Although the cardiovascular examination centers on the heart, peripheral signs often provide important information.
Although cardiac patients may appear healthy and comfortable at rest, many with acute MI appear anxious and restless. Diaphoresis may result from hypotension due to pericardial tamponade, tachyarrhythmias, MI, or the presence of a high vagal state. Cold and clammy skin or pallor suggests low cardiac output and may be a sign of cardiogenic shock or anemia. Patients with severe chronic heart failure or other long-standing low cardiac output states may appear cachectic.
Certain physical features may provide clues to underlying heart disease. Some examples include a person with Down syndrome who is likely to have an AV canal defect. Someone with the Marfan phenotype is likely to have aortic root disease or mitral valve prolapse. A bifid uvula may be a marker of Loeys-Dietz syndrome and diffuse aortic aneurysms. Tendon xanthomas or lipid deposits around the eyes may signal underlying atherosclerotic disease. Systemic inflammatory diseases, such as systemic lupus erythematosus or rheumatoid arthritis may be associated with underlying myocardial, pericardial, conduction system, or valvular heart disease. An obese patient with sleep apnea may suggest underlying pulmonary hypertension is present.
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. Clubbing may be present in chronic cyanotic states. Central cyanosis may be caused by pulmonary disease, left heart failure, or right-to-left intracardiac or intrapulmonary shunting; the latter will not be improved by increasing the inspired oxygen concentration. Differential clubbing of the toes but not the fingers suggest pulmonary hypertension related to a ductus arteriosus and a right to left shunt through the ductus. Edema may be present and its pitting nature and extent quantified. Note also if presacral edema is present. Severe right heart failure may also present with ascites and scrotal edema.
Although the normal resting 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 ECG should be performed to diagnose arrhythmia, conduction disturbance, or other abnormalities. The range of normal BP is wide, but even in asymptomatic individuals. Guidelines were issued in 2017 that updated the JNC 7. Blood pressure should be categorized as normal, elevated, or stage 1 or 2. Normal BP is defined as less than 120/80 mm Hg, elevated BP as 120–129/less than 80 mm Hg, hypertension stage 1 is 130–139/80–89 mm Hg and hypertension stage 2 as greater than or equal to 140/90 mm Hg. Out-of-office readings should be taken as accurate. Nonpharmacologic treatment for BP reduction with weight loss, sodium restriction, potassium supplementation and a structured physical activity program are recommended for all patients with hypertension. The benefit from pharmacologic treatment is related to atherosclerotic risk, and antihypertensive medications are recommended to achieve a BP of less than 130/80 mm Hg as secondary prevention and, likewise, as primary prevention if the estimated 10-year atherosclerotic cardiovascular disease risk is 10% or greater. Chlorthalidone has emerged as the preferred diuretic because of long half-life and proven reduction in atherosclerotic cardiovascular disease risk. Beta-blockers are generally not first-line therapy except in CAD, aortic root disease, and heart failure with reduced ejection fraction. ACE inhibitors or angiotensin receptor blockers (ARBs) should be used if albuminuria is present. The ready availability of home BP monitoring or drugstore monitoring units should be considered before beginning antihypertensive therapy if the BP is borderline elevated. Tachypnea is also nonspecific, but pulmonary disease and heart failure should be considered when respiratory rates exceed 16 breaths per min under resting conditions. Cheyne–Stokes respiration, a form of periodic breathing, is not uncommon in severe heart failure.
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Peripheral Pulses & Venous Pulsations
The quality or magnitude of the pulses palpated is a reflection of the pulse pressure. 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, especially if a delay is noted between the brachial or radial pulse and the femoral pulse. Exaggerated upper extremity pulses may indicate aortic regurgitation, the BP upstream from aortic coarctation, patent ductus arteriosus, or other conditions that increase stroke volume. The carotid pulse is a valuable aid to assessment of LV ejection. It has a delayed upstroke in aortic stenosis and a bisferiens quality (two palpable peaks) in mixed aortic stenosis and regurgitation or hypertrophic cardiomyopathy. The pulse may be difficult to feel in significant aortic stenosis or in low output states. Pulsus paradoxus (a decrease in systolic BP during inspiration) is a normal sign unless exaggerated to greater than 10 mm Hg. The most common cause of pulsus paradoxus is asthma and chronic obstructive pulmonary disease (COPD) (eFigure 10–6), though its presence may be a critical component to the diagnosis of pericardial tamponade. Pulsus alternans, in which the amplitude of the pulse alternates every other beat during sinus rhythm, occurs when cardiac contractility is very depressed. It is volume dependent and at times can only be elicited by feeling the pulse on standing.
Hemodynamic features of constrictive pericarditis. Enhancement of ventricular interdependence. Reciprocal respiratory changes in the filling of each ventricle occur, leading to discordance in pulse pressure, systolic pressure, or stroke volume between the right and left ventricles during respiration. (Reproduced, with permission, from Hall JB, Schmidt GA, Kress JP. Principles of Critical Care, 4th ed. McGraw-Hill, 2015.)
Jugular venous pulsations (JVP) provide insight into right atrial (RA) pressure (eFigure 10–7) and function. To identify the waveforms, it is important to palpate the opposite carotid pulse while simultaneously observing the JVP. During ventricular systole (a positive carotid pulse wave), the normal RA pressure falls due to both atrial diastole and the pulling of the tricuspid valve ring into the RV cavity (the x descent). The a wave is a prominent waveform in the JVP just prior to ventricular systole (timed with the opposite carotid pulse). It represents atrial systole into the RV. A prominent waveform just after ventricular systole is the v wave and reflects filling of the RA while the tricuspid valve is shut. Its height increases if the RA compliance worsens. A waveform during ventricular systole is the c-v wave. Prominent a waves imply poor RV compliance or atrial contraction against a closed tricuspid valve. This can be due to AV dissociation associated with ventricular arrhythmias, pacing, or tricuspid stenosis. A prominent v wave implies rapid filling of the RA in late ventricular systole or early ventricular diastole, such as in an atrial septal defect (ASD) or mild tricuspid regurgitation, and a c-v wave implies significant tricuspid regurgitation, since it is represented by a waveform that increases during ventricular systole (rather than decreases, which is the norm). The height of the JVP provides a measure of RA pressure with an elevated central venous pressure if it is visible above the angle of Louis with the patient upright. An increased central blood volume and reduced RV compliance can also be assumed if the JVP rises more than 1 cm above the sternal notch and is sustained (greater than 20 seconds) by right upper quadrant abdominal pressure (the hepatojugular reflux) (eFigure 10–8). Kussmaul sign (failure of jugular venous pressure to decrease with inspiration) is commonly seen with RV infarction, postoperatively after cardiac surgery, with tricuspid regurgitation, and with constrictive pericarditis.
Position of internal and external jugular veins. Pulsation in the internal jugular vein can be used to estimate central venous pressure. (Reproduced, with permission, from Thompson JM et al. Mosby’s Clinical Nursing, 5th ed. Mosby, 2002. Copyright © Elsevier.)
The ECG on the left indicates a negative hepatojugular reflux test. The ECG on the right represents a positive test. (Reproduced, with permission, from Sochowski RA et al. Clinical and hemodynamic assessment of the hepatojugular reflux. Am J Cardiol. 1990;66:1002–6. Copyright © Elsevier.)
Rales heard at the lung bases are a sign of heart failure but may be caused by similarly localized pulmonary disease (AUDIO 10–1). Cardiac rales tend to occur late in inspiration and be fine in nature, whereas pulmonary rales tend to be coarser and appear in early or mid-inspiration. Rales are loudest at the bases in heart failure, and the examiner should note how far up from the diaphragm they are audible. The so-called stress-relaxation quadruple hypothesis of crackle generation holds that expiratory crackles are caused by sudden airway closure events that are similar in mechanism but opposite in sign and far less energetic than the explosive opening events that generate inspiratory crackles. The most likely mechanism of crackle generation is sudden airway closing during expiration and sudden airway reopening during inspiration. Wheezing suggests obstructive pulmonary disease and only rarely occurs in left heart failure (AUDIO 10–2) (AUDIO 10–3). Pleural effusions with bibasilar percussion dullness and reduced breath sounds are common in heart failure and are more frequent or larger on the right. Egophony may be present due to pulmonary compression over a pleural effusion or to a pulmonary infiltration.
Audio 10-01. Recording of a person with early heart failure.
The lung sounds of early heart failure are very similar to those of pulmonary fibrosis. The fine end-inspiratory rales of the two diseases are difficult to distinguish. (Reproduced, with permission, from Murphy, RLH, Jr., A Simplified Introduction to Lung Sounds [audio tape], 1977.)
Audio 10-02. Lung sound: sonorous rhonchus.
(Reproduced, with permission, from Self-Assessment on Sounds of the Chest, narrated by Raymond Murphy, Jr., MD [vinyl record distributed by ACCP at 43rd Annual Scientific Assembly, Las Vegas, 1977].)
Audio 10-03. Lung sound: expiratory sibilant rhonchus or wheezing.
(Reproduced, with permission, from Self-Assessment on Sounds of the Chest, narrated by Raymond Murphy, Jr., MD [vinyl record distributed by ACCP at 43rd Annual Scientific Assembly, Las Vegas, 1977].)
A parasternal lift usually indicates right ventricular hypertrophy (RVH), pulmonary hypertension (pulmonary artery [PA] systolic pressure greater than 50 mm Hg), or LA enlargement; PA pulsations may also be visible. The examiner should feel the LV apical impulse in the left lateral position and note if it is sustained or enlarged and whether an early impulse (A wave) precedes the main apical thrust. The A wave implies poor LV compliance and corresponds to a fourth heart sound. If the second heart sound is palpable along the left sternal border, it may imply an increased P2 and pulmonary hypertension.
Auscultation is helpful in the diagnosis of many heart diseases and provides evidence for cardiac failure (eFigure 10–9). Specific findings are discussed under individual diseases below.
The timing of the principal cardiac murmurs. Heart murmurs can be either systolic or diastolic. During systole, while the left ventricle is contracting, the aortic valve is open and the mitral valve is closed. Turbulent flow can occur either because of an incompetent mitral valve, leading to regurgitation of blood back into the atrium, or from a narrowed aortic valve. In diastole, the situation is reversed, with filling of the left ventricle through an open mitral valve while the aortic valve is closed. Turbulent flow occurs when there is narrowing of the mitral valve or incompetence of the aortic valve. Stenosis of valves usually develops slowly over time; lesions that cause valvular regurgitation can be either chronic or acute. (Reproduced, with permission, from Hammer GD, McPhee SJ. Pathophysiology of Disease, 8th ed. McGraw-Hill, 2019.)
The first heart sound (S1), the closing of the mitral valve and tricuspid valve, may be diminished with severe LV dysfunction, long PR intervals, or premature mitral valve closure due to severe aortic regurgitation. It may be accentuated with mitral stenosis or short PR intervals. Separation of the components of the second heart sound is due to the RV ejection time being longer than the LV ejection time. This difference is due to the low resistance of the pulmonary vasculature compared to the systemic arterial system. The low pressure in the pulmonary circuit results in the pulmonary valve opening before the aortic valve and forward pulmonary flow starting before aortic flow and continuing even after the RV begins its diastole. The pulmonary valve thus opens earlier and closes later than the aortic valve (and results in P2 following A2). Inspiration increases flow to the lungs, increasing the RV ejection time, and reduces flow to the left heart, decreasing the LV ejection time. Thus, splitting is increased by increasing the RV stroke volume during inspiration. The events reverse during expiration. The splitting is less evident in expiration when flow from the lungs to the LV increases and flow from the RV decreases. Splitting may be fixed in ASD (AUDIO 10–4); wide with right bundle branch block; and absent or reversed (paradoxical splitting) with aortic stenosis, LV failure, or left bundle branch block. With normal or reduced splitting, an accentuated P2 is an important sign of pulmonary hypertension (AUDIO 10–5). Third and fourth heart sounds (ventricular and atrial gallops, respectively) indicate ventricular volume overload or impaired compliance and may be heard over either ventricle (AUDIO 10–6) (AUDIO 10–7). A right-sided gallop may increase with inspiration or may be confirmed if heard in the right subclavicular area (where a left-sided gallop does not usually radiate). A palpable LV A wave helps confirm an S4. An apical S3 is a normal finding in younger individuals and in high output states, such as 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 (AUDIO 10–8).
Audio 10-04. Atrial septal defect (ASD) and pulmonary hypertension.
Note S1 followed by a rough systolic murmur and fixed close splitting of A2-P2. P2 is louder than A2. (Reproduced, with permission, from T. Anthony Michael, MD, Mastering Auscultation [CD-ROM], McGraw-Hill, 2000.)
Audio 10-05. Pulmonary hypertension.
Note the rough mid-systolic murmur followed by a split S2 with a loud P2. (Reproduced, with permission, from T. Anthony Michael, MD, Mastering Auscultation [CD-ROM], McGraw-Hill, 2000.)
Audio 10-06. Heart failure due to valvular dysfunction.
Note the holosystolic murmur and S2 followed by S3. (Reproduced, with permission, from T. Anthony Michael, MD, Mastering Auscultation [CD-ROM], McGraw-Hill, 2000.)
Audio 10-07. An S4 precedes S1 and is an abnormal finding in this pregnant patient.
Peripartum cardiomyopathy must be considered. (Reproduced, with permission, from T. Anthony Michael, MD, Mastering Auscultation [CD-ROM], McGraw-Hill, 2000.)
Audio 10-08. Mitral valve prolapse with S1, nonejection click, late systolic murmur, and S2.
(Reproduced, with permission, from T. Anthony Michael, MD, Mastering Auscultation [CD-ROM], McGraw-Hill, 2000.)
Although 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 or aortic flow. Innocent murmurs often vary with inspiration, diminish in the upright position, and are most frequently heard in thin individuals. Systolic murmurs should be classified as “holosystolic” when they begin with S1 and persist through S2 or as “ejection” when they begin after S1 and end before S2. Holosystolic murmurs tend to have a uniform intensity during systole, while ejection murmurs have a peak at some part of the systolic cycle. Holosystolic murmurs usually represent AV valvular regurgitation and systolic ejection murmurs semilunar valve stenosis. Mitral regurgitation (AUDIO 10–9) is usually maximal at the apex or in the axilla and tricuspid regurgitation (AUDIO 10–10) or ventricular septal defect (VSD) (AUDIO 10–11) along the sternal border. Many patients with mitral regurgitation due to mitral valve prolapse may have an audible murmur only late in systole, generally following the ejection sound or click. A late systolic chest murmur is also common in pregnant women (mammary souffle). It may be continuous and represents increased flow in the engorged breast. Short aortic ejection murmurs with a preserved A2 are common in older individuals, especially when hypertension has been present; even if they are moderately loud, they usually reflect thickening (sclerosis) of the valve and may not imply an aortic stenosis gradient. The association of murmurs with palpable vibrations (“thrills”) is always clinically significant (except in the case of a tiny VSD where there is a high gradient between the LV and RV), as are diastolic murmurs. High-pitched diastolic murmurs imply flow from a high pressure to low-pressure chamber (eg, pulmonary valve regurgitation (AUDIO 10–12) in pulmonary hypertension, aortic regurgitation, or VSD) while low-pitched diastolic “rumbles” imply forward ventricular filling across an AV valve (eg, mitral stenosis). Continuous murmurs imply there is a pressure differential in both systole and diastole and are associated with fistula (such as coronary fistula to the RV or RA), large collaterals (such as collaterals around a coarctation of the aorta) or a patent ductus. Continuous murmurs are universal in the affected arteries of dialysis patients with a surgical AV fistula.
Audio 10-09. Mitral regurgitation causing heart failure.
Note the holosystolic murmur heard best at the apex, followed by S2 and an S3. (Reproduced, with permission, from T. Anthony Michael, MD, Mastering Auscultation [CD-ROM], McGraw-Hill, 2000.)
Audio 10-10. Tricuspid regurgitation due to tricuspid valve endocarditis.
A blowing holosystolic murmur is preceded by S1, followed by S2, and increases in loudness with inspiration. (Reproduced, with permission, from T. Anthony Michael, MD, Mastering Auscultation [CD-ROM], McGraw-Hill, 2000.)
Audio 10-11. Ventricular septal defect (VSD).
Blowing to rough grade 4/6 holosystolic murmur. A VSD may cause a loud rough murmur rather than a more characteristic blowing murmur. (Reproduced, with permission, from T. Anthony Michael, MD, Mastering Auscultation [CD-ROM], McGraw-Hill, 2000.)
Audio 10-12. Pulmonary valve regurgitation due to primary pulmonary hypertension.
Note the loud P2 followed by a rapidly attenuating early diastolic murmur. (Reproduced, with permission, from T. Anthony Michael, MD, Mastering Auscultation [CD-ROM], McGraw-Hill, 2000.)
Certain maneuvers can be used to help distinguish the origin of some murmurs. Murmurs arising from the right heart increase with inspiration and left-sided murmurs remain unchanged or decrease. There are a few notable exceptions: pulmonary murmurs of pulmonary hypertension or an ASD murmur may show no respiratory variation. The Valsalva maneuver may assist in defining a source; all murmurs, except in hypertrophic cardiomyopathy or occasionally the mitral regurgitation of mitral valve prolapse, decrease during the Valsalva maneuver, and upon release of the Valsalva the right heart murmurs increase a couple cycles before left heart murmurs. In the beat after a premature ventricular contraction (PVC), the aortic murmur is louder due to the higher stroke volume while there may be no change in a mitral regurgitation murmur (since the gradient between the LV and LA is so high regardless of whether a normal beat or post PVC beat). An echocardiogram should be ordered whenever a murmur is heard.
Subcutaneous fluid collections appear first in the lower extremities in ambulatory patients or in the sacral region of bedridden individuals. In heart disease, peripheral edema primarily results from elevated RA pressures or associated peripheral venous disease. Right heart failure most commonly results from left heart failure, pulmonary disease, RV dysfunction and tricuspid regurgitation, or constrictive pericarditis. Edema may also be due to venous insufficiency, nephrotic syndrome, low serum albumin, cirrhosis, premenstrual fluid retention, or medications (especially certain vasodilators such as calcium channel blockers or salt-retaining medications such as nonsteroidal anti-inflammatory agents or thiazolidinedione diabetic agents), or it may be idiopathic. The presence of ascites may predominate over the presence of peripheral edema, especially in constrictive pericarditis with associated cardiac cirrhosis, or following aggressive diuretic usage that reduces the peripheral edema but not the ascites. While diuretic usage has long been associated with ensuing hyponatremia, there is growing interest in the impact of hypochloremia because of an association with neurohormonal activation and diuretic resistance.
et al. Hypochloremia and diuretic resistance in heart failure: mechanistic insights. Circ Heart Fail. 2016 Aug;9(8):e003180.