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CHAPTER 8
Importance of the Physical
Examination, 000 Physical Examination of the Heart
The General Physical
Examination, 000 and Circulation
General Appearance, 000
Head and Face, 000 Eugene Braunwald • Joseph K. Perloff
Eyes, 000
Fundi, 000
Skin and Mucous
Membranes, 000
Extremities, 000
Clubbing of the Fingers and
Toes, 000
Importance of The General
Chest and Abdomen, 000
the Physical Examination
Jugular Venous Pulse, 000 Physical Examination
Sphygmomanometric A common pitfall in cardiovascular medi-
Measurement of Arterial cine is the failure by the cardiologist to rec- General Appearance
Pressure, 000 ognize that a patient’s heart disease is part
of a systemic illness. Equally important is An assessment of the patient’s general
Arterial Pulse, 000 the failure by the noncardiologist to recog- appearance is usually begun with a detailed
The Cardiac Examination, 000 nize the presence of a cardiac disorder that inspection at the time that the history is
is a component of a systemic illness whose being obtained.4-7 The general build and
Inspection, 000 major effect may be on other organ systems. appearance of the patient, the skin color, and
Palpation, 000 To avoid these two pitfalls, patients known the presence of pallor or cyanosis should be
Systolic Motion, 000 to have or suspected of having heart disease noted, as well as the presence of shortness of
Diastolic Motion, 000 require not only a detailed examination of breath, orthopnea, periodic (Cheyne-Stokes)
Right Ventricle, 000 the cardiovascular system but also a careful respiration (see Chap. 22), and distention of
Pulmonary Artery, 000 general physical examination. For example, the neck veins. If the patient is in pain, is he
Left Atrium, 000 the presence of coronary artery disease or she sitting quietly (typical of angina pec-
Thrills, 000 should prompt a careful search for frequent toris); moving about, trying to find a more
Percussion, 000 noncardiac concomitant conditions such as comfortable position (characteristic of acute
atherosclerosis of the carotid arteries and of myocardial infarction); or most comfortable
Cardiac Auscultation, 000 the arteries of the lower extremities and sitting upright (heart failure) or leaning
Principles and Technique, 000 aorta. Conversely, the very high incidence forward (pericarditis)? Simple inspection
Heart Sounds, 000 (approximately 50 percent) of coronary also reveals whether the patient’s whole
First Heart Sound, 000 artery disease in patients with cerebro- body shakes with each heartbeat and
Early Systolic Sounds, 000 vascular disorders must be considered in whether Corrigan pulses (bounding arterial
Midsystolic to Late Systolic dealing with patients with these conditions. pulsations, as occur with the large stroke
Sounds, 000 As stated by Mangione and coworkers,1 volume of severe aortic regurgitation, arteri-
Second Heart Sound, 000 “There are still many reasons to promote ovenous fistula, or complete atrioventricular
Abnormal Loudness (Intensity) of the teaching of bedside diagnostic skills [AV] block) are present in the head, neck,
the Two Components of S2, 000 such as cardiac auscultation. Among these and upper extremities. Malnutrition and
Early Diastolic Sounds, 000 are cost-effectiveness, the possibility of cachexia, which occur in severe chronic
Mid-diastolic and Late Diastolic making inexpensive serial observations, the heart failure (see Chap. 22), may also be
(Presystolic) Sounds, 000 early detection of critical findings, the intel- readily evident. The distinctive general
Heart Murmurs, 000 ligent and well-guided selection of costly appearance of the Marfan syndrome (see
Systolic Murmurs, 000 diagnostic technology, and the therapeutic Chap. 70) is often apparent: long extremities
Diastolic Murmurs, 000 value of the physical contact between with an arm span that exceeds the height; a
Continuous Murmurs, 000 physician and patient.” longer lower segment (pubis to foot) than
Approach to the Patient with a Shaver and Tavel have pointed out that upper segment (head to pubis); and arachn-
Heart Murmur, 000 in this era of cost containment in the prac- odactyly (spider fingers).
Pericardial Rubs, 000 tice of medicine, and the great expense of
Dynamic Auscultation, 000 many “high-tech” diagnostic procedures, HEAD AND FACE
the physical examination remains a rela- Examination of the face often aids in the recog-
Respiration, 000 tively inexpensive, useful “test.”2,3 An addi- nition of many disorders that can affect the cardio-
Postural Changes and tional benefit is that the actual physical vascular system. For example, myxedema (see
Exercise, 000 contact, that is, the “laying on of hands” by Chap. 79) is characterized by a dull, expressionless
Pharmacological Agents, 000 the physician creates a valued closer bond face, periorbital puffiness, loss of the lateral eye-
References, 000 with the patient at a time when the patient’s brows, a large tongue, and dry, sparse hair. An
encounter with the medical care system is earlobe crease occurs more frequently in patients
often so impersonal. with coronary artery disease than in those without Z
8-1
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8-2 this condition.8 Bobbing of the head coincident with each heartbeat (de type III hyperlipoproteinemia. Patients with xanthoma tendinosum
Musset sign) is characteristic of severe aortic regurgitation. Facial edema (i.e., nodular swellings of the tendons, especially of the elbows, exten-
may be present in patients with tricuspid valve disease or constrictive sor surfaces of the hands, and Achilles tendons) usually have type II
pericarditis. hyperlipoproteinemia. Eruptive xanthomas are tiny yellowish nodules,
1 to 2 mm in diameter on an erythematous base, that may occur
EYES anywhere on the body and are associated with hyperchylomicronemia
External ophthalmoplegia and ptosis due to muscular dystrophy of and are therefore often found in patients with type I and type V
the extraocular muscles occur in patients with the Kearns-Sayre syn- hyperlipoproteinemia.
drome, which may be associated with complete heart block. Exophthal- Hereditary telangiectases are multiple capillary hemangiomas occur-
mos and stare occur in patients with hyperthyroidism, an important ring in the skin, lips (Fig. 8–2), nasal mucosa, and upper respiratory and
cause of high-output cardiac failure (see Chaps. 22 and 79). Blue sclerae gastrointestinal tracts and resemble the spider nevi seen in patients with
CH 8 can be seen in patients with osteogenesis imperfecta, a disorder that may liver disease. When present in the lung, they are associated with pul-
be associated with aortic dilatation, regurgitation, and dissection and monary arteriovenous fistulas and cause central cyanosis.
with prolapse of the mitral valve (see Chap. 70).
EXTREMITIES
FUNDI A variety of congenital and acquired cardiac malformations are asso-
Examination of the fundi allows classification of arteriolar disease in ciated with characteristic changes in the extremities. Among the con-
patients with hypertension and may also be helpful in the recognition genital lesions, short stature, cubitus valgus, and medial deviation of the
of arteriosclerosis. Beading of the retinal artery may be present in extended forearm are characteristic of Turner syndrome (see Chap. 56).
patients with hypercholesterolemia. Hemorrhages near the discs with Patients with the Holt-Oram syndrome10 (atrial septal defect with skele-
white spots in the center (Roth spots) occur in patients with infective tal deformities) often have a thumb with an extra phalanx, a so-called fin-
endocarditis. Embolic retinal occlusions can occur in patients with rheu- gerized thumb, which lies in the same plane as the fingers, making it
matic heart disease, left atrial myxoma, and atherosclerosis of the aorta difficult to appose the thumb and fingers. In addition, they may exhibit
or arch vessels. Papilledema can be present not only in patients with deformities of the radius and ulna, causing difficulty in supination and
malignant hypertension (see Chap. 37) but also in those with cor pronation.
pulmonale with severe hypoxia (see Chap. 67). Arachnodactyly is characteristic of Marfan syndrome (see Chap. 70).
Normally, when a fist is made over a clenched thumb, the thumb does
SKIN AND MUCOUS MEMBRANES not extend beyond the ulnar side of the hand, but it usually does so in
Central cyanosis (due to intracardiac or intrapulmonary right-to-left patients with Marfan syndrome.
shunting) involves the entire body, including warm, well-perfused sites Systolic flushing of the nail beds, which can be readily detected by
such as the conjunctivae and the mucous membranes of the oral cavity. pressing a flashlight against the terminal digits (Quincke sign), is a sign
Peripheral cyanosis (due to reduction of peripheral blood flow, such as of aortic regurgitation and of other conditions characterized by a greatly
occurs in patients with heart failure and peripheral vascular disease) is widened pulse pressure. Differential cyanosis, in which the hands and
characteristically most prominent in cool, exposed areas that may not be fingers (especially on the right side) are pink and the feet and toes are
well perfused, such as the extremities, particularly the nail beds and nose. cyanotic, is indicative of patent ductus arteriosus with reversed shunt
Polycythemia can often be suspected from inspection of the conjuncti- due to pulmonary hypertension (see Chap. 67); this finding can often be
vae,lips,and tongue,which are darkly congested in cases of polycythemia brought out by exercise. On the other hand, reversed differential
and pale in cases of anemia. cyanosis, in which cyanosis of the fingers exceeds that of the toes, sug-
Bronze pigmentation of the skin and loss of axillary and pubic hair gests Taussig-Bing anomaly with pulmonary vascular disease and reversed
occur in patients with hemochromatosis (which may result in car- flow through a patent ductus arteriosus.Alternatively, it may occur with
diomyopathy owing to iron deposits in the heart). Jaundice may be transposition of the great arteries, pulmonary hypertension, preductal
observed in patients after pulmonary infarction as well as in patients with narrowing of the aorta, and reversed flow through a patent ductus
congestive hepatomegaly or cardiac cirrhosis. Lentigines, which are small arteriosus.11
brown macular lesions on the neck and trunk that begin at about age 6
and do not increase in number with sunlight, are observed in patients CLUBBING OF THE FINGERS AND TOES
with pulmonic stenosis and hypertrophic cardiomyopathy.9 Clubbing of the digits is characteristic of central cyanosis (cyanotic
Several types of xanthomas (cholesterol-filled nodules) are found congenital heart disease or pulmonary disease with hypoxia) (Fig. 8–3).
either subcutaneously or over tendons in patients with hyperlipopro- It may also appear within a few weeks of the development of infective
teinemia (see Chap. 39). Premature atherosclerosis frequently develops endocarditis. The earliest forms of clubbing are characterized by
in these individuals.Tuberoeruptive xanthomas, present subcutaneously increased glossiness and cyanosis of the skin at the root of the nail.12
or on the extensor surfaces of the extremities (Fig. 8–1), and xanthoma After obliteration of the normal angle between the base of the nail and
striatum palmare, which produce yellowish, orange, or pink discoloration the skin, the soft tissue of the pulp becomes hypertrophied, the nail root
of the palmar and digital creases, occur most commonly in patients with floats freely, and its loose proximal end can be palpated. In the more
severe forms of clubbing, bony changes occur (i.e., hypertrophic

FIGURE 8–1 Eruptive xanthomas on the elbow. Lipid deposition in the skin (xan-
thoma tuberosum) can be seen in young patients with homozygous familial hypercho-
lesterolemia. It affects the buttocks and palms. There is also joint involvement. (From FIGURE 8–2 Telangiectasia of the mouth and cheek (Osler-Weber-Rendu disease).
Zatouroff M: Physical Signs in General Medicine. 2nd ed. London, Mosby-Wolff, 1996, (From Zatouroff M: Physical Signs in General Medicine. 2nd ed. London, Mosby-Wolff,
Z p 99.) 1996, p 168.)
Ch08.qxd 3/26/04 07:00 PM Page 3

especially characteristic of tricuspid valve disease and 8-3

chronic constrictive pericarditis.

Splenomegaly can occur in the presence of severe congestive

hepatomegaly, most frequently in patients with constrictive pericarditis
or tricuspid valve disease. The spleen may be enlarged and painful in
patients with infective endocarditis as well as after splenic embolization.
Splenic infarction is frequently accompanied by an audible friction rub.
Both kidneys may be palpably enlarged in patients with hypertension
secondary to polycystic disease.Auscultation of the abdomen should be
carried out in all patients with hypertension; a systolic bruit secondary
to renal artery stenosis may be audible near the umbilicus or in the flank. CH 8
Atherosclerotic aneurysms of the abdominal aorta are usually readily
detected on palpation of the abdomen below the umbilicus (see Chap.

Physical Examination of the Heart and Circulation

FIGURE 8–3 Nail clubbing (right) and a normal nail (left). (From Zatouroff M: Phys-
ical Signs in General Medicine. 2d ed. London, Mosby-Wolff, 1996, p 239.) 53), except in markedly obese patients. In patients with coarctation of
the aorta, no abdominal pulsations are palpable despite the presence of
prominent arterial pulses in the neck and upper extremities; arterial
pulses in the lower extremities are reduced or absent.
osteoarthropathy); these changes involve the terminal digits and in rare
instances even the wrists, ankles, elbows, and knees. Unilateral clubbing
of the fingers is rare but can occur when an aortic aneurysm interferes
with the arterial supply to one arm. Jugular Venous Pulse
Osler nodes are small, tender, purplish erythematous skin lesions
caused by infected microemboli and occurring most frequently in the Important information concerning the dynamics of the
pads of the fingers or toes and in the palms of the hands or soles of the right side of the heart can be obtained by observation of the
feet,13 whereas Janeway lesions are slightly raised, nontender hemor- jugular venous pulse.5,18-21 The internal jugular vein is ordi-
rhagic lesions in the palms of the hands and soles of the feet; both of narily examined; the venous pulse can usually be analyzed
these lesions as well as petechiae occur in patients with infective endo- more readily on the right than on the left side of the neck,
carditis (see Chap. 58). When petechiae occur under the nail beds, they because the right innominate and jugular veins extend in an
are termed splinter hemorrhages.
EDEMA. The presence of edema of the lower extremities is a
almost straight line cephalad to the superior vena cava, thus
common finding in patients with congestive heart failure (see Chap. favoring transmission of hemodynamic changes from the
22)14; however, if it is present in only one leg, it is more likely due to right atrium, whereas the left innominate vein is not in a
obstructive venous or lymphatic disease than to heart failure. Firm pres- straight line and may be kinked or compressed by a variety
sure on the pretibial region for 10 to 20 seconds may be necessary for of normal structures, by a dilated aorta, or by an aneurysm.
the detection of edema. In patients confined to bed, edema appears first
in the sacral region. Edema may involve the face in children with heart During the examination, the patient should be lying comfortably.
failure of any cause and in adults with heart failure associated with Although the head should rest on a pillow, it must not be at a sharp angle
marked elevation of systemic venous pressure (e.g., constrictive peri- from the trunk. One can examine the jugular venous pulse effectively by
carditis and tricuspid valve disease). shining a light tangentially across the neck. Most patients with heart
disease are examined most effectively in the 45-degree position, but in
patients in whom venous pressure is high, a greater inclination (60 or
Chest and Abdomen even 90 degrees) is required to obtain visible pulsations,whereas in those
in whom jugular venous pressure is low, a lesser incline (30 degrees) is
desirable.
Examination of the thorax should begin with observations The internal jugular vein is located deep within the neck, where it is
of the rate, effort, and regularity of respiration. The shape of covered by the sternocleidomastoid muscle and is therefore not usually
the chest is important as well; thus, a barrel-shaped chest visible as a discrete structure except in the presence of venous hyper-
with low diaphragm suggests emphysema, bronchitis, and cor tension. However, its pulsations are transmitted to the skin of the neck,
pulmonale. Inspection of the chest is an integral part of the where they are usually easily visible. Sometimes examiners experience
cardiac examination. It may reveal a bulging to the right of difficulty in differentiating between the carotid and jugular venous pulses
the upper sternum caused by an aortic aneurysm. The latter in the neck, particularly when the latter exhibits prominent v waves, as
can also produce a venous collateral pattern caused by occurs in patients with tricuspid regurgitation, in whom the valves in the
obstruction of the superior vena cava. Kyphoscoliosis of any internal jugular veins may be incompetent.There are several helpful clues
to avoid this difficulty, however:
cause can cause cor pulmonale; this skeletal abnormality, 1. The arterial pulse is a sharply localized rapid movement that may
as well as pectus excavatum (funnel chest)15,16 and pectus not be readily visible but that strikes the palpating fingers with
carinatum (pigeon breast), is often present in patients with considerable force; in contrast, the venous pulse, although more
Marfan syndrome. readily visible, often disappears when the palpating finger is
Left ventricular failure and other causes of elevation of placed lightly on or below the pulsating area.
pulmonary venous pressure can cause pulmonary rales; 2. The arterial pulse usually exhibits a single upstroke, whereas (in
wheezing is sometimes audible in patients with pulmonary patients in sinus rhythm) the venous pulse has two peaks and two
edema (cardiac asthma). troughs per cardiac cycle.
Painful enlargement of the liver may be due to venous con- 3. The arterial pulsations do not change when the patient is in the
upright position or during respiration, whereas venous pulsations
gestion; the tenderness disappears in cases of long-standing usually disappear or diminish greatly in the upright position and
heart failure. Hepatic systolic expansile pulsations occur in during inspiration, unless the venous pressure is greatly elevated.
patients with severe tricuspid regurgitation, and presystolic 4. Compression of the root of the neck does not affect the arterial
pulsations can be felt in patients with tricuspid stenosis and pulse but usually abolishes venous pulsations, except in the pres-
sinus rhythm. Patients with constrictive pericarditis also ence of extreme venous hypertension.
often have pulsatile hepatomegaly, the contour of the pulsa-
tions resembling those of the jugular venous pulse in this con- Two principal observations can usually be made from
dition. When firm pressure over the abdomen causes cervical examination of the neck veins: the level of venous pressure
venous distention (that is, when there is abdominojugular and the type of venous wave pattern. To estimate jugular
reflux, right-sided heart failure17) constrictive pericarditis venous pressure, the height of the oscillating top of the dis-
(see later), or tricuspid valve disease is usually present. tended proximal portion of the internal jugular vein, which
Ascites is also characteristic of heart failure, but it is reflects right atrial pressure, should be determined. The Z
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8-4 upper limit of normal is 4 cm above the sternal angle, which

corresponds to a central venous pressure of approximately 9 A
cm H2O, since the right atrium is approximately 5 cm below V
the sternal angle. When the veins in the neck collapse in a C
subject breathing normally in the horizontal position, it is
likely that the central venous pressure is subnormal. When X Y
obstruction of veins in the lower extremities is responsible
for edema, pressure in the neck veins is not elevated and the 4 1 2
abdominal-jugular reflux is negative. A
ABDOMINAL-JUGULAR REFLUX. With the patient posi-
CH 8 tioned to make the jugular vein easily visible, steady, firm
pressure is supplied to the periumbilical region for 10 to 30 V
seconds with the patient breathing quietly17-20; increased
respiratory excursions, straining, and the Valsalva maneuver
should be avoided. In normal subjects, jugular venous pres- A
sure rises less than 3 cm H2O and only transiently while
abdominal pressure is continued, whereas in patients with Severe
right or left ventricular failure and/or tricuspid regurgitation, V
the jugular venous pressure remains elevated for more than A C Y
15 seconds. A positive abdominal-jugular reflux suggests
right ventricular systolic and/or diastolic dysfunction, tri- Mild X
A V Y
cuspid valve disease, constrictive pericarditis, or central C
venous pressure. Normal
PATTERN OF THE VENOUS PULSE. The events of the X Y
cardiac cycle, shown in Figure 19–19 provide an explanation
for the details of the jugular venous waveform (Fig. 8–4). The
A wave in the venous pulse results from venous distention 1 2 3
due to right atrial systole, whereas the X descent is due to
atrial relaxation and descent of the floor of the right atrium B
during right ventricular systole. The C wave, which occurs
simultaneously with the carotid arterial pulse, is an incon-
stant wave in the jugular venous pulse and/or interruption of
the X descent after the peak of the A wave. The continuation P
of the X descent after the C wave is referred to as the X¢ ECG
descent. The V wave results from the rise in right atrial pres-
sure when blood flows into this chamber during ventricular A
V
systole when the tricuspid valve is shut, and the Y descent A X
JVP
(i.e., the downslope of the V wave) is related to the decline
in right atrial pressure when the tricuspid valve reopens.
After the bottom of the Y descent (the Y trough) and begin-
ning of the A wave is a period of relatively slow filling of the
atrium or ventricle, the diastasis period, a wave termed the
H wave.
ALTERATIONS IN DISEASE. Elevation of jugular venous
Y
pressure reflects an increase in right atrial pressure and
occurs in cases of heart failure, reduced compliance of the 1 2 K
right ventricle, pericardial disease, hypervolemia, obstruc-
tion of the tricuspid orifice, and obstruction of the superior C
vena cava. During inspiration, the jugular venous pressure FIGURE 8–4 Common abnormalities of the venous pulse. A, Large A waves asso-
normally declines but the amplitude of the pulsations ciated with elevated right ventricular end-diastolic pressure or decreased right ventric-
increases. Kussmaul sign19,20 is a paradoxical rise in the ular compliance. Increased A wave size or giant A waves are seen when there is severe
height of the jugular venous pressure during inspiration, right ventricular hypertrophy, usually associated with right ventricular systolic hyper-
which typically occurs in patients with chronic constrictive tension. A right ventricular S4 is often present in such cases. B, Augmented V wave in
pericarditis and sometimes in patients with congestive heart tricuspid regurgitation. As reflux across the tricuspid valve increases in severity, the sys-
tolic V valve becomes higher as well as broader. The X descent disappears and the Y
failure and tricuspid stenosis. descent is progressively accentuated with increasing severity of tricuspid regurgitation.
The A wave is particularly prominent in patients with con- With severe tricuspid regurgitation, the systolic wave may be so dominant as to mimic
ditions in which the resistance to right atrial contraction is the carotid arterial pulsations; the entire lower neck will swell with each right ventric-
increased, such as right ventricular hypertrophy, pulmonary ular systole. C, Constrictive pericarditis. In this condition, right ventricular diastolic pres-
hypertension, and tricuspid stenosis (see Fig. 8–4A). The A sure is greatly elevated. This elevation results in a prominent Y descent following
wave can also be tall in cases of left ventricular hypertrophy tricuspid valve opening. The abrupt rise in venous pressure during right ventricular filling
when the thickened ventricular septum interferes with right is due to the noncompliant right ventricular chamber encased in an unyielding pericar-
ventricular filling. Tall A waves are present in patients with dial shell. The venous pulse contour in constrictive pericarditis often takes on an M or
sinus rhythm and tricuspid stenosis or atresia, right atrial W configuration. A pericardial knock (K), a high-frequency early diastolic filling sound,
typically is present. (From Abrams J: Synopsis of Cardiac Physical Diagnosis. 2nd ed.
myxoma, or reduced compliance and/or marked hypertrophy Boston, Butterworth Heinemann, 2001, pp 23-35.)
of the right ventricle. Cannon (amplified) A waves are noted
in patients with AV dissociation when the right atrium con-
tracts against a closed tricuspid valve. In cases of atrial fib-
rillation, the A wave and X descent disappear and the V wave
and Y descent become more prominent. In cases of right ven-
Z tricular failure and sinus rhythm, there may be increases in
Ch08.qxd 3/26/04 07:00 PM Page 5

prominence of both A and V waves. A steeply rising H wave BLOOD PRESSURE IN THE LOWER EXTREMITIES. With the 8-5
is observed (or recorded) in patients with restrictive car- patient lying on the abdomen, an 8-inch-wide cuff should be applied with
diomyopathy, constrictive pericarditis, and right ventricular the compression bag over the posterior aspect of the mid-thigh and
infarction. The X descent may be prominent in patients with should be rolled diagonally around the thigh to keep the edges snug
large A waves, as well as in patients with right ventricular against the skin. Auscultation should be carried out in the popliteal
volume overload (atrial septal defect). fossa.To measure pressure in the lower leg, an arm cuff is placed over the
calf and auscultation is carried out over the posterior tibial artery. Regard-
Constrictive pericarditis (see Fig. 8–4C) is characterized by less of where the cuff is applied, care must be taken to avoid letting the
a rapid and deep Y descent followed by a rapid rise to a dias- rubber part of the balloon of the cuff extend beyond its covering and to
tolic plateau (H wave) without a prominent A wave; occa- avoid placing the cuff on so loosely that central ballooning occurs.
sionally, the X descent is prominent in patients with this KOROTKOFF SOUNDS. There are five phases of Korotkoff sounds
condition as well, causing a W-shaped jugular venous pulse. (i.e., sounds produced by the flow of blood as the constricting blood CH 8
However, it is in patients with cardiac tamponade that the X pressure cuff is gradually released). The first appearance of a clear,
descent is most prominent. A prominent V wave or a C-V tapping sound (phase I) represents the systolic pressure. These sounds

Physical Examination of the Heart and Circulation

wave (i.e., fusion of the C and V waves in the absence or atten- are replaced by soft murmurs during phase II and by louder murmurs
uation of an X descent) occurs in patients with tricuspid during phase III, as the volume of blood flowing through the constricted
artery increases.The sounds suddenly become muffled in phase IV, when
regurgitation, sometimes causing a systolic movement of the constriction of the brachial artery diminishes as arterial diastolic pres-
earlobe (see Fig. 8–4B, center) and a right-to-left head move- sure is approached. Korotkoff sounds disappear in phase V, which is
ment with each ventricular systole. Equal A and V waves are usually within 10 mm Hg of phase IV.
seen in patients with atrial septal defect; the Y descent is Diastolic pressure measured directly through an intraarterial needle
gradual when right atrial emptying is impeded, as in tricus- and external manometer corresponds closely to phase V. In cases of
pid stenosis, and rapid when it is unimpeded, as in tricuspid severe aortic regurgitation, however, when the disappearance point is
regurgitation. A steep Y descent is seen in patients with any extremely low, sometimes 0 mm Hg, the sound of muffling (phase IV) is
condition in which there is myocardial dysfunction, ventric- much closer to the intraarterial diastolic pressure than is the disappear-
ular dilatation, and an elevated central venous pressure. ance point (phase V). When the difference between phases IV and V of
the Korotkoff sounds exceeds 10 mm Hg, both pressures should be
recorded (e.g., 142/54/10 mm Hg).
Sphygmomanometric Measurement of Korotkoff sounds may be difficult to hear and arterial pressure diffi-
cult to measure when arterial pressure rises at a slow rate (as in cases
Arterial Pressure of severe aortic stenosis), when the arteries are markedly constricted (as
in cases of shock), and when the stroke volume is reduced (as in cases
One can estimate systolic arterial pressure without a of severe heart failure). Very soft or inaudible Korotkoff sounds can
sphygmomanometer by gradually compressing the brachial often be accentuated by having the patient dilate the blood vessels
artery while palpating the radial artery; the force required to simply by opening and closing the fist repeatedly. Sometimes in states of
obliterate the radial pulse represents the systolic blood pres- shock, the indirect method of measuring blood pressure is unreliable and
sure, and, with practice, one can often estimate this level arterial pressure should be measured through an intraarterial needle.
The Auscultatory Gap. The auscultatory gap is a silence that some-
within 15 mm Hg. Ordinarily, however, a sphygmomanome- times separates the first appearance of the Korotkoff sounds from their
ter is used to obtain an indirect measurement of arterial pres- second appearance at a lower pressure.The phenomenon tends to occur
sure. The cuff should fit snugly around the arm, with its lower when there is venous distention or reduced velocity of arterial flow into
edge at least 1 inch above the antecubital space, and the the arm. If the first muffling of sounds is considered to be the diastolic
diaphragm of the stethoscope should be placed close to or pressure, it will be overestimated. If the second appearance is taken as
under the edge of the sphygmomanometer cuff. The width of the systolic pressure, it will be underestimated. On the other hand,
the cuff selected should be at least 40 percent of the circum- sounds transmitted through the arterial tree from prosthetic aortic valves
ference of the limb to be used. may be responsible for falsely high readings.
The standard size, with a 5-inch-wide cuff, is designed for BLOOD PRESSURE IN THE BASAL CONDITION. To determine
arterial pressure in the basal condition, the patient should have rested in
adults with an arm of average size. When this cuff is applied a quiet room for 5 to 10 minutes. It is desirable to record the arterial
to a large upper arm or a normal adult thigh, arterial pressure pressure in both arms at the time of the initial examination; differences
is overestimated, leading to spurious hypertension in the in systolic pressure between the two arms that exceed 10 mm Hg when
obese patient (arm circumference >35 cm)22; when it is measurements are made simultaneously or in rapid sequence24 suggest
applied to a small arm, the pressure is underestimated. The obstructive lesions involving the aorta or the origin of the innominate
cuff width should be approximately 1.5 inches in infants and and subclavian arteries or supravalvular aortic stenosis (in which pres-
small children, 3 inches in young children (2 to 5 years), and sure in the right arm exceeds that in the left). In patients with vertebral-
8 inches in obese adults. The rubber bag should be long basal artery insufficiency, a difference in pressure between the arms may
enough to extend at least halfway around the limb (10 inches signify that a subclavian “steal” is responsible for the cerebrovascular
symptoms.
in adults). In patients with rigid, sclerotic arteries, the sys- To be certain from physical examination that the systolic pressure is
tolic pressure may also be overestimated, by as much as different in the two arms or in the upper and lower extremities, two
30 mm Hg. Mercury manometers are, in general, more accu- examiners should measure the pressures simultaneously and then switch
rate and reliable than the aneroid type; the latter should be extremities and measure the pressures again.
calibrated at least once yearly. ORTHOSTATIC HYPOTENSION. To determine whether orthostatic
hypotension is present, arterial pressure should be determined with the
BLOOD PRESSURE IN THE UPPER EXTREMITIES. To measure patient in both the supine and the erect positions. Regardless of the
arterial pressure in an upper extremity,23,24 the patient should be seated patient’s posture, however, the brachial artery should be at the level of
or lying comfortably and relaxed, the arm should be slightly flexed and the heart to avoid superimposition of the effects of gravity on the
at heart level, and the arm muscles should be relaxed. The cuff should recorded pressure.
be inflated rapidly to approximately 30 mm Hg above the anticipated Normally, the systolic pressure in the legs is up to 20 mm Hg higher
systolic pressure. The cuff is then deflated slowly, no faster than than in the arms, but the diastolic pressures are usually virtually identi-
3 mm Hg/sec; the pressure at which the brachial pulse can be palpated cal. The recording of a higher diastolic pressure in the legs than in the
is close to the systolic pressure. arms suggests that the thigh cuff is too small.When systolic pressure in
The cuff should be deflated rapidly after the diastolic pressure is the popliteal artery exceeds that in the brachial artery by more than 20
noted and a full minute allowed to elapse before pressure is remeasured mm Hg (Hill sign), aortic regurgitation is usually present.25 Blood pres-
in the same limb. Although excessive pressure on the stethoscope head sure should be measured in the lower extremities in patients with hyper-
does not affect systolic pressure, it does erroneously lower diastolic tension to detect coarctation of the aorta or when obstructive disease of
readings. the aorta or its immediate branches is suspected. Z
 Ch08.qxd 3/26/04 07:00 PM Page 6

8-6 Arterial Pulse peripheral vessels. This artery is located at the medial aspect
of the elbow, and it may be helpful to flex the patient’s arm
The volume and contour of the arterial pulse are deter- to improve palpation; palpation of the artery should be
mined by a combination of factors, including the left ven- carried out with the thumb exerting pressure on the artery
tricular stroke volume, the ejection velocity, the relative until its maximal movement is detected. A normal rate of rise
compliance and capacity of the arterial system, and the pres- of the arterial pulse suggests that there is no obstruction to
sure waves that result from the antegrade flow of blood and left ventricular outflow, whereas a pulse wave of small ampli-
reflections of the arterial pressure pulse returning from the tude with normal configuration suggests a reduced stroke
peripheral circulation (Table 8–1).25,26 Bilateral palpation of volume.
the carotid, radial, brachial, femoral, popliteal, dorsalis pedis, THE NORMAL PULSE. The pulse in the ascending aorta
CH 8 and posterior tibial pulses should be part of the examination normally rises rapidly to a rounded dome (Fig. 8–6); this
of all cardiac patients (Fig. 8–5). The frequency, regularity, initial rise reflects the peak velocity of blood ejected from the
and shape of the pulse wave and the character of the arterial left ventricle. A slight anacrotic notch or pause is frequently
wall should be determined. recorded, but only occasionally felt, on the ascending limb of
The carotid pulse provides the most accurate representa- the pulse. The descending limb of the central aortic pulse is
tion of the central aortic pulse.26,27 The brachial artery is the less steep than is the ascending limb, and it is interrupted by
vessel ordinarily most suitable for appreciating the rate of rise the incisura, a sharp downward deflection related to closure
of the pulse and the contour, volume, and consistency of the of the aortic valve. Immediately thereafter, the pulse wave

TABLE 8–1 Classification of Abnormal Pulses

Name Meaning Comments
General Abnormalities
Hypokinetic Related to a decreased rate of LV pressure development, Low amplitude, may or may not have a slow
a decreased LV stroke volume, and/or obstruction of rate of rise
LV outflow
Hyperkinetic Related to an increased rate of LV pressure development Prominent fluctuation in the diameter of an
and/or to a large LV stroke volume with decreased artery
peripheral resistance Pulse pressure can be:
Increased (aortic regurgitation, patent
ductus arteriosus, arteriovenous fistulas,
fever, anemia, exercise)
Normal (HOCM, MR)

Specific Abnormalities
Pulsus parvus et tardus Pulse with slow rate of pressure increase, small pulse AS
pressure, late
Bisferiens pulse A pulse with two palpable beats during systole Occurs in HOCM and in mixed AS/AR.
Can also occur in cases of rapid ejection of
an increased stroke volume (e.g., exercise,
fever, patent ductus arteriosus)
Best appreciated in the carotid artery
Dicrotic pulse A twice-beating or double pulse produced by a Low-volume pulse, with shortened ejection
combination of the systolic wave followed by an period. Observed both in central and
exaggerated dicrotic (diastolic) wave peripheral arteries. Observed in cases of
cardiac tamponade, hypovolemic shock,
severe cardiac failure
Pulsus alternans Beats occur at constant intervals but with a regular Strong and weak pulses occur in
alternation of the peak of the pressure pulse and/or consecutive beats.
the rate of rise of the ascending limb. Pulses alternate in systolic pressure by
≥20 mm Hg
Caused by alternating strength of cardiac
contraction with consecutive beats,
signifies severely depressed cardiac
function
Best palpated in radial or femoral artery
Bigeminal pulse Regular coupling of two beats with the interval between Observed with premature ectopic beats
a pair of beats greater than between the coupled beats coupled to a sinus beat, 3 : 2 Wenckebach
themselves. atrioventricular block and nonconducted
atrial premature systole following every
second sinus beat
Pulsus paradoxus Abnormal exaggeration (>10 mm Hg) of the normal Observed in cases of cardiac tamponade,
decrease in systolic blood pressure during inspiration constrictive pericarditis, restrictive
cardiomyopathy, hypotensive shock,
severe obstructive pulmonary disease,
large pulmonary embolism
AR = aortic regurgitation; AS = aortic stenosis; HOCM = hypertrophic obstructive cardiomyopathy; LV = left ventricular; MR = mitral regurgitation.
Z Modified from Vlachopoulos C, O’Rourke M: Genesis of the normal and abnormal pulse. Curr Prob Cardiol 25:297, 2000.
Ch08.qxd 3/26/04 07:00 PM Page 7

8-7

CH 8

Physical Examination of the Heart and Circulation

FIGURE 8–5 A, Technique for evaluating the carotid artery pulsations. B, Technique for timing pulses in the femoral and radial arteries. C, Technique for palpation of the dor-
salis pedis arteries. D, Technique for palpation of the posterior tibial arteries. (From Swartz MH [ed]: Textbook of Physical Diagnosis: History and Examination. 3rd ed. Philadelphia,
WB Saunders, 1998, pp 300, 329, and 330.)

rises slightly and then declines gradually throughout dias- arterial pulsations occur in patients with carotid atheroscle-
tole. As the pulse wave is transmitted to the periphery, its rosis and with diseases of the aortic arch, including aortic
upstroke becomes steeper, the systolic peak becomes higher, dissection, aneurysm, and Takayasu disease (see Chap. 53).
the anacrotic shoulder disappears, and the sharp incisura is The pulses of the upper extremities may be reduced or
replaced by a smoother, later dicrotic notch followed by a unequal in a variety of conditions, including supravalvular
dicrotic wave.26-28 Normally, the height of this dicrotic wave aortic stenosis, arterial embolus or thrombosis, anomalous
diminishes with age, hypertension, and arteriosclerosis. In origin or aberrant path of the major vessels, and cervical rib
the central arterial pulse (central aorta and innominate and or scalenus anticus syndrome. Asymmetry of right and left
carotid arteries), the rapidly transmitted impact of left ven- popliteal pulses is characteristic of iliofemoral obstruction.
tricular ejection results in a peak in early systole, referred to Weakness or absence of radial, posterior tibial, or dorsalis
as the percussion wave; a second, smaller peak, the tidal pedis pulses on one side suggests arterial insufficiency. In
wave, presumed to represent a reflected wave from the cases of coarctation of the aorta, the carotid and brachial
periphery, can often be recorded but is not normally palpa- pulses are bounding, rise rapidly, and have large volumes,
ble. In older subjects, however, particularly those with whereas in the lower extremities, the systolic and pulse pres-
increased peripheral resistance, as well as in patients with sures are reduced, their rate of rise is slow, and there is a late
arteriosclerosis and diabetes, the tidal wave may be some- peak. This delay in the femoral arterial pulses can usually be
what higher than the percussion wave; that is, the pulse readily detected by simultaneous palpation of the femoral
reaches a peak in late systole. In peripheral arteries, the pulse and brachial arterial pulses (see Fig. 8–5B).
wave normally has a single sharp peak. In patients with fixed obstruction to left ventricular
ABNORMAL PULSES. When peripheral vascular resist- outflow (valvular aortic stenosis and congenital fibrous
ance and arterial stiffness are increased, as in patients with subaortic stenosis), the carotid pulse rises slowly (pulsus
hypertension or with the increased arterial stiffness that tardus) (see Fig. 8–6B); the upstroke is frequently character-
accompanies normal aging, there is an elevation in pulse ized by a thrill (the carotid shudder); and the peak is reduced,
wave velocity and the pulse contour has a more rapid occurs late in systole, and is sustained. There is a notch on
upstroke and greater amplitude.29 Reduced or unequal carotid the upstroke of the carotid pulse (anacrotic notch) that is so Z
 Ch08.qxd 3/26/04 07:00 PM Page 8

8-8 aorta) is usually normal but the fraction ejected during early systole is
greater than normal; hence, the arterial pulse is of normal volume (the
S4 P2 S4 P2 pulse pressure is normal) but the pulse may rise abnormally rapidly.30
S1 A2 S1 A2 Exaggerated or bounding arterial pulses may be observed in patients
with an elevated stroke volume, with sympathetic hyperactivity, and in
patients with a rigid, sclerotic aorta. In patients with aortic regurgitation,
there is a very brisk rate of rise with an increased pulse pressure.
AORTIC REGURGITATION. The Corrigan or water-hammer pulse
Dicrotic notch Dicrotic notch of aortic regurgitation consists of an abrupt upstroke (percussion wave)
A B followed by rapid collapse later in systole but no dicrotic notch. Corri-
gan pulse reflects a low resistance in the reservoir into which the left
CH 8 ventricle rapidly discharges an abnormally elevated stroke volume, and
it can be exaggerated by raising the patient’s arm. In cases of acute aortic
S4 P2 S4 P2 regurgitation, the left ventricle may not be significantly dilated, and pre-
S1 A2 mature closure of the mitral valve may occur and limit the volume of
S1 A2 aortic reflux; therefore, the aortic diastolic pressure may not be very low,
the arterial pulse not bounding, and the pulse pressure not widened
despite a serious abnormality of valve function (see Chap. 57).
Signs characteristic of severe chronic aortic regurgitation include
“pistol shot” sounds heard over the femoral artery when the stethoscope
Dicrotic notch Dicrotic notch is placed on it (Traube sign); a systolic murmur heard over the femoral
C D artery when the artery is gradually compressed proximally; a diastolic
murmur when the artery is compressed distally (Duroziez sign25), and
Quincke sign (phasic blanching of the nail bed). Of these, Duroziez sign
is the most predictive of severe aortic regurgitation. Bounding arterial
S4 P2 pulses are also present in patients with patent ductus arteriosus or large
S1 A2 arteriovenous fistulas; those in hyperkinetic states such as thyrotoxico-
sis, pregnancy, fever, and anemia; those in severe bradycardia; and in arter-
ies proximal to coarctation of the aorta. In patients with the Hill sign25
of aortic regurgitation (or any condition leading to an increased stroke
volume or the hyperkinetic circulatory state), the indirectly recorded sys-
Dicrotic notch tolic pressures in the lower extremities exceed that in the arms by more
E than 20 mm Hg. Other signs of increased pulse pressure include Becker
sign (visible pulsations of the retinal arterioles) and Mueller sign (pul-
FIGURE 8–6 Schematic diagrams of the configurational changes in carotid pulse sating uvula).
and their differential diagnoses. Heart sounds are also illustrated. A, Normal. BISFERIENS PULSE. A bisferiens pulse (see Fig. 8–6C) is character-
B, Anacrotic pulse with a slow initial upstroke. The peak is close to S2. These features ized by two systolic peaks, the percussion and tidal waves, separated by
suggest fixed left ventricular outflow obstruction, such as occurs with valvular aortic a distinct midsystolic dip; the peaks may be equal, or either one may be
stenosis. C, Pulsus bisferiens with both percussion and tidal waves occurring during larger. This type of pulse is detected most readily by palpation of the
systole. This type of carotid pulse contour is most frequently observed in patients with carotid and, less commonly, of the brachial arteries. It occurs in condi-
hemodynamically significant aortic regurgitation or combined aortic stenosis and regur- tions in which a large stroke volume is ejected rapidly31 and is observed
gitation with dominant regurgitation. It is rarely observed in patients with mitral valve most commonly in patients with pure aortic regurgitation or with a com-
prolapse or in normal individuals. D, Pulsus bisferiens in hypertrophic obstructive car- bination of aortic regurgitation and stenosis; it may disappear as heart
diomyopathy. It is rarely appreciated at the bedside by palpation. E, A dicrotic pulse failure supervenes (see Fig 8–6D).26,31
results from an accentuated dicrotic wave and tends to occur in patients with sepsis, A bisferiens pulse also occurs in patients with hypertrophic obstruc-
severe heart failure, hypovolemic shock, cardiac tamponade, and aortic valve replace- tive cardiomyopathy, but the bifid nature may only be recorded, not pal-
ment. A2 = aortic component of the second heart sound; P2 = pulmonic component of pated; on palpation, there may merely be a rapid upstroke. In these
the second heart sound; S1 = first heart sound; S4 = atrial sound. (From Chatterjee K: patients, the initial prominent percussion wave is associated with rapid
Bedside evaluation of the heart: The physical examination. In Chatterjee K, Parmley W ejection of blood into the aorta during early systole, followed by a rapid
[eds]: Cardiology: An Illustrated Text/Reference. Philadelphia, JB Lippincott, 1991, pp decline as obstruction becomes manifest in midsystole and by a tidal
3.11-3.51; and Braunwald E: The clinical examination. In Braunwald E, Goldman L [eds]: (reflected) wave. In some patients with hypertrophic cardiomyopathy
Primary Cardiology. 2nd ed. Philadelphia, Elsevier, 2003, pp 36.) with no or little obstruction to left ventricular outflow, the arterial pulse
is normal or simply hyperkinetic in the basal state, but obstruction and
a bisferiens pulse can be elicited by means of the Valsalva maneuver or
inhalation of amyl nitrite. Occasionally, a bisferiens pulse is observed in
distinct that two separate waves can be palpated in what is patients in hyperkinetic circulatory states, and very rarely it occurs in
termed an anacrotic pulse. Pulsus parvus is a pulse of small normal individuals.
amplitude, usually because of a reduction of stroke volume. DICROTIC PULSE. Not to be confused with a bisferiens pulse, in
Pulsus parvus et tardus refers to a small pulse with a delayed which both peaks occur in systole, is a dicrotic pulse, in which the
systolic peak, which is characteristic of severe aortic steno- second peak is in diastole immediately after S2 (see Fig. 8–6E).27-29,31-33 The
sis. This type of pulse is more readily appreciated by palpat- normally small wave that follows aortic valve closure (i.e., the dicrotic
ing the carotid rather than a more peripheral artery. Patients notch) is exaggerated and measures more than 50 percent of the pulse
with severe aortic stenosis and heart failure usually exhibit pressure on direct pressure recordings and in which the dicrotic notch
is low (i.e., near the diastolic pressure).A dicrotic wave may be present
simply a reduced pulse amplitude (i.e., pulsus parvus), and in normal hypotensive subjects with reduced peripheral resistance, as
the delay in the upstroke is not readily apparent. However, occurs in fever, and it may be elicited or exaggerated by inhalation alone
this delay is readily recorded. In elderly patients with inelas- or the inhalation of amyl nitrite. Rarely, a dicrotic pulse is noted in healthy
tic peripheral arteries, the pulse may rise normally despite adolescents or young adults, but it usually occurs in conditions such as
the presence of aortic stenosis. cardiac tamponade,29 severe heart failure, and hypovolemic shock, in
which a low stroke volume is ejected into a soft elastic aorta. In patients
The carotid arterial pulse may be prominent or exaggerated in a with these conditions, the dicrotic pulse is due to a reduction of the sys-
patient with any condition in which pulse pressure is increased, includ- tolic wave with preservation of the incisura.
ing anxiety, the hyperkinetic heart syndrome, anemia, fever, pregnancy, PULSUS ALTERNANS (ALTERNATING STRONG AND WEAK
or other high cardiac output states (see Chap. 22), as well as in patients PULSES). Mechanical alternans is a sign of depression of left ventricu-
with bradycardia and peripheral arteriosclerosis with reduction in arte- lar function (see Chap. 22).34,35 Although more readily recognized on
rial distensibility. In patients with mitral regurgitation or ventricular sphygmomanometry, when the systolic pressure alternates by more than
Z septal defect, the forward stroke volume (from the left ventricle into the 20 mm Hg, pulsus alternans can be detected by palpation of a periph-
Ch08.qxd 3/26/04 07:00 PM Page 9

eral (femoral or brachial) pulse more frequently than by a more central below the umbilicus suggests the presence of an aneurysm of 8-9
pulse. Palpation should be carried out with light pressure and with the the abdominal aorta. To diminish cold-induced vasocon-
patient’s breath held in mid-expiration to avoid the superimposition striction, peripheral pulses should be palpated after the
of respiratory variation on the amplitude of the pulse. Pulsus alternans patient has been in a warm room for at least 20 minutes.
is generally accompanied by alternation in the intensity of the Korotk- Absent or weak peripheral pulses usually signify obstruction.
off sounds and occasionally by alternation in intensity of the heart However, the dorsalis pedis and posterior tibial arteries may
sounds. Rarely, pulsus alternans is so marked that the weak beat is not
perceived at all.36 Aortic regurgitation, systemic hypertension, and reduc-
be absent in approximately 2 percent of normal persons
ing venous return by administration of nitroglycerin or by tilting the because they pursue an aberrant course.
patient into the upright position all exaggerate pulsus alternans and assist Arterial bruits should be sought at specific anatomical
in its detection. Pulsus alternans, which is frequently precipitated by a sites. When the lumen diameter is reduced by approximately
premature ventricular contraction, is characterized by a regular rhythm 50 percent, a soft short systolic bruit is heard; as the obstruc- CH 8
and must be distinguished from pulsus bigeminus, which is usually tion becomes more severe, the bruit becomes high pitched,
irregular. louder, and longer. With approximately 80 percent diameter

Physical Examination of the Heart and Circulation

PULSUS BIGEMINUS. A bigeminal rhythm is caused by the occur- reduction, the murmur spills into early diastole, but it dis-
rence of premature contractions, usually ventricular, after every other appears with more severe stenosis or complete occlusion.
beat and results in alternation of the strength of the pulse, which can
be confused with pulsus alternans. However, in contrast to the pulsus
Arterial bruits are augmented by elevation of the cardiac
alternans, in which the rhythm is regular, in pulsus bigeminus the weak output (e.g., as occurs in patients with anemia), by poor
beat always follows the shorter interval. In normal persons or in patients development of collaterals, and by increased arterial outflow
with fixed obstruction to left ventricular outflow, the compensatory (as occurs with regional exercise).
pause after a premature beat is followed by a stronger-than-normal
pulse. In patients with hypertrophic obstructive cardiomyopathy,
however, the post-premature ventricular contraction beat is weaker
than normal because of increased obstruction to left ventricular outflow
(see Chap. 59).37
The Cardiac Examination

PULSUS PARADOXUS. Pulsus paradoxus is an exagger- Inspection

ated reduction in the strength of the arterial pulse during
normal inspiration due to an exaggerated inspiratory fall in The cardiac examination proper should commence with
systolic pressure (more than 10 mm Hg during quiet breath- inspection of the chest, which can usually best be accom-
ing) (see Chap. 64). When marked (i.e., an inspiratory reduc- plished with the examiner standing at the side or foot of the
tion of pressure greater than 20 mm Hg), the paradoxical bed or examining table.4 Respirations—their frequency, regu-
pulse can be detected by simple palpation of the brachial arte- larity, and depth—as well as the relative effort required
rial pulse38; in severe cases, there is inspiratory disappear- during inspiration and exhalation, should be noted. Simulta-
ance of the pulse. Milder degrees of a paradoxical pulse can neously, one should search for cutaneous abnormalities, such
be readily detected on sphygmomanometry: the cuff is as spider nevi (seen in patients with hepatic cirrhosis and
inflated to suprasystolic levels and is deflated slowly at a rate Osler-Weber-Rendu disease). Dilation of veins on the anterior
of about 2 mm Hg per heartbeat; the peak systolic pressure chest wall with caudal flow suggests obstruction of the supe-
during exhalation is noted.39,40 The cuff is then deflated even rior vena cava, whereas cranial flow occurs in patients with
more slowly, and the pressure is again noted when Korotkoff obstruction of the inferior vena cava. Precordial prominence
sounds become audible throughout the respiratory cycle. is most striking if cardiac enlargement developed before
Normally, the difference between the two pressures should puberty, but it may also be present, although to a lesser
not exceed 10 mm Hg during quiet respiration. (Pulsus alter- extent, in patients in whom cardiomegaly developed in adult
nans can also be detected by this maneuver by noting whether life, after the period of thoracic growth.
peak systolic pressure or the intensity of the Korotkoff sounds
A heavy muscular thorax, contrasting to less developed lower extrem-
alternates when the breath is held.) ities, can occur in patients with coarctation of the aorta, in which col-
Pulsus paradoxus represents an exaggeration of the normal lateral arteries may be visible in the axillae and along the lateral chest
decline in systolic arterial pressure with inspiration. It results wall. The upper portion of the thorax exhibits symmetrical bulging in
from the reduced left ventricular stroke volume and the trans- children with stiff lungs in whom the inspiratory effort is increased.
mission of negative intrathoracic pressure to the aorta. It is A “shield chest” is a broad chest in which the angle between the
a frequent, indeed characteristic, finding in patients with manubrium and the body of the sternum is greater than normal, and it
cardiac tamponade,41,42 occurs less frequently (in about half) is associated with widely separated nipples; shield chest is frequently
in patients with chronic constrictive pericarditis,19 and is also observed in patients with Turner and Noonan syndromes (see Chap. 56).
Careful note should be made of other deformities of the thoracic cage,
observed in patients with emphysema and bronchial asthma
such as kyphoscoliosis, which may be responsible for cor pulmonale (see
(who have wide respiratory swings of intrapleural pressure),39 Chap. 67); and ankylosing spondylitis, sometimes associated with aortic
as well as in patients with hypovolemic shock, pulmonary regurgitation (see Chap. 82).
embolus, pregnancy, and extreme obesity. Aortic regurgita- Pectus excavatum,15,16 a condition in which the sternum is displaced
tion tends to prevent the development of pulsus paradoxus posteriorly, is commonly observed in patients with Marfan syndrome,
despite the presence of cardiac tamponade. Reversed pulsus homocystinuria, Ehlers-Danlos syndrome, and Hunter-Hurler syndrome
paradoxus (an inspiratory rise in arterial pressure) may occur and in a small fraction of patients with mitral valve prolapse. This tho-
in hypertrophic obstructive cardiomyopathy. racic deformity rarely compresses the heart or elevates the systemic and
THE ARTERIAL PULSE IN VASCULAR DISEASE (see pulmonary venous pressures, and the signs of heart disease are more
often apparent rather than real.44 Displacement of the heart into the left
Chap. 54). Examination of the arterial pulses is of critical
thorax, prominence of the pulmonary artery, and a parasternal midsys-
importance in the diagnosis of extracardiac obstructive arte- tolic murmur, all key features of this deformity, may falsely suggest the
rial disease. Systematic bilateral palpation of the common presence of organic heart disease. Lack of normal thoracic kyphosis (i.e.,
carotid, brachial, radial, femoral, popliteal, dorsalis pedis,42 the straight back syndrome) is often associated with expiratory splitting
and posterior tibial vessels (see Fig. 8–5C and D), as well as of S2, a parasternal midsystolic murmur, and prominence of the pul-
palpation of the abdominal aorta (both above and below the monary artery on radiography.
umbilicus), should be part of every examination in patients CARDIOVASCULAR PULSATIONS. Cardiovascular pulsations should
suspected of having ischemic heart disease.43 A normal aorta be looked for on the entire chest but specifically in the regions of the
is often palpable above the umbilicus, but a palpable aorta cardiac apex, the left parasternal region, and the third left and second Z
 Ch08.qxd 3/26/04 07:00 PM Page 10

8-10 visible lateral to the midclavicular

line; when present there, they
signify cardiac enlargement unless
there is thoracic deformity or con-
genital absence of the peri-
cardium. Shaking of the entire
precordium with each heartbeat
can occur in patients with severe
valvular regurgitation, large left-to-
right shunts, especially patent
ductus arteriosus, complete AV
CH 8 block, hypertrophic obstructive
cardiomyopathy, and various
hyperkinetic states. Aortic
aneurysms may produce visible
pulsations of one of the stern-
oclavicular joints of the right ante-
rior thoracic wall.
A B

Palpation
Pulsations of the heart and
great arteries that are trans-
mitted to the chest wall are
best appreciated when the
examiner is positioned on the
right side of a supine patient.
To palpate the movements of
the heart and great arteries,
the examiner should use the
fingertips or the area just
proximal thereto. Precordial
movements should be timed
C
D with the simultaneously
palpated carotid pulse or
auscultated heart sounds.45
The examination should be
carried out with the chest
completely exposed and ele-
vated to 30 degrees, with the
patient both supine and in
the partial left lateral decubi-
tus positions (Fig. 8–7).2
Rotating the patient into the
left lateral decubitus position
with the left arm elevated
over the head causes the heart
to move laterally and
increases the palpability of
E F both normal and pathological
thrusts of the left ventricle.
FIGURE 8–7 A, Palpation of the anterior wall of the right ventricle by applying the tips of three fingers in the third, fourth, and
fifth interspaces, and left sternal edge (arrows), during full held exhalation. Patient is supine with the trunk elevated 30 degrees. B,
The subxiphoid region,
Subxiphoid palpation of the inferior wall of the right ventricle (RV) with the relative position of the abdominal aorta (Ao) shown by which allows palpation of the
the arrow. C, The bell of the stethoscope is applied to the cardiac apex while the patient lies in a partial left lateral decubitus posi- right ventricle, should be
tion. The thumb of the examiner’s free left hand is used to palpate the carotid artery for timing purposes. D, The soft, high-frequency examined with the tip of the
early diastolic murmur of aortic regurgitation or pulmonary hypertensive regurgitation is best elicited by applying the stethoscopic index finger during held
diaphragm very firmly to the mid-left sternal edge. The patient leans forward with breath held in full exhalation. E, Palpation of the inspiration. Obese, muscular,
left ventricular impulse with a fingertip (arrow). The patient’s trunk is 30 degrees above the horizontal. The examiner’s right thumb emphysematous, and elderly
palpates the carotid pulse for timing purposes. F, Palpation of the liver. The patient is supine with knees flexed to relax the abdomen. persons may have weak or
The flat of the examiner’s right hand is placed on the right upper quadrant just below the expected inferior margin of the liver; the undetectable cardiac pulsa-
left hand is applied diametrically opposite. (From Perloff JK: Physical Examination of the Heart and Circulation. 3rd ed. Philadelphia,
WB Saunders, 2000.)
tions in the absence of
cardiac abnormality, and
thoracic deformities (e.g.,
kyphoscoliosis, pectus exca-
right intercostal spaces. Prominent pulsations in these areas suggest vatum) can alter the pulsations transmitted to the chest wall.
enlargement of the left ventricle, right ventricle, pulmonary artery, and In the course of cardiac palpation, precordial tenderness may
aorta, respectively.A thrusting apex exceeding 2 cm in diameter suggests be detected; this finding can result from costochondritis
left ventricular enlargement; systolic retraction of the apex may be visible (Tietze syndrome) and can be an important indication that
Z in cases of constrictive pericarditis. Normally, cardiac pulsations are not chest pain is not due to myocardial ischemia.
Ch08.qxd 3/26/04 07:00 PM Page 11

LEFT VENTRICLE. The left ventricular impulse, also referred to as when the patient is in the left lateral decubitus position, and it can be 8-11
the cardiac impulse, the apex beat, and the apical thrust, is normally pro- confirmed by detecting the motion of the stethoscope placed over the
duced by left ventricular contraction and is the lowest and most lateral left ventricular impulse or by observing the motion of an X mark over
point on the chest at which the cardiac impulse can be appreciated and the left ventricular impulse. Presystolic expansion of the left ventricle
is normally above the anatomical apex. Normally, the left ventricular can be enhanced by sustained handgrip. In patients with ischemic heart
impulse is medial and superior to the intersection of the left midclavic- disease, presystolic pulsation is usually associated with a reduction in left
ular line and the fifth intercostal space and is palpable as a single, brief ventricular compliance.
outward motion.Although it may not be palpable in the supine position
in as many as half of all normal subjects older than 50 years of age, the RIGHT VENTRICLE
left ventricular impulse can usually be felt in the left lateral decubitus Except in the first few months of life, the right ventricle normally is
position. Displacement of the apex beat lateral to the midclavicular line not palpable. A palpable anterior systolic movement (replacing systolic
or more than 10 cm lateral to the midsternal line is a sensitive but not retraction) in the left parasternal region, best felt by the proximal palm CH 8
specific indicator of left ventricular enlargement. However, when the or fingertips and with the patient supine, usually represents right
patient is in the left lateral decubitus position, a palpable apical impulse ventricular enlargement or hypertrophy.4 In patients with pulmonary

Physical Examination of the Heart and Circulation

that has a diameter of more than 3 cm is an accurate sign of left emphysema, even an enlarged right ventricle is not readily palpable at
ventricular enlargement.46 Thoracic deformities—particularly scoliosis, the left sternal edge but is better appreciated in the subxiphoid region.
straight back, and pectus excavatum—can result in the lateral displace- Exaggerated motion of the entire parasternal area (i.e., a hyperdynamic
ment of a normal-sized heart. impulse with normal contour) usually reflects increased right ventricu-
APEX CARDIOGRAM. This recording reflects the movement of the lar stroke volume, as occurs in patients with atrial septal defect or tri-
chest wall and represents the pulsation of the entire left ventricle. Its cuspid regurgitation.
contour differs from what is perceived on palpation of the apex.
PULMONARY ARTERY
SYSTOLIC MOTION Pulmonary hypertension and increased pulmonary blood flow fre-
During isovolumetric contraction, the heart normally rotates coun- quently produce a prominent systolic pulsation of the pulmonary trunk
terclockwise (as one faces the patient), and the lower anterior portion in the second intercostal space just to the left of the sternum.This pul-
of the left ventricle strikes the anterior chest wall, causing a brief sation is often associated with a prominent left parasternal impulse,
outward motion followed by medial retraction of the adjacent chest wall reflecting right ventricular enlargement, or with hypertrophy and a pal-
during ejection.The peak outward motion of the left ventricular impulse pable shock synchronous with the second heart sound, reflecting force-
occurs simultaneously with, or just after, aortic valve opening; then the ful closure of the pulmonic valve.
left ventricular apex moves inward. In asthenic persons, in patients with
LEFT ATRIUM
mild left ventricular enlargement, and in subjects with a normal left ven-
tricle but an augmented stroke volume, as occurs in anxiety and other An enlarged left atrium or a large posterior left ventricular aneurysm
hyperkinetic states, and in cases of mitral or aortic regurgitation, the can make right ventricular pulsations more prominent by displacing the
cardiac impulse may be overactive but with a normal contour; that is, the right ventricle anteriorly against the left parasternal area; in patients with
outward thrust during systole is exaggerated in amplitude but is not sus- severe mitral regurgitation, an expanding left atrium may be responsible
tained during ejection. for marked left parasternal movement, even in the absence of right ven-
HYPERTROPHY AND DILATATION. With moderate or severe left tricular hypertrophy. Movement imparted by the systolic expansion of
ventricular concentric hypertrophy, the outward systolic thrust persists the left atrium can be appreciated by placing the index finger of one
throughout ejection, often lasting up to the second heart sound,47 and hand at the left ventricular apex and the index finger of the other in the
this motion is accompanied by retraction of the left parasternal region. left parasternal region in the third intercostal space.
The left ventricular heave or lift, which is more prominent in patients AORTA. Enlargement or aneurysm of the ascending aorta or aortic
with concentric hypertrophy than in those with left ventricular dilata- arch may cause visible or palpable systolic pulsations of the right or left
tion without volume overload, is characterized by a sustained outward sternoclavicular joint and may also cause a systolic impulse in the
movement of an area that is larger than the normal apex; that is, it is more suprasternal notch or the first or second right intercostal space.4
than 2 to 3 cm in diameter. In patients with left ventricular enlargement,
THRILLS
the systolic impulse is displaced laterally and downward into the sixth
or seventh interspaces. In patients with volume overload and/or sympa- The flat of the hand or the fingertips usually best appreciate thrills,
thetic stimulation, the left ventricular impulse is hyperkinetic; that is, it which are vibratory sensations that are palpable manifestations of loud,
is brisker and larger than normal. harsh murmurs having low- to medium-frequency components. Because
OTHER CONDITIONS. Left ventricular aneurysm produces a larger- the vibrations must be quite intense before they are felt, far more infor-
than-normal area of pulsation of the left ventricular apex.Alternatively, it mation can be obtained from the auscultatory than from the palpatory
may produce a sustained systolic bulge several centimeters superior to features of heart murmurs. High-pitched murmurs such as those pro-
the left ventricular impulse, sometimes termed an ectopic impulse. duced by valvular regurgitation, even when loud, are not usually associ-
A double systolic outward thrust of the left ventricle is characteris- ated with thrills.
tic of patients with hypertrophic obstructive cardiomyopathy (see Chap.
PERCUSSION
54), who may also often exhibit a typical presystolic cardiac expansion,
thus resulting in three separate outward movements of the chest wall Palpation is far more helpful than is percussion in determining
during each cardiac cycle.48 Constrictive pericarditis is characterized by cardiac size. However, in the absence of an apical beat, as occurs in
systolic retraction of the chest, particularly of the ribs in the left axilla patients with pericardial effusion or in some patients with dilated car-
(Broadbent sign). diomyopathy, heart failure, and marked displacement of a hypokinetic
apical beat, the left border of the heart can be approximately outlined
DIASTOLIC MOTION by means of percussion. Also, percussion of dullness in the right lower
The outward motion of the apex characteristic of rapid left ventric- parasternal area may, in some instances, aid in the detection of a greatly
ular diastolic filling is most readily palpated with the patient in the left enlarged right atrium. Percussion aids materially in determining visceral
lateral decubitus position and in full exhalation. The outward motion is situs, that is, in ascertaining the side on which the heart, stomach, and
accentuated when the inflow of blood into the left ventricle is acceler- liver are located.
ated.This occurs in cases of mitral regurgitation, when the volume of the
left ventricle is increased or when its function is impaired.4 This motion
is the mechanical equivalent of and occurs simultaneously with a third
heart sound (S3).
PRESYSTOLIC EXPANSION. When the atrial contribution to Cardiac Auscultation
ventricular filling is augmented, as occurs in patients with reduced left
ventricular compliance associated with concentric left ventricular hyper- Principles and Technique
trophy, myocardial ischemia, and myocardial fibrosis, a presystolic pulsa-
tion (usually accompanying a fourth heart sound [S4]) is palpable, The modern binaural stethoscope is a well-crafted, airtight
resulting in a double outward movement of the left ventricular impulse. instrument with earpieces selected for comfort, with metal
This presystolic expansion is most readily discernible during exhalation, tubing joined to single flexible 12-inch-long, thick-walled Z
 Ch08.qxd 3/26/04 07:00 PM Page 12

8-12 rubber tubing (internal diameter of 1/8 inch), and with dual Heart Sounds
chest pieces—diaphragm for high frequencies, bell for low or
lower frequencies—designed so that the examiner can readily Heart sounds are relatively brief, discrete auditory vibra-
switch from one chest piece to the other.49,50 When the bell is tions that can be characterized by intensity (loudness), fre-
applied with just enough pressure to form a skin seal, low quency (pitch), and quality (timbre). S1 identifies the onset of
frequencies are accentuated; when the bell is pressed firmly, ventricular systole, and S2 identifies the onset of diastole.
the stretched skin becomes a diaphragm, damping low fre- These two auscultatory events establish a framework within
quencies. Variable pressure with the bell provides a range of which other heart sounds and murmurs can be placed and
frequencies from low to medium. timed.4,48,50
Cardiac auscultation is best accomplished in a quiet room The basic heart sounds are the S1, S2, S3, and S4 (Fig. 8–9).
CH 8 with the patient comfortable and the chest fully exposed. The Each of these events can be normal or abnormal. Other heart
topographical areas for auscultation (Fig. 8–8) are best desig- sounds are, with few exceptions, abnormal or iatrogenic (e.g.,
nated by descriptive terms: cardiac apex, left and right sternal prosthetic valve sounds, pacemaker sounds). Heart sounds
borders interspace by interspace, and subxiphoid. Ausculta- within the framework established by S1 and S2 are designated
tion should begin at the cardiac apex (best identified in the as “early systolic, midsystolic, late systolic,” and “early dias-
left lateral decubitus) and contiguous lower left sternal edge tolic, mid-diastolic, late diastolic (presystolic).”2
(inflow), proceeding interspace by interspace up the left For example, an early systolic sound might be an ejection
sternal border to the left base and then to the right base sound (aortic or pulmonary) or an aortic prosthetic sound.
(outflow). In addition, the stethoscope should be applied reg- Midsystolic and late systolic sounds are typified by the
ularly to the axillae, the back, the anterior chest on the oppo- click or clicks of mitral valve prolapse but occasionally are
site side, and above the clavicles. In patients with increased “remnants” of pericardial rubs. Early diastolic sounds are re-
anteroposterior chest dimensions (emphysema), auscultation presented by opening snaps (usually mitral), an early S3 (con-
is often best achieved by applying the stethoscope in the strictive pericarditis, less commonly mitral regurgitation), the
epigastrium (subxiphoid). opening of a mechanical inflow prosthesis, or the abrupt
seating of a pedunculated mobile atrial myxoma (“tumor
During auscultation, the examiner is generally on the patient’s right; plop”). Mid-diastolic sounds are generally S3 or summation
three positions are routinely employed: left lateral decubitus (assuming
left thoracic heart), supine, and sitting. One should begin auscultation by
applying the stethoscope to the cardiac apex with the patient in the left
lateral decubitus position (see Fig. 8–7C). Identification of S1 can usually The basic heart sounds
be established by simultaneous palpation of the carotid artery with the
thumb of the free left hand. Once the S1 is identified, analysis then pro-
ceeds by systematic, methodical, sequential attention to early, middle, and
late systole; S2; then early, middle, and late diastole (presystole); and
returning to S1. When auscultation at the apex has been completed, the S1 S2 S3 S4
patient is turned into the supine position. Each topographical area—
lower to upper left sternal edge interspace by interspace and then the
A
right base—is interrogated using the same systematic sequence of analy-
sis (see Fig. 8–7D).
Assessment of pitch or frequency ranging from low to moderately The heart sounds: expanded terminology
high can be achieved by variable pressure of the stethoscopic bell,
whereas for high frequencies the diaphragm should be employed. It is ES
practical to begin by using the stethoscopic bell with varying pressure MS LS ED MD LD
at the apex and lower left sternal edge, changing to the diaphragm when
the base is reached. Low frequencies are best heard by applying the bell
just lightly enough to achieve a skin seal. High-frequency events are best S1 S2
elicited with firm pressure of the diaphragm, often with the patient
sitting, leaning forward in full, held exhalation.
B

S4

Aortic Pulm
S1 S2

VSD
MR
Vibratory

HCM C
FIGURE 8–9 A, The basic heart sounds consist of the first heart sound (S1), the
second heart sound (S2), the third heart sound (S3), and the fourth heart sound (S4).
B, Heart sounds within the auscultatory framework established by S1 and S2. The addi-
FIGURE 8–8 Maximal intensity and radiation of six isolated systolic murmurs. tional heart sounds are designated as early systolic (ES), midsystolic (MS), late systolic
HCM = hypertrophic cardiomyopathy; MR = mitral regurgitation; Pulm = pulmonary; (LS), early diastolic (ED), mid-diastolic (MD), and late diastolic (LD) or presystolic.
VSD = ventricular septal defect. (From Barlow JB: Perspectives on the Mitral Valve. C, Upper tracing illustrates a low-frequency S4, and the lower tracing illustrates a split
Z Philadelphia, FA Davis, 1987, p 140.) S1, the two components of which are of the same quality.
Ch08.qxd 3/26/04 07:00 PM Page 13

TABLE 8–2 Factors Affecting the Intensity of S1 TABLE 8–3 Conditions Associated with Ejection 8-13
Sound or Click
Loud S1
Short PR interval (<160 msec) Aortic
Tachycardia or hyperkinetic states Congenital valvular aortic stenosis
“Stiff” left ventricle Bicuspid aortic valve
Mitral stenosis Aortic regurgitation
Left atrial myxoma Aortic aneurysm
Holosystolic mitral valve prolapse Aortic root dilatation
Systemic hypertension
Soft S1 Severe tetralogy of Fallot
Long PR interval (>200 msec)
Depressed left ventricular contractility
CH 8
Pulmonic
Premature closure of mitral valve (e.g., acute aortic Pulmonary valve stenosis

Physical Examination of the Heart and Circulation

regurgiation) Idiopathic dilatation of the pulmonary artery
Left bundle branch block Atrial septal defect
Extracardiac factors (e.g., obesity, muscular chest, chronic Chronic pulmonary hypertension
obstructive pulmonary disease, large breasts) Tetralogy of Fallot (with pulmonic valve stenosis)
Flail mitral leaflet
Pseudo-ejection sound
From Abrams J: Synopsis of Cardiac Physical Diagnosis. 2nd ed. Boston, Prominent splitting of S1
Butterworth Heinemann, 2001, p 60. Increased T1 (Ebstein’s anomaly; atrial septal defect)
Hypertrophic cardiomyopathy
Early nonejection click of holosystolic mitral valve prolapse
sounds (synchronous occurrence of S3 and S4). Late diastolic High-pitched S4 (S1 confused for ejection sound)
or presystolic sounds are almost always S4 sounds, rarely
From Abrams J: Synopsis of Cardiac Physical Diagnosis. 2nd ed. Boston,
pacemaker sounds. Butterworth Heinemann, 2001, p 100.

First Heart Sound

S1 consists of two components (see Fig. 8–9C). The initial
component is most prominent at the cardiac apex when the Aortic Ejection Click of
Aortic Stenosis
apex is occupied by the left ventricle. The second component,
if present, is normally confined to the lower left sternal edge, x
is less commonly heard at the apex, and is seldom heard at Aorta Diastole SM A2
the base. The first major component is associated with closure Aortic S1
of the mitral valve and coincides with abrupt arrest of leaflet valve
motion when the cusps, especially the larger and more LV
mobile anterior mitral cusp, reach their fully closed posi- Carotid
tions. The origin of the second component of S1 has been pulse
debated but is generally assigned to closure of the tricuspid Early
valve based on an analogous line of reasoning.4,48-51 systole

Opening of the semilunar valves with ejection of blood into the aortic X
root or pulmonary trunk usually produces no audible sound in the LV
normal heart. In cases of complete right bundle branch block, S1 is widely
split as a result of delay of the tricuspid component.52 In cases of com-
plete left bundle branch block, S1 is single as a result of delay of the mitral
ECG
component.53
When S1 is split, its first component is normally louder. The softer
second component is confined to the lower left sternal edge but may FIGURE 8–10 Ejection click associated with aortic stenosis due to a congenitally
also be heard at the apex. Only the louder first component is heard at bicuspid valve. Note the high-frequency, high-amplitude sound that follows S1 and is
the base.The intensity of the S1, particularly its first major audible com- coincident with the onset of ejection into the aorta. The aortic ejection sound is formed
ponent, depends chiefly on the position of the bellies of the mitral by sudden cessation of the opening motion of the abnormal valve leaflets (doming). Note
leaflets, especially the anterior leaflet, at the time the left ventricle begins also the delayed carotid upstroke and long systolic murmur. (From Abrams J: Synopsis
to contract. S1 is therefore loudest when the onset of left ventricular of Cardiac Physical Diagnosis. 2nd ed. Boston, Butterworth Heinemann, 2001, p 135.)
systole finds the mitral leaflets maximally recessed into the left ventric-
ular cavity, as in the presence of a rapid heart rate, a short PR interval
(Table 8–2),54 short cycle lengths in atrial fibrillation, or mitral stenosis
with a mobile anterior leaflet.When this mobility is lost, the intensity of
S1 decreases. sound originating in the aortic valve (congenital aortic steno-
sis or bicuspid aortic valve) or in the pulmonary valve (con-
genital pulmonary valve stenosis) indicates that the valve is
Early Systolic Sounds mobile because the ejection sound is caused by abrupt cepha-
Aortic or pulmonary ejection sounds are the most common lad doming.56 Less certain is the origin of an ejection sound
early systolic sounds (Table 8–3).55 Ejection sound is pre- within a dilated arterial trunk distal to a normal semilunar
ferred to the term ejection click, with the latter designation valve (Fig. 8–11A). Origin of the sound is assigned either to
best reserved for the midsystolic to late systolic clicks of opening movement of the leaflets that resonate in the arterial
mitral valve prolapse (see Chap. 57). Ejection sounds coin- trunk or to the wall of the dilated great artery. Aortic ejection
cide with the fully opened position of the relevant semilunar sounds do not vary with respiration.
valve, as in congenital aortic valve stenosis (Fig. 8–10), bicus-
pid aortic valve in the left side of the heart, or pulmonary
valve stenosis in the right side of the heart.4,48,50 Ejection
Midsystolic to Late Systolic Sounds
sounds are relatively high frequency events and, depending The most common midsystolic to late systolic sounds are
on intensity, have a pitch similar to that of S1. An ejection associated with mitral valve prolapse (see Chap. 57).4,57 The Z
 Ch08.qxd 3/26/04 07:00 PM Page 14

8-14
Supine

S1
S2
C

CH 8
Standing

S1
S2
C

FIGURE 8–11 A, Tracings from a 32-year-old woman with an ostium secundum

atrial septal defect, pulmonary hypertension, and a small right-to-left shunt. In the
second left intercostal space (2 LICS), the first heart sound is followed by a prominent
pulmonary ejection sound (E). The second sound remains split. The pulmonic compo-
nent (P2) is very loud and is transmitted to the apex. CAR = carotid pulse. B, Phono-
cardiogram recorded in the left lateral decubitus position over the left ventricular Squatting
impulse in a patient with pure rheumatic mitral stenosis. The first heart sound (S1)
is loud. The second heart sound (S2) is followed by an opening snap (OS). There is a S1
mid-diastolic murmur (MDM). The prominent presystolic murmur (PM) goes up to the S2
subsequent loud S1. C

term click is appropriate because these midsystolic to late

systolic sounds are of relatively high frequency. Midsystolic
to late systolic clicks of mitral valve prolapse coincide with FIGURE 8–12 A midsystolic nonejection sound (C) occurs during mitral valve pro-
maximal systolic excursion of a prolapsed anterior leaflet (or lapse and is followed by a late systolic murmur that crescendos to the second heart
scallop of the posterior leaflet) into the left atrium and are sound (S2). Standing decreases venous return; the heart becomes smaller; C moves
ascribed to sudden tensing of the redundant leaflets and elon- closer to the first heart sound (S1) and the mitral regurgitant murmur has an earlier
gated chordae tendineae. Physical or pharmacological inter- onset. With prompt squatting, venous return increases; the heart becomes larger; C
moves toward S2 and the duration of the murmur shortens. (From Shaver JA, Leonard
ventions that reduce left ventricular volume, such as the JJ, Leon DF: Examination of the Heart. Part IV: Auscultation of the Heart. Dallas,
Valsalva maneuver, or a change in position from squatting to American Heart Association, 1990, p 13. Copyright 1990, American Heart Association.)
standing (Fig. 8–12) causes the clicks to occur earlier in
systole.57 Conversely, physical or pharmacological interven-
tions that increase left ventricular volume, such as squatting
or sustained hand grip, delay the clicks. Multiple clicks are
thought to arise from asynchronous tensing of different por- resistance, inspiratory splitting of S2 narrows and, if present
tions of redundant mitral leaflets, especially the triscalloped at all, reflects an increase in right ventricular ejection time
posterior leaflet. and/or earlier timing of A2.
The frequency compositions of the aortic and pulmonary
components of S2 are similar, but their normal amplitudes
Second Heart Sound (Table 8–4)
differ appreciably, the aortic component being the louder,
S2, like S1, has two components. The first component of reflecting the differences in systemic (aortic) and pulmonary
the second heart sound is designated “aortic” (A2) and the arterial closing pressures. Splitting of S2 is most readily iden-
second “pulmonic” (P2) (Fig. 8–13).58,59 Each component coin- tified in the second left intercostal space, because the softer
cides with the incisura of its great arterial pressure pulse. P2 is normally confined to that site, whereas the louder A2 is
Inspiratory splitting of S2 is due chiefly to a delay in P2, less heard at the base, sternal edge, and apex.4,58
to earlier timing of A2.60 During inspiration, the pulmonary ABNORMAL SPLITTING OF THE SECOND HEART
arterial incisura moves away from the descending limb of the SOUND (Fig. 8–14). Three general categories of abnormal
right ventricular pressure pulse because of an inspiratory splitting are recognized: (1) persistently single, (2) persist-
increase in capacitance of the pulmonary vascular bed, delay- ently split (fixed or nonfixed), and (3) paradoxically split
ing P2.61 Exhalation has the opposite effect. The earlier inspi- (reversed). When S2 remains single throughout the respira-
ratory timing of A2 is attributed to a transient reduction in tory cycle, one component is absent or the two components
left ventricular volume coupled with unchanged impedance are persistently synchronous. The most common cause of
(capacitance) in the systemic vascular bed. Normal respira- a single S2 is inaudibility of the P2 in older adults with
tory variations in the timing of S2 are therefore ascribed increased anteroposterior chest dimensions. In the setting of
principally to the variations in impedance characteristics congenital heart disease, a single S2 due to absence of the pul-
(capacitance) of the pulmonary vascular bed and secondarily monary component is a feature of pulmonary atresia, severe
to an inspiratory increase in right ventricular volume as orig- pulmonary valve stenosis, dysplastic pulmonary valve, or
inally proposed. When an increase in capacitance of the pul- complete transposition of the great arteries. Conversely, a
Z monary bed is lost because of a rise in pulmonary vascular single S2 due to inaudibility of the A2 occurs when the aortic
Ch08.qxd 3/26/04 07:00 PM Page 15

TABLE 8–4 Causes of Splitting of the Second Heart Sound 8-15

Normal Splitting Reversed Splitting
Delayed pulmonic closure Delayed aortic closure
Delayed electrical activation of the right ventricle Delayed electrical activation of the left ventricle
Complete right bundle branch block (proximal type) Complete left bundle branch block (proximal type)
Left ventricular paced beats Right ventricular paced beats
Left ventricular ectopic beats Right ventricular ectopic beats
Prolonged right ventricular mechanical systole Prolonged left ventricular mechanical systole
Acute massive pulmonary embolus Complete left bundle branch block (peripheral type)
Pulmonary hypertension with right-sideed heart failure Left ventricular outflow tract obstruction
Pulmonic stenosis with intact septum (moderate to severe) Hypertensive cardiovascular disease
CH 8
Decreased impedance of the pulmonary vascular bed (increased Arteriosclerotic heart disease

Physical Examination of the Heart and Circulation

hangout) Chronic ischemic heart disease
Normotensive atrial septal defect Angina pectoris
Idiopathic dilatation of the pulmonary artery Decreased impedance of the systemic vascular bed (increased
Pulmonic stenosis (mild) hangout)
Atrial septal defect, postoperative (70%) Poststenotic dilatation of the aorta secondary to aortic stenosis or
insufficiency
Early aortic closure Patent ductus arteriosus
Shortened left ventricular mechanical systole (left ventriculer
ejection time) Early puimonic closure
Mitral regurgitation Early electrical activation of the right ventricle
Ventricular septal defect Wolff-Parkinson-White syndrome, type B
Modified from Shaver JA, O’Toole JD: The second heart sound: Newer concepts. Parts 1 and 2. Mod Concepts Cardiovasc Dis 46:7 and 13, 1977.

valve is immobile (severe calcific aortic stenosis) or atretic

EXPIRATION INSPIRATION (aortic atresia).
Normal Physiological Splitting Persistent Splitting of S2. This term applies when the two
components remain audible (or recordable) during both
A2
P2 inspiration and exhalation (see Fig. 8–14). Persistent splitting
may be due to a delay in P2, as in cases of simple complete
right bundle branch block,58 or to early timing of the A2, as
S1 S2 S1 S2 occasionally occurs in cases of mitral regurgitation. Normal
directional changes in the interval of the split (greater with
Audible Expiratory Splitting inspiration, lesser with exhalation) in the presence of per-
A2 P A2 P sistent audibility of both components defines the split as per-
Wide physiological
2 2 sistent but not fixed.
splitting Fixed Splitting of the S2. This term applies when the
interval between the A2 and P2 is not only wide and persist-
S1 S2 S1 S2 ent but also remains unchanged during the respiratory
cycle.50 Fixed splitting is an auscultatory hallmark of uncom-
A2 P2 A2
P2 plicated ostium secundum atrial septal defect (Fig. 8–15; see
Reversed splitting Chap. 56). A2 and P2 are widely separated during exhalation
and exhibit little or no change in the degree of splitting
S1 S2 S1 S2 during inspiration or with the Valsalva maneuver. The wide
splitting is caused by a delay in the P2 because a marked
A2 P2
increase in pulmonary vascular capacitance prolongs the
Narrow physiological interval between the descending limbs of the pulmonary arte-
splitting ( P2) rial and right ventricular pressure pulses (“hangout”), and
therefore delays the pulmonary incisura and the P2. The
S1 S2 S1 S2 capacitance (impedance) of the pulmonary bed is apprecia-
bly increased, and the right ventricular stroke volume is not
FIGURE 8–13 Top, Normal physiological splitting. During expiration (left), the influenced by respiration, so there is little or no additional
aortic (A2) and pulmonic (P2) components of the second heart sound are separated by increase during inspiration and little or no inspiratory delay
less than 30 milliseconds and are appreciated as a single sound. During inspiration in the P2. Phasic changes in systemic venous return during
(right), the splitting interval widens, and A2 and P2 are clearly separated into two dis-
tinct sounds. Bottom, Audible expiratory splitting. In contrast to normal physiological
respiration in patients with atrial septal defect are associated
splitting, two distinct sounds are easily heard during expiration. Wide physiological with reciprocal changes in the volume of the left-to-right
splitting is caused by a delay in P2. Reversed splitting is caused by a delay in A2, result- shunt, minimizing respiratory variations in right ventricular
ing in paradoxical movement; that is, with inspiration P2 moves toward A2, and the split- filling. The net effect is the characteristic wide, fixed split-
ting interval narrows. Narrow physiological splitting occurs in patients with pulmonary ting of the two components of the S2.55
hypertension, and both A2 and P2 are heard during expiration at a narrow splitting inter- Paradoxical (Reversed) Splitting of S2. This term refers
val because of the increased intensity and high-frequency composition of P2. (From to a reversed sequence of semilunar valve closure, the P2 pre-
Shaver JA, Leonard JJ, Leon DF: Examination of the Heart, Part IV, Auscultation of the ceding the A2. Common causes of paradoxical splitting are
Heart. Dallas, American Heart Association, 1990, p 17. Copyright 1990, American Heart complete left bundle branch block62 or a right ventricular
Association.)
pacemaker, both of which are associated with initial activa-
tion of the right side of the ventricular septum, and delayed
activation of the left ventricle owing to transseptal (right-to-
left) depolarization.63 When the S2 splits paradoxically, its Z
 Ch08.qxd 3/26/04 07:00 PM Page 16

8-16 normal P2 is responsible for its

Splitting? localization in the second left
intercostal space, whereas the rel-
Normal Narrow fixed Wide fixed Reversed ative loudness of the normal A2
accounts for its audibility at all
Normal Pulm HT RBBB PDA (L to R shunt) precordial sites (see earlier). An
PS TI increase in intensity of the A2
ASD LBBB occurs with systemic hyperten-
PAPVR AS sion. The intensity of A2 also
MI IHD increases when the aorta is closer
VSD and L to R shunt to the anterior chest wall, owing
CH 8 Pseudo:
to root dilatation or transposition
of the great arteries or when an
S2+OS
anterior pulmonary trunk is small
S2+S3
or absent, as in pulmonary
S2+pericardial knock
atresia.55
S2+tumor plop
A loud P2 is a feature of pul-
monary hypertension, and the
loudness is enhanced by dilata-
tion of a hypertensive pulmonary
A2 versus P2? trunk. An accentuated P2 can be
A2>P2 P2>A2 transmitted to the middle or
lower left sternal edge and, when
very loud, throughout the pre-
Normal Pulm HT (any cause) cordium to the apex and right
AS base. A moderate increase in
loudness of the P2 sometimes
occurs in the absence of pul-
FIGURE 8–14 Decision tree for splitting of the second heart sound (S2). A2 = aortic valve closure; AS = aortic stenosis; ASD = monary hypertension when the
atrial septal defect; IHD = ischemic heart disease; L to R shunt = left-to-right shunt; LBBB = left bundle branch block; MI = mitral pulmonary trunk is dilated, as in
insufficiency; OS = opening snap; P2 = pulmonic valve closure; PAPVR = partial anomalous pulmonary venous return; PDA = patent cases of ostium secundum atrial
ductus arteriosus; PS = pulmonic stenosis; Pulm HT = pulmonary hypertension; RBBB = right bundle branch block; S3 = third heart septal defect or when there is a
sound; TI = tricuspid insufficiency; VSD = ventricular septal defect. (From Braunwald E: The clinical examination. In Braunwald E, decrease in anteroposterior chest
Goldman L [eds]: Primary Cardiology. 2nd ed. Philadelphia, Elsevier, 2003; and Sapira JD: The Art and Science of Bedside Diagnosis. dimensions (loss of thoracic
Baltimore, Urban and Schwartzenberg, 1990.) kyphosis) that places the pul-
monary trunk closer to the chest
wall.64

A2 P P2 Early Diastolic Sounds

2
Base
The opening “snap” of rheumatic
SEM mitral stenosis is the best known early
P2 50 msec diastolic sound (see Fig. 8–11B). The
50 msec S1
diagnostic value derived from the
pitch, loudness, and timing of the
opening snap in the assessment of
rheumatic mitral stenosis was estab-
Inspiration
lished by Wood in his classic mono-
Carotid graph, An Appreciation of Mitral
Stenosis.65 An audible opening snap
Expiration indicates that the mitral valve is
EKG
mobile, or at least its longer anterior
leaflet is. The snap is generated when
superior systolic bowing of the anterior
mitral leaflet is rapidly reversed toward
FIGURE 8–15 Simultaneous base and apex phonocardiograms recorded with the carotid pulse during quiet res- the left ventricle in early diastole in
piration in a young woman with a large atrial septal defect. Wide fixed splitting of the second heart sound (S2) is response to high left atrial pressure.
present, and the pulmonic component (P2) is easily recorded at the apex. A prominent systolic ejection murmur (SEM) The mechanism of the opening snap is
is recorded at the base and is attributable to the large stroke volume across the right ventricular outflow tract. The tri- therefore a corollary to the loud S1,
cuspid component of S1 is prominent at the apex. EKG = electrocardiogram. (From Shaver JA: Innocent murmurs. Hosp which is generated by abrupt superior
Med 14:8, 1978. Copyright 1999, Quadrant Healthcom, Inc.)
systolic displacement of a mobile ante-
rior mitral leaflet that was recessed into
the left ventricle during diastole by
two components separate during exhalation and become high left atrial pressure until the onset of left ventricular iso-
single (synchronous) during inspiration (see Fig. 8–13). Inspi- volumetric contraction (see earlier). The designation “snap”
ratory synchrony is achieved as the two components fuse is appropriate because of the relatively high frequency of the
because of a delay in the P2, less to earlier timing of the aortic sound.
component. The timing of the opening snap relative to the A2 has
important physiological meaning.4 A short A2/opening snap
ABNORMAL LOUDNESS (INTENSITY) OF THE TWO interval generally reflects the high left atrial pressure of
COMPONENTS OF S2
severe mitral stenosis. In older subjects with systolic hyper-
Assessment of intensity requires that both components be compared tension, however, mitral stenosis of appreciable severity can
Z when heard simultaneously at the same site.The relative softness of the occur without a short A2/opening snap interval because the
Ch08.qxd 3/26/04 07:00 PM Page 17

elevated left ventricular systolic pressure takes longer to fall relatively unobstructed) AV orifice on the side of the heart in which 8-17
below the left atrial pressure. In the presence of atrial fibril- the sound originates. An S3 or S4 originating from the right ventricle
lation, the A2/opening snap interval varies inversely with often responds selectively and distinctively to respiration, becoming
cycle length, because (all else being equal) the higher the left more prominent during inspiration.4 The inspiratory increase in right
atrial pressure (short cycle length), the earlier the stenotic atrial flow is converted into an inspiratory augmentation of both mid-
valve opens and vice versa. diastolic and presystolic filling.
S3 and S4, either normal or abnormal, are relatively low frequency
Early diastolic sounds are not confined to the opening snap of rheu- events that vary considerably in intensity (loudness), that originate in
matic mitral stenosis but include the pericardial “knock” of chronic con-
strictive pericarditis.66 The term “knock” has also been applied to an
early diastolic sound in patients with pure severe mitral regurgitation
with reduced left ventricular compliance. Both the pericardial knock and CH 8
S4 S1 S2 S1 S2
the knock of mitral regurgitation are rapid filling sounds that are early Atrial gallop

Physical Examination of the Heart and Circulation

and loud because a high-pressure atrium rapidly decompresses across an Presystolic
unobstructed mitral valve into a recipient ventricle whose compliance S4 S4
gallop
is impaired.
Early diastolic sounds are sometimes caused by atrial myxomas (see A
Chap. 63).67 The generation of such a sound, called a tumor “plop,”
requires a mobile myxoma attached to the atrial septum by a long stalk.
The “plop”is believed to result from abrupt diastolic seating of the tumor
within the right or left AV orifice.67 S3 S1 S2 S1 S2
An early diastolic sound can also be generated by the opening move- Ventricular
ment of a mechanical prosthesis in the mitral position. This opening gallop S3 S3
sound is especially prominent with a ball-in-cage prosthesis (Starr-
Edwards) and less prominent with a tilting disc prosthesis (Bjork-Shiley).
B
Mid-diastolic and Late Diastolic (Presystolic)
Sounds (Fig. 8–16) S1 S2 S1 S2
Pericardial
Mid-diastolic sounds are, for all practical purposes, either knock (K)
normal or abnormal S3 sounds, and most, if not all, late dias-
K K
tolic or presystolic sounds are S4 sounds. Each sound coin-
cides with its relevant diastolic filling phase.68 In sinus C
rhythm, the ventricles receive blood during two filling
phases. The first phase occurs when ventricular pressure
drops sufficiently to allow the AV valve to open; blood then
S1 S2 S1 S2
flows from atrium into ventricle. This flow is designated the Quadruple
“rapid filling phase,” accounting for about 80 percent of rhythm
normal ventricular filling. The rapid filling phase is not S4 S3 S4 S3
a passive event in which the recipient ventricle merely
expands in response to augmented inflow volume. Rather, D
ventricular relaxation is an active, complex, energy-
dependent process (see Chaps. 19 and 20).
S3 is generated during the rapid filling phase.69 The second S1 S2 S1 S2
filling phase—diastasis—is variable in duration, usually Incomplete
accounting for less than 5 percent of ventricular filling. The summation
third phase of diastolic filling is in response to atrial con- gallop S4 S3 S4 S3
traction, which accounts for about 15 percent of normal ven-
tricular filling. S4 is generated during the atrial filling phase. E
Both S3 and S4 occur within the recipient ventricle as that
chamber receives blood. The addition of either an S3 or an S4
to the cardiac cycle produces a triple rhythm. If both S3 and S1 S2 S1 S2
S4 are present, a quadruple rhythm is produced. When dias- Summation
gallop (SG)
tole is short or the PR interval is long, S3 and S4 occur simul-
taneously to form a summation sound.4 SG
Children and young adults often have a normal (physiological) S3 but F
do not have a normal S4.A normal S3 sometimes persists beyond the age FIGURE 8–16 Diastolic filling sounds. A, the fourth heart sound (S4) occurs in
of 40 years, especially in women. After that age, however, especially in presystole and is frequently called an atrial or presystolic gallop. B, The third heart
men, S3 is likely to be abnormal.An S4 is sometimes heard in healthy older sound (S3) occurs during the rapid phase of ventricular filling. It is a normal finding that
adults without clinical evidence of heart disease, particularly after exer- is commonly heard in children and young adults but disappears with increasing age.
cise.4 Such observations have led to the conclusion, still debated, that When it is heard in a patient with cardiac disease, it is called a pathologic S3 or ven-
such an S4 may be normal in the elderly. tricular gallop and usually indicates ventricular dysfunction or atrioventricular valvular
ATRIAL CONTRIBUTION TO FILLING. Because an S4 requires active incompetence. C, In constrictive pericarditis, a sound in early diastole, the pericardial
atrial contribution to ventricular filling, the sound disappears when coor- knock (K) is heard earlier and is louder and higher pitched than the usual pathologic S3.
dinated atrial contraction ceases, as in atrial fibrillation. When the atria D, A quadruple rhythm results if both S4 and S3 are present. E, At faster heart rates, S3
and ventricles contract independently as in complete heart block, an S4 and S4 occur in rapid succession and may give the illusion of a mid-diastolic rumble.
or summation sound occurs randomly in diastole because the relation- F, When the heart rate is sufficiently rapid, the two rapid phases of ventricular filling
ship between the P wave and the QRS of the electrocardiogram is reinforce each other, and a loud summation gallop (SG) may appear; this sound may be
random. S3 and S4 are events caused by rapid ventricular filling, so louder than either S3 or S4 alone. S1 = first heart sound; S2 = second heart sound. (From
obstruction of an AV valve, by impeding ventricular inflow, removes Braunwald E: The clinical examination. In Braunwald E, Goldman L [eds]: Primary Car-
one of the prime preconditions for the generation of these filling sounds. diology. 2nd ed. Philadelphia, Elsevier, 2003, pp 29-46; and Shaver JA: Examination of
Accordingly, the presence of an S3 or S4 implies an unobstructed (or the Heart. Part 4: Auscultation. Dallas, American Heart Association, 1990.) Z
 Ch08.qxd 3/26/04 07:00 PM Page 18

8-18 either the left or right ventricle, and that are best elicited when the bell TABLE 8–5 Principal Causes of Heart Murmurs
of the stethoscope is applied with just enough pressure to provide a
skin seal. An S3 or S4 originating from the left ventricle should be A. Organic Systolic Murmurs
sought over the left ventricular impulse identified with the patient in the 1. Midsystolic (ejection)
left lateral decubitus position.An S3 or S4 originating from the right ven- a. Aortic
tricle should be sought over the right ventricular impulse (lower left (1) Obstructive
sternal edge, occasionally subxiphoid) with the patient supine.An under- (a) Supravalvular—supraaortic stenosis, coarction
standing of these simple principles sets the stage for bedside detection. of the aorta
The same principles can be used to advantage to distinguish an S4 pre- (b) Valvular—aortic stenosis and sclerosis
ceding a single S1 from splitting of the two components of the S1 (see (c) Infravalvular—HOCM
Fig. 8–9C). The two components of S1 are similar in frequency (pitch) (2) Increased flow, hyperkinetic states, aortic
CH 8 although not in intensity (loudness) but differ in pitch from a preceding regurgitation, complete heart block
S4. Selective pressure with the bell of the stethoscope enhances these (3) Dilatation of ascending aorta, atheroma, aortitis,
distinctions. aneurysm of aorta
AUDIBILITY OF S3. This is improved by isotonic exercise that aug- b. Pulmonary
ments venous return and mid-diastolic AV flow. A few sit-ups usually (1) Obstructive
suffice to produce the desired increase in venous return and accelera- (a) Supravalvular—pulmonary arterial stenosis
tion in heart rate that increase the rate and volume of AV flow. Venous (b) Valvular—pulmonic valve stenosis
return can be increased by simple passive raising of both legs with the (c) Infravalvular—infundibular stenosis
patient supine. The heart rate is also transiently increased by vigorous (2) Increase flow, hyperkinetic states, left-to-right shunt
coughing. Left ventricular S4, especially in patients with ischemic heart (e.g., ASD, VSD)
disease, can be induced or augmented when resistance to left ventricu- (3) Dilatation of pulmonary artery
lar discharge is increased by sustained hand-grip (isometric exercise; see 2. Pansystolic (regurgitant)
later). a. Atrioventricular valve regurgitation (MR, TR)
In the presence of sinus tachycardia, atrial contraction may coincide b. Left-to-right shunt to ventricular level
with the rapid filling phase, making it impossible to determine whether
a given filling sound is an S3, an S4, or a summation sound. Carotid sinus B. Early Diastolic Murmurs
massage transiently slows the heart rate, so the diastolic sound or sounds 1. Aortic regurgitation
can be assigned their proper timing in the cardiac cycle.4 a. Valvular: rheumatic deformity; perforation
CAUSES OF S3 AND S4. The normal S3 is believed to be caused by postendocarditis, posttraumatic, postvalvulotomy
sudden limitation of longitudinal expansion of the left ventricular wall b. Dilatation of valve ring: aorta dissection, annulectasia,
during brisk early diastolic filling.70-73 The majority of abnormal S3 sounds cystic medial necrosis, hypertension
are generated by altered physical properties of the recipient ventricle c. Widening of commissures: syphilis
and/or an increase in the rate and volume of AV flow during the rapid d. Congenital: biscuspid valve, with VSD
filling phase of the ventricle. An abnormal S4 occurs when augmented 2. Pulmonic regurgitation
atrial contraction generates presystolic ventricular distention (an a. Valvular: postvalvulotomy, endocarditis, rheumatic
increase in end-diastolic segment length) so that the recipient chamber fever, carcinoid
can contract with greater force.74-76 Typical substrates are the left ven- b. Dilatation of valve ring: pulmonary hypertension;
tricular hypertrophy of aortic stenosis or systemic hypertension or the Marfan syndrome
right ventricular hypertrophy of pulmonary stenosis or pulmonary c. Congenital: isolated or associated with tetralogy of
hypertension in the right side of the heart.74 S4 sounds are also common Fallot, VSD, pulmonic stenosis
in ischemic heart disease and are almost universal during angina pectoris C. Mid-Diastolic Murmurs
or acute myocardial infarction. 1. Mitral stenosis
2. Carey-Coombs murmur (mid-diastolic apical murmur in
acute rheumatic fever)
Heart Murmurs 3. Increased flow across nonstenotic mitral valve (e.g., MR,
VSD, PDA, high-output states, and complete heart block)
A cardiovascular murmur is a series of auditory vibrations 4. Tricuspid stenosis
5. Increased flow across nonstenotic tricuspid valve (e.g.,
that are more prolonged than a sound and are characterized TR, ASD, and anomalous pulmonary venous return)
according to timing in the cardiac cycle, intensity (loudness), 6. Left and right atrial tumors
frequency (pitch), configuration (shape), quality, duration,
and direction of radiation.4,50,77 When these features are estab- D. Continuous Murmurs
lished, the stage is set for diagnostic conclusions.2,76,78 The 1. PDA
principal causes of heart murmurs are listed in Table 8–5. 2. Coronary arteriovenous fistula
3. Ruptured aneurysm of sinus of Valsalva
Intensity or loudness is graded from 1 to 6, based on the 4. Aortic septal defect
original recommendations of Samuel A. Levine in 1933. A 5. Cervical venous hum
grade 1 murmur is so faint that it is heard only with special 6. Anomalous left coronary artery
effort. A grade 2 murmur is soft but readily detected; a grade 7. Proximal coronary artery stenosis
3 murmur is prominent but not loud; a grade 4 murmur is 8. Mammary souffle
loud (and usually accompanied by a thrill); a grade 5 murmur 9. Pulmonary artery branch stenosis
is very loud. A grade 6 murmur is loud enough to be heard 10. Bronchial collateral circulation
with the stethoscope just removed from contact with the 11. Small (restrictive) ASD with mitral stenosis
chest wall. The factors affecting the loudness of heart 12. Intercostal arteriovenous fistula
murmurs are listed in Table 8–6. Frequency or pitch varies A and C, Modified from Oram S (ed): Clinical Heart Disease. London,
from high to low. The configuration or shape of a murmur is Heinemann, 1981. D, Modified from Fowler NO (ed): Cardiac Diagnosis and
best characterized as crescendo, decrescendo, crescendo- Treatment. Hagerstown, MD, Harper & Row, 1980.
ASD = atrial septal defect; HOCM = hypertrophic obstructive cardiomyopathy;
decrescendo (diamond-shaped), plateau (even), or variable MR = mitral regurgitation; PDA = patent ductus arteriosus; TR = tricuspid
(uneven). The duration of a murmur varies from short to long, regurgitation; VSD = ventricular septal defect.
with all gradations in between. A loud murmur radiates from From Norton PJ, O’Rourke RA: Approach to the patient with a heart murmur.
its site of maximal intensity, and the direction of radiation is In Braunwald E, Goldman L, (eds): Primary Cardiology. 2nd ed. Philadel-
phia, Elsevier, 2003, pp 151–168.
sometimes diagnostically useful.
There are three broad categories of murmurs: systolic,
diastolic, and continuous. A systolic murmur begins with
Z or after S1 and ends at or before S2 on its side of origin. A
Ch08.qxd 3/26/04 07:00 PM Page 19

TABLE 8–6 Factors Affecting the Loudness of Heart component of S2. Accordingly, midsystolic murmurs origi- 8-19
Murmurs nating in the left side of the heart end before A2; midsystolic
murmurs originating in the right side of the heart end before
Increased intensity P2. A holosystolic murmur begins with S1, occupies all of
High cardiac output (hyperdynamic) states systole, and ends with the S2 on its side of origin. Holosys-
Thin chest wall tolic murmurs originating in the left side of the heart end with
Narrow thoracic diameter; for example, “straight back,” pectus
excavatum
A2, and holosystolic murmurs originating in the right side of
Anemia (decreased blood viscosity) the heart end with P2.
Tortuous aorta (close to chest wall) The term regurgitant systolic murmur, originally applied
to murmurs that occupied all of systole, has fallen out of use
Decreased intensity because “regurgitation” can be accompanied by holosystolic, CH 8
Obesity midsystolic, early systolic, or late systolic murmurs.2 Simi-
Muscular or thick chest wall
larly, the term ejection systolic murmur, originally applied to

Physical Examination of the Heart and Circulation

Obstructive lung disease
Barrel chest (increased anteroposterior diameter) midsystolic murmurs, should be discarded, because midsys-
Pericardial thickening or fluid tolic murmurs are not necessarily due to “ejection.”4
Decreased cardiac output (congestive heart failure, low ejection MIDSYSTOLIC MURMURS. Midsystolic murmurs occur
fraction) in five settings: (1) obstruction to ventricular outflow, (2)
dilatation of the aortic root or pulmonary trunk, (3) acceler-
From Abrams J: Synopsis of Cardiac Physical Diagnosis. 2nd ed. Boston,
Butterworth Heinemann, 2001, p 115. ated systolic flow into the aorta or pulmonary trunk, (4) inno-
cent (normal) midsystolic murmurs,55 and (5) some forms of
mitral regurgitation. The physiological mechanism of outflow
midsystolic murmurs reflects the pattern of phasic flow
diastolic murmur begins with or after S2 and ends before the
across the left or right ventricular outflow tract as originally
subsequent S1. A continuous murmur begins in systole and
described by Leatham (Fig. 8–18).58 Isovolumetric contraction
continues without interruption through the S2 into all or part
generates S1. Ventricular pressure rises, the semilunar valve
of diastole. The following classification of murmurs is based
opens, flow commences, and the murmur begins. As flow pro-
on their timing relative to S1 and S2.
ceeds, the murmur increases in crescendo; as flow decreases,
the murmur decreases in decrescendo. The murmur ends
Systolic Murmurs before ventricular pressure drops below the pressure in the
central great artery, at which time the aortic and pulmonary
Systolic murmurs are classified according to their time of
valves close, generating A2 and P2.
onset and termination as midsystolic, holosystolic, early sys-
tolic, or late systolic (Fig. 8–17).77,79,80 A midsystolic murmur AORTIC VALVE STENOSIS (See Chap. 57). This is associated with a
begins after S1 and ends perceptibly before S2. The termina- midsystolic murmur, which may have an early systolic peak and a short
tion of a systolic murmur must be related to the relevant duration, a relatively late peak and a prolonged duration, or all gradations
in between.Whether long or short, however, the murmur retains a sym-
metrical diamond shape beginning after S1 (or with an aortic ejection
sound), rising in crescendo to a systolic peak, and declining in
Systolic Murmurs decrescendo to end before A2.The high-velocity jet within the aortic root
results in radiation of the murmur upward, to the right (second right
Midsystolic intercostal space), and into the neck. An important variation occurs in
older adults with previously normal trileaflet aortic valves rendered scle-
Left sided Right sided rotic or stenotic by fibrocalcific changes.The accompanying murmur in
the second right intercostal space is harsh, noisy, and impure (see Fig.

S1 A2 S1 A2 P2
Holosystolic
Left sided Right sided

GA
S1 A2 S1 A2 P2

Early systolic

S1 S2 V
Late systolic

S1 S2 S1 S2

FIGURE 8–17 Systolic murmurs as illustrated here are descriptively classified FIGURE 8–18 Illustration of the physiological mechanism of a midsystolic murmur
according to their time of onset and termination as midsystolic, holosystolic, early sys- generated by phasic flow into aortic root or pulmonary trunk. Ventricular (V) and great
tolic, and late systolic. The termination of the murmur must be related to the compo- arterial (GA) pressure pulses are shown with phonocardiogram. The midsystolic murmur
nent of the second heart sound on its side of origin, that is, the aortic component (A2) begins after the first heart sound (S1), rises in crescendo to a peak as flow proceeds,
for systolic murmurs originating in the left side of the heart and the pulmonic compo- then declines in decrescendo as flow diminishes, ending just before the second heart
nent (P2) for systolic murmurs originating in the right side of the heart. sound (S2) as ventricular pressure falls below the pressure in the great artery. Z
 Ch08.qxd 3/26/04 07:00 PM Page 20

8-20 8–10), whereas the murmur over the left ventricular impulse is pure and INNOCENT (NORMAL) MURMURS. These are, except for the sys-
often musical. tolic mammary souffle, all midsystolic.53 The normal vibratory midsystolic
The high-frequency apical midsystolic murmur of aortic sclerosis or murmur (Still murmur) is short, buzzing, pure, and medium in frequency
stenosis should be distinguished from the high-frequency apical murmur (Fig. 8–20) and is believed to be generated by low-frequency periodic
of mitral regurgitation, a distinction that may be difficult or impossible, vibrations of normal pulmonary leaflets at their attachments or periodic
especially if A2 is soft or absent. However, when premature ventricular vibrations of a left ventricular false tendon.81,82 A second type of inno-
contractions are followed by pauses longer than the dominant cycle cent midsystolic murmur occurs in children, adolescents, and young
length, the apical midsystolic murmur of aortic stenosis or sclerosis adults and represents an exaggeration of normal ejection vibrations
increases in intensity in the beat after the premature contraction, within the pulmonary trunk.This normal pulmonary midsystolic murmur
whereas the intensity of the murmur of mitral regurgitation (whether is relatively impure and is best heard in the second left intercostal space,
midsystolic or holosystolic) remains relatively unchanged.The same pat- in contrast to the vibratory midsystolic murmur of Still, which is typically
CH 8 terns hold after longer cycle lengths in atrial fibrillation. heard between the lower left sternal edge and apex. Normal pulmonary
PULMONARY VALVE STENOSIS (See Chap. 56). This is prototypical midsystolic murmurs are also heard in patients with diminished antero-
of a midsystolic murmur originating in the right side of the heart.55 The posterior chest dimensions (e.g., loss of thoracic kyphosis).
murmur begins after S1 or with a pulmonary ejection sound, rises in The most common form of “innocent” midsystolic murmur in older
crescendo to a peak, then decreases in a slower decrescendo to end adults has been designated the “aortic sclerotic” murmur (see earlier).
before a delayed or soft P2.The length and configuration of the murmur The cause of this functionally benign murmur is fibrous or fibrocalcific
are useful signs of the severity of obstruction.55 When the ventricular thickening of the bases of otherwise normal aortic cusps as they insert
septum is intact (Fig. 8–19, left), as obstruction becomes more severe, into the sinuses of Valsalva.55 As long as the fibrous or fibrocalcific thick-
the murmur lengthens and envelops A2, and P2 becomes softer. When ening is confined to the base of the leaflets, the free edges remain mobile.
obstruction to right ventricular outflow is accompanied by a ventricular No commissural fusion and no obstruction occur. The Gallavardin
septal defect (tetralogy of Fallot), the midsystolic murmur becomes dissociation phenomenon associated with such an aortic valve was
shorter with increased severity of obstruction (see Fig. 8–19, right). described earlier.
ACCELERATED FLOW. Short, soft midsystolic murmurs originate MIDSYSTOLIC MURMUR OF MITRAL REGURGITATION. The clin-
within a dilated aortic root or dilated pulmonary trunk. Midsystolic ical setting is usually ischemic heart disease associated with left ventric-
murmurs are also generated by rapid ejection into a normal aortic root ular regional wall motion abnormalities. The physiological mechanism
or pulmonary trunk,as during pregnancy,fever,thyrotoxicosis,or anemia. responsible for the midsystolic murmur of mitral regurgitation in this
The pulmonary midsystolic murmur of ostium secundum atrial septal setting reflects impaired integrity of the muscular component of the
defect results from rapid ejection into a dilated pulmonary trunk (see mitral apparatus, with early systolic competence of the valve, and midsys-
Fig. 8–17). tolic incompetence, followed by a late systolic decline in regurgitant
flow.These midsystolic murmurs are unrelated to “ejection.”

Pulmonic Stenosis Tetralogy of Fallot HOLOSYSTOLIC MURMURS. Just as the

term midsystolic is preferable to ejection sys-
S1 S2 S1 S2 tolic, the term holosystolic is preferable to regur-
gitant because holosystolic murmurs are not
necessarily due to regurgitant flow. A holosys-
Mild

tolic murmur begins with S1 and occupies all of

systole up to the S2 on its side of origin (see Figs.
A2 P2 A2 P2 8–17 and 8–21).4,50 Such murmurs are generated
P.Ej
by flow from a vascular bed whose pressure or
S1 S2 S1 S2
resistance throughout systole is higher than the
pressure or resistance in the vascular bed receiv-
Moderate

ing the flow. Holosystolic murmurs occur in the

left side of the heart with mitral regurgitation,
in the right side of the heart with high-pressure
A2 P2 A2 tricuspid regurgitation, between the ventricles
P.Ej through a restrictive ventricular septal defect,
S1 S2 S1 S and between the great arteries through aorto-
pulmonary connections.
Severe

The timing of holosystolic murmurs reflects

the physiological and anatomical mechanisms
S4 responsible for their genesis. Figure 8–21 illus-
A2 P2 A.Ej A2 trates the mechanism of the holosystolic murmur
of mitral regurgitation or high-pressure tricuspid
P.Ej=Pulmonary Ejection A.Ej=Aortic Ejection regurgitation. Ventricular pressure exceeds atrial
(Valvular) (Root) pressure at the very onset of systole (isovolu-
metric contraction), so regurgitant flow begins
FIGURE 8–19 Left, In cases of valvular pulmonic stenosis with intact ventricular septum, right ven- with the S1. The murmur persists up to or
tricular systolic ejection becomes progressively longer, with increasing obstruction to flow. As a result, slightly beyond the relevant component of the
the murmur becomes louder and longer, enveloping the aortic component of the second heart sound (A2). S2, provided that ventricular pressure at end
The pulmonic component (P2) occurs later, and splitting becomes wider but more difficult to hear because
A2 is lost in the murmur and P2 becomes progressively fainter and lower pitched. As pulmonic diastolic
systole exceeds atrial pressure and provided that
pressure progressively decreases, isometric contraction shortens until the pulmonary valvular ejection the AV valve remains incompetent.
sound fuses with the first heart sound (S1). In cases of severe pulmonic stenosis with concentric hyper-
trophy and decreasing right ventricular compliance, a fourth heart sound appears. Right, In cases of tetral- Direction of radiation of the intraatrial jet of mitral
ogy of Fallot with increasing obstruction at the pulmonic infundibular area, an increasing amount of right regurgitation determines the chest wall distribution of
ventricular blood is shunted across the silent ventricular septal defect, and flow across the obstructed the murmur.83 When the direction of the intraatrial jet is
outflow tract decreases. Therefore, with increasing obstruction the murmur becomes shorter, earlier, and forward and medial against the atrial septum near the
fainter. P2 is absent in patients with severe tetralogy of Fallot. A large aortic root receives almost all origin of the aorta, the murmur radiates to the left sternal
cardiac output from both ventricular chambers, and the aorta dilates and is accompanied by a root ejec- edge, to the base, and even into the neck.When the flow
tion sound that does not vary with respiration. (From Shaver JA, Leonard JJ, Leon DF: Examination of the generating the murmur of mitral regurgitation is directed
Heart. Part IV: Auscultation of the Heart. Dallas, American Heart Association, 1990, p 45. Copyright 1990, posterolaterally within the left atrial cavity, the murmur
Z American Heart Association.) radiates to the axilla, to the angle of the left scapula, and
Ch08.qxd 3/26/04 07:00 PM Page 21

8-21

LV

LA
FIGURE 8–20 Four vibratory midsystolic murmurs (SM) from healthy children.
These murmurs, designated Still murmur, are pure, medium frequency, relatively brief
in duration, and maximal along the lower left sternal border (LSB). The last of the four CH 8
murmurs was from a 5-year-old girl who was febrile. After defervescence, the murmur
decreased in loudness and duration.

Physical Examination of the Heart and Circulation

GA SM
B
FIGURE 8–22 A, Phonocardiogram recorded from the cardiac apex of a patient
with acute severe mitral regurgitation due to ruptured chordae tendineae. There is an
early systolic decrescendo murmur (SM) diminishing if not ending before the aortic com-
VENT ponent (A2) of the second heart sound. B, Left ventricular (LV) and left atrial (LA) pres-
sure pulses with schematic illustration of the phonocardiogram showing the relationship
between the decrescendo configuration of the early systolic murmur and late systolic
approximation of the tall left atrial v wave and left ventricular end-systolic pressure.
V Regurgitant flow diminishes or ceases. The murmur therefore is early systolic and
decrescendo, paralleling the hemodynamic pattern of regurgitation. P2 = pulmonic com-
Atrium ponent of the second heart sound; S1 = first heart sound; S3 = third heart sound.

8–17). Certain types of mitral regurgitation, tricuspid regur-

gitation, or ventricular septal defects are the substrates.
S1 S2 Acute severe mitral regurgitation is accompanied by an
early systolic murmur or a holosystolic murmur that is
FIGURE 8–21 Illustration of great arterial (GA), ventricular (VENT), and atrial pres- decrescendo, diminishing if not ending before S2 (Fig.
sure pulses with phonocardiogram showing the physiological mechanism of a holosys- 8–22A).84 The physiological mechanism responsible for this
tolic murmur in some forms of mitral regurgitation and in high-pressure tricuspid early systolic decrescendo murmur is acute severe regurgita-
regurgitation. Ventricular pressure exceeds atrial pressure at the very onset of systole, tion into a relatively normal-sized left atrium with limited
so regurgitant flow and murmur commence with the first heart sound (S1). The murmur distensibility. A steep rise in left atrial V wave approaches
persists up to or slightly beyond the second heart sound (S2) because regurgitation per- the left ventricular pressure at end systole; a late systolic
sists to the end of systole (ventricular pressure still exceeds atrial pressure). V = atrial decline in left ventricular pressure favors this tendency (see
v wave.
Fig. 8–22B). The stage is set for regurgitant flow that is
maximal in early systole and minimal in late systole. The sys-
tolic murmur parallels this pattern, declining or vanishing
before S2.
occasionally to the vertebral column, with bone conduction from the cer-
vical to the lumbar spine. An early systolic murmur is a feature of tricuspid regurgitation with
The murmur of tricuspid regurgitation is holosystolic when there normal right ventricular systolic pressure.85 An example is tricuspid
is a substantial elevation of right ventricular systolic pressure, as schemat- regurgitation caused by infective endocarditis in drug abusers.The mech-
ically illustrated in Figure 8–21.A distinctive and diagnostically important anisms responsible for the timing and configuration of the early systolic
feature of the tricuspid murmur is its selective inspiratory increase in murmur of low-pressure tricuspid regurgitation are analogous to those
loudness—Carvallo sign. The tricuspid murmur is occasionally audible just described for mitral regurgitation. The crest of the right atrial V
only during inspiration. The increase in intensity occurs because the wave reaches the level of normal right ventricular pressure in later
inspiratory augmentation in right ventricular volume is converted into systole; the regurgitation and murmur are therefore chiefly, if not exclu-
an increase in stroke volume and in the velocity of regurgitant flow. sively, early systolic. These murmurs are of medium frequency because
When the right ventricle fails, this capacity is lost; thus, Carvallo sign normal right ventricular systolic pressure generates comparatively low
vanishes. velocity regurgitant flow, in contrast to elevated right ventricular systolic
The murmur of an uncomplicated restrictive ventricular septal defect pressure, which generates a high-frequency holosystolic murmur (see
(see Chap. 56) is holosystolic because left ventricular systolic pressure earlier).
and systemic resistance exceed right ventricular systolic pressure and Early systolic murmurs also occur through ventricular septal defects,
pulmonary resistance from the onset to the end of systole. Holosystolic but under two widely divergent anatomical and physiological circum-
murmurs are perceived as such in patients with large aortopulmonary stances. A soft, pure, high-frequency, early systolic murmur localized to
connections (aortopulmonary window, patent ductus arteriosus) when the middle or lower left sternal edge is typical of a very small ventricu-
a rise in pulmonary vascular resistance abolishes the diastolic portion lar septal defect in which the shunt is confined to early systole.55 A
of the continuous murmur, leaving a murmur that is holosystolic or murmur of similar timing and configuration occurs through a nonre-
nearly so.55 strictive ventricular septal defect when an elevation in pulmonary vas-
cular resistance decreases or abolishes late systolic shunting.
EARLY SYSTOLIC MURMURS. Murmurs confined to
early systole begin with S1, diminish in decrescendo, and end LATE SYSTOLIC MURMURS. The term late systolic
well before S2, generally at or before midsystole (see Fig. applies when a murmur begins in middle to late systole and Z
 Ch08.qxd 3/26/04 07:00 PM Page 22

8-22 proceeds up to the S2 (see Fig. 8–17). The late systolic murmur appreciably exceeds left ventricular diastolic pressure, so the
of mitral valve prolapse is prototypical (see Fig. 8–12).86 One decrescendo is subtle and the murmur is well heard through-
or more middle to late systolic clicks often introduce the out diastole. In cases of chronic severe aortic regurgitation,
murmur. The responses of the late systolic murmur and clicks the decrescendo is more obvious, paralleling the dramatic
to postural maneuvers are illustrated in Figure 8–12. decline in aortic root diastolic pressure. Selective radiation
of the murmur of aortic regurgitation to the right sternal edge
The late systolic murmur of mitral valve prolapse is occasionally implies aortic root dilatation, as in patients with Marfan syn-
replaced by an intermittent, striking, and sometimes disconcerting sys- drome. When an inverted cusp is set into high-frequency
tolic “whoop” or “honk,” either spontaneously or in response to physical periodic vibration by aortic regurgitation, the accompanying
maneuvers.The whoop is of high frequency, musical, widely transmitted,
and occasionally loud enough to be disturbing to the patient.The musical
murmur is musical, early diastolic, and decrescendo (see Fig.
CH 8 whoop is thought to arise from mitral leaflets and chordae tendineae set 8–24B).
into high-frequency periodic vibration.
SYSTOLIC ARTERIAL MURMURS. Systolic murmurs can originate ACUTE AORTIC REGURGITATION. The diastolic murmur of acute
in anatomically normal arteries in the presence of normal or increased severe aortic regurgitation differs importantly from the murmur of
flow or in abnormal arteries because of tortuosity or luminal narrowing. chronic severe aortic regurgitation as just described (Fig. 8–25). When
Detection of systolic arterial murmurs requires auscultation at non- regurgitant flow is both sudden and severe (as may occur in cases of
precordial sites. infective endocarditis or aortic dissection), the diastolic murmur is rela-
The supraclavicular systolic murmur, often heard in children and tively short because the aortic diastolic pressure rapidly equilibrates with
adolescents, is believed to originate at the aortic origins of normal major the steeply rising diastolic pressure in the unprepared, nondilated left
brachiocephalic arteries.55 The configuration of these murmurs is ventricle; the pitch of the murmur is likely to be medium and it may
crescendo-decrescendo, the onset is abrupt, the duration is brief, and the be quite soft (grade 2). These auscultatory features are in contrast to
intensity at times is surprisingly loud, with radiation below the clavicles. the long, pure, high-frequency, blowing and often loud (grade 4) early
Normal supraclavicular systolic murmurs decrease or vanish in response diastolic murmur of chronic severe aortic regurgitation (see Figs. 8–24
to hyperextension of the shoulders, which is achieved by bringing the and 8–25).
elbows back until the shoulder girdle muscles are drawn taut. Pulmonary Regurgitation. The Graham Steell murmur of pul-
In older adults, the most common cause of a systolic arterial murmur monary hypertensive pulmonary regurgitation begins with a loud P2
is atherosclerotic narrowing of a carotid, subclavian, or iliofemoral artery. because the elevated pressure exerted on the incompetent pulmonary
A variation on this theme is the “compression artifact” that can be valve begins at the moment that right ventricular pressure drops below
induced in the femoral artery in the presence of free aortic regurgita- the pulmonary arterial incisura. The high diastolic pressure generates
tion. When the femoral artery is moderately compressed by the exam- high-velocity regurgitant flow and results in a high-frequency blowing
iner’s stethoscopic bell, a systolic arterial murmur is generated. Further murmur that may last throughout diastole. Because of the persistent and
compression causes the systolic murmur to continue into diastole, a sign appreciable difference between pulmonary arterial and right ventricular
described in 1861 by Duroziez.55 The eponym is still in use. diastolic pressures, the amplitude of the murmur is usually relatively
A systolic “mammary souffle” is sometimes heard over the breasts uniform throughout most, if not all, of diastole.
because of increased flow through normal arteries during late pregnancy
or more especially in the postpartum period in lactating women.55 The Mid-Diastolic Murmurs
murmur begins well after S1 because of the interval between left ven-
tricular ejection and the arrival of flow at the artery of origin. By definition, mid-diastolic murmurs begin at a clear inter-
A systolic arterial murmur is present in the interscapular region over val after S2 (Figs. 8–23 and 8–26). The majority of mid-
the site of coarctation of the aortic isthmus.55 Transient systolic arterial diastolic murmurs originate across mitral or tricuspid valves
murmurs originating in the pulmonary artery and its branches are occa- during the rapid filling phase of the cardiac cycle (AV valve
sionally heard in normal neonates because the angulation and disparity obstruction or abnormal patterns of AV flow) or across an
in size between the pulmonary trunk and its branches set the stage for incompetent pulmonary valve in the absence of pulmonary
turbulent systolic flow. These normal or innocent pulmonary arterial hypertension.
systolic murmurs disappear with maturation of the pulmonary bed,
generally within the first few weeks or months of life.55 Similar if not
identical pulmonary arterial systolic murmurs are generated at sites of
congenital stenosis of the pulmonary artery and its branches. Rarely, a
pulmonary arterial systolic murmur is caused by luminal narrowing after
a pulmonary embolus.74 Diastolic Murmurs

Early diastolic

Diastolic Murmurs Left sided Right sided

Diastolic murmurs, like systolic murmurs, are classified
according to their time of onset as early diastolic, mid-dias- S1 A2 S1 A2P2
tolic, or late diastolic (presystolic) (Fig. 8–23). An early dias-
tolic murmur begins with A2 or P2, depending on its side of
Mid-diastolic
origin. A mid-diastolic murmur begins at a clear interval after
S2. A late diastolic or presystolic murmur begins immediately
before S1.
S1 S2
Early Diastolic Murmurs
CHRONIC AORTIC REGURGITATION. An early dias- Late diastolic (presystolic)
tolic murmur originating in the left side of the heart occurs
in cases of aortic regurgitation (see Chap. 57). This murmur Left sided Right sided
is heard best with the diaphragm of the stethoscope, with the
patient leaning forward and during a held, deep exhalation
(see Fig. 8–7D). The murmur begins with the aortic compo- S1 S2 S1 S1 S2
nent of S2 (Fig. 8–24A), that is, as soon as left ventricular pres-
sure falls below the aortic incisura. The configuration of the
murmur tends to reflect the volume and rate of regurgitant FIGURE 8–23 Diastolic murmurs are descriptively classified according to their
flow. In cases of chronic aortic regurgitation of moderate time of onset as early diastolic, mid-diastolic, or late diastolic (presystolic). Diastolic
Z severity, the aortic diastolic pressure consistently and murmurs originate in either the left or the right side of the heart.
Ch08.qxd 3/26/04 07:00 PM Page 23

in two important respects: (1) the loudness of the tricuspid 8-23

murmur increases with inspiration, and (2) the tricuspid
murmur is confined to a relatively localized area along the
left lower sternal edge. The inspiratory increase in loudness
occurs because inspiration is accompanied by an augmenta-
tion in right ventricular volume, by a fall in right ventricular
diastolic pressure, and by an increase in gradient and flow
rate across the stenotic tricuspid valve.4 The murmur is local-
ized to the lower left sternal edge because it originates within
the inflow portion of the right ventricle and is transmitted to
the overlying chest wall. CH 8
Mid-diastolic murmurs across unobstructed AV valves occur in the

Physical Examination of the Heart and Circulation

presence of augmented volume and velocity of flow. Examples in the left
side of the heart are the mid-diastolic flow murmur of pure mitral regur-
gitation and the mid-diastolic mitral flow murmur that accompanies a
large left-to-right shunt through a ventricular septal defect (Fig. 8–27A).
Mid-diastolic murmurs due to augmented flow across unobstructed tri-
cuspid valves are generated by severe tricuspid regurgitation or by a large
left-to-right shunt through an atrial septal defect (see Fig. 8–27B).These
mid-diastolic murmurs indicate appreciable AV valve incompetence or
large left-to-right shunts and are often preceded by an S3, especially in
the presence of mitral or tricuspid regurgitation.
Short, mid-diastolic AV flow murmurs occur intermittently in patients
with complete heart block when atrial contraction coincides with the
phase of rapid diastolic filling. These murmurs are believed to result
from antegrade flow across AV valves that are closing rapidly during filling
of the recipient ventricle.A similar mechanism is believed to be respon-
sible for the Austin Flint murmur (see Fig. 8–25).88,89
A mid-diastolic murmur is a feature of pulmonary valve regurgitation,
provided that the pulmonary arterial pressure is not elevated. The
diastolic murmur typically begins at a perceptible interval after P2 is
crescendo-decrescendo, and ends well before the subsequent S1.55 The
diastolic pressure exerted on the incompetent pulmonary valve is negli-
gible at the inception of P2, so regurgitant flow is minimal. Regurgitation
FIGURE 8–24 A, Phonocardiogram recorded from the mid-left sternal edge of a accelerates as right ventricular pressure dips below the diastolic pres-
patient with chronic pure severe aortic regurgitation. An early diastolic murmur (EDM) sure in the pulmonary trunk; at that point, the murmur reaches its
proceeds immediately from the aortic component of the second heart sound (A2). The maximum intensity. Late diastolic equilibration of pulmonary arterial and
murmur has an early crescendo followed by a late long decrescendo. There is a promi- right ventricular pressures eliminates regurgitant flow and abolishes the
nent midsystolic flow murmur (SM) across an unobstructed aortic valve. B, Phonocar- murmur before the next S1.
diogram in the third left intercostal space (3 LICS) records a high-frequency, musical,
early diastolic decrescendo murmur (EDM) caused by eversion of an aortic cusp. S1 = Late Diastolic or Presystolic Murmurs
first heart sound; SM = midsystolic murmur.
A late diastolic murmur occurs immediately before S1, that
is, in presystole (see Fig. 8–23). With few exceptions, the late

The mid-diastolic murmur of rheumatic

mitral stenosis is a prime example.87 The Aortic Regurgitation
murmur characteristically follows the mitral Chronic Acute
opening snap (see Fig. 8–11B). Because the
murmur originates within the left ventricular SEM SEM
cavity, transmission to the chest wall is
Base

maximal over the left ventricular impulse.

Care must be taken to place the bell of the
stethoscope lightly against the skin precisely
over the left ventricular impulse with the S1 S2 S1 S1 S2 S1
patient turned into the left lateral decubitus
position (see Fig. 8–7C). Soft mid-diastolic S3 S3
murmurs are reinforced when the heart rate
Apex

and mitral valve flow are transiently

increased by vigorous voluntary coughs or a AF AF
few sit-ups. In patients with atrial fibrillation,
the duration of the mid-diastolic murmur is FIGURE 8–25 Contrast between the auscultatory findings in patients with chronic and acute aortic regur-
a useful sign of the degree of obstruction at gitation. In a patient with chronic aortic regurgitation, a prominent systolic ejection murmur resulting from
the mitral orifice. A murmur that lasts up to the large forward stroke volume is heard at the base and the apex and ends well before the second heart
S1 even after long cycle lengths indicates that sound (S2). The aortic diastolic regurgitant murmur begins with S2 and continues in a decrescendo fashion,
the stenosis is severe enough to generate a terminating before the first heart sound (S1). At the apex, the early diastolic component of Austin Flint murmur
persistent gradient even at the end of long (AF) is introduced by a prominent third heart sound (S3). A presystolic component of the AF is also heard. In
cases of acute aortic regurgitation, there is a significant decrease in the intensity of the systolic ejection
diastoles. murmur compared with that of chronic aortic regurgitation because of the decreased forward stroke volume.
The mid-diastolic murmur of tricuspid The S1 is markedly decreased in intensity because of preclosure of the mitral valve, and at the apex the
stenosis occurs in the presence of atrial fibril- presystolic component of the AF murmur is absent. The early diastolic murmur at the base ends well before
lation. The tricuspid mid-diastolic murmur S1 because of equilibration of the left ventricle and aortic end-diastolic pressures. Significant tachycardia is
differs from the mitral mid-diastolic murmur usually present. (From Shaver JA: Diastolic murmurs. Heart Dis Stroke 2:100, 1994.) Z
 Ch08.qxd 3/26/04 07:00 PM Page 24

8-24 TRICUSPID STENOSIS. In patients with tricuspic steno-

Diastolic Filling Murmur (Rumble) sis who are in sinus rhythm, a late diastolic or presystolic
Mitral Stenosis murmur typically occurs in the absence of a perceptible mid-
S1 S2 S1 S2 diastolic murmur (see Fig. 8–28B). This is so because the
timing of tricuspid diastolic murmurs reflects the maximal
O.S. O.S. acceleration of flow and gradient, which is usually negligible
Mild

until a powerful right atrial contraction occurs.4 The presys-

tolic murmur of tricuspid stenosis is crescendo-decrescendo
A2 P2 A2 P2 and relatively discrete, fading before S1 (see Fig. 8–28B). This
is in contrast to the presystolic murmur of mitral stenosis,
which tends to rise in a crescendo up to S1 (see Fig. 8–28A).
ECG

CH 8 The most valuable auscultatory sign of tricuspid stenosis in

S1 S2 S1 S2 sinus rhythm is the effect of respiration on the intensity of the
presystolic murmur. Inspiration increases right atrial volume,
O.S. O.S. provoking an increase in right atrial contractile force that
Severe

coincides with a fall in right ventricular end-diastolic pressure.

The result is an increase in the tricuspid gradient, in the veloc-
ity of tricuspid flow, and in the intensity of the tricuspid
A2 P2 A2 P2 stenotic presystolic murmur (Fig. 8–29).
THE AUSTIN FLINT MURMUR (see Fig. 8–25). In 1862,
FIGURE 8–26 Diastolic filling murmur (rumble) in mitral stenosis. In cases of mild mitral steno- Austin Flint described a presystolic murmur in patients with
sis, the diastolic gradient across the valve is limited to the two phases of rapid ventricular filling in aortic regurgitation and proposed a mechanism that was
early diastole and presystole. The rumble may occur during either period or during both periods. As astonishingly perceptive88-91: “Now in cases of considerable
the stenotic process becomes severe, a large pressure gradient exists across the valve during the aortic insufficiency, the left ventricle is rapidly filled with
entire diastolic filling period, and the rumble persists throughout diastole. As the left atrial pressure blood flowing back from the aorta as well as from the auricle,
becomes greater, the interval between aortic component of the second heart sound (A2) and the before the auricular contraction takes place.The distention of
opening snap (O.S.) shortens. In cases of severe mitral stenosis, secondary pulmonary hypertension the ventricle is such that the mitral curtains are brought into
develops and results in a loud pulmonic component of the second heart sound (P2) and the splitting coaptation; and when the auricular contraction takes place,
interval usually narrows. S1 = first heart sound; S2 = second heart sound; ECG = electrocardiogram. the mitral direct current passing between the curtains throws
(From Shaver JA, Leonard JJ, Leon DF: Examination of the Heart. Part IV: Auscultation of the Heart. them into vibration and gives rise to the characteristic blub-
Dallas, American Heart Association, 1990, p 55. Copyright 1990, American Heart Association.) bering murmur.”88

Continuous Murmurs
The term continuous appropriately applies to murmurs
that begin in systole and continue without interruption
through S2 into all or part of diastole (Fig. 8–30). The pres-
ence of murmurs throughout both phases of the cardiac cycle
(holosystolic followed by holodiastolic) is not the criterion
for the designation “continuous.” Conversely, a murmur that
fades completely before the subsequent S1 may be continu-
ous, provided that the systolic portion of the murmur pro-
ceeds without interruption through S2.
Continuous murmurs are generated by uninterrupted flow
from a vascular bed of higher pressure or resistance into a
A B vascular bed of lower pressure or resistance without phasic
interruption between systole and diastole. Such murmurs are
FIGURE 8–27 A, Phonocardiogram recorded at the apex of a patient with a mod- due chiefly to (1) aortopulmonary connections, (2) arteriove-
erately restrictive ventricular septal defect and increased pulmonary arterial blood flow.
nous connections, (3) disturbances of flow patterns in arter-
The mid-diastolic murmur (DM) results from augmented flow across the mitral valve.
B, Phonocardiogram at the lower left sternal edge of a patient with an ostium secun- ies, and (4) disturbances of flow patterns in veins (Table 8–7).
dum atrial septal defect and increased pulmonary arterial blood flow. A mid-diastolic The best known continuous murmur is associated with the
murmur resulted from augmented flow across the tricuspid valve. SM = holosystolic aortopulmonary connection of patent ductus arteriosus (see
murmur; S1 = first heart sound; S2 = second heart sound; A2 and P2 = aortic and pul- Chap 56; Fig. 8–31). The murmur characteristically peaks just
monic components of a conspicuously split S2. before and after S2, which it envelops, decreases in late dias-
tole (often appreciably), and may be soft or even absent before
the subsequent first heart sound.55 George Gibson’s descrip-
diastolic timing of the murmur coincides with the phase of tion in 1900 was even more precise.92 “It persists through S2
ventricular filling that follows atrial systole and implies the and dies away gradually during the long pause. The murmur
presence of sinus rhythm and coordinated atrial contraction. is rough and thrilling. It begins softly and increases in inten-
Late diastolic or presystolic murmurs usually originate at the sity so as to reach its acme just about, or immediately after,
mitral or tricuspid orifice because of obstruction, but occa- the incidence of the second sound, and from that point grad-
sionally because of abnormal patterns of presystolic AV flow. ually wanes until its termination.”
The best known presystolic murmur accompanies rheu-
ARTERIOVENOUS CONTINUOUS MURMURS. These can be con-
matic mitral stenosis in sinus rhythm as AV flow is aug-
genital or acquired and are represented in part by arteriovenous fistulas,
mented in response to an increase in the force of left atrial coronary arterial fistulas, anomalous origin of the left coronary artery
contraction (Figs. 8–11B and 8–28A).65 Presystolic accentua- from the pulmonary trunk, and communications between the sinus of
tion of a mid-diastolic murmur is occasionally heard in Valsalva and the right side of the heart.55 The configuration, location, and
patients with mitral stenosis with atrial fibrillation, espe- intensity of arteriovenous continuous murmurs vary considerably among
cially during short cycle lengths; however, the timing is actu- these different lesions. Acquired systemic arteriovenous fistulas are
ally early systolic, and the mechanism differs from the true created surgically by forearm shunts for hemodialysis. Congenital arteri-
presystolic murmur as described earlier and as shown in ovenous continuous murmurs occur when a coronary arterial fistula
Z Figure 8–28A. enters the pulmonary trunk, right atrium, or right ventricle. At the right
Ch08.qxd 3/26/04 07:00 PM Page 25

ventricle, the continuous murmur can be either softer or 8-25

louder in systole, depending on the degree of compression
exerted on the fistulous coronary artery by right ventricu-
lar contraction.55 Rupture of a congenital aortic sinus
aneurysm into the right side of the heart results in a con-
tinuous murmur that tends to be louder in either systole or
diastole, sometimes creating a to-and-fro impression.55
ARTERIAL CONTINUOUS MURMURS. These originate
in either constricted or nonconstricted arteries.A common
example of a continuous murmur arising in a constricted
artery is carotid or femoral arterial atherosclerotic obstruc-
tion. Not surprisingly, these murmurs are characteristically CH 8
louder in systole and more often than not are purely
systolic.

Physical Examination of the Heart and Circulation

Disturbances of flow patterns in normal, nonconstricted A B
arteries sometimes produce continuous murmurs. The FIGURE 8–28 A, Phonocardiogram from the cardiac apex of a patient with pure rheumatic mitral
“mammary souffle” described earlier,4 an innocent murmur stenosis. A presystolic murmur (PM) rises in a crescendo that is interrupted by a loud first heart sound
heard during late pregnancy and the puerperium, is an arte- (S1). B, Phonocardiogram from the lower left sternal edge of a patient with rheumatic tricuspid steno-
rial murmur that, when continuous, is typically louder in sis. The first cycle is during inspiration and is accompanied by a prominent presystolic murmur (PM)
systole and maximal over either lactating breast. that is crescendo-decrescendo, decreasing before the S1. During exhalation (second cycle), the presys-
Continuous murmurs in nonconstricted arteries origi- tolic murmur all but vanishes. S2 = second heart sound; OS = mitral opening snap.
nate in the large systemic-to-pulmonary arterial collaterals
in certain types of cyanotic congenital heart disease, typi-
cally tetralogy of Fallot with pulmonary atresia. These continuous
murmurs are randomly located throughout the thorax because of the Continuous Murmur vs. To-Fro Murmur
random location of the aortopulmonary collaterals.55 They are also heard S1 S2 S1 S2
in coarctation of the aorta (see Chap. 56).

Continuous
murmur
CONTINUOUS VENOUS MURMURS. These are well represented by
the innocent cervical venous “hum” (Fig. 8–32). The hum is by far the
most common type of normal continuous murmur, universal in healthy
children, and frequently present in healthy young adults, especially
during pregnancy. Thyrotoxicosis and anemia, by augmenting cervical
S1 S2 S1 S2
venous flow, initiate or reinforce the venous hum. The term hum does
murmur
not necessarily characterize the quality of these cervical venous
To-Fro
murmurs, which may be rough and noisy and are occasionally accom-
panied by a high-pitched whine.55 The hum is truly continuous, although

FIGURE 8–30 Comparison of continuous murmurs and to-fro murmurs. During

abnormal communication between high-pressure and low-pressure systems, a large
pressure gradient exists through the cardiac cycle, producing a continuous murmur. A
classic example is patent ductus arteriosus. At times, this type of murmur is confused
with a to-fro murmur, which is a combination of systolic ejection murmur and a murmur
of semilunar valve incompetence. A classic example of a to-fro murmur is aortic steno-
sis and regurgitation. A continuous murmur crescendos to around the second heart
sound (S2), whereas a to-fro murmur has two components. The midsystolic ejection com-
ponent decrescendos and disappears as it approaches S2. S1 = first heart sound. (From
Shaver JA, Leonard JJ, Leon DF: Examination of the Heart. Part IV: Auscultation of the
Heart. Dallas, American Heart Association, 1990, p 55. Copyright 1990, American Heart
Association.)

FIGURE 8–29 Pressure pulses and phonocardiogram illustrating the physiological

mechanism of the respiratory variation in the presystolic murmur of tricuspid stenosis.
During inhalation, a fall in intrathoracic pressure and an increase in systemic venous FIGURE 8–31 The classic continuous murmur of patent ductus arteriosus recorded
return result in an increase in the right atrial (RA) A wave and a decline in right ven- from within the main pulmonary artery (upper tracing) and simultaneously on the chest
tricular (RV) end-diastolic pressure, so the presystolic murmur (PSM) increases in loud- wall at the second left intercostal space (2LICS). The murmur “begins softly and
ness. During exhalation, the right atrial A wave declines, the RV diastolic pressure increases in intensity so as to reach its acme just about, or immediately after, the inci-
increases, the tricuspid gradient is at its minimum, and the PSM all but vanishes. LSE dence of the second sound, and from that point gradually wanes until its termination,”
= left sternal edge; S1 = first heart sound; S2 = second heart sound; INS = inspiration; as originally described by Gibson in 1900.92 Pulm. Art. = pulmonary artery; S1 = first
EXP = expiration. heart sound; S2 = second heart sound. Z
 Ch08.qxd 3/26/04 07:00 PM Page 26

8-26 TABLE 8–7 Differential Diagnosis of Continuous

Thoracic Murmurs (in Order of
Frequency)
Diagnosis Key Findings
Cervical venous hum Disappears on compression of
the jugular vein
Hepatic venous hum Often disappears with
epigastric pressure
CH 8 Mammary souffle Disappears on pressing hard
with stethoscope
Patent ductus arteriosus Loudest at second left
intercostal space
Coronary arteriovenous fistula Loudest at lower sternal
borders
Ruptured aneurysm of sinus Loudest at upper right sternal
of Valsalva border, sudden onset
Bronchial collaterals Associated signs of congenital
heart disease
High-grade coarctation
Brachial pedal arterial FIGURE 8–32 The phonocardiogram shows the continuous murmur of a normal
pressure gradient venous hum. The diastolic component is louder (paired arrows). Digital pressure over
the right internal jugular vein (vertical arrow) abolishes the murmur. The photographs
Anomalous left coronary artery Electrocardiographic changes show maneuvers used to elicit or abolish the venous hum. Left, The bell of the stetho-
arising from pulmonary of myocardial infarction scope is applied to the medial aspect of the right supraclavicular fossa as the exam-
artery iner’s left hand grasps the patient’s chin from behind and pulls it tautly to the left and
upward, stretching the neck. Right, The patient’s head has returned to a more neutral
Truncus arteriosus position, and digital compression of the right internal jugular vein (arrow) abolishes
Pulmonary artery branch Heard outside the area of the hum.
stenosis cardiac dullness
Pulmonary arteriovenous fistula Same as above
cardiomyopathy or mitral valve prolapse respectively); (4)
Atrial septal defect with mitral Altered by the Valsalva
stenosis or atresia maneuver
other systolic murmurs in patients with clinical findings sug-
gesting infective endocarditis (see Chap. 58), thromboem-
Aortic-atrial fistulas bolism, or syncope; (5) a systolic murmur accompanied by an
Adapted from Sapira JD: The Art and Science of Bedside Diagnosis. Baltimore,
abnormal electrocardiogram.
Urban & Schwartzenberg, 1990. According to this schema, a large majority of patients with
heart murmurs (i.e., patients with grade 1 or grade 2 midsys-
tolic murmurs) without any other clinical manifestations of
cardiac disease ordinarily do not require extensive work-up.
typically louder in diastole.The mechanism of the venous hum is unset-
tled. Silent laminar flow in the internal jugular vein may be disturbed by
deformation of the vessel at the level of the transverse process of the
Pericardial Rubs (See Chap. 64)
atlas during head rotation designed to elicit the hum.93 In sinus rhythm, the typical pericardial “rub” is triple
phased, that is, midsystolic, mid-diastolic, and presystolic.
Recognition is simplest when all three phases are present and
Approach to the Patient with a Heart Murmur when the characteristic superficial scratchy, leathery quality
Although a careful physical examination with emphasis is evident. Pericardial rubs may be more readily detected
on detailed auscultation is useful in establishing a cardiac when the patient is on elbows and knees (Fig. 8–34), a phys-
diagnosis or excluding serious cardiac disease in a patient ical maneuver designed to increase the contact of visceral and
with a heart murmur, echocardiography is decisive in con- parietal pericardium (see earlier). The term rub is appropri-
firming the diagnosis and determining the severity of the ate because the auscultatory sign is generated by abnormal
condition (Fig. 8–33). As delineated by O’Rourke,77 the visceral and parietal pericardial surfaces “rubbing” against
approach to the patient with a heart murmur depends on its each other. In the supine position, firm pressure with the
intensity, timing, location, response to maneuvers, and the stethoscopic diaphragm during full held exhalation rein-
presence of other cardiac and noncardiac symptoms and forces visceral and parietal pericardial contact and accentu-
signs. Patients with diastolic murmurs, or continuous ates the rub. Apposition of visceral and parietal pericardium
murmurs that are not cervical venous hums, or mammary can be even better achieved by examination while the patient
souffles of pregnancy, should ordinarily go to two- rests on elbows and knees.
dimensional and Doppler echocardiography, and subsequent Of the three phases of the pericardial rub, the systolic
work-up, including cardiac consultation, is guided by the phase is the most consistent,94 followed by the presystolic
echocardiographic findings. In general, echocardiography is phase. In atrial fibrillation, the presystolic component neces-
also advised for patients with systolic murmurs having the sarily disappears. The diagnosis of a pericardial rub is least
following characteristics: (1) loud murmur (i.e., grade 3 or secure when only one phase remains, which is typically the
higher); (2) holosystolic or late systolic murmur, especially at midsystolic. The most common clinical setting in which peri-
the left sternal edge or apex; (3) systolic murmurs that become cardial rubs are heard is immediately after open heart surgery.
louder or longer during the strain of the Valsalva maneuver However, auscultation often detects instead a “crunch” syn-
Z (suggesting the diagnosis of hypertrophic obstructive chronous with the heartbeat, especially in the left lateral
Ch08.qxd 3/26/04 07:00 PM Page 27

decubitus position. This is 8-27

not a pericardial rub but is Presence of
Hamman sign caused by air cardiac murmur
in the mediastinum.95 Peri-
cardial rubs are frequently Systolic murmur Diastolic or
audible in patients with continuous murmur
acute pericarditis. They may
become softer or even disap- Grade I+II Grade III or>,
pear in the presence of a and midsystolic holosystolic, or
large pericardial effusion. late systolic
Asymptomatic Other signs or CH 8
and no symptoms of cardiac
Dynamic Auscultation associated findings disease, infective

Physical Examination of the Heart and Circulation

Echocardiography
Dynamic auscultation endocarditis,
thromboembolism, or
refers to the technique of syncope
altering circulatory dynam- No further
workup Cardiac consult
ics by a variety of physiolog- if appropriate
ical and pharmacological
maneuvers and determining
the effects of these maneu- FIGURE 8–33 A schematic approach to the work-up of a patient with a cardiac murmur according to whether the murmur is
vers on heart sounds and probably innocent or secondary to cardiac pathology. This algorithm is particularly relevant to children and adults younger than 40
murmurs. 96,97
The conditions years, and echocardiography is recommended before cardiac consultation. (From Norton PJ, O’Rourke RA: Approach to the patients
with a heart murmur. In Braunwald E, Goldman L [eds]: Primary Cardiology. 2nd ed. Philadelphia, Elsevier, 2003.)
and interventions most com-
monly employed in dynamic
auscultation include respira- during exhalation, owing to respiratory alterations in venous
tion, postural changes, the Valsalva maneuver, premature return, whereas the opening snap of the tricuspid valve
ventricular contractions, isometric exercise, and one of behaves in the opposite fashion. Inspiration also diminishes
the vasoactive agents—amyl nitrite, methoxamine, or the intensity of ejection sounds in pulmonary valve stenosis
phenylephrine. because the elevation of right ventricular diastolic pressure
causes partial presystolic opening of the pulmonary valve
Respiration and therefore less upward motion of the valve during systole.
On the other hand, respiration does not affect the intensity
SECOND HEART SOUND. The splitting of S2 is most of aortic ejection sounds, except in cases of tetralogy of Fallot
audible along the left sternal border and can usually be appre- with pulmonary atresia.
ciated when A2 and P2 are separated by more than 0.02 MURMURS. Respiration exerts more pronounced and
second. The effects of respiration on the splitting of the consistent alterations on murmurs originating from the right
second heart sound were discussed earlier (see Second Heart than from the left side of the heart. During inspiration, the
Sound). diastolic murmurs of tricuspid stenosis (see Fig. 8–29) and
DIASTOLIC SOUNDS AND EJECTION SOUNDS. When low-pressure pulmonary regurgitation, the systolic murmurs
S3 and S4 originate from the right ventricle, they are charac- of tricuspid regurgitation (Carvallo sign),98 and the presystolic
teristically augmented during inspiration and diminished murmur of Ebstein anomaly may all be accentuated. The
during exhalation, whereas they exhibit the opposite inspiratory reduction in left ventricular size in patients with
response when they originate from the left side of the heart. mitral valve prolapse increases the redundancy of the mitral
Like other left-sided events, the opening snap of the mitral valve and therefore the degree of valvular prolapse; conse-
valve may become softer during inspiration and louder quently, the midsystolic click and the systolic murmurs occur
earlier during systole and may become accentuated.99

THE VALSALVA MANEUVER. This maneuver consists of a relatively

deep inspiration followed by forced exhalation against a closed glottis
for 10 to 20 seconds. The patient should first be instructed on how to
perform the maneuver. Simulation by the examiner is a simple means of
doing so.The examiner then places the flat of the hand on the abdomen
to provide the patient with a force against which to strain and to permit
assessment of the degree and duration of the straining effort.100,101
The normal response to the Valsalva maneuver consists of four
phases. Phase I is associated with a transient rise in systemic arterial pres-
sure as straining commences. Phase II is accompanied by a perceptible
decrease in systemic venous return, systolic pressure, and pulse pressure
(small pulse) and by reflex tachycardia. Phase III begins promptly with
cessation of straining and is associated with an abrupt, transient decrease
in arterial pressure. Phase IV is characterized by an overshoot of systemic
arterial pressure and reflex bradycardia. During phase II, S3 and S4 are
attenuated and the A2-P2 interval narrows or is abolished. As stroke
volume and systemic arterial pressure fall, the systolic murmurs of aortic
and pulmonary stenosis and of mitral and tricuspid regurgitation dimin-
ish and the diastolic murmurs of aortic and pulmonary regurgitation and
of tricuspid and mitral stenosis soften. As left ventricular volume is
reduced, the systolic murmur of hypertrophic obstructive cardiomyopa-
thy amplifies and the click and late systolic murmur of mitral valve pro-
FIGURE 8–34 A technique for eliciting a pericardial rub. The diaphragm of the lapse begin earlier. In phase III, the sudden increase in systemic venous
stethoscope is firmly applied to the precordium (arrow) while the patient rests on elbows return is accompanied by wide splitting of the S2 and by augmentation
and knees. of murmurs and filling sounds in the right side of the heart. Murmurs Z
 Ch08.qxd 3/26/04 07:00 PM Page 28

8-28 and filling sounds in the left side of the heart return to control levels and SQUATTING. A sudden change from standing to squatting increases
may transiently increase during the overshoot of phase IV. venous return and systemic resistance simultaneously. Stroke volume and
In patients with atrial septal defect, mitral stenosis, or heart failure, arterial pressure rise, and the latter may induce a transient reflex brady-
the Valsalva maneuver provokes a “square wave” response, negating the cardia.The auscultatory features include augmentation of S3 and S4 (from
four phases and their auscultatory equivalents. The Valsalva maneuver both ventricles) and as a consequence of an increase in stroke volume,
should not be performed in patients with ischemic heart disease because the systolic murmurs of pulmonary and aortic stenosis and the diastolic
of the accompanying fall in coronary blood flow. murmurs of tricuspid and mitral stenosis become louder, with right-sided
THE MULLER MANEUVER. This maneuver is the converse of the events preceding left-sided events. Squatting may make audible a previ-
Valsalva maneuver but is less frequently employed because it is not as ously inaudible murmur of aortic regurgitation.
useful. In this maneuver, the patient forcibly inspires while the nose is The elevation of arterial pressure increases blood flow through the
held closed and the mouth is firmly sealed for about 10 seconds. The right ventricular outflow tract of patients with tetralogy of Fallot and
CH 8 Muller maneuver exaggerates the inspiratory effort, widens the split S2, increases the volume of mitral regurgitation and of the left-to-right shunt
and augments murmurs and filling sounds originating in the right side through a ventricular septal defect, thereby increasing the intensity of
of the heart. the systolic murmur in these conditions. Also, the diastolic murmur of
aortic regurgitation is augmented consequent to an increase in aortic
POSTURAL CHANGES AND EXERCISE (Fig. 8–35) reflux. The combination of elevated arterial pressure and increased
Sudden assumption of the lying position from the standing or sitting venous return increases left ventricular size, which reduces the obstruc-
position or sudden passive elevation of both legs results in an increase tion to outflow and thus the intensity of the systolic murmur of hyper-
in venous return, which augments first right ventricular and, several trophic obstructive cardiomyopathy; the midsystolic click and the late
cardiac cycles later, left ventricular stroke volume.The principal auscul- systolic murmur of mitral valve prolapse are delayed.
tatory changes include widening of the splitting of S2 in all phases of res- OTHER POSITIONAL CHANGES. Assumption of the left lateral
piration and augmentations of right-sided S3 and S4 and, several cardiac recumbent position accentuates the intensity of S1, S3, and S4 originating
cycles later, left-sided S3 and S4.The systolic murmurs of pulmonic valve from the left side of the heart; the opening snap and the murmurs asso-
stenosis and aortic stenosis, the systolic murmurs of mitral and tricuspid ciated with mitral stenosis and regurgitation; the midsystolic click and
regurgitation and ventricular septal defect, and most functional systolic late systolic murmur of mitral valve prolapse;and the Austin Flint murmur
murmurs are augmented. On the other hand, because left ventricular end- associated with aortic regurgitation. Sitting up and leaning forward (see
diastolic volume is increased, the systolic murmur of hypertrophic Fig. 8–10D) make the diastolic murmurs of aortic and pulmonary regur-
obstructive cardiomyopathy is diminished and the midsystolic click and gitation more readily audible.
late systolic murmur associated with mitral valve prolapse are delayed Stretching the neck to elicit a venous hum is illustrated in Figure
and sometimes attenuated (see Fig. 8–12). 8–32. Passive elevation of the legs with the patient supine transiently
Rapid standing or sitting up from a lying position or rapid standing increases venous return and augments S3.
from a squatting posture has the opposite effect; in patients in whom ISOMETRIC EXERCISE. This can be carried out simply and repro-
there is relatively wide splitting of S2 during exhalation—a finding that ducibly using a calibrated handgrip device or hand ball. (It is useful to
may be confused with fixed splitting—the width of the splitting is carry out isometric exercise bilaterally simultaneously.) Isometric exer-
reduced, so that a normal pattern emerges during the respiratory cycle. cise should be avoided in patients with ventricular arrhythmias and
No change in splitting occurs in patients with true fixed splitting. myocardial ischemia, both of which can be intensified by this activity.
The decrease in venous return reduces stroke volume and innocent Handgrip should be sustained for 20 to 30 seconds, but a Valsalva maneu-
pulmonary flow murmurs as well as the murmurs of semilunar valve ver during the handgrip must be avoided. Isometric exercise results in
stenosis and of AV valve regurgitation. The auscultatory changes in transient but significant increases in systemic vascular resistance, arterial
hypertrophic cardiomyopathy and mitral valve prolapse are opposite to pressure, heart rate, cardiac output, left ventricular filling pressure, and
those on assumption of the lying posture just described. heart size.
As a consequence, (1) S3 and S4
originating from the left side of the
Systolic Second Effect of Posture Amyl Phenyl- heart become accentuated; (2) the
Diagnosis
Murmur Sound Erect Squatting Nitrite ephrine systolic murmur of aortic stenosis is
diminished as a result of reduction
Variable ie - Changes in intensity of systolic murmur
1. Hypertrophic of the pressure gradient across the
obstructive reversed aortic valve102; (3) the diastolic
cardiomyopathy partially reversed murmur of aortic regurgitation and
narrow or normal the systolic murmurs of rheumatic
2. Mitral regurgitation mitral regurgitation and ventricular
a. Pure severe widely split septal defect increase in intensity;
(4) the diastolic murmur of mitral
b. Papillary muscle normal or stenosis becomes louder conse-
dysfunction partially reversed quent to the increase in cardiac
output; and (5) the systolic murmur
c. Billowing posterior of hypertrophic obstructive car-
normal
leaflet diomyopathy diminishes and the sys-
d. Rheumatic of tolic click and late systolic murmur
slightly wide of mitral valve prolapse are delayed
moderate degree
because of the increased left ven-
mild to mod narrow or tricular volume.
3. Valvular
partially reversed
aortic PHARMACOLOGICAL
stenosis marked reversed AGENTS (See Fig. 8–35)
AMYL NITRITE. Inhalation of
4. Ventricular septal
slightly wide amyl nitrite is carried out by placing
defect
an ampule in gauze near the supine
5. Innocent vibratory patient’s nose and then crushing the
normal ampule.The patient is asked to take
systolic murmur
three or four deep breaths over 10
to 15 seconds, after which the amyl
No change from control Degree of increase Degree of decrease nitrite is removed. The drug pro-
duces marked vasodilatation, result-
ing in the first 30 seconds in a
FIGURE 8–35 Diagrammatic representation of the character of the systolic murmur and of the second heart sound in five
reduction of systemic arterial pres-
conditions. The effects of posture, amyl nitrite inhalation, and phenylephrine injection on the intensity of the murmur are shown.
Z sure and 30 to 60 seconds later in a
(Modified from Barlow JB: Perspectives on the Mitral Valve. Philadelphia, FA Davis, 1987, p 138.)
Ch08.qxd 3/26/04 07:00 PM Page 29

8. Kirkham N, Murrels T, Melcher SH, Morrison EA: Diagonal ear lobe creases and fatal 8-29
reflex tachycardia, followed in turn by a reflex increase in cardiac output,
cardiovascular disease: A necropsy study. Br Heart J 61:361, 1989.
velocity of blood flow, and heart rate.4,97,101,103 The major auscultatory 9. Woywodt A, Welzel J, Haase H, et al: Cardiomyopathic lentiginosis/LEOPARD syn-
changes occur in the first 30 seconds after inhalation. S1 is augmented, drome presenting as sudden cardiac arrest. Chest 113:1415, 1998.
and A2 is diminished.The opening snaps of the mitral and tricuspid valves 10. Basson CT, Cowley GS, Solomon SD, et al: The clinical and genetic spectrum of the
become louder, and as arterial pressure falls, the A2/opening snap inter- Holt-Oram syndrome (heart-hand syndrome). N Engl J Med 330:885, 1994.
val shortens.An S3 originating in either ventricle is augmented, owing to 11. Buckley MJ, Mason DT, Ross J Jr, Braunwald E: Reversed differential cyanosis
greater rapidity of ventricular filling; but because mitral regurgitation is with equal desaturation of the upper limbs: Syndrome of complete transposition of
reduced, the S3 associated with this lesion is diminished. The systolic the great vessels with complete interruption of the aortic arch. Am J Cardiol 15:111,
1965.
murmurs of aortic valve stenosis, pulmonary stenosis, hypertrophic
12. Fishman AP: Approach to the patient with respiratory symptoms. In Fishman AP (ed):
obstructive cardiomyopathy, tricuspid regurgitation, and functional sys- Pulmonary Diseases and Disorders. New York, McGraw-Hill, 1998, pp. 361-394.
tolic murmurs are all accentuated. 13. Yee J, McAllister CK: The utility of Osler’s nodes in the diagnosis of infective endo-
The response to amyl nitrite is useful in distinguishing (1) the sys- carditis. Chest 92:751, 1987. CH 8
tolic murmur of aortic stenosis (which is augmented) from that of mitral 14. Braunwald E: Edema. In Kasper DL, et al (eds): Harrison’s Principles of Internal Med-
regurgitation (which is diminished)103; (2) the systolic murmur of tricus- icine. 16th ed. New York, McGraw-Hill, 2005.

Physical Examination of the Heart and Circulation

pid regurgitation (augmented) from that of mitral regurgitation (dimin- 15. Willekes CL, Backer CL, Mavroudis C: A 26-year review of pectus deformity repairs,
ished); (3) the systolic murmur of isolated pulmonary stenosis including simultaneous intracardiac repair. Ann Thorac Surg 67:511, 1999.
16. Fonkalsrud EW, Bustorff-Silva J: Repair of pectus excavatum and carinatum in adults.
(augmented) from that of tetralogy of Fallot (diminished); (4) the dias-
Am J Surg 177:121, 1999.
tolic rumbling murmur of mitral stenosis (augmented) from the Austin 17. Wiese J: The abdominojugular refllux sign. Am J Med 109:59, 2000.
Flint murmur of aortic regurgitation (diminished); and (5) the early 18. Butman SM, Ewy GA, Standen JR, et al: Bedside cardiovascular examination in
blowing diastolic murmur of pulmonary regurgitation (augmented) from patients with severe chronic heart failure: Importance of rest or inducible jugular
that of aortic regurgitation (diminished). venous distension. J Am Coll Cardiol 22:968, 1993.
In patients with tetralogy of Fallot, the reduction of arterial pressure 19. Perloff JK: The jugular venous pulse and third heart sound in patients with heart
increases the right-to-left shunt and decreases the blood flow from failure. N Engl J Med 345:612, 2001.
the right ventricle to the pulmonary artery and diminishes the midsys- 20. Bilchick KC, Wise RA: Paradoxical physical fiindings described by Kussmaul: Pulsu
paradoxus and Kussmaul’s sign. Lancet 359:1940, 2002.
tolic murmur. The increase in cardiac output augments the diastolic
21. Drazner MH, Rame JE, Stevenson LW, Dries DL: Prognostic importance of elevated
murmurs of mitral and tricuspid stenosis and of pulmonary regurgitation jugular venous pressure and a third heart sound in patients with heart failure. N Engl
and the systolic murmur of tricuspid regurgitation. However, as a result J Med 345:574, 2001.
of the fall in systemic arterial pressure, the systolic murmurs of mitral 22. Linfors EW, Feussner JR, Blessing CL, et al: Spurious hypertension in the obese patient:
regurgitation and ventricular septal defect, the diastolic murmurs of Effect of sphygmomanometer cuff size on prevalence of hypertension. Arch Intern Med
aortic regurgitation, and the Austin Flint murmur as well as the continu- 144:1482, 1984.
ous murmurs of patent ductus arteriosus and of systemic arteriovenous 23. Nelson WP, Egbert AM: How to measure blood pressure accurately. Prim Cardiol 10:14,
fistula are all diminished. The reduction of cardiac size results in an 1984.
24. Gould BA, Hornung RS, Kieso HA, et al: Is the blood pressure the same in both arms?
earlier appearance of the midsystolic click and late systolic murmur
Clin Cardiol 8:423, 1985.
of mitral valve prolapse; the intensity of the systolic murmur exhibits a 25. Sapira JD: Quincke, de Musset, Duroziez, and Hill: Some aortic regurgitations. South
variable response. Med J 74:459, 1981.
METHOXAMINE AND PHENYLEPHRINE. These agents increase 26. Vlachopoulos C, O’Rourke M: Genesis of the normal and abnormal pulse. Curr Prob
systemic arterial pressure and exert an effect opposite to that of amyl Cardiol 25:297, 2000.
nitrite. Phenylephrine is preferred because of its shorter duration of 27. Perloff JK: The physiologic mechanisms of cardiac and vascular physical signs. J Am
action; when administered intravenously it elevates systolic pressure by Coll Cardiol 1:184, 1983.
approximately 30 mm Hg for only 3 to 5 minutes. Both drugs cause reflex 28. Brown DV: Dicrotic pulse in pericardial tamponade. J Cardiothorac Vasc Anesth
16:742, 2002.
bradycardia and decreased contractility and cardiac output.They should
29. Safar ME, Levy BI, Struijker-Boudier H: Current perspectives on arterial stiffness and
not be used in the presence of congestive heart failure and systemic pulse pressure in hypertension and cardiovascular diseases. Circulation 107:2864,
hypertension. 2003.
After administration, the intensity of S1 is usually reduced, and the 30. Elkins RC, Morrow AG, Vasko JS, Braunwald E: The effects of mitral regurgitation on
A2/mitral opening snap interval becomes prolonged. The responses of the pattern of instantaneous aortic blood fllow: Clinical and experimental observations
S3 and S4 are variable. As a result of the increased arterial pressure, the Circulation 36:45, 1967.
diastolic murmur of aortic regurgitation, the systolic murmurs of mitral 31. Talley JD: Recognition, etiology, and clinical implications of pulsus bisferiens. Heart
regurgitation, ventricular septal defect, and tetralogy of Fallot, and the Dis Stroke 3:309, 1994.
32. Smith D, Craige E: Mechanisms of the dicrotic pulse. Br Heart J 56:531, 1986.
continuous murmurs of patent ductus arteriosus and systemic arteri-
33. Talley JD: Dicrotism: Examples and review of the dicrotic pulse. J Ark Med Soc 92:507,
ovenous fistula all become louder. On the other hand, as a consequence 1996.
of the increase in left ventricular size, the systolic murmur of 34. Morpurgo M, Boutarin J: Right-sided pulsus alternans: A neglected phenomenon.
hypertrophic obstructive cardiomyopathy becomes softer and the click Cardiologia 40:803, 1995.
and late systolic murmur of mitral valve prolapse are delayed. The 35. Lab MJ, Seed WA: Pulsus alternans. Cardiovasc Res 27:1407, 1993.
reduction in cardiac output diminishes the systolic murmur of aortic 36. Rosenthal E: Extreme pulsus alternans presenting as 2:1 electromechanical dissocia-
valve stenosis, functional systolic murmurs, and the diastolic murmur of tion. Br Heart J 74:695, 1995.
mitral stenosis. The rumbling diastolic murmurs of mitral regurgitation 37. Brockenbrough EC, Braunwald E, Morrow AG: A hemodynamic technic for the detec-
tion of hypertrophic subaortic stenosis. Circulation 23:189, 1961.
and the Austin Flint murmur also diminish.
38. Fowler NO: Pulsus paradoxus. Heart Dis Stroke 3:68, 1994.
39. Pearson MG, Spence DP, Ryland I, Harrison BD: Value of pulsus paradoxus in assess-
ing acute severe asthma. BMJ 307:659, 1993.
REFERENCES 40. Jay GD, Onuma K, Davis R, et al: Analysis of physician ability in the measurement of
pulsus paradoxus by sphygmomanometry. Chest 118:348, 2000.
The General Physical Examination 41. Swami A, Spodick DH: Pulsus paradoxus in cardiac tamponade: A pathophysiologic
continuum. Clin Cardiol 26:215, 2003.
1. Mangione S, Nieman LZ, Gracely E, et al: The teaching and practice of cardiac aus-
42. Mowlavi A, Whiteman J, Wilhelmi BJ, et al: Dorsalis pedis arterial pulse: Palpation
cultation during internal medicine and cardiology training: A nationwide survey. Ann
using a bony landmark. Postgrad Med J 78:746, 2002.
Intern Med 119:47, 1993.
43. Hirsch AT: Recognition and management of peripheral arterial disease. In Braunwald
2. Shaver JA: Cardiac auscultation: A cost-effective diagnostic skill. Curr Probl Cardiol
E, Goldman L (eds): Primary Cardiology. 2nd ed. Philadelphia: Elsevier, 2003.
20:441, 1995.
44. Beiser GD, Epstein SE, Stampfer M, et al: Impairment of cardiac function in patients
3. Tavel M: Cardiac auscultation: A glorious past—but does it have a future? Circulation
with pectus excavatum. N Engl J Med 287:267, 1972.
93:1250, 1996.
4. Perloff JK: Physical Examination of the Heart and Circulation. 3rd ed. Philadelphia,
WB Saunders, 2000.
The Cardiac Examination
5. Roldan CA, Abrams J (eds): Evaluation of the Patient with Heart Disease: Integrating 45. Abrams J: Precordial palpation. In Horwitz LD, Groves BM (eds): Signs and Symptoms
the Physical Exam and Echocardiography. Philadelphia: Lippincott Williams & in Cardiology. Philadelphia, JB Lippincott, 1985, pp. 156-177.
Wilkins, 2002, pp 383. 46. Ellen SD, Crawford MH, O’Rourke RA: Accuracy of precordial palpation for detecting
6. Swartz MH (ed): Textbook of Physical Diagnosis: History and Examination. 3rd ed. increased left ventricular volume. Ann Intern Med 99:628, 1983.
Philadelphia, WB Saunders, 1998. 47. Ellen SD, et al: Accuracy of precordial palpation for detecting increased left ventricu-
7. O’Rourke RA, Braunwald E: Physical Examination of the Cardiovascular System. In lar volume. Ann Intern Med 99:628, 1983.
Kasper DL et al (eds): Harrison’s Principles of Internal Medicine. 16th ed. New York: 48. Ranganathan N, Juma Z, Sivaciyan V: The apical impulse in coronary heart disease.
McGraw Hill, 2005. Clin Cardiol 8:20, 1985. Z
 Ch08.qxd 3/26/04 07:00 PM Page 30

8-30 49. Adolph RJ: In defense of the stethoscope. Chest 114:1235, 1998. 76. Ishikawa M, Sakata K, Maki A, et al: Prognostic signifiicance of a clearly audible fourt
50. Abrams J: Synopsis of cardiac physical diagnosis. 2nd ed. Boston: Butterworth Heine- heart sound detected a month after an acute myocardial infarction. Am J Cardiol
mann, 2001. 80:619, 1997.

Heart Sounds Heart Murmurs

51. O’Toole JD, Reddy PS, Curtiss EL, et al: The contribution of tricuspid valve closure
77. O’Rourke R: Approach to the patient with a heart murmur. In Braunwald E, Goldman
to the fiirst heart sound: An intracardiac micromanometer study. Circulation 53:752
L (eds): Primary Cardiology. 2nd ed. Philadelphia: Elsevier, 2003, pp 155-173.
1976.
78. Grewe K, et al: Differentiation of cardiac murmurs by auscultation. Curr Probl Cardiol
52. Brooks N, Leech G, Leatham A: Complete right bundle branch block: Echophonocar-
13:699, 1988.
diographic study of the fiirst heart sound and right ventricular contraction times. B
79. Lembo NJ, et al: Bedside diagnosis of systolic murmurs. N Engl J Med 318:1572, 1988.
Heart J 41:637, 1979.
80. Ecchells E, et al: Does this patient have an abnormal systolic murmur? JAMA 277:564,
53. Burggraf GW: The fiirst heart sound in left bundle branch block: An echophonocardi-
1997.
graphic study. Circulation 63:429, 1981.
CH 8 81. Joffe HS: Genesis of Still’s innocent systolic murmur. Br Heart J 67:206, 1992
54. Leech G, Brooks N, Green-Wilkinson A, Leatham A: Mechanism of inflluence of P
82. Donnerstein RL, Thomsen VS: Hemodynamic and anatomic factors affecting the fre-
interval on loudness of fiirst heart sound. Br Heart J 43:138, 1980.
quency content of Still’s innocent murmur. Am J Cardiol 74:508, 1994.
55. Perloff JK: The Clinical Recognition of Congenital Heart Disease. 5th ed. Philadelphia,
83. Perloff JK, Roberts WC: The mitral apparatus: Functional anatomy of mitral regurgita-
WB Saunders, 2003.
tion. Circulation 46:227, 1972.
56. Mills PG, Brodie B, McLaurin L, et al: Echocardiographic and hemodynamic relation-
84. Ronan JA, Steelman RB, DeLeon AC, et al: The clinical diagnosis of acute severe mitral
ships of ejection sounds. Circulation 56:430, 1977.
insuffiiciency. Am J Cardiol 27:284, 1971.
57. Lembo NJ, Dell’Italia JL, Crawford MH, O’Rourke RA: Bedside diagnosis of systolic
85. Rios JC, Massumi RA, Breesman WT, Sarin RK: Auscultatory features of acute tricus-
murmurs. N Engl J Med 318:1572, 1988.
pid regurgitation. Am J Cardiol 23:4, 1969.
58. Leatham A: Splitting of the fiirst and second heart sounds. Lancet 2:607, 1954.
86. Fontana ME: Mitral valve prolapse and flloppy mitral valve: Physical examination.In
59. Kupari M: Aortic valve closure and cardiac vibrations in the genesis of the second
Mitral Valve: Floppy Mitral Valve, Mitral Valve Prolapse, Mitral Valvular Regurgita-
heart sound. Am J Cardiol 52:152, 1983.
tion. 2nd ed. Armouk, NY, Futura, 2000, pp 283-304.
60. Curtiss EI, Matthews DG, Shaver JA: Mechanism of normal splitting of the second heart
87. Fortuin NJ, Craige E: Echocardiographic studies of genesis of mitral diastolic murmurs.
sound. Circulation 51:157, 1975.
Br Heart J 35:75, 1973.
61. Shaver JA, Nadolny RA, O’Toole JD, et al: Sound-pressure correlates of the second
88. Flint A: On cardiac murmurs. Am J Med Sci 44:23, 1862.
heart sound. Circulation 49:316, 1974.
89. Landzberg JS, Tfllugfelder PW, Cassidy MM, et al: Etiology of the Austin Flint murmur
62. Xiao HB, Faiek AH, Gibson DG: Re-evaluation of normal splitting of the second heart
J Am Coll Cardiol 20:408, 1992.
sound in patients with classical left bundle branch block. Int J Cardiol 45:163, 1994.
90. Reddy PS, Curtiss EL, Salerni R: Sound-pressure correlates of the Austin Flint murmur:
63. Hultgren HN, Craige E, Nakamura T, Bilisoly J: Left bundle branch block and mechan-
An intracardiac sound study. Circulation 53:210, 1976.
ical events of the cardiac cycle. Am J Cardiol 52:755, 1985.
91. Berman P: Austin Flint—America’s Laennec revisited. Arch Intern Med 148:2053,
64. Tokushima T, Utsunomiya T, Ogawa T, et al: Contrast-enhanced radiographic com-
1988.
puted tomographic fiindings in patients with straight back syndrome. Am J Car
92. Gibson GA: Persistence of the arterial duct and its diagnosis. Edinb Med J 8:1, 1900.
Imaging 10:228, 1996.
93. Cutforth R, Wideman J, Sutherland RD: The genesis of the cervical venous hum. Am
65. Wood P: An appreciation of mitral stenosis: I. Clinical features. BMJ 1:1051, 1954; II.
Heart J 80:488, 1970.
Investigations and results. BMJ 1:1113, 1954.
94. Spodick DH: Auscultatory phenomena in pericardial disease. In Spodick DH: The Peri-
66. Tyberg TI, Goodyer AVN, Langou RA: Genesis of the pericardial knock in constrictive
cardium: A Comprehensive Textbook. New York, Marcel Dekker, 1997, pp 27-39.
pericarditis. Am J Cardiol 46:570, 1980.
95. Hamman L: Mediastinal emphysema. JAMA 128:1, 1945.
67. Bass NM, Sharatt GJP: Left atrial myxoma diagnosed by echocardiography with obser-
vations on tumor movement. Br Heart J 35:1332, 1973.
68. Van de Werf F, Minten J, Carmeliet P, et al: Genesis of the third and fourth heart sounds.
Dynamic Auscultation
J Clin Invest 73:1400, 1984. 96. Grewe K, Crawford MH, O’Rourke RA: Differentiation of cardiac murmurs by dynamic
69. Van de Werf F, Boel A, Geboers J, et al: Diastolic properties of the left ventricle in auscultation. Curr Probl Cardiol 13:671, 1988.
normal adults and in patients with third heart sounds. Circulation 69:1070, 1984. 97. Lembro NJ, Dell’Italia LJ, Crawford MH, O’Rourke RA: Bedside diagnosis of systolic
70. Drzewiecki GM, Wasicko MJ, Li JK: Diastolic mechanics and the origin of the third murmurs. N Engl J Med 318:1572, 1988.
heart sound. Ann Biomed Eng 19:651, 1991. 98. Cha SD, Gooch AS: Diagnosis of tricuspid regurgitation. Arch Intern Med 143:1763,
71. Glower DD, Murrah RL, Olsen CO, et al: Mechanical correlates of the third heart sound. 1983.
J Am Coll Cardiol 19:450, 1992. 99. Barlow JB: Perspectives on the Mitral Valve. Philadelphia, FA Davis, 1987.
72. Downes TR, Dunson W, Stewart K, et al: Mechanism of physiologic and pathologic S3 100. Vrewe K, Crawford MH, O’Rourke RA: Differentiation of cardiac murmurs by dynamic
gallop sounds. Am Soc Echocardiol 5:211, 1992. auscultation. Curr Probl Cardiol 13:671, 1988.
73. Tribouilloy CM, Enriquez-Sarano M, Mohty D, et al: Pathophysiologic determinants of 101. Nishimura RA, Tajik AJ: The Valsalva maneuver and response revisited. Mayo Clin
third heart sounds: A prospective clinical and Doppler echocardiographic study. Am Proc 61:211, 1986.
J Med 111:96, 2001. 102. McCraw DB, Siegel W, Stonecipher HK, et al: Response of the heart murmur intensity
74. Adolph RJ: The fourth heart sound. Chest 115:1480, 1999. to isometric (handgrip) exercise. Br Heart J 34:605, 1972.
75. Baracca E, Scorzoni D, Brunazzi MC, et al: Genesis and acoustic quality of the physi- 103. Barlow J, Shillingford J: The use of amyl nitrite in differentiating mitral and aortic sys-
ological fourth heart sound. Acta Cardiol 50:23, 1995. tolic murmurs. Br Heart J 20:162, 1958.