Chapter 110: Physical Examination of the Heart

General examination of a pt with suspected heart disease should include vital signs (respiratory rate, pulse, blood pressure) and observation of skin color (e.g., cyanosis, pallor, jaundice), clubbing, edema, evidence of decreased perfusion (cool and diaphoretic skin), and hypertensive changes in optic fundi. Examine abdomen for evidence of hepatomegaly, ascites, or abdominal aortic aneurysm. An ankle-brachial index (systolic bp at ankle divided by arm systolic bp) <0.9 indicates lower extremity arterial obstructive disease. Important findings on cardiovascular examination include:

• Pulsus parvus: Weak upstroke due to decreased stroke volume (hypovolemia, LV failure, aortic or mitral stenosis [MS]) (Fig. 110-1)

• Pulsus tardus: Delayed upstroke (aortic stenosis)

• Bounding (hyperkinetic) pulse: Hyperkinetic circulation, aortic regurgitation, patent ductus arteriosus, marked vasodilation

• Pulsus bisferiens: Double systolic pulsation (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 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 sign) in constrictive pericarditis. Abnormalities in examination include:

• Large “a” wave: Tricuspid stenosis (TS), pulmonic stenosis (PS), atrioventricular (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: TS

Cardiac apical impulse is normally localized at the fifth intercostal space, midclavicular line. Abnormalities include:

• 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

HEART SOUNDS

S₁

Loud: Mitral stenosis (MS), short PR interval, hyperkinetic heart, thin chest wall (Fig. 110-2). 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, PS, 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, heart failure

• 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 coronary artery disease (CAD).

Opening Snap (OS)

High-pitched; follows S₂ (by 0.06–0.12 s), heard at lower left sternal border and apex in MS; the more severe the MS, the shorter the S₂–OS interval.

Ejection Clicks

High-pitched sounds following S₁ typically loudest at left sternal border; observed in dilation of aortic root or pulmonary artery, congenital AS or PS; when due to the latter, click decreases with inspiration.

Midsystolic Clicks

At lower left sternal border and apex, often followed by late systolic murmur in mitral valve prolapse.

HEART MURMURS

Systolic Murmurs

May be “crescendo-decrescendo” ejection type, pansystolic, or late systolic; right-sided murmurs (e.g., tricuspid regurgitation) typically increase with inspiration (Fig. 110-3; Tables 110-1 and 110-2).

Diastolic Murmurs

• 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.