7 Physical Examination of the Heart and Circulation

Chapter 7 / Physical Examination of the Heart and Circulation

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Physical Examination of the Heart and Circulation Jonathan Abrams, MD CARDIAC EXAMINATION

The examination of the heart and circulation has a long and rich tradition in clinical medicine. Most of the cardinal signs of cardiovascular disease detectable on the physical examination were described and documented by master physicians during the 19th and early 20th centuries. Subsequently, echocardiography and cardiac catheterization have demonstrated that the presumed pathogenesis of many to most cardiovascular abnormalities on the physical examination were accurately and presciently described before these modern techniques became available. In the past, generations of internists and cardiologists were well trained in the skills of cardiac examination; the absence of our current ultrasound technology providing “immediate” answers contributed to the emphasis of expertise in cardiac physical diagnosis. Unfortunately, clinical skills in this area are no longer emphasized in medical education, in part due to the burgeoning of other aspects of medical science that must be taught in the medical student curriculum. The advent of readily available two-dimensional echocardiography has clearly contributed to the demise of cardiac physical diagnosis capability among physicians, a phenomenon well documented in recent published studies. This chapter will highlight the core components of the cardiac physical examination, and will focus on a practical assessment of the heart and circulation in health and disease. The author’s assumption is that the reader will already possess a basic knowledge of one cardiac exam and structural heart disease. It is hoped that physicians will redouble their efforts in applying the well-known components of the cardiac examination to their patients. The rewards are many—in particular, a feeling of real satisfaction in making a diagnosis of organic heart disease with one’s hands and ears.

Limitation of the Cardiac Examination Echocardiography has clearly demonstrated that much cardiovascular disease is not detectable or accurately quantifiable, even to the expert, on the physical examination. For instance, mitral and aortic regurgitation are often missed; left ventricular function may be significantly depressed without a detectable abnormality on examination. Thus, it is best to consider the physical examination and the echo as complementary. For the experienced clinician, the findings on the cardiac exam often predict what will be noted on the echo. Nevertheless, if significant heart disease is suspected, a complete 2-D echo-Doppler examination is often indicated. Conversely, with a negative cardiac physical examination in the setting of a normal electrocardiogram, an echo can be avoided in many instances.

The Cardiac Exam The components of the cardiac physical examination are standard (Table 1). As with the more general physical examination, physicians are urged to conduct the cardiac exam in a systematic From: Essential Cardiology: Principles and Practice, 2nd Ed. Edited by: C. Rosendorff © Humana Press Inc., Totowa, NJ

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Abrams Table 1 Cardiac Pysical Examination Overall assessment of the patient General features, e.g., dyspnea, cyanosis, edema Special features, e.g., unusual facies, lipid deposits Blood pressure Supine, upright Leg pressure (if coarctation suspected) Arterial pulses Contour, volume Precordial motion LV apex impulse (PMI) RV activity Ectopic impulses Thrills (loud murmur) Heart Sounds Characteristics of S1, S2 Is an S3 or S4 present? Ejection or nonejection clicks Opening snap Heart Murmurs Systolic Diastolic Continuous Timing in cardiac cycle Quality Length Radiation Table 2 Blood Pressure and Peripheral Arterial Examination Clues to Cardiovascular Disease

Coarctation of aorta Aortic regurgitation Pulsus or mechanical alternans Pulsus paradoxus Hypertension

Hypertension in upper extremities; brachial–femoral delay Wide pulse pressure with increased systolic and decreased diastolic pressure Increased volume, rate of rise of arterial pulses with exaggerated collapse Beat-to-to beat alternation in peak pressure and pulse volume (detect by palpation, not cuff) Exaggerated inspiratory decline (>10 mmHg) in peak systolic pressure measured carefully by cuff; palpation may pick up if severe Elevated systolic and diastolic pressure; increased systolic pressure with normal diastolic (isolated systolic hypertension of the elderly)

and sequential fashion. After a general assessment of the patient, the arterial pulses and pressure and venous pulsations are evaluated, followed by careful inspection and palpation of the precordium. Auscultation is the last but most important component of the cardiac exam.

EVALUATION OF ARTERIAL PULSE An accurate determination of arterial pressure is part of the cardiac physical examination. Careful attention to the details of the technique of taking blood pressure are important. Abnormalities of blood pressure are not usually a component of structural heart disease except in selected instances (Table 2). Assessment of the severity of aortic regurgitation or detection of pulsus paradoxus are two situations in which the blood pressure can provide important information.


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Fig. 1. The arterial pulse in aortic stenosis. Note the delayed upstroke and the jagged contour representing a palpable shudder or transmitted thrill. The pulse volume is usually decreased as well.

The Examination The physician must become familiar with the normal volume and rate of rise of the arterial pulse. In general, the carotid artery is the only artery that should be utilized for detection of cardiovascular abnormalities. Because of delay of transmission of the pulse wave in the periphery, as well as the distal decrease in arterial diameter, assessment of the radial or brachial arterial pulses usually is of little value (except in the assessment of pulsus alternans, pulsus paradoxus, and cardiogenic shock). In hypertensive patients, simultaneous assessment of the brachial and femoral arterial pulses is useful to rule out a significant coarctation of the aorta. In such cases, the femoral peak of the pulse wave peak will clearly follow the palpable brachial artery impulse; a delay indicates a probable obstruction in the aorta. The contour of the aortic pulse is important in the assessment of aortic valve disease. Aortic stenosis characteristically produces a small volume, late peaking, or delayed carotid upstroke, often with a palpable shudder or thrill (anacrotic notch, transmitted murmur) (see Fig. 1). Remember that in the healthy older subject, decreased compliance and increased arterial stiffness typically result in an increase in the arterial pulse amplitude as well as the pulse pressure. This can readily mask the typical abnormalities of aortic stenosis. Aortic regurgitation, when significant (e.g., 2+/4), typically results in an arterial pulse with an increased amplitude and rate of rise and a collapsing quality. In severe aortic regurgitation, the aortic pulsations are abnormal throughout the arterial system (see Table 3). A prominent (often visible), high-amplitude, full-volume carotid arterial pulse, coupled with a wide pulse pressure (diastolic blood pressure 60 mmHg) is highly suggestive of severe aortic regurgitation. A double peaking or bisferiens pulse is common in advanced aortic regurgitation (Fig. 2).

PULSUS PARADOXUS A greater-than-normal difference in systolic blood pressure between inspiration and expiration is known as pulsus paradoxus. This is common whenever there are major fluctuations of intrathoracic pressure or in pericardial tamponade. Careful palpation and auscultation is mandatory to detect significant pulsus paradoxus (>10 mmHg). Normally, there is a slight physiologic respiratory difference between inspiration and expiration, typically 6 to 8 mmHg or less during quiet respiration. Pulsus paradoxus may be detected in severe congestive heart failure, decompensated chronic obstructive lung disease, asthma, and in an occasional very obese individual. PULSUS ALTERNANS In setting of severe left ventricular systolic dysfunction, beat-to-beat alteration in the peak amplitude of the arterial pulse may be noted (Fig. 3). This can be palpated in the brachial or radial

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Abrams Table 3 Peripheral or Nonauscultatory Signs of Severe Aortic Regurgitation: A Glossary

Bisferiens pulse Corrigan’s sign Pistol shot of Traube Palmar click Quincke’s pulse

Duroziez’s sign

DeMusset’s sign Hill’s sign Water-hammer pulse

Miller’s sign

A double or bifid systolic impulse felt in the carotid arterial pulse. Visible pulsations of the supraclavicular and carotid arteries. A loud systolic sound heard with the stethoscope lightly placed over a femoral artery. A palpable, abrupt flushing of the palms in systole. Exaggerated sequential reddening and blanching of the fingernail beds when light pressure is applied to the tip of the fingernail. A similar effect can be induced by pressing a glass slide to the lips. A to-and-fro bruit heard over the femoral artery when light pressure is applied to the artery by the edge of the stethoscope head. This bruit is caused by the exaggerated reversal of flow in diastole. Visible oscillation or bobbing of the head with each heartbeat. Abnormal accentuation of leg systolic blood pressure, with popliteal pressure 40 mmHg or higher than brachial artery pressure. The high-amplitude, abruptly collapsing pulse of aortic regurgitation. (This term refers to a popular Victorian toy producing a slapping impact on being turned over.) Visible pulsations of the uvula.

arteries. This phenomenon, usually undetected, is most likely to be associated with a left ventricular heave and third heart sound. Careful palpation of the radial artery is recommended. Determination of pulsus paradoxus and/or mechanical pulsus alternans are two exceptions to the rule of always using the carotid arteries for arterial pulse analysis. Table 2 lists the conditions where arterial pulse wave analysis is particularly valuable.

EVALUATION OF VENOUS PULSE Most physicians do a poor job of the venous examination and many are intimidated by the presumed difficulty in assessment of the jugular venous pulse (JVP). The following key points should help make the JVP examination straightforward: 1. The A wave (produced by right atrial contraction) is normally larger or taller than the V wave in normal subjects. Expect to visualize a dominant A wave in most instances (Fig. 4). 2. Conditions of decreased right ventricular compliance, such as right ventricular hypertrophy or pulmonary disease, may augment the A wave amplitude and prominence, particularly the setting of pulmonary hypertension. 3. Detection of the A wave is easy if one remembers that it immediately precedes the palpable carotid arterial pulse (one must use simultaneous inspection and palpation of the carotid upstroke). Conversely, the V wave of the jugular venous pulse occurs simultaneous with the carotid upstroke (systolic in timing). 4. When the V wave is the predominant wave form and is greater than the A wave (in the absence of atrial fibrillation), it is likely that significant tricuspid regurgitation is present even in the absence of a typical murmur of tricuspid regurgitation. 5. Mean jugular pressure is relatively easy to measure (Fig. 5). It is most important to determine if the mean venous pressure is normal or elevated; quantification of the precise degree of venous pressure elevation is less important, although this can be often accomplished.

Dr. Gordon Ewy has emphasized the use of abdominal or hepatic compression to bring out latent or borderline elevation of the jugular venous pressure, which may be important to assess if a volume overload state or heart failure is suspected. The technique is simple and employs steady


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Fig. 2. Bisferiens pulse of aortic regurgitation. Note the bifid systolic pulse wave, which is best detected using light finger pressure over the carotid arteries. This contour is usually associated with an increased pulse volume. The bisferiens pulse must be differentiated from a transmitted systolic murmur or palpable thrill. Note the soft S1 and S2. SM, systolic murmur; DM, diastolic murmur; 2 LIC, 2nd left intercostal space.

Fig. 3. Pulsus alternans. Note that every other beat has a lower systolic pressure. The rate of rise of the second pulse wave is slower, relating to decreased contractile force in alternate beats. Pulsus alternans is an important sign of severe left ventricular dysfunction. It is best detected in a peripheral vessel, such as the radial artery. Heart sounds and murmurs may also alternate in intensity.

pressure with the hand over the upper abdomen for 60 s while carefully observing the jugular venous pulsations. The normal response is a brief rise and a decline in the mean jugular venous pressure. An abnormal test consists of progressive and sustained rise in the mean venous pressure for up to 1 min. Remember that abnormalities of the venous contour or pressure reflect right heart events. While it is true that left heart disease, particular left ventricular failure, is the most common cause of right ventricular failure, an increased level of venous pressure does not necessarily imply left ventricular systolic failure. Fluid or volume overload in the setting of normal cardiac function, left ventricular diastolic dysfunction, pulmonary hypertension, severe tricuspid regurgitation, or isolated right heart failure (cor pulmonale) can all produce an increase in jugular venous pressure in the absence of left ventricular pathology. Nevertheless, an increased jugular venous pressure is one of the hallmarks of congestive heart failure, usually a left heart problem in adults.

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Fig. 4. Normal jugular venous pulse. Note the biphasic venous waveform with a large A wave immediately preceding the carotid arterial upstroke and roughly coinciding with S1, and a smaller V wave that peaks almost coincident with S2. The jugular X descent occurs during systole and in some individuals may be quite prominent. The Y descent occurs during early diastole; the nadir of the Y descent times with S3. The C wave and H wave are not visible to the eye but are often recordable in venous pulse tracings.

PRECORDIAL MOTION Left Ventricle By far the most important aspect of inspection and palpation of the heart is a determination as to whether the left ventricle is grossly normal or abnormal. Left ventricular hypertrophy and dilation are the commonest causes of an abnormal PMI (point of maximal impulse—an oldfashioned term that is still useful), also known as the left ventricular apical impulse. The normal left ventricle is felt over a small area (<3 cm), not displaced beyond the midclavicular line, not sustained into late systole, and not hyperdynamic (Table 4, Fig. 6). Often, the left ventricle is not palpable in the supine position; the examiner must then ask the patient to turn onto the left side with the left arm elevated for optimal assessment of the precordium (Fig. 7). Commonly, the left ventricular impulse will then become apparent in this position, although not always. Older subjects (>50 years of age), those with large chests, prominent musculature or obesity, or large breasts, all have a decreased likelihood of a detectable the PMI. Abnormalities of the apical impulse are listed in Table 5. Palpable third and fourth heart sounds are more commonly present than physicians realize (particularly in the left lateral position), and represent important findings suggesting abnormal left ventricular size, function, or compliance. In coronary artery disease, an ectopic or bifid (double) left ventricular impulse is related to dyskinesis/akinesis caused by a prior myocardial infarction. A palpable S4 is an important observation in aortic valve disease (suggesting severe aortic stenosis or regurgitation), as well as coronary artery disease (suggesting decreased LV compliance). A meticulous search for the impulse can be quite rewarding, and may suggest increased LV size or LV hypertrophy with high specificity. Absence of an abnormal left ventricular impulse in a thin


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Fig. 5. Estimation of mean venous pressure. The right atrium is approximately 5 cm below the sternal angle of Louis with the subject in any body position. Thus with a patient supine or erect, the height of the venous pulsations from the sternal angle can be measured; by adding 5 cm to this value, one can estimate the actual venous pressure. The thorax and neck should be positioned until the peak of the venous column is readily identified. In subjects with a normal venous pressure, only the peaks of the A and V waves may be seen when the patient is sitting up at 45 degrees or greater; the neck veins are often in this position. When the venous pressure is abnormally high, the thorax and head must be elevated in order to accurately identify the true peak of the venous column.

Table 4 Normal Supine Apical Impulse A gentle, nonsustained tap Early systolic anterior motion that ends before the last third of systole Located within 10 cm of the midsternal line in the fourth or fifth left intercostal space A palpable area <2 to 2.5 cm2 and detectable in only one intercostal space Right ventricular motion normally not palpable Diastolic events normally not palpable May be completely absent in older persons

individual is useful in excluding significant aortic stenosis, hypertrophic cardiomyopathy, or severe mitral regurgitation in an individual with a prominent systolic murmur.

Right Ventricle Right ventricular activity is not usually detectable in normal subjects, except in young or thin individuals where a gentle parasternal impulse may be found. Technique is important in the detection of a right ventricular impulse; firm pressure over the lower parasternal region is the key, with the hand held in end-expiration (Fig. 8). The examining hand should be observed for an upward or anterior motion, which can be quite subtle. Subxiphoid palpation with two or three fingers may be employed in patients with a large chest or chronic obstructive pulmonary disease (COPD).

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Fig. 6. Major variants of left ventricular precordial motion. (A) Normal. (B) Hyperdynamic. (C) Sustained. With the patient in the supine position, sustained left ventricular activity detectable in the latter half of systole is distinctly abnormal. Some experts believe that palpation of a sustained impulse when patients are in the left lateral decubitus position may have less specificity for underlying left ventricular enlargement. (Adapted from Abrams J. Precordial palpation. In: Horwitz LD, Groves BM, eds. Signs and Symptoms of Cardiology. J. B. Lippincott, Philadelphia, 1985.)

Fig. 7. Palpation of the apex impulse, left lateral decubitus position. This maneuver should be used in any patient with suspected left ventricular disease. The patient should be turned 45 to 60 degrees onto the left side with the left arm extended above the head.

Table 5 Causes of Palpable Precordial Abnormalities Left ventricular hypertrophy and/or dilation Left ventricular wall motion abnormalities (fixed or transient) Increased force of left atrial contraction (palpable S4) Accentuated diastolic rapid filling (palpable S3) Anterior thrust of the heart from severe mitral regurgitation Right ventricular hypertrophy and/or dilation Loud murmurs (thrills) Loud heart sounds (normal and abnormal) Dilated or hyperkinetic pulmonary artery Dilated aorta

Detection of right ventricular hypertrophy generally implies pulmonary hypertension in an adult. Severe mitral regurgitation can occasionally result in a recoil phenomenon related to left atrial expansion, with the regurgitant jet of blood “pushing” the heart forward.


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Fig. 8. Precordial palpation for detection of parasternal or right ventricular activity. Use firm downward pressure with the heel of the had while the patient’s breath is held in end-expiration.

Palpable Heart Sounds The experienced examiner is familiar with palpable heart sounds that can be felt with the hand or fingers as discrete deflections. Thus, a loud S1, S2, or opening snap are often palpable. An S3 or S4 may be detectable in the left lateral position. For instance, mitral stenosis can be strongly suspected solely by detection of a palpable S1, opening snap, diastolic apical thrill, and a right ventricular lift.

HEART SOUNDS Normal and Abnormal Abrupt intracardiac pressure changes and the subsequent valve motion related to alterations hemodynamic are responsible for most normal and abnormal heart sounds. Thus, closure of the A-V and semilunar valves (S1, S2) and the opening motion of thickened and noncompliant aortic and mitral valve leaflets (aortic ejection click, mitral opening snap) produce commonly heard sounds. The S3 and S4 are due to left ventricular filling transients produced by left atrial contraction (S4) and passive left ventricular inflow after mitral valve opening (S3). These sounds are lowfrequency and dull, and are best heard with the bell of the stethoscope (light pressure) with the patient in the left lateral position. Conversely, the first and second heart sounds, aortic and pulmonary ejection clicks and opening snap, are high-frequency, and best heard with the diaphragm of the stethoscope (firm pressure).

First Heart Sound (S1) The S1 is directly related to vibrations of the A-V valves and myocardium produced by A-V closure and in general has little diagnostic usefulness. A loud S1 is common in mitral stenosis and in individuals with a short PR interval. A soft S1 is common in individuals with decreased left ventricular systolic function or first-degree AV block.

Second Heart Sound (S2) Although assessment of respiratory movement and intensity of the two components of S2 is a well-emphasized aspect of auscultation, for practical purposes, analysis of S2 is helpful in relatively few conditions (Table 6). The physician should focus on the relative intensity of aortic and pulmonary components (A2, P2) and the possible presence of reversed or paradoxic splitting, characterized by inspiratory narrowing and expiratory widening of the two components of S2. Paradoxic

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Abrams Table 6 Assessment of Second Heart Sound (S2): A Practical Approach

Character a

Significance

Abnormalities of respiratory variation Wide splitting, inspiratory increase in A2–P2 interval Wide splitting, fixed A2–P2 interval Single S2

Reversed or paradoxical splitting

Abnormalities of intensity Loud A2 Loud P2 Soft A2 Soft P2

Right ventricular conduction delay (e.g., incomplete or total right bundle branch block—important clue) Idiopathic dilation of pulmonary artery Small atrial septal defect (unusual) Pulmonic stenosis Atrial septal defect (important clue) Often normal in older patients Aortic stenosis Mild left ventricular conduction delay Severe pulmonary hypertension (A2 “masked”) Left bundle branch block (important clue) Left ventricular systolic dysfunction (important in acute ischemia) Dilated aorta Hypertension Tetralogy of Fallot Pulmonary hypertension (important clue) Atrial septal defect Dilated pulmonary artery Aortic sclerosis or stenosis Hypotension Pulmonic stenosis

a The physician must differentiate between decreased intensity of all cardiac sounds vs a selective decrease in the loudness of A2 or P2.

splitting is an important clue to an underlying left bundle branch block or significant aortic stenosis in a patient with a systolic ejection murmur. A loud P2, particularly when P2 is louder than A2 at the base and apex, is predictive of significant pulmonary hypertension.

Third Heart Sound (S3) The low-pitched early diastolic third heart sound can be a normal finding or a significant cardiovascular abnormality. The S3 is most easily heard by turning the patient into the left lateral position, identifying the apex impulse with a finger, and carefully applying the bell of the stethoscope with light pressure (Fig. 7).

Fourth Heart Sound (S4) The atrial sound or S4 is caused by augmentation of late LV diastolic filling resulting from left atrial contraction. Audibility is correlated with increased left ventricular stiffness or decreased compliance; thus, S4 is a useful finding in hypertension, or coronary artery disease, where its presence suggests increased LV end-diastolic pressure and/or LV hypertrophy. The S4 (and S3) may be palpable. The S4 is felt as a presystolic outward thrust just before the palpable LV impulse, and is noted as a double early systolic left ventricular impulse. It is important to use the left lateral position for optimal detection by palpation or auscultation of both the S3 and S4 (Fig. 7).

Ejection Sounds These are high-frequency, discrete audible sounds that occur immediately after S1 (Fig. 9). They are usually caused by stiff or malformed semilunar leaflets, such as a bicuspid aortic valve,


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Fig. 9. Aortic ejection sound. This phonocardiogram and carotid arterial pulse tracing demonstrates a prominent, discrete aortic ejection sound that is better heard and recorded at the apex than at the base. This is characteristic of aortic ejection sounds or clicks. Note the prominent separation of the ejection sound from S1 by approx 40 to 50 ms. (Adapted from Shaver JA, Griff FW, Leonard JJ. Ejection sounds of left-sided origin. In: Leon DF, Shaver JA, eds. Physiologic Principles of Heart Sounds and Murmurs. American Heart Association Monograph No. 46, 1975.)

or a valvar pulmonic stenosis. Importantly, ejection sounds may be detected in the setting of a dilated great vessel (aorta or pulmonary artery), particularly if systolic pressure is elevated. An isolated ejection sound or click in a patient with or without a systolic ejection murmur suggests a congenitally deformed aortic valve, typically biscuspid.

HEART MURMURS Physicians are more knowledgeable about heart murmurs than about any other aspect of the cardiac physical examination. Nevertheless, recent studies confirm that physician skills in cardiac auscultation are poor, probably worse than in earlier decades. The widespread availability and utilization of two-dimensional echocardiography certainly is a significant factor relating to this decline in expertise. In addition, the teaching of the cardiac physical examination in medical schools takes up an increasingly limited amount of the curriculum. Murmurs are a result of turbulence of blood flow; thus, systolic murmurs are by far the most common and are related to ejection of blood across the aortic and pulmonic valves in the normal or structurally abnormal heart. Abnormal similar valves frequently produce systolic ejection murmurs that must be differentiated from functional or flow murmurs. Mitral valve incompetence with regurgitation of blood into the left or right atrium commonly produces audible cardiac sound. Thus, a systolic murmur may be normal or abnormal. On the other hand, all diastolic murmurs are abnormal, as there is no physiologic explanation for normal flow of sufficient turbulence during diastole to produce a heart murmur.

Classification of Murmurs (Fig. 10) SYSTOLIC MURMUR The classic heart murmur is a systolic ejection murmur, characterized by a crescendo contour and a gap between the end of audible sound and S2. This sound-free period represents the critical distinction from a regurgitant systolic murmur, in which sound continues up to S2 (holosystolic, pansystolic) (Fig. 11). Distinguishing between the two is not always possible, even by an expert in cardiac physical diagnosis. Nevertheless, the large majority of systolic murmurs can be identified correctly by a careful cardiac examination.

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Fig. 10. Intracardiac pressures and heart murmurs of the major cardiac valve abnormalities. See text for discussion of specific murmurs. LVP, left ventricular pressure; LAP, left atrial pressure; AOP, aortic pressure; HSM, holosystolic murmur; PSM, presystolic murmur; OS, opening snap; MDM, mid-diastolic murmur; C, mid-systolic click; LSM + late systolic murmur; ES, ejection sound; SEM, systolic ejection murmur; EDM, early diastolic murmur; CM, continuous murmur. (Adapted from Crawford MH, O’Rourke RA. A systematic approach to the bedside differentiation of cardiac murmurs and abnormal sound. Curr Prob Cardiol 1979;1:1.)

Fig. 11. Importance of late systole in evaluation of systolic murmurs. It is essential to assess the last part of systole to determine whether a murmur is ejection in nature or is holosystolic. On the left, an early peaking murmur ends before the last third of systole. This is the rule in functional murmurs or with mild semilunar valve stenosis. On the right, a long ejection murmur is shown, which peaks later in systole. Sound vibrations extend to S2, suggesting severe obstruction to ventricular outflow. In severe semilunar valve stenosis, the vibrations may extend beyond S2.

The functional heart murmur, also known as an innocent or physiologic murmur, is usually not very loud (grade 1–2 intensity), is best heard at or near the base of the heart, and is unassociated with other cardiac abnormalities. It is thought that functional murmurs are related to normal turbulent blood flow across semilunar valves. Thus, anxiety, fever, anemia, excitement, pregnancy, or exercise can all accentuate murmur intensity. Younger individuals (children, teens, young adults) commonly have innocent or functional systolic murmurs.

DIASTOLIC MURMUR The most common audible diastolic murmur is the blowing or high-pitched decrescendo murmur of aortic regurgitation (Fig. 2). This can be difficult to hear and should be sought out by the clinician. Examination in a quiet room with the subject sitting up and leaning forward with the


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Fig. 12. Echocardiographic correlates of the loud first sound and opening snap in mitral stenosis. S1 is produced by mitral valve closure and is accentuated and delayed due to elevation of left atrial pressure and the loss of valve compliance. A prominent presystolic diastolic murmur merges with S1; this represents augmented transmitral flow with left atrial contraction. The opening snap (OS) times precisely with the maximum opening excursion of the anterior leaflet of the mitral valve and is produced by tensing of the valve cusps during early diastole. Left ventricular filling and the resultant early to mid-diastolic murmur (DM) follows the OS. (From Reddy PS, Salerni R, Shaver JA. Normal and abnormal heart sounds in cardiac diagnosis. Part II. Diastolic sound. Curr Prog Cardiol 1985;10:1.)

breath held in end-expiration will enhance detection of these murmurs, which can be quite soft and are typically high-frequency. Thus, the inexperienced or distracted physician will often miss a grade 1–2 aortic regurgitation murmur. Furthermore, echocardiography confirms that mild to moderate aortic regurgitation is often silent to examination. Mitral stenosis produces with a diastolic murmur, which is different from the murmur of aortic regurgitation. The classic “mitral rumble” is low-frequency, begins after the early diastolic opening snap, and is often heard only at the cardiac apex in the left lateral position (Fig. 12).

CONTINUOUS MURMUR These unusual murmurs are caused by late systolic flow and persistent blood flow from one cardiac chamber or great vessel to another after ventricular ejection has been completed. Thus, a continuous murmur typically is heard in late systole extending into diastole. These murmurs are often phasic in intensity and may be audible at sites away from the classic valve areas. Table 7 lists some of the more common continuous murmurs. The murmur of a patent ductus arteriosus is usually very loud and harsh, maximal at the upper left infraclavicular area and left scapular area. Aortic valve disease with both stenosis and regurgitation may simulate a continuous murmur, especially at fast heart rates.

CARDIAC PHYSICAL EXAMINATION IN SPECIFIC CARDIOVASCULAR CONDITIONS The cardinal physical findings in a variety of common cardiac syndromes and conditions are summarized below. It is important to recognize that typical or classic features of structural heart disease on examination are not always present. In many instances, atypical characteristics or no

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Abrams Table 7 Common Causes of a Continuous Murmur a

Patient ductus arteriosus Arteriovenous fistula, congenital or acquired, systemic or pulmonary Ruptured aneurysm of the sinus of Valsalva (communication usually into right atrium or right ventricle) Venous hum (innocent finding in children) Anomalous origin of the coronary artery from the pulmonary artery Coronary arteriovenous fistula “Mammary soufflé” of pregnancy Systemic arterial-pulmonary arterial collaterals or bronchial arterial collaterals in congenital defects Coarctation of the aorta: coarctation site and/or collateral vessel flow a Pseudocontinuous

murmur suggests aortic stenosis and regurgitation.

specific features may be present (e.g., “silent” valve disease), resulting in considerable diagnostic confusion or error.

Congestive Heart Failure Overt or decompensated heart failure is a very common clinical condition; the cardiac physical examination can confirm this diagnosis suggested by the patient’s history. Importantly, the absence of features of heart failure on examination may suggest another etiology for the patient’s complaints, such as chronic obstructive lung disease or pneumonia.

GENERAL APPEARANCE The patient is often tachypneic and orthopneic, with lower extremity peripheral edema. Rales may be heard at the lung bases; percussion dullness and decreased breath sounds suggest pleural effusions. JUGULAR VENOUS PULSE Elevation of the mean venous pulse is the sine qua non of right heart failure. The A-wave may be prominent, suggesting right arterial (and right ventricular) pressure elevation (Fig. 4). Tricuspid regurgitation in subjects with heart failure is common and may produce a dominant systolic jugular V wave, typically seen simultaneous with the palpable carotid arterial upstroke (Fig. 13). A large systolic V wave is often present in heart failure, but is frequently missed by the examiner. PRECORDIAL IMPULSE The examiner should actively seek out an abnormally prominent LV impulse and/or a parasternal heave. Look for findings on the examination that confirm structural heart disease and/or cardiac enlargement. On occasion, an S3 can be palpated in the left lateral position. In the presence of hypertensive heart disease or coronary artery disease, a hypertrophic or dilated LV may result in a prominent LV thrust. Displacement of the PMI leftward indicates LV enlargement. Remember, heart failure may be due to diastolic dysfunction (a stiff left ventricle with normal systolic function). HEART SOUNDS An S4 or S3 are common. The latter has adverse prognostic implications. Conversely, an S4 (audible or palpable) indicates decreased LV compliance and LV hypertrophy. S1 may be diminished in heart failure. MURMURS Mitral and tricuspid regurgitation are common in heart failure, but often these regurgitant murmurs are nondescript or inaudible. If congestive heart failure is due to an underlying valve lesion, specific features of that structural abnormality may be prominent. Remember that in the setting of heart failure due to decreased left ventricular systolic function, the murmur of severe


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Fig. 13. The large V wave of tricuspid regurgitation. As reflux across the tricuspid wave increases in severity, the systolic V wave becomes higher as well as broader. The X descent disappears and the Y descent is progressively accentuated with increasing severity of tricuspid regurgitation. With severe tricuspid regurgitation, the systolic wave may be so dominant as to mimic the carotid arterial pulsations; the entire lower neck will swell with each right ventricular systole.

aortic regurgitation, aortic stenosis, or mitral regurgitation may be unimpressive or even inaudible, in spite of a major hemodynamic burden due to the valve lesion.

Coronary Artery Disease Unless there is left ventricular damage from prior infarction or episodes of prior myocardial stunning and/or hibernation, the cardiac exam in patients with coronary disease is usually unremarkable. Signs of hypercholesterolemia should be sought, such as arcus senilus, xanthelasma, or tendon xanthomata. In patients with left ventricular dysfunction, an ectopic cardiac impulse or enlarged apical impulse may be noted. An S4 is common, but this finding is not specific enough to be diagnostically helptful. A third heart sound may be heard, but only if severe LV dysfunction is present. Mitral regurgitation is common in patients with depressed systolic function; the late systolic murmur of papillary muscle dysfunction should be sought. It is important to examine all subjects with coronary heart disease in the left lateral position to “bring out” the left ventricular impulse as well as the third and fourth heart sounds (Fig. 7).

Mitral Stenosis Mitral stenosis is easily identified by the experienced examiner but is usually missed by the inexperienced practitioner. The classic features include a very loud S1, often palpable, as well as an increased P2, and an early diastolic sound, the opening snap. The typical murmur of mitral stenosis is a mid-late diastolic, low-frequency “rumble,” that is best (or only) heard at the left ventricular apex in the left lateral position (Fig. 10). A right ventricular lift is common; in pure mitral stenosis, the LV impulse is not abnormal and may be undetectable. Coexisting mitral regurgitation may confuse the auscultatory findings, usually producing an apical murmur that is typically holosystolic. Many physicians have difficulty assessing the timing of the acoustic events in mitral stenosis, confusing systole for diastole.

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Fig. 14. The classic late systolic murmur of mitral valve prolapse. Note the crescendo configuration of the murmur, which begins in midsystole following the first systolic click. The frequency of this murmur is usually relatively pure. SM, systolic murmur; SC, systolic click. (Adapted from Delman AJ, Stein E. Dynamic cardiac auscultation and phonocardiography. W. B. Saunders, Philadelphia, 1979.)

Mitral Regurgitation This lesion is ubiquitous and occurs in many forms. In longstanding severe mitral regurgitation, the left ventricle dilates. Thus, careful evaluation of the apical impulse is important, with the examiner seeking a left ventricular heave, palpable S3, or apical systolic thrill. A right ventricular lift is common in chronic severe mitral regurgitation. The murmur of mitral regurgitation is typically holosystolic at the apex, but variants of the classic murmur can confuse the picture. Myxomatous mitral valve prolapse may produce a mid-late systolic murmur that can radiate to the aortic area in the setting of selective posterior leaflet prolapse. Mitral regurgitation murmur may be variable in intensity, particularly in the setting of left ventricular dysfunction; when mitral regurgitation is secondary to left ventricular disease, the murmur is loudest during the decompensated heart failure state. Conversely, organic mitral regurgitation murmurs are usually loudest after heart failure has been effectively treated and left ventricular function has improved.

MITRAL VALVE PROLAPSE The cardinal features of mitral valve prolapse include a mid-late systolic murmur and one or more mid-late systolic clicks (Fig. 14). The latter may or may not be present, or can be variably heard from day to day. The clicks are often confusing to the uninitiated; they may be “close to the ear,” quite high-frequency, sounding like extracardiac events. Typically the systolic murmur begins well after S1 and may be variable in length and intensity, especially with specific maneuvers that alter left ventricular volume or systemic resistance (e.g., going from supine to upright position, squatting, Valsalva maneuver, sustained hand grip).


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Aortic Stenosis Classic features of valvar aortic stenosis include a small and slow-rising carotid arterial upstroke (Fig. 1); a left ventricular lift; a palpable S4; a palpable basal systolic thrill; and a loud, often harsh systolic murmur at the aortic area radiating into the neck. The murmur of aortic stenosis is often more high-frequency and pure pitched at the apex (where it is often confused with mitral regurgitation). The length of the murmur is key; functional or aortic sclerosis murmurs are not very long and late-peaking; moderate to severe aortic stenosis murmurs typically take up much of systole and their peak intensity is later than normal. These murmurs can be quite harsh and grunting above the right clavicle, and usually radiate into the carotids.

HYPERTROPHIC CARDIOMYOPATHY These patients have an extremely prominent left ventricular heave, a very loud and usually palpable fourth heart sound, and a loud, long systolic murmur that is best heard at the left sternal region and apex. The murmur classically changes with body position, Valsalva, or following postventricular contraction (PVC). The murmur often has characteristics of mitral regurgitation and aortic stenosis. The carotid upstrokes are brisk and not delayed. Experienced examiners should be able to differentiate valvular aortic stenosis from hypertrophic cardiomyopathy.

Aortic Regurgitation The first clue to the recognition of significant aortic regurgitation is an abnormal carotid arterial pulse, characterized by a full-volume, high-amplitude impulse, often with a double or bisferiens contour (Fig. 2). Signs of left ventricular enlargement signify a major degree of regurgitation. A third heart sound is a poor prognostic finding. Fourth heart sounds are commonly heard. A highfrequency blowing decrescendo diastolic murmur beginning with S2 is the typical finding in aortic regurgitation. This valve or aortic root lesion uncommonly produces a loud murmur. Careful technique is necessary to hear the often-soft murmur of aortic regurgitation; the optimal patient position for examination is sitting up, leaning forward, with the breath held in endexpiration. An accompanying aortic systolic murmur is common.

RECOMMENDED READING Roldan C, Abrams J. Evaluation of the Patient with Heart Disease: Integrating the Physical Exam and Echocardiography. Lippincott Williams & Wilkins, Philadelphia, 2002. Abrams J. Synopsis of Cardiac Physical Diagnosis. Butterworth Heinemann, Boston, 2001. Otto C. Valvular Heart Disease, W. B. Saunders, Philadelphia, 1999. Don, Michael A. Auscultation of the Heart: A Cardiophonetic Approach. McGraw Hill, New York, 1998. Criley J. Beyond Heart Sounds, vol. 1 (CD-ROM). Armus (www.armus.com), 2000.

7 Physical Examination of the Heart and Circulation

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