|Inspection ||Malar flush, precordial bulge, and diffuse pulsation in young patients. ||Usually prominent and hyperdynamic apical impulse to left of MCL. ||Sustained PMI, prominent atrial filling wave. ||Hyperdynamic PMI to left of MCL and downward. Visible carotid pulsations. Pulsating nailbeds (Quincke sign), head bob (deMusset sign). ||Giant a wave in jugular pulse with sinus rhythm. Peripheral edema or ascites, or both. ||Large v wave in jugular pulse; time with carotid pulsation. Peripheral edema or ascites, or both. |
|Palpation ||“Tapping” sensation over area of expected PMI. Right ventricular pulsation in left third to fifth ICS parasternally when pulmonary hypertension is present. P2 may be palpable. ||Forceful, brisk PMI; systolic thrill over PMI. Pulse normal, small, or slightly collapsing. ||Powerful, heaving PMI to left and slightly below MCL. Systolic thrill over aortic area, sternal notch, or carotid arteries in severe disease. Small and slowly rising carotid pulse. If bicuspid AS, check for delay at femoral artery to exclude coarctation. ||Apical impulse forceful and displaced significantly to left and downward. Prominent carotid pulses. Rapidly rising and collapsing pulses (Corrigan pulse). ||Pulsating, enlarged liver in ventricular systole. ||Right ventricular pulsation. Systolic pulsation of liver. |
|Heart sounds, rhythm, and blood pressure ||S1 loud if valve mobile. Opening snap following S2. The worse the disease, the closer the S2-opening snap interval. ||S1 normal or buried in early part of murmur (exception in mitral prolapse where murmur may be late). Prominent third heart sound when severe MR. Atrial fibrillation common. Blood pressure normal. Midsystolic clicks may be present and may be multiple. ||A2 normal, soft, or absent. Prominent S4. Blood pressure normal, or systolic pressure normal with high diastolic pressure. || |
S1 normal or reduced, A2 loud. Wide pulse pressure with diastolic pressure < 60 mm Hg.
When severe, gentle compression of femoral artery with diaphragm of stethoscope may reveal diastolic flow (Duroziez) and pressure in leg on palpation > 40 mm Hg than arm (Hill).
|S1 often loud. ||Atrial fibrillation may be present. |
|Location and transmission ||Localized at or near apex. Diastolic rumble best heard in left lateral position; may be accentuated by having patient do sit-ups. Rarely, short diastolic murmur along lower left sternal border (Graham Steell) in severe pulmonary hypertension. ||Loudest over PMI; posteriorly directed jets (ie, anterior mitral prolapse) transmitted to left axilla, left infrascapular area; anteriorly directed jets (ie, posterior mitral prolapse) heard over anterior precordium. Murmur unchanged after premature beat. ||Right second ICS parasternally or at apex, heard in carotid arteries and occasionally in upper interscapular area. May sound like MR at apex (Gallaverdin phenomenon), but murmur occurs after S1 and stops before S2. ||Diastolic: louder along left sternal border in third to fourth interspace. Heard over aortic area and apex. May be associated with low-pitched mid-diastolic murmur at apex (Austin Flint) due to functional mitral stenosis. If due to an enlarged aorta, murmur may radiate to right sternal border. ||Third to fifth ICS along left sternal border out to apex. Murmur increases with inspiration. ||Third to fifth ICS along left sternal border. Murmur hard to hear but increases with inspiration. Sit-ups can increase cardiac output and accentuate murmur. |
|Timing ||Relation of opening snap to A2 important. The higher the LA pressure, the earlier the opening snap. Presystolic accentuation before S1 if in sinus rhythm. Graham Steell begins with P2 (early diastole) if associated pulmonary hypertension. ||Pansystolic: begins with S1 and ends at or after A2. May be late systolic in mitral valve prolapse. ||Begins after S1, ends before A2. The more severe the stenosis, the later the murmur peaks. ||Begins immediately after aortic second sound and ends before first sound (blurring both); helps distinguish from MR. ||Rumble often follows audible opening snap. ||At times, hard to hear. Begins with S1 and fills systole. Increases with inspiration. |
|Character ||Low-pitched, rumbling; presystolic murmur merges with loud S1. ||Blowing, high-pitched; occasionally harsh or musical. ||Harsh, rough. ||Blowing, often faint. ||As for mitral stenosis. ||Blowing, coarse, or musical. |
|Optimum auscultatory conditions ||After exercise, left lateral recumbency. Use stethoscope bell, lightly applied. ||After exercise; use stethoscope diaphragm. In prolapse, findings may be more evident while standing. ||Use stethoscope diaphragm. Patient resting, leaning forward, breath held in full expiration. ||Use stethoscope diaphragm. Patient leaning forward, breath held in expiration. ||Use stethoscope bell. Murmur usually louder and at peak during inspiration. Patient recumbent. ||Use stethoscope diaphragm. Murmur usually becomes louder during inspiration. |
|Radiography ||Straight left heart border from enlarged LA appendage. Elevation of left mainstem bronchus. Large right ventricle and pulmonary artery if pulmonary hypertension is present. Calcification in mitral valve in rheumatic mitral stenosis or in annulus in calcific mitral stenosis. ||Enlarged left ventricle and LA. ||Concentric left ventricular hypertrophy. Prominent ascending aorta. Calcified aortic valve common. ||Moderate to severe left ventricular enlargement. Aortic root often dilated. ||Enlarged right atrium with prominent SVC and azygous shadow. ||Enlarged right atrium and right ventricle. |
|ECG ||Broad P waves in standard leads; broad negative phase of diphasic P in V1. If pulmonary hypertension is present, tall peaked P waves, right axis deviation, or right ventricular hypertrophy appears. ||Left axis deviation or frank left ventricular hypertrophy. P waves broad, tall, or notched in standard leads. Broad negative phase of diphasic P in V1. ||Left ventricular hypertrophy. ||Left ventricular hypertrophy. ||Tall, peaked P waves. Possible right ventricular hypertrophy. ||Right axis usual. |
|Two-dimensional echocardiography ||Thickened, immobile mitral valve with anterior and posterior leaflets moving together. “Hockey stick” shape to opened anterior leaflet in rheumatic mitral stenosis. Annular calcium with thin leaflets in calcific mitral stenosis. LA enlargement, normal to small left ventricle. Orifice can be traced to approximate mitral valve orifice area. ||Thickened mitral valve in rheumatic disease; mitral valve prolapse; flail leaflet or vegetations may be seen. Dilated left ventricle in volume overload. Operate for left ventricular end-systolic dimension < 4.5 cm. ||Dense persistent echoes from the aortic valve with poor leaflet excursion. Left ventricular hypertrophy late in the disease. Bicuspid valve in younger patients. ||Abnormal aortic valve or dilated aortic root. Diastolic vibrations of the anterior leaflet of the mitral valve and septum. In acute aortic regurgitation, premature closure of the mitral valve before the QRS. When severe, dilated left ventricle with normal or decreased contractility. Operate when left ventricular end-systolic dimension > 5.0 cm. ||In rheumatic disease, tricuspid valve thickening, decreased early diastolic filling slope of the tricuspid valve. In carcinoid, leaflets fixed, but no significant thickening. ||Enlarged right ventricle with paradoxical septal motion. Tricuspid valve often pulled open by displaced chordae. |
|Continuous and color flow Doppler and TEE ||Prolonged pressure half-time across mitral valve allows estimation of gradient. MVA estimated from pressure half-time. Indirect evidence of pulmonary hypertension by noting elevated right ventricular systolic pressure measured from the tricuspid regurgitation jet. ||Regurgitant flow mapped into LA. Use of PISA helps assess MR severity. TEE important in prosthetic mitral valve regurgitation. ||Increased transvalvular flow velocity; severe AS when peak jet > 4 m/sec (64 mm Hg). Valve area estimate using continuity equation is poorly reproducible. ||Demonstrates regurgitation and qualitatively estimates severity based on percentage of left ventricular outflow filled with jet and distance jet penetrates into left ventricle. TEE important in aortic valve endocarditis to exclude abscess. Mitral inflow pattern describes diastolic dysfunction. ||Prolonged pressure half-time across tricuspid valve can be used to estimate mean gradient. Severe tricuspid stenosis present when mean gradient > 5 mm Hg. ||Regurgitant flow mapped into right atrium and venae cavae. Right ventricular systolic pressure estimated by tricuspid regurgitation jet velocity. |