Chapter 7 / Physical Examination of the Heart and Circulation 99
99
From: Essential Cardiology: Principles and Practice, 2nd Ed.
Edited by: C. Rosendorff © Humana Press Inc., Totowa, NJ
7 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. Subse- quently, echocardiography and cardiac catheterization have demonstrated that the presumed patho- genesis of many to most cardiovascular abnormalities on the physical examination were accurately and presciently described before these modern techniques became available. In the past, genera- tions 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-dimen- sional echocardiography has clearly contributed to the demise of cardiac physical diagnosis capabil- ity 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 struc- tural 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 with- out 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
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. Abnormali- ties 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 para- doxus are two situations in which the blood pressure can provide important information.
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 S
1, S
2Is an S
3or S
4present?
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 Hypertension in upper extremities; brachial–femoral delay
Aortic regurgitation Wide pulse pressure with increased systolic and decreased diastolic pressure Increased volume, rate of rise of arterial pulses with exaggerated collapse Pulsus or mechanical Beat-to-to beat alternation in peak pressure and pulse volume (detect by
alternans palpation, not cuff)
Pulsus paradoxus Exaggerated inspiratory decline (>10 mmHg) in peak systolic pressure measured carefully by cuff; palpation may pick up if severe
Hypertension Elevated systolic and diastolic pressure; increased systolic pressure with
normal diastolic (isolated systolic hypertension of the elderly)
Chapter 7 / Physical Examination of the Heart and Circulation 101
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 cardio- vascular 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).
P
ULSUSP
ARADOXUSA 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 intratho- racic pressure or in pericardial tamponade. Careful palpation and auscultation is mandatory to detect significant pulsus paradoxus (>10 mmHg). Normally, there is a slight physiologic respira- tory 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.
P
ULSUSA
LTERNANSIn 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
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.
Table 3
Peripheral or Nonauscultatory Signs of Severe Aortic Regurgitation: A Glossary Bisferiens pulse A double or bifid systolic impulse felt in the carotid arterial pulse.
Corrigan’s sign Visible pulsations of the supraclavicular and carotid arteries.
Pistol shot of Traube A loud systolic sound heard with the stethoscope lightly placed over a femoral artery.
Palmar click A palpable, abrupt flushing of the palms in systole.
Quincke’s pulse 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.
Duroziez’s sign 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.
DeMusset’s sign Visible oscillation or bobbing of the head with each heartbeat.
Hill’s sign Abnormal accentuation of leg systolic blood pressure, with popliteal pressure 40 mmHg or higher than brachial artery pressure.
Water-hammer pulse 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.)
Miller’s sign Visible pulsations of the uvula.
arteries. This phenomenon, usually undetected, is most likely to be associated with a left ventricu- lar 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 pre- sumed 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). Con- versely, 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
Chapter 7 / Physical Examination of the Heart and Circulation 103
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 iso- lated 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.
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 vol- ume. The bisferiens pulse must be differentiated from a transmitted systolic murmur or palpable thrill. Note the soft S
1and S
2. 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.
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 S
1, and a smaller V wave that peaks almost coincident with S
2. The jugular X descent occurs during systole and in some individuals may be quite prom- inent. The Y descent occurs during early diastole; the nadir of the Y descent times with S
3. 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 old- fashioned 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 sus- tained into late systole, and not hyperdynamic (Table 4, Fig. 6). Often, the left ventricle is not pal- pable 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 ventric- ular 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 S
4is an important observa- tion 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
Chapter 7 / Physical Examination of the Heart and Circulation 105
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 cm
2and 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).
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.
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.
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.)
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 S
4) Accentuated diastolic rapid filling (palpable S
3)
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
Chapter 7 / Physical Examination of the Heart and Circulation 107
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 S
1, S
2, or opening snap are often palpable. An S
3or S
4may be detectable in the left lateral position. For instance, mitral stenosis can be strongly suspected solely by detection of a palpable S
1, 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 (S
1, S
2) and the opening motion of thickened and noncompliant aortic and mitral valve leaflets (aortic ejection click, mitral opening snap) produce commonly heard sounds. The S
3and S
4are due to left ventricular filling transients produced by left atrial contrac- tion (S
4) and passive left ventricular inflow after mitral valve opening (S
3). These sounds are low- frequency 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 (S
1)
The S
1is 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 S
1is common in mitral stenosis and in individuals with a short PR interval. A soft S
1is common in individuals with decreased left ventricular systolic function or first-degree AV block.
Second Heart Sound (S
2)
Although assessment of respiratory movement and intensity of the two components of S
2is a well-emphasized aspect of auscultation, for practical purposes, analysis of S
2is helpful in rela- tively few conditions (Table 6). The physician should focus on the relative intensity of aortic and pulmonary components (A
2, P
2) and the possible presence of reversed or paradoxic splitting, char- acterized by inspiratory narrowing and expiratory widening of the two components of S
2. Paradoxic
Fig. 8. Precordial palpation for detection of parasternal or right ventricular activity. Use firm downward pres-
sure with the heel of the had while the patient’s breath is held in end-expiration.
Table 6
Assessment of Second Heart Sound (S
2): A Practical Approach
Character
aSignificance
Abnormalities of respiratory variation Right ventricular conduction delay (e.g., incomplete or Wide splitting, inspiratory increase total right bundle branch block—important clue)
in A
2–P
2interval Idiopathic dilation of pulmonary artery Small atrial septal defect (unusual) Pulmonic stenosis
Wide splitting, fixed A
2–P
2interval Atrial septal defect (important clue)
Single S
2Often normal in older patients
Aortic stenosis
Mild left ventricular conduction delay Severe pulmonary hypertension (A
2“masked”)
Reversed or paradoxical splitting Left bundle branch block (important clue)
Left ventricular systolic dysfunction (important in acute ischemia)
Abnormalities of intensity
Loud A
2Dilated aorta
Hypertension Tetralogy of Fallot
Loud P
2Pulmonary hypertension (important clue)
Atrial septal defect Dilated pulmonary artery
Soft A
2Aortic sclerosis or stenosis
Hypotension
Soft P
2Pulmonic stenosis
a
The physician must differentiate between decreased intensity of all cardiac sounds vs a selective decrease in the loudness of A
2or P
2.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 P
2, particularly when P
2is louder than A
2at the base and apex, is predictive of significant pulmonary hypertension.
Third Heart Sound (S
3)
The low-pitched early diastolic third heart sound can be a normal finding or a significant car- diovascular abnormality. The S
3is most easily heard by turning the patient into the left lateral posi- tion, identifying the apex impulse with a finger, and carefully applying the bell of the stethoscope with light pressure (Fig. 7).
Fourth Heart Sound (S
4)
The atrial sound or S
4is 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, S
4is a useful finding in hypertension, or coronary artery disease, where its presence suggests increased LV end-diastolic pressure and/or LV hypertrophy. The S
4(and S
3) may be palpable. The S
4is 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 S
3and S
4(Fig. 7).
Ejection Sounds
These are high-frequency, discrete audible sounds that occur immediately after S
1(Fig. 9).
They are usually caused by stiff or malformed semilunar leaflets, such as a bicuspid aortic valve,
Chapter 7 / Physical Examination of the Heart and Circulation 109
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 com- mon and are related to ejection of blood across the aortic and pulmonic valves in the normal or struc- turally abnormal heart. Abnormal similar valves frequently produce systolic ejection murmurs that must be differentiated from functional or flow murmurs. Mitral valve incompetence with regurgi- tation 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 abnor- mal, as there is no physiologic explanation for normal flow of sufficient turbulence during diastole to produce a heart murmur.
Classification of Murmurs (Fig. 10) S
YSTOLICM
URMURThe classic heart murmur is a systolic ejection murmur, characterized by a crescendo contour and a gap between the end of audible sound and S
2. This sound-free period represents the critical distinction from a regurgitant systolic murmur, in which sound continues up to S
2(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.
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 S
1by 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.)
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 S
2, suggesting severe obstruction to ventricular outflow. In severe semilunar valve stenosis, the vibra- tions may extend beyond S
2.
Fig. 10. Intracardiac pressures and heart murmurs of the major cardiac valve abnormalities. See text for dis- cussion 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.)
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 turbu- lent 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.
D
IASTOLICM
URMURThe 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
Chapter 7 / Physical Examination of the Heart and Circulation 111
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).
C
ONTINUOUSM
URMURThese 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 usu- ally 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
Fig. 12. Echocardiographic correlates of the loud first sound and opening snap in mitral stenosis. S
1is pro- duced 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 S
1; this represents augmented transmitral flow with left atrial contraction. The opening snap (OS) times precisely with the maximum open- ing 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.)
Table 7
Common Causes of a Continuous Murmur
aPatient 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