112 PHYSICAL EXAMINATION OF THE HEART
Harrison’s Manual of Medicine
PHYSICAL EXAMINATION OF THE HEART
General examination of a pt with suspected heart disease should include vital signs (respiratory rate, pulse, blood pressure), skin color, clubbing, edema, evidence of decreased perfusion (cool and sweaty skin), and hypertensive changes in optic fundi. Important findings on cardiovascular examination include:
CAROTID ARTERY PULSE (Fig. 112-1)
FIGURE 112-1. Carotid artery pulse patterns.
Pulsus parvus: Weak upstroke due to decreased stroke volume (hypovolemia, LV failure, aortic or mitral stenosis).
Pulsus tardus: Delayed upstroke (aortic stenosis).
Bounding pulse: Hyperkinetic circulation, aortic regurgitation, patent ductus arteriosus, marked vasodilatation.
Pulsus bisferiens: Double systolic pulsation in aortic regurgitation, hypertrophic cardiomyopathy.
Pulsus alternans: Regular alteration in pulse pressure amplitude (severe LV dysfunction).
Pulsus paradoxus: Exaggerated inspiratory fall (>10 mmHg) in systolic bp (pericardial tamponade, severe obstructive lung disease).
JUGULAR VENOUS PULSATION (JVP) (Fig. 112-2) Jugular venous distention develops in right-sided heart failure, constrictive pericarditis, pericardial tamponade, obstruction of superior vena cava. JVP normally falls with inspiration but may rise (Kussmaul’s sign) in constrictive pericarditis. Abnormalities in examination include:
FIGURE 112-2. Normal jugular venous pressure recording.
Large “a” wave: Tricuspid stenosis (TS), pulmonic stenosis, AV dissociation (right atrium contracts against closed tricuspid valve).
Large “v” wave: Tricuspid regurgitation, atrial septal defect.
Steep “y” descent: Constrictive pericarditis.
Slow “y” descent: Tricuspid stenosis.
PRECORDIAL PALPATION Cardiac apical impulse is normally localized in the fifth intercostal space, midclavicular line (Fig. 112-3). Abnormalities include:
FIGURE 112-3. A. Schematic representation of electrocardiogram, aortic pressure pulse (AOP), phonocardiogram recorded at the apex, and apex cardiogram (ACG). On the phonocardiogram, S1, S2, S3, and S4 represent the first through fourth heart sounds; OS represents the opening snap of the mitral valve, which occurs coincident with the O point of the apex cardiogram. S3 occurs coincident with the termination of the rapid-filling wave (RFW) of the ACG, while S4 occurs coincident with the a wave of the ACG. B. Simultaneous recording of electrocardiogram, indirect carotid pulse (CP), phonocardiogram along the left sternal border (LSB), and indirect jugular venous pulse (JVP). ES, ejection sound; SC, systolic click.
Forceful apical thrust: Left ventricular hypertrophy.
Lateral and downward displacement of apex impulse: Left ventricular dilatation.
Prominent presystolic impulse: Hypertension, aortic stenosis, hypertrophic cardiomyopathy.
Double systolic apical impulse: Hypertrophic cardiomyopathy.
Sustained “lift” at lower left sternal border: Right ventricular hypertrophy.
Dyskinetic (outward bulge) impulse: Ventricular aneurysm, large dyskinetic area post MI, cardiomyopathy.M
HEART SOUNDS (Fig. 112-3) S1 Loud: Mitral stenosis, short PR interval, hyperkinetic heart, thin chest wall. Soft: Long PR interval, heart failure, mitral regurgitation, thick chest wall, pulmonary emphysema.
S2 Normally A2 precedes P2 and splitting increases with inspiration; abnormalities include:
Widened splitting: Right bundle branch block, pulmonic stenosis, mitral regurgitation.
Fixed splitting (no respiratory change in splitting): Atrial septal defect.
Narrow splitting: Pulmonary hypertension.
Paradoxical splitting (splitting narrows with inspiration): Aortic stenosis, left bundle branch block, CHF.
Loud A2: Systemic hypertension.
Soft A2: Aortic stenosis (AS).
Loud P2: Pulmonary arterial hypertension.
Soft P2: Pulmonic stenosis (PS).
S3 Low-pitched, heard best with bell of stethoscope at apex, following S2; normal in children; after age 30–35, indicates LV failure or volume overload.
S4 Low-pitched, heard best with bell at apex, preceding S1; reflects atrial contraction into a noncompliant ventricle; found in AS, hypertension, hypertrophic cardiomyopathy, and CAD.
Opening Snap (OS) High-pitched; follows S2 (by 0.06–0.12 s), heard at lower left sternal border and apex in mitral stenosis (MS); the more severe the MS, the shorter the S2–OS interval.
Ejection Clicks High-pitched sounds following S1; observed in dilatation of aortic root or pulmonary artery, congenital AS (loudest at apex) or PS (upper left sternal border); the latter decreases with inspiration.
Midsystolic Clicks At lower left sternal border and apex, often followed by late systolic murmur in mitral valve prolapse.
HEART MURMURS (Table 112-1, Fig. 112-4) Systolic Murmurs May be “crescendo-decrescendo” ejection type, pansystolic, or late systolic; right-sided murmurs (e.g., tricuspid regurgitation) typically increase with inspiration. A number of simple maneuvers produce characteristic changes depending on cause of murmur (Table 112-2).
Table 112-1 Heart Murmurs
FIGURE 112-4. A. Schematic representation of ECG, aortic pressure (AOP), left ventricular pressure (LVP), and left atrial pressure (LAP). The hatched areas indicated a transvalvular pressure difference during systole. HSM, holosystolic murmur; MSM, midsystolic murmur. B. Graphic representation of ECG, aortic pressure (AOP), left ventricular pressure (LVP), and left atrial pressure (LAP) with hatched areas indicating transvalvular diastolic pressure difference. EDM, early diastolic murmur; PSM, presystolic murmur; MDM, middiastolic murmur.
Table 112-2 Heart Murmurs and Responsible Lesions
Early diastolic murmurs: Begin immediately after S2, are high-pitched, and are usually caused by aortic or pulmonary regurgitation.
Mid-to-late diastolic murmurs: Low-pitched, heard best with bell of stethoscope; observed in MS or TS; less commonly due to atrial myxoma.
Continuous murmurs: Present in systole and diastole (envelops S2); found in patent ductus arteriosus and sometimes in coarctation of aorta; less common causes are systemic or coronary AV fistula, aortopulmonary septal defect, ruptured aneurysm of sinus of Valsalva.
For a more detailed discussion, see O’Gara PT, Braunwald E: Approach to the Patient with a Heart Murmur, Chap. 34, p. 207; and O’Rourke RA, Braunwald E: Physical Examination of the Cardiovascular System, Chap. 225, p. 1255, in HPIM-15.