitting outside it.",
"related": [
"Q177",
"Q179",
"Q181",
"Q287",
"Q353"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "secundum ASD",
"discriminator": "A secundum defect sits in the fossa ovalis and is well seen subcostally with a rim you can measure for device closure; sinus venosus and primum defects sit outside the fossa, need TEE or CMR, and are surgical rather than device lesions."
},
"delta": null
},
{
"id": "Q388",
"orig": 388,
"title": "Patent foramen ovale and paradoxical embolism",
"lesions": [
"ASD",
"CONTRAST",
"MASS"
],
"lens": "procedure",
"items": [
{
"id": "Q388.1",
"q": "A 38-year-old with a cryptogenic stroke has an interatrial septum that visibly swings back and forth between the atria. Why does that mobility make a PFO both more likely and more dangerous?",
"a": "An atrial septal aneurysm and a patent foramen ovale share the septum primum/secundum overlap zone; the hypermobile, redundant aneurysm tissue both predisposes to and enlarges an associated PFO, creating a hypermobile complex with larger right-to-left shunting on Valsalva and a higher paradoxical-embolism risk. In a young patient with cryptogenic stroke and a wobbling septum, a bubble study is non-negotiable: image during and immediately after release of a Valsalva strain and count bubbles crossing within 3–5 beats. Atrial septal aneurysm is present in about 2 percent of people and a patent foramen in about a quarter, but PFO size and prevalence are substantially higher when an aneurysm is there. Document the septal excursion from the subcostal and apical four-chamber views and state that the two findings were seen together, because the combination is what drives management."
},
{
"id": "Q388.2",
"q": "Bubbles arrive in the left atrium. Which part of the study localizes the shunt and which part grades it, and why does that distinction decide management?",
"a": "A venous thrombus (or right-sided septic embolus) crosses a right-to-left interatrial shunt through the PFO, bypassing the pulmonary filter and entering the systemic arterial circulation to cause paradoxical embolism and cryptogenic stroke. Risk rises with a large shunt, PFO size, and a coexisting atrial septal aneurysm. In cryptogenic stroke, perform an agitated-saline bubble study with Valsalva. Distinguish two criteria: early left-heart microbubble appearance (within ~3-6 cardiac cycles of RA opacification) localizes an intracardiac shunt, while microbubble COUNT grades shunt size. A PFO plus atrial septal aneurysm markedly raises recurrent-stroke risk (OR ~24) and strengthens the case for closure. A patent foramen sits in about a quarter of adults, so it is over-represented but not always causal in cryptogenic stroke; attributable risk concentrates in younger patients with large shunts and a septal aneurysm, which is what the RoPE score formalizes."
}
],
"numbers": [],
"pearl": "A PFO is a finding in a quarter of the population; a large PFO with a wobbling septum in a young stroke patient is a diagnosis.",
"related": [
"Q26",
"Q289",
"Q290",
"Q333"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "an intrapulmonary shunt",
"discriminator": "Bubbles crossing the septum appear in the left atrium within about three beats of right atrial opacification; bubbles from a pulmonary arteriovenous malformation arrive after five or more beats and enter through the pulmonary veins."
},
"delta": null
},
{
"id": "Q389",
"orig": 389,
"title": "Shunt physiology progressing to Eisenmenger",
"lesions": [
"VSD",
"ASD",
"PH"
],
"lens": "chamber-effects",
"items": [
{
"id": "Q389.1",
"q": "An ASD floods the lungs with extra flow for decades. Why does pulmonary pressure usually stay normal anyway, and what do you measure to prove it has not?",
"a": "A long-standing large shunt raises pulmonary flow and, in a minority of cases, pressure — occasionally progressing to Eisenmenger physiology if uncorrected. As a pre-tricuspid shunt, an ASD raises pulmonary pressure later and less often than a VSD. An atrial defect sits before the tricuspid valve, so the lungs get the extra volume without the systemic pressure behind it. Estimate RVSP from the peak TR velocity with the IVC-derived right atrial pressure added, and report RV size and function beside it, since a volume-loaded RV and a pressure-loaded RV are two different problems that can share one patient."
},
{
"id": "Q389.2",
"q": "Why does an unrepaired ventricular septal defect threaten the pulmonary vasculature sooner than an atrial one, and what do you measure at each study to track it?",
"a": "A large VSD shunt increases pulmonary blood flow and pressure; without repair it can drive irreversible pulmonary vascular disease. A VSD sits downstream of the tricuspid valve, so the pulmonary arteries see left ventricular systolic pressure directly rather than extra volume alone. Size and locate the defect in parasternal short axis, take the peak shunt velocity with CW, and compute Qp:Qs from the RVOT and LVOT stroke volumes. That shunt velocity doubles as a pressure gauge: subtract 4v² from the systolic cuff pressure for an RV systolic pressure that cross-checks the TR estimate, valid only when there is no aortic stenosis or LVOT obstruction to lift LV pressure above the cuff."
},
{
"id": "Q389.3",
"q": "An adult with an unrepaired secundum ASD is newly hypoxemic, and color across the septum has turned bidirectional. What has happened, and how does it change what can be offered?",
"a": "A large, long-standing left-to-right shunt delivers chronic excess flow and pressure to the pulmonary circulation. Over years this drives progressive pulmonary vascular remodeling and a rise in pulmonary vascular resistance to systemic levels. When PVR exceeds SVR the shunt reverses to right-to-left or bidirectional (Eisenmenger physiology), producing cyanosis and severe, irreversible pulmonary arterial hypertension. In any adult with an unrepaired shunt, bidirectional or right-to-left color/spectral flow across the defect, severe RVH, a markedly dilated main pulmonary artery, and RV-systemic pressures signal shunt reversal; do not attribute new desaturation to lung disease. A bubble study showing early left-heart opacification confirms it. Once established, defect closure is contraindicated. This end point develops in a minority, roughly 10 percent, of large unrepaired atrial defects, later and less often than in post-tricuspid shunts such as VSD and PDA."
},
{
"id": "Q389.4",
"q": "On serial studies of a large unrepaired VSD, the peak shunt velocity has fallen from 4.8 m/s to 2.0 m/s. Is the defect closing?",
"a": "A large unrepaired VSD is a post-tricuspid (high-pressure) shunt that transmits systemic pressure directly to the pulmonary circulation. This produces earlier and more aggressive pulmonary vascular remodeling than an ASD, raising pulmonary vascular resistance until it meets or exceeds systemic resistance and the shunt reverses to right-to-left (Eisenmenger physiology with cyanosis and severe fixed PAH). In an adult with a known large VSD, a falling shunt velocity on CW Doppler is ominous: it means the LV-RV gradient is equalizing as PVR climbs, not that the defect is closing. Look for severe RVH, a dilated pulmonary artery, and bidirectional flow across the VSD; once the shunt reverses, the defect must not be closed. Large unrepaired ventricular defects carry roughly a 50 percent risk of progressing to Eisenmenger physiology, and VSD is the single most common cause of the syndrome."
}
],
"numbers": [
{
"label": "Eisenmenger physiology in large unrepaired ASD",
"value": "~ 10",
"unit": "%"
},
{
"label": "Eisenmenger physiology in large unrepaired VSD",
"value": "~ 50",
"unit": "%"
}
],
"pearl": "Pre-tricuspid shunts send the lungs volume and spare most patients; post-tricuspid shunts send them systemic pressure and take half.",
"related": [
"Q130",
"Q181",
"Q186",
"Q196",
"Q293"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "a restrictive VSD with a low-velocity jet from poor Doppler alignment",
"discriminator": "A malaligned jet gives a low velocity with a normal RV, normal pulmonary artery and unidirectional color; a genuinely equalized VSD comes with severe RV hypertrophy, a dilated pulmonary artery and bidirectional flow."
},
"delta": null
},
{
"id": "Q390",
"orig": 390,
"title": "Tetralogy of Fallot and pulmonary regurgitation",
"lesions": [
"PR",
"VSD",
"CONGENITAL"
],
"lens": "anatomy",
"items": [
{
"id": "Q390.1",
"q": "In an unrepaired tetralogy study, what makes the septal defect a malalignment VSD rather than an ordinary hole, and how do you demonstrate it?",
"a": "A large malalignment VSD is one of the four defining components of tetralogy of Fallot, with the aorta overriding the defect. The malalignment is anterocephalad deviation of the outlet septum, one embryologic event that both leaves a hole in the septum and crowds the right ventricular outflow tract, so the defect and the obstruction are the same lesion seen from two angles. Show it in the parasternal long axis, where the anterior aortic wall fails to line up with the interventricular septum and the aorta sits astride the defect, and estimate the override percentage there. Then sweep to parasternal short axis and subcostal for the outflow tract and take the gradient with CW, because it is the obstruction, not the defect, that decides how blue the patient is."
},
{
"id": "Q390.2",
"q": "A 31-year-old repaired in infancy comes in for a routine study. Which lesion should you assume is present before you put the probe down?",
"a": "Surgical repair of tetralogy of Fallot relieves RVOT obstruction, often via a transannular patch that disrupts pulmonary valve competence. The resulting chronic free pulmonary regurgitation imposes progressive RV volume overload, driving RV dilation, dysfunction, exercise intolerance, and ventricular arrhythmias over years to decades. In any adult with a history of TOF repair, severe PR is the rule, not the exception: look for a broad, low-velocity, rapidly decelerating diastolic flow in the RVOT (a wide, laminar to-and-fro that can look deceptively unimpressive on color). Serially track RV size and TAPSE/RV S'; progressive RV dilation is the trigger for pulmonary valve replacement, and CMR is the gold standard for RV volumes. Significant regurgitation is nearly universal after a transannular patch and is the leading indication for late pulmonary valve replacement."
}
],
"numbers": [],
"pearl": "One deviated outlet septum builds all four features, and the patch that relieves the obstruction trades it for a lifetime of free pulmonary regurgitation.",
"related": [
"Q176",
"Q244",
"Q246"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "physiologic pulmonary regurgitation",
"discriminator": "Physiologic PR is a narrow, brief, high-velocity jet with a normal RV; free PR after a transannular patch is broad and laminar, decelerates to baseline in early diastole, and comes with a progressively dilating RV."
},
"delta": null
},
{
"id": "Q391",
"orig": 391,
"title": "Endocarditis and perivalvular extension",
"lesions": [
"ENDOCARDITIS",
"PROSTHETIC",
"AORTA"
],
"lens": "best-method",
"items": [
{
"id": "Q391.1",
"q": "Blood cultures are positive and your transthoracic study looks clean. What has that clean study actually proved?",
"a": "Vegetations — mobile masses on the upstream valve surface — are the defining echocardiographic lesion of endocarditis. A normal TTE does not exclude endocarditis; proceed to TEE when suspicion is high. Upstream of normal flow is where the regurgitant jet lands: the atrial side of the mitral valve, the ventricular side of the aortic. Record the size in its longest dimension, the mobility, and the attachment site from every window that shows it, because those three descriptors are what the surgical conversation runs on."
},
{
"id": "Q391.2",
"q": "Your febrile patient with aortic valve endocarditis develops new first-degree AV block on the monitor overnight. What does the rhythm change predict, and where do you point the probe?",
"a": "Infection extending beyond the leaflets into annular tissue forms a perivalvular abscess — most common with aortic and prosthetic valve IE and in the relatively avascular mitral-aortic intervalvular fibrosa. It appears as perivalvular thickening or an echolucent cavity that does NOT flow on color Doppler (unlike a pseudoaneurysm), and is a surgical indication. In any aortic or prosthetic valve IE, deliberately interrogate the aortic root and intervalvular fibrosa. TTE sensitivity is poor (~50%) so a persistently febrile patient needs TEE; new PR prolongation or AV block means infection has reached the conduction tissue — escalate immediately. Abscess complicates roughly 10 to 30 percent of endocarditis, markedly more with aortic and prosthetic valves. Color is the discriminator: a periannular cavity that stays black is an abscess, and one that fills with flow has already ruptured into a pseudoaneurysm."
},
{
"id": "Q391.3",
"q": "Why does a prosthetic valve turn a routine endocarditis question into a TEE question, and which single 2D observation is a surgical emergency?",
"a": "Prosthetic material is a nidus for infection, and prosthetic valve endocarditis manifests as new paravalvular regurgitation, vegetations, ring abscess, or dehiscence with a rocking/unstable prosthesis. Conversely, infection causes the dysfunction, so the two findings drive each other and both demand TEE. Acoustic shadowing from the prosthesis hides vegetations on TTE; TEE is 2-3x more sensitive and can detect 1-2 mm vegetations, paravalvular leak, and abscess. A prosthesis that ROCKS (>15 degrees motion) signals >40% dehiscence from ring infection and is a surgical emergency. Prosthetic valves account for a substantial minority of all endocarditis and carry higher rates of abscess and dehiscence than native valves."
}
],
"numbers": [
{
"label": "Perivalvular abscess complicating endocarditis",
"value": "10–30",
"unit": "%"
}
],
"pearl": "Once infection leaves the leaflet it becomes a surgical problem, and the chest wall is the wrong window from which to find it.",
"related": [
"Q99",
"Q111",
"Q318",
"Q319",
"Q321"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "a paravalvular pseudoaneurysm",
"discriminator": "An abscess is an echolucent periannular cavity with no color flow entering it; once color fills the space it has ruptured and become a pseudoaneurysm, and flow crossing between two chambers makes it a fistula."
},
"delta": null
},
{
"id": "Q392",
"orig": 392,
"title": "Right-sided vegetations and their emboli",
"lesions": [
"ENDOCARDITIS",
"TR",
"MASS"
],
"lens": "pitfall",
"items": [
{
"id": "Q392.1",
"q": "Before you can say where a vegetation will travel, you have to say which side it sits on. What happens with a left-sided vegetation, and which features set the risk?",
"a": "Friable, mobile vegetations on left-sided valves shed septic emboli into the systemic circulation, most consequentially the brain (stroke, mycotic aneurysm), but also spleen, kidneys, and coronaries. Embolic risk rises sharply with vegetation size, mobility, and mitral location. Size the largest vegetation in its longest dimension across multiple views. Vegetations >10 mm roughly double embolic risk (OR ~2.3) and >15 mm with high mobility are highest risk, often prompting earlier surgery to prevent stroke. Use TEE when TTE is nondiagnostic, especially for mitral and prosthetic valves. Risk is highest before/early in antibiotic therapy. Above 15 mm, or above 10 mm with a prior embolus despite adequate therapy, is what turns the size into a surgical conversation. The date of your study is part of its meaning, so say where in the antibiotic course it was performed."
},
{
"id": "Q392.2",
"q": "A febrile 27-year-old who injects drugs has a quick bedside study called normal. Which views were probably skipped, and what were they hiding?",
"a": "Right-sided (tricuspid) endocarditis, classically from IV drug use or indwelling lines/leads, produces bulky vegetations that prevent leaflet coaptation and can cause leaflet destruction/perforation, resulting in tricuspid regurgitation. In a febrile IV drug user, interrogate the tricuspid valve in the RV-inflow and apical 4-chamber views; tricuspid vegetations are often large and mobile but easily missed on a quick scan. New or worsening TR plus septic-appearing lungs should trigger a dedicated right-heart and TEE look. The tricuspid valve is the most commonly affected valve in right-sided endocarditis, and tricuspid disease accounts for the majority of endocarditis related to injection drug use."
},
{
"id": "Q392.3",
"q": "The chest CT shows peripheral cavitating nodules and your study shows a mobile mass on the tricuspid valve. Why is this not a bland pulmonary embolism?",
"a": "Right-sided (tricuspid or pulmonic) vegetations shed septic emboli that travel antegrade through the RV and pulmonary artery to lodge in the lungs, producing septic pulmonary emboli with multifocal peripheral nodular/cavitary infiltrates (feeding-vessel sign) rather than bland thromboembolism. Right-sided vegetations embolize to the LUNG, not the systemic circulation (unless a PFO permits paradoxical crossover). When you find a tricuspid/pulmonic vegetation, the embolic target to anticipate is SEPTIC PE; correlate with chest imaging showing peripheral cavitating nodules. Do not equate this with bland/thrombotic PE. Chest imaging consistent with septic emboli is seen in roughly 75 to 87 percent of right-sided endocarditis patients, so the lung findings are expected rather than incidental."
}
],
"numbers": [
{
"label": "Septic emboli on chest imaging in right-sided endocarditis",
"value": "75–87",
"unit": "%"
}
],
"pearl": "Which side the vegetation sits on decides where it lands: left goes to the brain, right goes to the lung, and only a PFO lets it cross over.",
"related": [
"Q99",
"Q100",
"Q320",
"Q321"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "bland thromboembolic pulmonary embolism",
"discriminator": "Bland emboli give wedge-shaped peripheral infarcts with a proximal clot burden; septic emboli give multifocal peripheral cavitating nodules with a feeding-vessel sign and a right-sided vegetation to account for them."
},
"delta": null
},
{
"id": "Q393",
"orig": 393,
"title": "Cardiac sources of systemic embolism",
"lesions": [
"MASS",
"ENDOCARDITIS",
"CONTRAST"
],
"lens": "best-method",
"items": [
{
"id": "Q393.1",
"q": "A stroke patient's transthoracic study is signed out as 'no cardiac source of embolism.' Which of the four sources has that sentence actually addressed?",
"a": "One, and only conditionally. A plain transthoracic study interrogates the left ventricular cavity, and it does that badly at the apex, where near-field clutter and foreshortening hide exactly the clot you are hunting, so without an enhancing agent even that source is not excluded. The appendage sits behind the aorta and is essentially invisible from the chest wall, a 2 mm vegetation is below transthoracic resolution, and a foramen that opens only on the release of a strain shows nothing at rest. Name the sources you assessed and the sources you did not, because 'no cardiac source' read by a neurologist closes a workup that has barely started."
},
{
"id": "Q393.2",
"q": "Anticoagulation was started five days ago and today's contrast study shows no apical thrombus. Does that clear the ventricle as the source of last week's stroke?",
"a": "It does not, because every one of these sources shrinks under the treatment the patient has already been given. Ventricular thrombus organizes and resolves on anticoagulation, vegetations regress once effective antibiotics start, and appendage emptying velocity climbs as soon as sinus rhythm returns, so a study performed after treatment answers a different question from the one the stroke asked. Date the study against the start of therapy in one line of the impression. When the timing has already made the search futile, report the substrate instead of the mass: an akinetic apex, an atrium emptying below 20 cm/s, or a destroyed leaflet all say the source was there even after the clot has gone."
},
{
"id": "Q393.3",
"q": "Your bubble study in a 34-year-old with a cryptogenic stroke is negative. Before you accept it, what could have made it falsely negative?",
"a": "A bubble study fails from technique far more often than from anatomy. The strain has to be held long enough to raise right atrial pressure and the bubbles have to arrive during its release, because that is the only moment the interatrial gradient reverses, so a badly coached strain or a sedated patient who cannot perform one gives a negative study on a septum that shunts every day. The right atrium must also opacify densely, which needs a large-bore antecubital cannula and a brisk flush. Record continuously through the release and count bubbles reaching the left atrium within about three beats; arrival after five beats through the pulmonary veins is an intrapulmonary shunt, not a foramen. If suspicion stays high, repeat it on TEE with the strain rehearsed before the probe goes in."
},
{
"id": "Q393.4",
"q": "You find a patent foramen ovale in a 78-year-old with atrial fibrillation and a middle cerebral artery stroke. Is it the source?",
"a": "Almost certainly not, and saying so is part of the report. A foramen sits in about a quarter of the population, so finding one in a patient who already has a stronger explanation adds a finding rather than a diagnosis, and in atrial fibrillation the appendage is the source until a TEE says otherwise. Attributable risk for a foramen concentrates in younger patients with a large shunt or a septal aneurysm and no competing cause, which is what the RoPE score formalizes. When two candidates are present, rank them in the impression rather than listing them, because an unranked list sends the patient toward a closure device instead of an anticoagulant."
}
],
"numbers": [],
"pearl": "'No cardiac source' is not a finding, it is a list of the sources you did not look for.",
"related": [
"Q26",
"Q329",
"Q331",
"Q333",
"Q353"
],
"reviewed": "2026-09-07",
"lookalike": {
"vs": "a cardiac finding that is incidental rather than causal",
"discriminator": "A source has to fit the patient: a foramen in a young patient with a large shunt, a septal aneurysm and no competing cause is causal, while the same foramen alongside atrial fibrillation or an akinetic apex is a bystander."
},
"delta": null
},
{
"id": "Q394",
"orig": 394,
"title": "Wavelength and the 1540 m/s assumption",
"lesions": [
"US_PHYSICS",
"INSTRUMENTATION"
],
"lens": "formula",
"reviewed": "2026-09-07",
"items": [
{
"id": "Q394.1",
"q": "What sets the speed of sound in tissue, and can you change it from the console?",
"a": "Sound travels by compressing the medium ahead of it, so its speed is fixed by how stiff that medium is and how dense it is, c = √(K/ρ), with stiffness dominant. Fat runs at about 1450 m/s, soft tissue at 1540 m/s, muscle near 1580 m/s, cortical bone at 4080 m/s, and air collapses to roughly 330 m/s. At diagnostic amplitudes and body temperature nothing on the console moves c: output power, depth, gain, focus and probe selection all leave it where it was. Swapping a 2 MHz probe for a 10 MHz probe changes f, and wavelength falls from 0.77 mm to 0.154 mm to keep λ = c/f satisfied. The only way to change c is to point the beam at a different tissue."
},
{
"id": "Q394.2",
"q": "Why does the machine assume 1540 m/s, and what does it do with the number?",
"a": "A conventional B-mode beamformer does not measure propagation speed; it assumes it. It measures the go-and-return time of each echo and converts that time to depth with d = c·t/2, so it must supply c from somewhere, and 1540 m/s is the working average across liver, muscle, fat, blood and kidney. It is also the value written into the AIUM and IEC specifications for tissue-mimicking material, which is why the phantom and the scanner agree. In imaging units that is 1.54 mm per microsecond: 13 microseconds of round trip per centimeter of depth. A structure at 10 cm returns its echo 130 microseconds after transmission, and that timing is all the machine knows about where it is."
},
{
"id": "Q394.3",
"q": "What happens on the image when the true speed is not 1540 m/s?",
"a": "Because the machine converts time to depth at a fixed 1.54 mm/µs, a slower medium returns its echo late and the reflector is painted too deep, while a faster medium paints it too shallow. Taking fat at the 1450 m/s this deck uses, it is 5.8% slower than the assumption, so everything behind it lands 6.2% too deep: a true 5 cm layer of epicardial fat is drawn as 5.3 cm, shifting what lies beyond it about 3 mm deeper. The same mismatch breaks the delays the beamformer calculated on the way out, so the focus smears — the phase aberration you see in a large patient. When a measurement matters, get the target on-axis and as free of intervening fat as the window allows, because you cannot correct this from the panel."
}
],
"numbers": [
{
"label": "Speed of sound in soft tissue, imaging units",
"value": "1.54",
"unit": "mm/µs"
},
{
"label": "Wavelength in soft tissue at 2 MHz",
"value": "0.77",
"unit": "mm"
},
{
"label": "Wavelength in soft tissue at 3.5 MHz",
"value": "0.44",
"unit": "mm"
},
{
"label": "Wavelength in soft tissue at 5 MHz",
"value": "0.31",
"unit": "mm"
},
{
"label": "Wavelength in soft tissue at 10 MHz",
"value": "0.154",
"unit": "mm"
},
{
"label": "Propagation speed in fat",
"value": "1450",
"unit": "m/s"
},
{
"label": "Propagation speed in cortical bone",
"value": "4080",
"unit": "m/s"
},
{
"label": "Propagation speed in air",
"value": "330",
"unit": "m/s"
},
{
"label": "Depth overestimation for echoes behind fat",
"value": "6.2",
"unit": "%"
}
],
"pearl": "You pick the frequency, the tissue owns the speed, and the machine assumes 1540 either way.",
"equation": "λ = c / f; in soft tissue λ(mm) = 1.54 / f(MHz). Depth comes from d = c·t/2 with c held at 1540 m/s.",
"related": [],
"delta": null,
"lookalike": null
},
{
"id": "Q395",
"orig": 395,
"title": "Acoustic impedance and why gel is mandatory",
"lesions": [
"US_PHYSICS",
"INSTRUMENTATION"
],
"lens": "definition",
"reviewed": "2026-09-07",
"items": [
{
"id": "Q395.1",
"q": "What is acoustic impedance, and what changes it?",
"a": "Impedance is the opposition a medium presents to the passage of sound, and it is the product of exactly two properties of that medium, Z = ρ × c: density times propagation speed. The unit is the rayl, and tissue values are quoted in megarayl — soft tissue 1.63, fat 1.33, blood 1.61, muscle 1.69, cortical bone 7.75, and air 0.0004 MRayl, which is 396 rayl. Frequency does not appear in the equation, so moving from 2 MHz to 10 MHz changes nothing, and neither does gain, output power, depth or focus. Substituting c = √(K/ρ) gives Z = √(ρK): impedance is fixed by the density and the stiffness of the tissue in front of you. No console control adjusts it — the only way to change the impedance the beam sees is to change what is in the beam, which is what an enhancing agent does to the blood pool."
},
{
"id": "Q395.2",
"q": "Why is gel mandatory, and what is it actually doing?",
"a": "A film of air between the transducer face and the skin puts 0.0004 MRayl against tissue's 1.63 MRayl, and that mismatch reflects 99.9% of the intensity straight back at the element. Gel works by displacement first: remove the air and the air–skin interface no longer exists in the beam path. Its impedance matters second — formulated near 1.5 to 1.7 MRayl against skin at about 1.6, the interface it does create reflects a few tenths of a percent at worst. What gel is not is the quarter-wave matching layer inside the probe, which steps the beam from the element's roughly 30 MRayl toward tissue at an ideal 7 MRayl. Press firmly enough that no rim of air survives at the edge of a small footprint, because a dropout you blame on the window is often a millimeter of trapped air."
}
],
"numbers": [
{
"label": "Acoustic impedance of soft tissue",
"value": "1.63",
"unit": "MRayl"
},
{
"label": "Acoustic impedance of fat",
"value": "1.33",
"unit": "MRayl"
},
{
"label": "Acoustic impedance of blood",
"value": "1.61",
"unit": "MRayl"
},
{
"label": "Acoustic impedance of muscle",
"value": "1.69",
"unit": "MRayl"
},
{
"label": "Acoustic impedance of cortical bone",
"value": "7.75",
"unit": "MRayl"
},
{
"label": "Acoustic impedance of air",
"value": "396",
"unit": "rayl"
},
{
"label": "Coupling gel, formulated near skin",
"value": "1.5–1.7",
"unit": "MRayl"
},
{
"label": "PZT transducer element",
"value": "≈ 30",
"unit": "MRayl"
},
{
"label": "Ideal quarter-wave matching layer",
"value": "≈ 7",
"unit": "MRayl"
}
],
"pearl": "Impedance is density times speed and nothing else, so the echo belongs to the boundary, never to the knob.",
"equation": "Z = ρ × c = √(ρK), in rayl (kg·m⁻²·s⁻¹); tissue values are quoted in megarayl.",
"related": [],
"delta": null,
"lookalike": null
},
{
"id": "Q396",
"orig": 396,
"title": "Reflection at an interface: R and T",
"lesions": [
"US_PHYSICS",
"INSTRUMENTATION"
],
"lens": "formula",
"reviewed": "2026-09-07",
"items": [
{
"id": "Q396.1",
"q": "What sets the size of the echo from a boundary?",
"a": "At normal incidence an echo exists only because the two media present different acoustic impedances, and the fraction of intensity sent back is R = ((Z₂ − Z₁)/(Z₂ + Z₁))², with whatever is not reflected transmitted, so R + T = 1. Because the bracket is squared, the intensity is identical in either direction: blood into myocardium and myocardium into blood both reflect 0.06%. The amplitude is not identical — reflecting off the higher-impedance medium inverts the pulse — so order matters to phase even though it does not matter to brightness. Neither density alone nor speed alone predicts the echo, and two media differing in both can share an impedance and give you nothing. An anatomically real boundary can be sonographically invisible."
},
{
"id": "Q396.2",
"q": "How much of the beam comes back at a typical soft-tissue boundary?",
"a": "Soft tissues cluster tightly between about 1.33 and 1.69 MRayl, so the mismatches are tiny: soft tissue into liver reflects 0.002%, blood into myocardium 0.06%, soft tissue into muscle 0.03%, and fat into muscle, one of the largest, still only 1.4%. More than 98% carries on past each boundary, so the pulse is not destroyed at every interface it crosses — what limits how deep you can image is attenuation, not these reflection losses. Push one impedance out of the cluster and the picture inverts: soft tissue to air reflects 99.9%, soft tissue to cortical bone about 43%. Blood against soft tissue reflects 0.005%, so there is no boundary echo to see; blood looks anechoic because red cells are weak scatterers, and that same scattering gives you the Doppler signal."
},
{
"id": "Q396.3",
"q": "Air and bone both shadow. Is it the same mechanism?",
"a": "No, and the exam separates them. Air shadows by reflection: 99.9% comes back at the interface and 0.1% goes on, so essentially nothing survives to image with, which is the whole argument for coupling gel and the reason lung and bowel gas stop the beam dead. Bone reflects about 43%, which means 57% does get through — more than half — so reflection alone cannot explain a rib shadow. Bone shadows because it absorbs what enters it, at roughly 10 dB/cm/MHz against soft tissue's 0.7, and whatever survives must cross the bone twice. Read a shadow by asking which of the two is doing the work, because the fix differs: slide off a rib, but no amount of sliding gets you through gas."
}
],
"numbers": [
{
"label": "Intensity reflected, soft tissue → air",
"value": "99.9",
"unit": "%"
},
{
"label": "Intensity reflected, soft tissue → cortical bone",
"value": "42.5",
"unit": "%"
},
{
"label": "Intensity reflected, fat → muscle",
"value": "1.4",
"unit": "%"
},
{
"label": "Intensity reflected, soft tissue → fat",
"value": "1.0",
"unit": "%"
},
{
"label": "Intensity reflected, blood → myocardium",
"value": "0.06",
"unit": "%"
},
{
"label": "Intensity reflected, soft tissue → muscle",
"value": "0.03",
"unit": "%"
},
{
"label": "Intensity reflected, soft tissue → liver",
"value": "0.002",
"unit": "%"
},
{
"label": "Attenuation coefficient of cortical bone",
"value": "10",
"unit": "dB/cm/MHz"
}
],
"pearl": "Reflection is a mismatch, not a tissue: swap the two media and the brightness is identical.",
"equation": "At normal (perpendicular, 0°) incidence: R = ((Z₂ − Z₁)/(Z₂ + Z₁))² and T = 1 − R = 4Z₁Z₂/(Z₁ + Z₂)². Both are intensity coefficients and R + T = 1.",
"related": [],
"delta": null,
"lookalike": null
},
{
"id": "Q397",
"orig": 397,
"title": "Attenuation and the half-value layer",
"lesions": [
"US_PHYSICS",
"INSTRUMENTATION"
],
"lens": "formula",
"reviewed": "2026-09-07",
"items": [
{
"id": "Q397.1",
"q": "Is the 0.5 dB/cm/MHz figure the loss down to the reflector, or the loss the echo has suffered by the time it gets back?",
"a": "It is one way. The coefficient is 0.5 dB for every centimeter traveled at every megahertz, so a 3 MHz beam loses 1.5 dB per centimeter and the total is that coefficient times path length. A pulse returning from a reflector at 15 cm has covered 30 cm, not 15, so the round trip costs 45 dB while the one-way figure is only 22.5 dB. Since the round trip is exactly twice the one-way figure, round-trip loss in decibels equals frequency in MHz times depth in centimeters. Forty-five decibels leaves 0.003% of the transmitted intensity, which is the number behind the receiver's gain reserve and the steepness of the TGC ramp. Read any quoted attenuation as one way unless the question says the sound went down and back."
},
{
"id": "Q397.2",
"q": "What is the half-value layer, and what number goes with each probe?",
"a": "Halving the intensity is a loss of 3 dB, so the half-value layer is 3 dB divided by the attenuation coefficient at that frequency, which in soft tissue collapses to 6 divided by the frequency in megahertz, in centimeters. A 2 MHz phased array halves its intensity every 3 cm, a 3 MHz probe every 2 cm, a 5 MHz probe every 1.2 cm, and a 12 MHz linear probe every 5 mm. It is fixed by the tissue and the transmit frequency, not by gain and not by output power, and frequency is the only control that moves it. When a large patient goes dark beyond 12 cm, dropping from 3 MHz to 2 MHz stretches every halving from 2 cm to 3 cm, which buys more penetration than gain can, because gain amplifies the noise with the echo."
},
{
"id": "Q397.3",
"q": "Where does the energy go, and what does that predict on the image?",
"a": "Attenuation is absorption, scattering and reflection together, and in soft tissue absorption — sound energy converted to heat — dominates, which makes it a bioeffects question as much as an image-quality one. Absorption rises roughly linearly with frequency, which is why the coefficient is written per megahertz, while Rayleigh scattering from targets much smaller than a wavelength rises with the fourth power. Compensation is set for uniformly attenuating tissue, so anything that attenuates differently from its neighbors announces itself. A fluid-filled cyst attenuates far less and the tissue behind it is over-amplified into posterior enhancement, while a calcified leaflet or rib attenuates far more and casts a shadow. Read those two as measurements of what sits in front of them."
}
],
"numbers": [
{
"label": "Attenuation coefficient of soft tissue, one way",
"value": "0.5",
"unit": "dB/cm/MHz"
},
{
"label": "Round-trip loss, 3 MHz at 15 cm depth",
"value": "45",
"unit": "dB"
},
{
"label": "Intensity loss that halves intensity",
"value": "3",
"unit": "dB"
},
{
"label": "Half-value layer at 2 MHz",
"value": "3.0",
"unit": "cm"
},
{
"label": "Half-value layer at 3 MHz",
"value": "2.0",
"unit": "cm"
},
{
"label": "Half-value layer at 5 MHz",
"value": "1.2",
"unit": "cm"
},
{
"label": "Half-value layer at 12 MHz",
"value": "0.5",
"unit": "cm"
},
{
"label": "Useful receiver dynamic range budget",
"value": "60",
"unit": "dB"
}
],
"pearl": "Half a decibel per centimeter per megahertz each way, so the echo pays frequency times depth.",
"equation": "One-way loss (dB) = 0.5 × f(MHz) × path(cm). Round-trip loss from a reflector at depth d = f × d dB. Half-value layer = 3 dB ÷ (0.5 × f) = 6/f cm.",
"widgets": [
"attenuation"
],
"related": [],
"delta": null,
"lookalike": null
},
{
"id": "Q398",
"orig": 398,
"title": "Refraction and the critical angle",
"lesions": [
"US_ARTIFACTS",
"US_PHYSICS",
"INSTRUMENTATION"
],
"lens": "pitfall",
"reviewed": "2026-09-07",
"items": [
{
"id": "Q398.1",
"q": "Under what conditions does the beam bend at all?",
"a": "Refraction is transmission with a bend, and it needs two things at once: the beam must strike the boundary obliquely, and the two media must have different propagation speeds. Remove either and the transmitted beam goes straight on — a beam meeting a fat–muscle boundary head-on is not refracted despite a 130 m/s speed difference, and a beam meeting a boundary at 40 degrees between media of identical speed is not refracted either. Snell's law then fixes the size of the bend, sin θt / sin θi = c₂ / c₁, so a faster second medium swings the beam away from the normal and a slower one pulls it toward the normal. Hold the two ideas apart: impedance decides whether you get an echo, speed decides where the transmitted part travels."
},
{
"id": "Q398.2",
"q": "How large are these bends in a patient, and what does the scanner do with the result?",
"a": "Human soft tissues sit within about 100 m/s of the 1540 m/s average, so the bends are small: crossing from soft tissue into fat at 30 degrees of incidence gives a transmitted angle of 28.1 degrees, a deflection of 1.9 degrees. The scanner writes every echo along the straight line it believes it fired, so the structure is drawn in the wrong place — about 3.3 mm off at 10 cm beyond the interface, and misplaced in depth too, since the same fat also violates the 1540 m/s assumption. When only part of the aperture crosses a lens-shaped refracting layer you get a duplicate, the double aorta seen through the fat between the rectus muscles. Fix it with the probe: slide or rotate so the beam no longer crosses that oblique interface."
},
{
"id": "Q398.3",
"q": "When does the transmitted beam disappear entirely?",
"a": "Increase the incident angle and the transmitted angle grows faster still, until Snell's law would demand a transmitted angle beyond 90 degrees, which is impossible. At that incidence — the critical angle, θc = arcsin(c₁/c₂) — the transmitted ray grazes the boundary, and beyond it nothing crosses. It exists only when the second medium is the faster one, so going from fast into slow there is no critical angle at any incidence. Soft tissue into cortical bone puts it at 22.2 degrees, so the curved flanks of a rib transmit nothing — though the shadow behind a rib is mostly the 43% reflected at its near surface plus the absorption inside the bone. Fat into muscle sits at 66.6 degrees, and near-critical incidence at the wall of a cyst is one accepted mechanism for edge shadows."
}
],
"numbers": [
{
"label": "Propagation speed range across soft tissue",
"value": "1400–1640",
"unit": "m/s"
},
{
"label": "Transmitted angle, soft tissue → fat at 30° incidence",
"value": "28.1",
"unit": "degrees"
},
{
"label": "Displacement 10 cm beyond a 1.9° bend",
"value": "≈ 3.3",
"unit": "mm"
},
{
"label": "Critical angle, soft tissue → cortical bone",
"value": "22.2",
"unit": "degrees"
},
{
"label": "Critical angle, fat → muscle",
"value": "66.6",
"unit": "degrees"
}
],
"pearl": "Impedance decides whether you get an echo; speed decides where the machine draws it.",
"equation": "sin θt / sin θi = c₂ / c₁. Refraction needs BOTH oblique incidence AND c₁ ≠ c₂. A critical angle exists only when c₂ > c₁: θc = arcsin(c₁/c₂). All angles are measured from the normal, so perpendicular incidence is 0°.",
"related": [],
"delta": null,
"lookalike": null
},
{
"id": "Q399",
"orig": 399,
"title": "Axial resolution is half the pulse",
"lesions": [
"IMAGE_OPT",
"INSTRUMENTATION"
],
"lens": "formula",
"reviewed": "2026-09-07",
"items": [
{
"id": "Q399.1",
"q": "Why is axial resolution half the spatial pulse length rather than the whole pulse length?",
"a": "Two reflectors separated by a distance d along the beam return echoes separated in time by 2d/c, because the pulse travels down to the deeper one and back again. Those echoes stay distinct only if that gap exceeds the pulse duration, so d must exceed c × PD / 2, and since c × PD is the spatial pulse length, the resolvable separation is SPL/2. The round trip is what supplies the factor of two; it has nothing to do with the shape of the wave. With a 3-cycle pulse at 3 MHz the spatial pulse length is 1.54 mm, so you can separate reflectors 0.77 mm apart and no closer. Anything nearer than that arrives inside the pulse and is written as a single echo."
},
{
"id": "Q399.2",
"q": "What sets the number of cycles in a pulse?",
"a": "The crystal rings after it is excited, and the backing or damping layer bonded behind it absorbs that ringing to cut the transmit pulse short — which is also why imaging probes are low-Q and wide-bandwidth, and why Q-factor is roughly the cycle count. Damped pulses run 2 to 3 cycles in the registry model, and modern broadband probes get to about 1.5, but never to 1, so axial resolution is nλ/2 and never λ/2. At 5 MHz, where λ is 0.31 mm, a 2-cycle pulse gives 0.31 mm of axial resolution and a 3-cycle pulse 0.46 mm. In soft tissue the arithmetic collapses to axial resolution in mm = 0.77 × cycles ÷ frequency in MHz."
},
{
"id": "Q399.3",
"q": "What can you change at the machine to improve axial resolution?",
"a": "Only the two terms in nλ/2. Raising the transmit frequency shortens λ in direct proportion, so with a 2-cycle pulse axial resolution goes 0.77 mm at 2 MHz, 0.31 mm at 5 MHz and 0.15 mm at 10 MHz, at the price of penetration. The backing block sets a floor on how short the pulse can be — you cannot get shorter than the probe rings — but you can get longer, because a penetration transmit setting or coded excitation lengthens the burst and costs you axial resolution. Moving the focus, widening the aperture, changing depth or adding focal zones does nothing to it, because the pulse is the same length at every depth along the beam."
}
],
"numbers": [
{
"label": "Cycles per damped B-mode transmit pulse",
"value": "2–3",
"unit": "cycles"
},
{
"label": "Axial resolution, 3 MHz, 2-cycle pulse",
"value": "0.51",
"unit": "mm"
},
{
"label": "Axial resolution, 3 MHz, 3-cycle pulse",
"value": "0.77",
"unit": "mm"
},
{
"label": "Axial resolution, 5 MHz, 2-cycle pulse",
"value": "0.31",
"unit": "mm"
},
{
"label": "Axial resolution, 5 MHz, 3-cycle pulse",
"value": "0.46",
"unit": "mm"
},
{
"label": "Spatial pulse length, 3 MHz, 3-cycle pulse",
"value": "1.54",
"unit": "mm"
},
{
"label": "Spatial pulse length, adult cardiac at 2–3.5 MHz",
"value": "0.9–2.3",
"unit": "mm"
}
],
"pearl": "Axial resolution is half a pulse, not half a wavelength: the crystal rings two or three times, and that ringing is your limit.",
"equation": "AR = SPL/2 = (n × λ)/2 = 0.77n / f  [mm, soft tissue, f in MHz, n = cycles per pulse]",
"widgets": [
"axialres"
],
"related": [],
"delta": null,
"lookalike": null
},
{
"id": "Q400",
"orig": 400,
"title": "Lateral resolution is the beam width",
"lesions": [
"IMAGE_OPT",
"INSTRUMENTATION"
],
"lens": "formula",
"reviewed": "2026-09-07",
"items": [
{
"id": "Q400.1",
"q": "Why is lateral resolution simply the beam width?",
"a": "Every echo is written onto the image at the position of the scan line, not the position of the reflector that made it, so while two side-by-side structures both sit inside the beam the machine cannot separate them and paints them as one wide smear — the point spread artifact. They resolve only once the beam is narrower than the gap between them, so the numerical value of lateral resolution is the beam diameter at that depth. The transmit beam is not a constant width: it leaves the face at the aperture width, converges to a waist at the focus, then diverges beyond it, though dynamic receive focusing narrows the received beam at every depth. That is the whole difference from axial resolution, which is a property of the pulse and the same at every depth."
},
{
"id": "Q400.2",
"q": "What sets the beam width at the focus, and how bad does it get with depth?",
"a": "Diffraction at the aperture sets it: the waist is proportional to the wavelength times the f-number, where the f-number is focal depth divided by active aperture width, so LR ≈ λ × F#. A cardiac phased array with a 20 mm aperture focused at 6 cm is running F# 3, and at 3 MHz the waist is about 1.5 mm. Push the focus to 15 cm on that same fixed footprint and F# becomes 7.5 and the waist grows to about 3.8 mm. In echo the aperture cannot grow past the rib space, so the f-number rises in direct proportion to depth and lateral resolution degrades linearly the deeper you look."
},
{
"id": "Q400.3",
"q": "How much worse is lateral than axial, and what do you do about it?",
"a": "Take the ratio directly: LR/AR = 2 × F# / n, so at the f-numbers cardiac imaging runs — 3 at 6 cm and 7.5 at 15 cm on a rib-limited aperture — lateral is roughly 3 to 5 times worse than axial with a 3-cycle pulse. At the low f-numbers a wide linear array can reach, the two converge and lateral can even win at the focus, so the ratio is the fact and \"lateral is always worse\" is not. On a phased array with a fixed elevation lens the real ceiling is neither: elevational resolution, the slice thickness, is usually the worst of the three axes and is what fills small cavities with spurious echoes. Put the focus at the depth you are interrogating, reduce depth and narrow the sector."
}
],
"numbers": [
{
"label": "F# for a 20 mm cardiac aperture focused at 6 cm",
"value": "3.0",
"unit": ""
},
{
"label": "F# for a 20 mm cardiac aperture focused at 15 cm",
"value": "7.5",
"unit": ""
},
{
"label": "F#, adult cardiac phased array, minimum",
"value": "3.5–4.5",
"unit": ""
},
{
"label": "Beam width at focus, 3 MHz, F# 3",
"value": "≈ 1.5",
"unit": "mm"
},
{
"label": "Beam width at focus, 3 MHz, F# 7.5",
"value": "≈ 3.8",
"unit": "mm"
},
{
"label": "Frame-rate cost per added focal zone",
"value": "1",
"unit": "extra pulse per scan line"
}
],
"pearl": "Axial resolution is what your pulse is; lateral resolution is where your focus is; elevation is the one you never set.",
"equation": "LR ≈ beam diameter at that depth; at the focus LR ≈ λ × F#, where F# = focal depth / active aperture. Against axial: LR/AR = 2 × F# / n.",
"related": [],
"delta": null,
"lookalike": null
},
{
"id": "Q401",
"orig": 401,
"title": "Near field length and the focus ceiling",
"lesions": [
"IMAGE_OPT",
"TRANSDUCER",
"INSTRUMENTATION"
],
"lens": "formula",
"reviewed": "2026-09-07",
"items": [
{
"id": "Q401.1",
"q": "What does the near field length mark?",
"a": "The beam leaves the transducer face at the aperture width, converges through the near or Fresnel zone to its narrowest point, then diverges into the far zone. The near field length is the depth of that natural waist, D²/(4λ), equivalently r²/λ with r the radius, and since λ = c/f it can be written D²f/(4c). Aperture enters squared while frequency enters only linearly, so doubling the aperture quadruples the near field length while doubling the frequency merely doubles it. For an unfocused disc the beam diameter at the near field length is half the transducer diameter — the best lateral resolution that aperture gives without a lens — and by two near field lengths it has diverged back out to the full diameter."
},
{
"id": "Q401.2",
"q": "Why does this number cap where focusing helps?",
"a": "A lens or an electronic delay pattern can pull the waist shallower than the natural focus, but it cannot push it deeper: a beam cannot be focused beyond the end of its near field. The focus control will still move there — nothing on the machine refuses — it just stops buying you anything, because past the near field the beam is no narrower than it would be unfocused. A 20 mm cardiac aperture at 3.5 MHz gives 400 / (4 × 0.44) = 227 mm, or 22.7 cm, deeper than any transthoracic study, so you may usefully place the focus anywhere on the depth scale. Halve the aperture to 10 mm and the near field length falls fourfold to 5.7 cm, and a focus at 12 cm buys nothing."
},
{
"id": "Q401.3",
"q": "How does this apply to a cardiac phased array rather than a disc?",
"a": "D²/(4λ) and the D/2 landmark are the unfocused circular-disc result, so on a rectangular phased-array footprint treat them as an order-of-magnitude tool rather than a specification. Run it on both apertures, because they differ: a 20 × 14 mm adult cardiac footprint at 3.5 MHz gives about 21 cm in the azimuthal plane but only 11 cm in elevation, and elevation is exactly the plane where slice-thickness artifact lives. So the plane that runs out first is the one you never control. Choose aperture and frequency so the depth you care about sits at or shallower than the natural waist, and read an inability to sharpen a deep structure as the aperture running out rather than the focus control failing."
}
],
"numbers": [
{
"label": "Near field length, 20 mm aperture at 3.5 MHz",
"value": "22.7",
"unit": "cm"
},
{
"label": "Near field length, 20 mm aperture at 2.5 MHz",
"value": "16.2",
"unit": "cm"
},
{
"label": "Near field length, 10 mm aperture at 3.5 MHz",
"value": "5.7",
"unit": "cm"
},
{
"label": "Near field length, 14 mm elevation aperture at 3.5 MHz",
"value": "11.1",
"unit": "cm"
},
{
"label": "Beam diameter at one near zone length",
"value": "half the transducer diameter",
"unit": ""
},
{
"label": "Effect on near field length of doubling the aperture",
"value": "×4",
"unit": ""
}
],
"pearl": "You can pull the focus shallower than the near field ends, never usefully deeper.",
"equation": "NZL = D²/(4λ) = r²/λ = D²f/(4c) ≈ D²(mm) × f(MHz) / 6.16  [mm, soft tissue]",
"related": [],
"delta": null,
"lookalike": null
},
{
"id": "Q402",
"orig": 402,
"title": "Depth, pulse repetition period and the 13 microsecond rule",
"lesions": [
"PULSE_ECHO",
"INSTRUMENTATION"
],
"lens": "formula",
"reviewed": "2026-09-07",
"items": [
{
"id": "Q402.1",
"q": "Why does pulse repetition frequency set the deepest reflector the system can place correctly?",
"a": "A pulsed system transmits once and then listens, and it cannot tell which transmission an arriving echo belongs to, so it must wait for the deepest echo it cares about before firing again. That listening window is the pulse repetition period, and the deepest reflector it accommodates sits at d_max = c / (2 × PRF): 15.4 cm at a PRF of 5 kHz and 7.7 cm at 10 kHz. An echo arriving after the next pulse has already left is assigned to that new pulse and painted far too shallow, which is the range ambiguity artifact. In 2D you never dial PRF directly — you set the depth of view and the system computes the highest PRF it allows. In pulsed and color Doppler it runs the other way: the scale control is the PRF control."
},
{
"id": "Q402.2",
"q": "How long does a pulse take to reach a reflector 1 cm deep and return?",
"a": "Sound travels at 1540 m/s in soft tissue, which is 1.54 mm per microsecond, so 1 cm of one-way travel takes 6.5 µs. The echo makes that trip twice, so every centimeter of depth costs 13 µs of go-return time. Read it in either direction: a reflector at 10 cm returns its echo 130 µs after transmission, and a go-return time of 195 µs places a reflector at 15 cm. The same constant sets the listening window, so the minimum pulse repetition period is 13 µs × depth in cm and the maximum PRF is 77,000 ÷ depth in cm, which is where the roughly 5 kHz ceiling of a 15 cm cardiac image comes from."
},
{
"id": "Q402.3",
"q": "Which depth matters — the depth of view or the sample volume?",
"a": "They are different controls and the exam separates them. In 2D the depth of view sets the PRF ceiling, so doubling depth from 8 cm to 16 cm doubles the minimum pulse repetition period from 104 µs to 208 µs and halves the maximum PRF from 9.6 kHz to 4.8 kHz, spent on frame rate. In pulsed wave spectral Doppler the ceiling is set by sample volume depth instead: pulling the sector out to 20 cm to see the whole heart does not lower your mitral inflow Nyquist limit as long as the gate stays put. Keep the two apart, or you will give up depth you need for velocity range you never lost."
}
],
"numbers": [
{
"label": "One-way travel time per centimeter",
"value": "6.5",
"unit": "µs"
},
{
"label": "Go-return time per centimeter of depth",
"value": "13",
"unit": "µs/cm"
},
{
"label": "Range constant (c/2)",
"value": "77,000",
"unit": "cm/s"
},
{
"label": "Minimum pulse repetition period at 15 cm depth of view",
"value": "195",
"unit": "µs"
},
{
"label": "Maximum PRF at 15 cm depth of view",
"value": "5.1",
"unit": "kHz"
},
{
"label": "Maximum unambiguous depth at PRF 5 kHz",
"value": "15.4",
"unit": "cm"
},
{
"label": "Maximum unambiguous depth at PRF 10 kHz",
"value": "7.7",
"unit": "cm"
},
{
"label": "Typical clinical imaging PRF",
"value": "1–10",
"unit": "kHz"
}
],
"pearl": "Every centimeter of depth costs 13 microseconds of listening, and that bill is paid in frame rate.",
"equation": "d_max = c / (2 × PRF). In centimeters and microseconds: PRP_min = 13 µs × d(cm) and PRF_max = 77,000 / d(cm).",
"related": [],
"delta": null,
"lookalike": null
},
{
"id": "Q403",
"orig": 403,
"title": "Frame rate and temporal resolution",
"lesions": [
"IMAGE_OPT",
"INSTRUMENTATION"
],
"lens": "formula",
"reviewed": "2026-09-07",
"items": [
{
"id": "Q403.1",
"q": "What sets the ceiling on frame rate?",
"a": "A frame is finished only when every scan line has been fired and listened to, and each line costs the same 13 µs per centimeter of depth that any other pulse costs. Multiply that up and frame time is depth × lines × 13 µs, so frame rate is 77,000 ÷ (depth in cm × lines per frame). A 15 cm sector built from 128 lines tops out near 40 frames per second, and the same 128 lines at 20 cm fall to 30. This is a ceiling for conventional one-receive-line-per-transmit acquisition rather than a conservation law: parallel receive beamforming reconstructs four to eight receive lines per transmit and legitimately multiplies the rate, at the cost of block artifact and some lateral resolution."
},
{
"id": "Q403.2",
"q": "Which controls trade what for frame rate?",
"a": "Lines per frame is not one quantity but two multiplied together — line density, the scan lines per degree of sector, times the sector width in degrees — and frame rate is inversely proportional to each. Narrowing the sector from 90 degrees to 45 at constant line density halves the pulses and doubles the frame rate, costing you nothing but field of view, which is why it is the first control you reach for. Cutting line density doubles the rate the same way but coarsens lateral sampling, so the picture itself degrades. Turning off multi-focus buys frame rate a third way, because every extra focal zone needs its own pulse down every line: two zones halve the rate, three cut it to a third."
},
{
"id": "Q403.3",
"q": "Why do color Doppler and harmonic imaging cost frame rate on top of depth and line count?",
"a": "The full expression carries a third factor, pulses per line, and every mode needing more than one pulse per line pays there. Color Doppler fires a packet of 8 to 16 pulses down each line inside the color box to extract phase shift, so an 8 cm, 40-line box with a packet of 12 consumes enough of the budget to cap the composite image below about 20 frames per second — lower still once the 2D background lines are added back. Pulse inversion harmonic imaging transmits two pulses per line and halves the frame rate outright. M-mode is the opposite extreme, one line per frame, which is why it resolves motion no 2D frame rate can touch."
}
],
"numbers": [
{
"label": "Frame rate, 15 cm sector, 128 lines, single focus",
"value": "40",
"unit": "frames/s"
},
{
"label": "Frame rate, 20 cm sector, 128 lines, single focus",
"value": "30",
"unit": "frames/s"
},
{
"label": "Pulses per frame, 90° versus 30° sector",
"value": "3",
"unit": "× more"
},
{
"label": "Pulses per line, pulse inversion harmonic imaging",
"value": "2",
"unit": "pulses"
},
{
"label": "Parallel receive beamforming, receive lines per transmit",
"value": "4–8",
"unit": "lines"
}
],
"pearl": "Frame rate, depth and pulses per frame draw on one budget of 77,000 cm/s, so temporal resolution is only ever traded for.",
"equation": "FR = 77,000 / (d(cm) × lines per frame × pulses per line), where lines per frame = line density × sector width.",
"related": [],
"delta": null,
"lookalike": null
},
{
"id": "Q404",
"orig": 404,
"title": "The Doppler equation and its factor of two",
"lesions": [
"DOPPLER_PRIN",
"DOPPLER_PHYSICS"
],
"lens": "formula",
"reviewed": "2026-09-07",
"items": [
{
"id": "Q404.1",
"q": "Where does the factor of two come from?",
"a": "A red cell moving toward the transducer meets the outgoing wavefronts more often than a stationary cell would, so it receives an already-shifted frequency rather than the transmitted one. It then scatters that shifted wave back while still moving toward the probe, which compresses the returning wave a second time. The shift is applied twice on a single round trip, which is why the equation carries a factor of two where a passing siren would carry none. The sign follows direction of travel: flow toward the transducer raises the returning frequency and is drawn above the baseline, flow away lowers it and sits below. Nothing in the numerator involves depth, so moving the sample volume along the same vessel changes signal strength but not the shift for a given velocity."
},
{
"id": "Q404.2",
"q": "How large is the Doppler shift, and why does the machine play it as sound?",
"a": "The shift is smaller than the carrier by the ratio 2v/c — about 1 in 770 at 1 m/s — so a megahertz carrier yields a kilohertz shift. A 2 MHz probe aligned with 1 m/s flow returns 2.6 kHz, a 5 m/s aortic stenosis jet on the same probe returns 13 kHz, and myocardial tissue moving at 8 cm/s returns only 208 Hz. Every one of those falls inside the 20 Hz to 20 kHz band the human ear resolves, which is why the scanner hands you the shift as audio as well as a spectral trace. Use it while you steer, because the audio peaks before the trace does when you find the jet."
},
{
"id": "Q404.3",
"q": "What does raising the transmit frequency do to the shift?",
"a": "Δf is directly proportional to f₀, so a 5 MHz probe returns two and a half times the shift a 2 MHz probe returns from the same 1 m/s flow — 6.5 kHz against 2.6 kHz. A larger shift is easier to detect and resolves low velocities better, which is why superficial vascular work runs at 5 to 10 MHz. The same proportionality works against you in pulsed Doppler, where the shift must stay below half the pulse repetition frequency, so on a 5 MHz probe you alias at 40% of the velocity a 2 MHz probe tolerates. That is the argument for the lowest transmit frequency that still returns a usable signal — not the argument for the 2 MHz pencil probe, which you reach for because its dedicated crystals give better sensitivity on a weak jet."
}
],
"numbers": [
{
"label": "Doppler shift, 2 MHz probe, 1 m/s, aligned",
"value": "2.6",
"unit": "kHz"
},
{
"label": "Doppler shift, 2 MHz probe, 5 m/s stenotic jet",
"value": "13",
"unit": "kHz"
},
{
"label": "Doppler shift, 5 MHz probe, 1 m/s, aligned",
"value": "6.5",
"unit": "kHz"
},
{
"label": "Doppler shift, 2 MHz probe, tissue at 8 cm/s",
"value": "208",
"unit": "Hz"
},
{
"label": "Audible band the Doppler shift falls in",
"value": "20–20,000",
"unit": "Hz"
}
],
"pearl": "The red cell is shifted twice on one round trip, and that double shift is the 2 in the equation.",
"equation": "Δf = 2 f₀ v cosθ / c  (positive = flow toward the transducer)",
"related": [],
"delta": null,
"lookalike": null
},
{
"id": "Q405",
"orig": 405,
"title": "Velocity from the shift: three assumptions, one measurement",
"lesions": [
"DOPPLER_PRIN",
"DOPPLER_PHYSICS"
],
"lens": "formula",
"reviewed": "2026-09-07",
"items": [
{
"id": "Q405.1",
"q": "Of the four quantities in the equation, which one does the machine actually measure?",
"a": "Only Δf. The speed of sound is hard-coded at 1540 m/s regardless of what the beam is passing through, the transmit frequency is a property of the probe you selected, and cosθ is set to 1 unless you steer an angle-correct cursor — three assumptions and one measurement. A 2 kHz shift on a 3.5 MHz probe with the beam aligned works out to 0.44 m/s, and that number is exactly as trustworthy as the assumption that the beam is parallel to flow. When a displayed velocity looks wrong, suspect the geometry or the signal: either the beam is not on the flow, or it is on a different flow, such as an MR jet contaminating an AS envelope. The shift itself is rarely the liar."
},
{
"id": "Q405.2",
"q": "How does a velocity error propagate into the pressure gradient?",
"a": "The simplified Bernoulli equation squares the velocity, ΔP = 4v², so a fractional velocity error becomes roughly twice that fraction in the gradient. An uncorrected 20 degree angle underestimates velocity by 6% but the gradient by 12%; at 30 degrees the velocity is 13% low and the gradient 25% low; at 60 degrees you lose half the velocity and three quarters of the gradient. A true mean gradient of 40 mmHg recorded 30 degrees off axis is reported as 30 mmHg, which moves aortic stenosis from severe to moderate on the strength of a beam angle. The error you tolerate on the trace is not the error that reaches the report, because gradient and, through the continuity equation, valve area are both built on velocity squared."
},
{
"id": "Q405.3",
"q": "When do you use the angle-correct cursor, and when do you refuse it?",
"a": "Angle correction divides the measured shift by cosθ, so it recovers the true velocity only if the angle you drew on screen is the real angle between beam and flow in three dimensions. In peripheral vascular work the walls are visible and flow runs parallel to them, so you lay the cursor along the vessel and keep the angle at or below 60 degrees, beyond which a single degree of cursor error already costs about 3% of the velocity. In cardiac Doppler you do not angle-correct: a jet is eccentric and its direction in the imaging plane is not its direction in space, so you move to whatever window aligns the beam and report the highest velocity you find. Applying vascular angle correction to an intracardiac jet manufactures velocity that was never measured."
}
],
"numbers": [
{
"label": "Velocity from a 2 kHz shift on a 3.5 MHz probe, aligned",
"value": "0.44",
"unit": "m/s"
},
{
"label": "Gradient underestimate, uncorrected 20°",
"value": "12",
"unit": "%"
},
{
"label": "Gradient underestimate, uncorrected 30°",
"value": "25",
"unit": "%"
},
{
"label": "Gradient underestimate, uncorrected 60°",
"value": "75",
"unit": "%"
},
{
"label": "Vascular angle-correction ceiling",
"value": "60",
"unit": "degrees"
},
{
"label": "Velocity error per 1° of cursor error at 60°",
"value": "3",
"unit": "%"
}
],
"pearl": "The scanner measures the shift and assumes the rest; the only assumption you can get wrong is the angle.",
"equation": "v = Δf × c / (2 f₀ cosθ). Only Δf is measured; c, f₀ and cosθ are supplied.",
"related": [],
"delta": null,
"lookalike": null
},
{
"id": "Q406",
"orig": 406,
"title": "The Nyquist limit and the range-velocity budget",
"lesions": [
"DOPPLER_PRIN",
"DOPPLER_PHYSICS"
],
"lens": "formula",
"reviewed": "2026-09-07",
"items": [
{
"id": "Q406.1",
"q": "Why is the ceiling exactly half the pulse repetition frequency?",
"a": "Pulsed Doppler never watches the returning wave continuously; each transmitted pulse returns one phase measurement from the sample volume, so the machine must reconstruct a shift of several kilohertz from samples arriving only at the pulse repetition frequency. Recovering both the rate and the direction of a rotating phase needs at least two samples per cycle, so the highest shift that can be resolved is PRF/2 — a frequency, which is the form the exam asks for. Push that limit back through the Doppler equation and you get the Nyquist velocity, PRF × c / (4 f₀), which at a PRF of 5 kHz on a 3.5 MHz probe is 0.55 m/s. That number is printed at the ends of the spectral scale and the color bar, so your ceiling is always on screen."
},
{
"id": "Q406.2",
"q": "Why can you not simply raise the PRF until nothing aliases?",
"a": "The machine must wait for the deepest echo of one pulse before firing the next, so the sample volume depth imposes a hard ceiling of PRF = c/2d — 5.1 kHz at 15 cm, and no scale control pushes past it. Multiply the two constraints and the PRF cancels: v_Nyquist × d = c²/8f₀, a fixed budget you spend on either range or velocity. On a 2 MHz probe that budget is about 15 in units of meters per second times centimeters, so roughly 1.2 m/s with the gate at 12 cm, where mitral leaflet tips sit from an apical window. Normal mitral E fits there with little to spare, a baseline shift makes it comfortable, and a mitral stenosis jet does not fit at all."
},
{
"id": "Q406.3",
"q": "What actually raises the Nyquist limit, and what does not?",
"a": "Two controls move it cleanly: raise the PRF, which on the scanner is the scale knob and which in turn demands a shallower gate or a smaller color box; or drop the transmit frequency, since the Nyquist velocity is inversely proportional to f₀, so moving from 3.5 MHz to 2 MHz lifts the same 5 kHz PRF from 0.55 to 0.96 m/s. Two more move it at a price: a larger beam-to-flow angle shrinks the shift but throws away the velocity you came to measure, and High-PRF mode fires faster than the depth allows and accepts two or three ambiguous sample gates in exchange. Continuous wave is on neither list — it has no pulse repetition frequency, so it removes the ceiling rather than raising it."
}
],
"numbers": [
{
"label": "Nyquist velocity, PRF 5 kHz on a 3.5 MHz probe",
"value": "0.55",
"unit": "m/s"
},
{
"label": "Nyquist velocity, PRF 5 kHz on a 2 MHz probe",
"value": "0.96",
"unit": "m/s"
},
{
"label": "PRF ceiling at a 15 cm sample volume depth",
"value": "5.1",
"unit": "kHz"
},
{
"label": "Nyquist velocity, 2 MHz probe, gate at 12 cm",
"value": "1.2",
"unit": "m/s"
},
{
"label": "Range-velocity budget on a 2 MHz probe",
"value": "≈ 15",
"unit": "(m/s)·cm"
}
],
"pearl": "Depth and velocity draw on one budget: the deeper you listen, the slower the fastest flow you can still read.",
"equation": "Nyquist limit = PRF/2 (a frequency). v_Nyquist = PRF × c / (4 f₀), with PRF ≤ c/2d, so v_Nyquist × d ≤ c²/8f₀.",
"widgets": [
"nyquist"
],
"related": [],
"delta": null,
"lookalike": null
},
{
"id": "Q407",
"orig": 407,
"title": "Aliasing: recognition and repair",
"lesions": [
"DOPPLER_PRIN",
"DOPPLER_PHYSICS"
],
"lens": "pitfall",
"reviewed": "2026-09-07",
"items": [
{
"id": "Q407.1",
"q": "How do you recognize aliasing, and separate it from genuine flow reversal?",
"a": "Aliasing is a wrap, not a measurement: a shift beyond PRF/2 is indistinguishable from one a full PRF lower, so the system reassigns it to the opposite channel. On a spectral trace the top of the envelope is cut off at the ceiling of the scale and reappears at the floor of the reverse channel, and the two pieces line up continuously across the baseline instead of meeting at zero. In color, aliasing runs from bright red through yellow straight into bright blue by wrapping around the outside of the color bar, whereas true flow reversal passes through the dark center where velocity is zero. If red touches blue with no black between them you are looking at aliasing, and PISA uses that boundary deliberately as a hemisphere of known velocity."
},
{
"id": "Q407.2",
"q": "Which fixes raise the aliasing threshold, and which only rearrange the display?",
"a": "Three genuinely raise it: increase the scale, which is the PRF control on the scanner; move the sample volume shallower or shrink the color box, which is what allows the higher PRF; or select a lower-frequency transducer, since the Nyquist velocity is inversely proportional to f₀. A fourth removes it altogether — continuous wave has no PRF, so there is no ceiling to raise. Shifting the baseline raises nothing and the Nyquist limit stays at PRF/2, but by handing the whole display window to one direction it shows close to twice the Nyquist velocity when flow is unidirectional, which unwraps most mildly aliased traces. Increasing the beam-to-flow angle also clears the alias and you should recognize it as a listed answer, but it has no place in cardiac Doppler."
},
{
"id": "Q407.3",
"q": "How does an aliased velocity relate to the true one?",
"a": "The display wraps in steps of twice the Nyquist velocity, as many times as needed. With a Nyquist velocity of 0.55 m/s, a true forward velocity of 0.70 m/s is drawn as 0.40 m/s of reverse flow, and a true 1.20 m/s wraps back onto the correct side of the baseline but reads only 0.10 m/s forward — the direction looks right and the number is nonsense. A single wrap can be unwrapped by eye and read; past that the wraps are uncountable and the peak is gone, so never report a peak velocity off a multiply-wrapped envelope. Fix the scale, shift the baseline, or move to continuous wave and read the true peak from an unambiguous trace."
}
],
"numbers": [
{
"label": "Nyquist velocity 0.55 m/s: true 0.70 m/s displays as",
"value": "−0.40",
"unit": "m/s"
},
{
"label": "Nyquist velocity 0.55 m/s: true 1.20 m/s displays as",
"value": "0.10",
"unit": "m/s"
},
{
"label": "Unidirectional range after a full baseline shift",
"value": "2",
"unit": "× Nyquist velocity"
}
],
"pearl": "Raising the scale lifts the ceiling; shifting the baseline only spends the same ceiling all in one direction.",
"equation": "Aliased when |Δf| > PRF/2, equivalently |v cosθ| > v_Nyquist. The display wraps in steps of 2 v_Nyquist.",
"widgets": [
"nyquist"
],
"related": [],
"delta": null,
"lookalike": null
}
]