Although the cardiovascular examination centers on the heart, peripheral signs are often invaluable.
While cardiac patients may appear healthy and comfortable at rest, many with acute myocardial infarction appear anxious and restless. Diaphoresis suggests hypotension or a hyperadrenergic state, such as during pericardial tamponade, tachyarrhythmias, or myocardial infarction. Patients with severe congestive heart failure or other chronic low cardiac output states may appear cachectic.
Cyanosis may be central, due to arterial desaturation, or peripheral, reflecting impaired tissue delivery of adequately saturated blood in low-output states, polycythemia, or peripheral vasoconstriction. Central cyanosis may be caused by pulmonary disease, left heart failure, or right-to-left shunting; the latter will not be improved by increasing the inspired oxygen concentration. Pallor usually indicates anemia but may be a sign of low cardiac output.
Although the normal heart rate usually ranges from 50 to 90 beats/min, both slower and more rapid rates may occur in normal individuals or may reflect noncardiac conditions such as anxiety or pain, medication effect, fever, thyroid disease, pulmonary disease, anemia, or hypovolemia. If symptoms or clinical suspicion warrants, an electrocardiogram (ECG) should be performed to diagnose arrhythmia, conduction disturbance, or other abnormality. The range of normal blood pressure is wide, but even in asymptomatic individuals systolic pressures below 90 mm Hg or above 140 mm Hg and diastolic pressures above 90 mm Hg warrant further clinical evaluation and follow-up. Initially elevated pressures may decline if the patient is allowed to relax and rest comfortably. Tachypnea is also nonspecific, but pulmonary disease and heart failure should be considered when respiratory rates exceed 16/min under resting conditions. Periodic breathing (Cheyne-Stokes respiration) is not uncommon in severe heart failure.
Peripheral Pulses & Venous Pulsations
Diminished peripheral pulses most commonly result from arteriosclerotic peripheral vascular disease and may be accompanied by localized bruits. Asymmetry of pulses should also arouse suspicion of coarctation of the aorta or aortic dissection. Exaggerated pulses may indicate aortic regurgitation, coarctation, patent ductus arteriosus, or other conditions that increase stroke volume. The carotid pulse is a valuable aid to assessment of left ventricular ejection. It has a delayed upstroke in aortic stenosis and a bisferiens quality (two palpable peaks) in mixed aortic stenosis and regurgitation or hypertrophic obstructive cardiomyopathy. Pulsus paradoxus (a decrease in systolic blood pressure during inspiration greater than the normal 10 mm Hg) is a valuable sign of pericardial tamponade, though it also occurs in asthma and chronic obstructive pulmonary disease. Pulsus alternans, in which the amplitude of the pulse alternates every other beat during sinus rhythm, occurs when cardiac contractility is very depressed or with large pericardial effusions.
Jugular venous pulsations provide insight into right atrial pressure. They indicate (1) elevated central venous pressure if they are more than 3 vertical centimeters above the angle of Louis, (2) increased central blood volume if they rise more than 1 cm with sustained (30 seconds) right upper quadrant abdominal pressure (hepatojugular reflux), (3) tricuspid obstruction or pulmonary hypertension if the a wave is exaggerated, and (4) Tricuspid regurgitation if large cv waves are seen. The latter may be associated with hepatic pulsations. Atrioventricular dissociation due to conduction block or ventricular arrhythmia can be recognized by intermittent cannon a waves.
Constant J: Using internal jugular pulsations as a manometer for right atrial pressure measurements. Cardiology 2000;93:26.
Drazner MH et al: Prognostic importance of elevated jugular venous pressure and a third heart sound in patients with heart failure. N Engl J Med 2001;345:574.
Rales heard at the lung bases are a sign of congestive heart failure but may be caused by similarly localized pulmonary disease. Wheezing and rhonchi suggest obstructive pulmonary disease but may occur in left heart failure. Pleural effusions with bibasilar percussion dullness and reduced breath sounds are common in congestive heart failure and are more frequent or larger on the right.
A parasternal lift usually indicates right ventricular hypertrophy, pulmonary hypertension (pulmonary artery systolic pressure > 50 mm Hg), or left atrial enlargement; pulmonary artery pulsations may also be visible. The left ventricular apical impulse, if sustained and enlarged, suggests myocardial hypertrophy or dysfunction. If it is very prominent but not sustained, the apical impulse may indicate volume overload or high-output states. Additional precordial pulsations may reflect regional abnormalities of left ventricular contraction.
The first heart sound (S1), the closing of the mitral valve and tricuspid valve, may be diminished with severe left ventricular dysfunction or accentuated with mitral stenosis or short PR intervals. S2, the closing of the atrioventricular valve and pulmonary valve, is usually split, with the two components (aortic preceding pulmonary) being separated more during inspiration; splitting is fixed in atrial septal defect, wide with right bundle branch block, and absent or reversed (paradoxic splitting) with aortic stenosis, left ventricular failure, or left bundle branch block. With normal splitting, an accentuated P2 is an important sign of pulmonary hypertension. Third and fourth heart sounds (ventricular and atrial gallops, respectively) indicate ventricular volume overload or impaired compliance and may be heard over either ventricle. An apical S3 is a normal finding in younger individuals and in pregnancy. Additional auscultatory findings include sharp, high-pitched sounds classified as “clicks.” These may be early systolic and represent ejection sounds (as with a bicuspid aortic valve or pulmonary stenosis) or may occur in mid or late systole, indicating myxomatous changes in the mitral valve.
While many murmurs indicate valvular disease, a soft, short systolic murmur, usually localized along the left sternal border or toward the apex, may be innocent, reflecting pulmonary flow. Innocent murmurs often vary with inspiration, diminish in the upright position, and are most frequently heard in thin individuals. Systolic murmurs are pansystolic (holosystolic) when they merge with the first sound and persist through all of systole or “ejection” murmurs when they begin after the first sound and end before the second sound, with a peak in early or mid systole. The former represent mitral regurgitation if maximal at the apex or in the axilla and Tricuspid regurgitation or Ventricular septal defect if best heard at the sternal border. Short aortic ejection murmurs with a preserved A2 are common in older individuals, especially when hypertension has been present, and even if they are moderately loud they usually reflect thickening (sclerosis) of the valve rather than stenosis. Association of murmurs with palpable vibrations (”thrills”) is always clinically significant, as are diastolic murmurs. Further evaluation is warranted when the patient has symptoms of possible cardiac origin. Some studies suggest that one should have a low threshold for evaluating murmurs with echocardiograms.
Attenhofer Jost CG et al: Echocardiography in the evaluation of systolic murmurs of unknown cause. Am J Med 2000;108: 614.
Richardson TR et al: Bedside cardiac examination: constancy in a sea of change. Curr Probl Cardiol 2000;25:783.
Subcutaneous fluid collections appear first in the lower extremities in ambulatory patients or in the sacral region of bedridden individuals. In heart disease, edema results from elevated right atrial pressures. Right heart failure most commonly results from left heart failure, although the right-sided signs may predominate. Other cardiogenic causes of edema include pericardial disease, right-sided valve lesions, and cor pulmonale. Edema may also be due to peripheral venous insufficiency, venous obstruction, nephrotic syndrome, cirrhosis, premenstrual fluid retention, drugs (especially vasodilators such as calcium channel blockers or salt-retaining medications such as nonsteroidal anti-inflammatory agents), or it may be idiopathic.
Cho S et al: Peripheral edema. Am J Med 2002;113:580.
Rasool A et al: Treatment of edematous disorders with diuretics. Am J Med Sci 2000;319:25.
Revision date: June 20, 2011
Last revised: by Andrew G. Epstein, M.D.