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316 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
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aortic stenosis, aortic regurgitation, mitral regurgitation) and/or increased
contractility (exertion, emotion, hyperthyroidism).
Decreased amplitude. Reduced contractility, as in congestive heart failure,
weakens the PMI, and, if accompanied by LV dilatation, it becomes more
diffuse.
Enlarged, sustained apical impulse. Contraction against increased afterload
prolongs left ventricular ejection time. Therefore, rather than the normal brief
tap, aortic stenosis and systemic hypertension produce an enlarged sustained
apical impulse.
Displaced to the left. Volume overload dilates the LV. If contractility is normal, the PMI is enlarged, brisk, and displaced laterally, but is not sustained.
Causes of LV volume overload are aortic or mitral regurgitation and intracardiac shunts. Other causes of leftward displacement are right pneumothorax,
left pleural adhesions, or left lung volume loss.
Displaced to the right. This is seen with left pneumothorax, right pleural adhesions, right lung volume loss, and dextrocardia.
Shifted downward. Severe emphysema attens the diaphragm pulling the
heart and mediastinum downward. The PMI may be felt just inferior to the
xiphoid.
Right ventricular impulse.
produce a palpable impulse. A dilated, hypertrophied or forward displaced
RV may produce a palpable impulse. A palpable precordial impulse near the
left sternal edge in the third, fourth or fth interspace and medial to the apex
impulse almost always reects right ventricular pressure or volume overload.
With severe mitral insufciency, the enlarged left atrium produces a sternal or
parasternal impulse peaking with S2, whereas true right ventricular impulses
peak during systole. Slight impulses move just the interspaces, while more
advanced disease lifts the lower sternum with each beat.
CLINICAL OCCURRENCE: Right Ventricular Hypertrophy (pressure over-
load): Pulmonic stenosis, pulmonary hypertension, mitral stenosis; Right
Ventricular Dilation (volume overload):
ciency, left-to-right intracardiac shunts; Forward Displacement of the Heart:
Tumors behind the heart, enlarged left atrium; Right Ventricle Protuberance:
Right ventricular aneurysm; Hyperdynamic Circulation: Exertion, emotion,
hyperthyroidism.
Other impulses
Epigastric pulsation. Normal in thin people after exertion, it is also seen
with inferior displacement of the heart in emphysema. Most frequently, it
reects normal aortic pulsation. Abdominal aortic aneurysm (AAA) should
be considered.
Pulsations at the Base. An impulse may be felt over the pulmonary conus,
just to the left of the sternum in the second or third interspace, in pulmonary
hypertension and/or with increased pulmonary blood ow from large left to
Normal right ventricular contraction does not
Tricuspid or pulmonary valve insuf-
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right shunts. Ascending aortic aneurysm may produce pulsations in the right
second interspace.
Thrills.
when transmitted to peripheral structures.
a purring cat. Since auscultation is more sensitive than palpation, thrills are
associated with more intense murmurs (grade IV/VI). Thrills must be localized and timed to the cardiac cycle. DDX: In mitral stenosis, diastolic and
presystolic thrills may be felt at the apex. Severe aortic stenosis causes a systolic thrill in the second right interspace and carotid arteries. The thrill from a
ventricular septal defect (VSD) is felt in the fourth and fth interspaces near
the sternum.
Palpable friction rubs (friction fremitus). Occasionally a pleural or pericardial friction rub is palpable (see Acute Pericarditis, page 352).
Percussion
Shifted cardiac dullness. Estimating the distance of the cardiac apex from the
midsternal line (MSL) by percussion only detects gross changes in heart size.
Left border shifted leftward. The LBCD is normally 7–9 cm left of the MSL.
DDX: Leftward shift is caused by LV dilatation (RBCD normal or right-
shifted), pericardial effusion (RBCD right-shifted, mufed heart sounds,
paradoxical pulse), and displacement of a normal-sized heart to left by right
pneumothorax, right hydrothorax, left pleural adhesions, or left lung atelectasis with left-shifted mediastinum.
Left border shifted rightward. Consider pulmonary emphysema with a normal midline heart, a prominent lingula anterior to the heart preventing accurate percussion of LBCD, and displacement rightward from right lung brosis or atelectasis, left pneumothorax, or left hydrothorax.
Turbulent blood ow produces audible murmurs and palpable thrills
The vibrations feel like holding
Right border shifted rightward. Causes include cardiac dilatation, pericardial effusion, left pneumothorax, left hydrothorax, right lung atelectasis, right
pleural adhesions, and dextrocardia.
Right border shifted leftward. Causes include left lung atelectasis, left pleural
adhesions, right pneumothorax, and right hydrothorax.
Enlarged cardiac dullness. The area of cardiac dullness expands when the
right or left border is displaced laterally without the other moving, or both
borders are displaced in opposite directions, e.g., by cardiac dilatation and
pericardial effusion.
Wide manubrial dullness. Dullness >6 cm suggests aortic aneurysm,
retrosternal goiter, thymus tumor, lymphoma, or metastatic carcinoma.
Auscultating Heart Sounds
First (S1) and second (S2) heart sounds. During ventricular systole intraven-
tricular pressure rises rapidly closing the mitral and tricuspid valves and,
318 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
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shortly thereafter, opening the aortic and pulmonic valves (Fig. 8-19). Tensing
of the AV valves is associated with S1; tensing of the aortic and pulmonic
valves is associated with S2. The normal heart sounds are NOT caused by the leaf-
lets slapping together.
are probably caused by the closed valves tensing producing abrupt deceleration of blood that vibrates the heart, vessels, and blood column. The contracting ventricles force blood silently into the aorta and pulmonary artery. When
the ventricles relax, intraventricular pressure falls. Initial aortic and pulmonic
valve leaet apposition occurs prior to the high-frequency components of S2.
The pressure gradient between each artery and the more rapidly declining
intraventricular pressures abruptly stretches elastic leaet tissue producing
the second heart sound. S2 is heard when arterial ow is near zero but just
before brief retrograde ow occurs.
on the precordium nearest their origin: S1 from the AV valves at the apex
and lower left sternal border; S2 from the semilunar valves at the base. S2 is
louder than S1at the base. Occasionally, S2 at the apex may be as loud or
louder than S1. The intensity of S1 and S2 varies with the stress on the valve
leaets.
First heart sound, S1—onset of ventricular systole. S1 marks the beginning of
ventricular systole, approximately synchronous with the apical impulse. S1 is
usually louder than S2 at the cardiac apex and can be heard throughout the
precordium. At the base, S1 is less loud than S2.
Splitting of S1. S1 splits with asynchronous tricuspid and mitral valves tensing. Slight splitting of S1 is a common normal nding. Wide splitting occurs
with right bundle-branch block, which delays right ventricular contraction.
Rather, the high-frequency components of these sounds
The heart sounds are usually loudest
Accentuated S1. Thickened mitral valve leaets with preserved mobility and
increased force of LV contraction accentuate S1. This occurs in mitral stenosis,
tachycardia from fever, hyperthyroidism, exercise, emotion, and hypertension.
Diminished S1. When the mitral and tricuspid valves are closely approximated at the onset of systole, their tensing is less forceful as seen with weak
ventricular contraction, aortic insufciency, prolonged PR interval, and heavily calcied mitral valve leaets. Attenuation of heart sounds by obesity, emphysema, and pericardial and/or pleural effusion also diminishes S1.
Variable and intermittently very loud S1 (Bruit de Canon). Variable ventricular diastolic lling and asynchronous atrial and ventricular contraction
change the intensity of S1 from beat to beat. Atrial brillation, atrial utter
with varying block, complete AV block, frequent premature beats, and ventricular tachycardia are each a cause.
Second heart sound, S2—onset of ventricular diastole.
semilunar aortic (A2) and pulmonic (P2) valves produces S2, normally A2
slightly preceding P2. The more compliant and distensible an artery, the less
closely the arterial pressure follows the pressure in the ventricle ejecting into
that artery, a phenomenon known as hangout. Thus, the aorta’s lower com-
pliance compared to the PA causes the interval between completion of LV
systole and A2 to be shorter than that between the completion of RV systole
Tensing of the closed
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FIG. 8-37 Normal Physiologic Variations in the Heart Sounds. Duration is represented on the horizontal axis
and intensity of the heart sounds on the vertical axis. The S1 is prolonged during inspiration. The aortic component of the
second sound (A2) is audible over the entire precordium, but (P2) the weaker pulmonic component is heard only in the left
second intercostal space. During expiration, the aortic and pulmonic components of S2 fuse. With inspiration the splitting of
S2 widens. Splitting of S2 is normal only in the pulmonic area; it is pathologic elsewhere.
and P2, so A2 precedes P2 (Fig. 8-37). Aortic pressure is much higher than PA
pressure making A2 louder than P2. Compare the intensity of A2 and P2 in
the second left intercostal space. In adults, only A2 is heard at the apex; hearing both A2 and P2 suggests that P2 is abnormally loud.
Effect of respiration on S2. Inspiration delays PV closure resulting in inspiratory splitting of S2 by decreasing intrathoracic pressure leading to
increased venous return and pulmonary compliance. In children and adolescents, the inspiratory split of S2 is wider than in older adults. In recumbent young persons, S2 may not fuse into a single sound with expiration. Fusion should occur during expiration when sitting, so failure to fuse suggests
an unusually wide split. With advancing age, the normal split narrows and
inspiratory splitting of S2 may not be detectable, even in recumbency. The
variable splitting of S2 with the respiratory cycle distinguishes the triple
S1-A2-P2 sounds from other sounds such as lower pitched noises including
S3 and S4.
Accentuated A2. Increased pressure on the closed aortic valve increases A2.
Arterial hypertension is most common, but it can occur with ascending aortic
aneurysm.
Diminished A2. A2 is decreased when the valve is rigid and immobile or the
pressure on the valve and aortic root at end systole is lower. Arterial hypotension and a heavily calcied AV in aortic stenosis diminish A2.
Accentuated P2. P2 is accentuated in primary or secondary pulmonary hypertension, atrial septal defect (ASD), truncus arteriosus, and in adolescence
(Fig. 8-38).
320 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
Heart sounds S
S2S
S
(parad
(paradoxical splitting)
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1
Pulmonary
hypertension
Right-bundlebranch block
Pulmonary
stenosis
Left-bundle-
branch block
oxical splitting)
Aortic
stenosis
Tetralogy ofTT
Fallot
Protodiastolic
gallop
Presystolic
gallop
FIG. 8-38 Pathologic Variations in the Heart Sounds. Pulmonary hypertension causes an increased P2.
A and P
P
A and P
A
P
A
AP
A
P
A
P
A
P
A
AP
3
4
Inspiration
Expiration
Inspiration
Expiration
Inspiration
Expiration
Inspiration
Expiration
Inspiration
Expiration
Inspiration
Expiration
Right bundle-branch block delays right ventricular emptying, increasing the normal split and accentuating P2. Pul-
monic stenosis also delays P2 but decreases its intensity. In left bundle-branch block and aortic stenosis, LV ejec-
tion is d elayed so A2 co incides wit h P2 and the norm al expirator y movement of P 2 causes para doxic split ting during ex piration.
Diminished P2. Diminished pulmonary artery pressure reduces tension on
the pulmonic valve. Pulmonic stenosis is the most common cause (Fig. 8-38).
Widened inspiratory S2 split. This indicates either delayed PV tensing or
early AV tensing. P2 delay occurs with right bundle-branch block, ASD, and
pulmonic stenosis. Early AV closure valve occurs with severe MR (Fig. 8-38).
Reversed or paradoxic S2 split. Delays in LV ejection cause A2 to occur with
or after P2. During inspiration there is a single sound, or closely approximated sounds; expiration increases the split. This is seen in hypertrophic cardiomyopathy with dynamic LV outow obstruction, valvular aortic stenosis,
left bundle-branch block, and RV pacing (Fig. 8-38).
Triple rhythms and gallops. These low-pitched sounds are best heard in a
quiet room. Listen specically for triple heart sounds (couplets alternating
with single sounds) resembling a horse’s gallop. The couplet may be either
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a normal S2 followed closely by an audible S3 or an audible S4 preceding a
normal S1. Differentiating S3 from S4 requires correctly identifying S1 and S2.
The galloping rhythm is most evident at rates >100 bpm. Some reserve “gallop” for an S3 and/or S4 and a rate >100 bpm. At very fast rates S3 and S4 fuse
creating a mid-diastolic summation gallop.
S3, ventricular or protodiastolic gallop. Reverberation of ventricular muscle
and blood, decelerating at the end of rapid early ventricular lling, produces
the S3 (Figs. 8-20
cadence of Kentucky: ken. . . . TUCK..eh. By whispering “ken . . . . TUCK..eh” to
yourself as you listen, timing “ken” to S1 and “TUCK” to S2 you can train your
ear to listen for the low-pitched S3 coincident with “eh.” A left ventricular S3 is
best heard at the apex with the patient lying 45 degrees to the left side; a right
ventricular S3 is best heard near the lower left sternal border. S3 is best heard in
expiration and is accentuated by increasing venous return by exercise, abdominal pressure, or exing the knees on the abdomen. An S3 is normal in children,
young adults, and in pregnancy. After the third decade it may indicate myocardial systolic dysfunction with increased LV end-diastolic pressure and elevated
left atrial pressure. It is also seen, although of less concern, in hyperkinetic circulatory states (fever, anemia, and hyperthyroidism) or by very rapid ventricular
lling from mitral regurgitation or a large left-to-right shunt with a VSD.
and 8-38). S3 closely follows S2 in early diastole. It has the
S4, presystolic or atrial gallop.
tral valve apparatus, and LV outow tract produced by atrial contraction
(Figs. 8-20 and 8-38). S4 occurs after atrial contraction but before S1. The ca-
dence is Tennessee: “te..NUH … ..see.” This is the most difcult to hear of all
heart sounds; listen at apex with patient in left lateral decubitus position. As
you listen, whisper to yourself “te..NUH … .see,” timing “NUH” to S1 and
“see” to S2; train your ear for the S4 coincident with “te.” S4 is low pitched,
identical to S3. The S4 always indicates a high pressure, powerful atrial contraction, most often associated with decreased ventricular compliance. S4 is
heard with a thickened and/or noncompliant left ventricle, as with LVH, aortic stenosis, subaortic stenosis, hypertension, and acute ischemia or infarction
from coronary artery disease (CAD).
Summation gallop, mid-diastolic gallop. High heart rates compress diastole
moving S3 and S4 together giving the impression of a single sound or a rumbling murmur. Vagus stimulation may slow the rate enough to reveal the four
sounds.
Early systolic ejection sound—ejection click, aortic ejection sound.
tic root suddenly tensing at the onset of LV ejection and sudden doming of a
stenotic yet exible noncalcied aortic valve are causes (Fig. 8-20, page 284).
At the onset of LV ejection in early systole, a click is heard at the base and
apex. It is unaffected by inspiration and usually loudest at the base. Ejection clicks occur with a dilated aortic root from ascending aortic aneurysm,
coarctation, hypertension, valvular aortic stenosis, a bicuspid aortic valve, or
aortic regurgitation.
Early systolic ejection sound—ejection click, pulmonic ejection sound. See
Aortic ejection sound above and Fig. 8-20. This is a click at the onset of right
S4 is caused by the vibrating LV muscle, mi-
The aor-
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ventricular ejection, occurring with pulmonary valve stenosis or dilatation. It
is best heard in the left second interspace during early systole. In some cases,
a loud click fuses with S1 making S1 sound louder. The closer the sound is to
S1, the more severe the stenosis. Pulmonic clicks may decrease or disappear
with inspiration.
Mid or late systolic click—mitral valve prolapse. This click is heard
at the apex in mid or late systole; it can be intermittent (Fig. 8-20). It is unchanged by respiration but can be delayed or abolished by squatting from
standing or raising the legs, both of which increase LV end-diastolic volume.
The click may rst become apparent or, if already audible, will move toward
S1 as the LV end-diastolic volume decreases with standing or Valsalva. It
is sometimes associated with a late systolic murmur of mitral insufciency.
Most individuals are otherwise normal, although mitral prolapse occurs
with increased frequency in Marfan syndrome and myxomatous mitral valve
degeneration.
Diastolic snap—mitral opening snap. When LV pressure drops below LA
pressure, stenotic but still exible (noncalcied) mitral valve leaets that are
tethered at their commissures buckle or bow into the left ventricle producing
a snap. The diastolic rumble begins a few hundredths of a second later (Fig.
8-20). The snap is best heard at the apex but may radiate to the base and left
sternal border, simulating a widely split S2. This sign is characteristic of rheumatic mitral stenosis.
Diastolic snap—tricuspid opening snap. See mitral opening snap above.
Usually associated with other rheumatic valvular abnormalities, this snap is
difcult to identify.
Prosthetic heart valves. Prosthetic heart valves are common. It is advisable
to be familiar with the various valve types and their auscultatory features.
Auscultating Extracardiac Sounds: These relatively uncommon precordial
sounds are often mistaken for murmurs. Extracardiac sounds may move
about within a specic part of the cardiac cycle, distinguishing them from the
S1, S2, S3, and S4.
Diastolic sound—pericardial knock. With constrictive pericarditis ventricular lling stops abruptly in early diastole producing vibrations known as a
pericardial knock. Knocks are higher pitched than S3 and are heard widely
over the precordium. They can be earlier than S3 and increase with inspiration (Fig. 8-20).
Pericardial friction rub. Two inamed pericardial surfaces rubbing together
create a sound which seems closer to the ear than a murmur. Pericardial effusions often do not cover the entire pericardium, so rub and effusion can coexist. Listen during full expiration with the patient prone or sitting and leaning
forward. Rubs are scratchy, grating, rasping, or squeaky. In ~50% of cases
the rub is triphasic, in systole and early and late diastole. In one-third it is
systolic and late diastolic. The rest are heard only in systole. Rubs are often
intermittent.
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Mediastinal crunch (Hamman sign). See Subcutaneous and mediastinal
emphysema page 302 and Spontaneous esophageal rupture page 355.
Venous hum. High-velocity ow in the internal jugular veins, especially the
right, produces a humming sound. Hums are usually heard in both supraclavicular fossae and often in the second and third interspaces near the sternum.
They are low pitched, persist throughout the cardiac cycle, and frequently
increase during diastole. Hums are intensied by sitting or standing; they
do not vary with respirations. The hum is readily abolished by light pressure
on the jugular veins beside the trachea. They are frequently mistaken for an
intracardiac murmur. Venous hums can be normal. They are more common
with hyperthyroidism and anemia.
Auscultating Heart Murmurs: In normal vessels and heart chambers, blood
ow at rest is laminar and silent. Murmurs result from turbulence (vortices)
developing near the vessel wall–bloodstream interface as the blood passes
an obstruction or dilatation (vortex-shedding theory). Imagine 60 cm of pliable rubber tubing attached to a water faucet. When the faucet is turned on,
a ow velocity can be attained that will not vibrate the tubing, because the
ow is laminar and smooth. At this ow, slightly constricting the tubing
causes vibrations distally. Similarly, increasing the ow without constriction
induces turbulence. In a normal heart, murmurs are induced when the velocity of blood ow is increased by high output states such as exercise, anemia,
pregnancy, or hyperthyroidism, that is, a ow murmur. Blood owing over
obstructions or through unusual openings in the circulation creates turbulence and collision currents resulting in murmurs.
Murmurs should be described by their location, pitch, and timing in the
cardiac cycle. The quality of a murmur is of some diagnostic value. Ventricular
lling murmurs involving diastolic ow across the AV valves are relatively
low pitched because of the pressure gradients are low; blood owing through
narrow orices with higher pressure gradients cause high-pitched murmurs.
Accurate categorization of these features is necessary to establish the likely
diagnosis. Figures 8-39 to 8-41 show the anatomy and murmur of each major
condition.
Systolic Murmurs: Systolic murmurs may occur in early, mid, or late sys-
tole. Murmurs heard throughout systole are pansystolic or holosystolic. Blood
moving across a rising then falling pressure gradient produces a crescendo–
decrescendo murmur reecting accelerating then slowing ow, e.g., aortic
stenosis. The murmur, starting soon after S1, intensies to a maximum at
mid-systole, then tapers off disappearing before S2. Blood owing continuously from a high-pressure region to one of low pressure produces a pansystolic murmur of almost uniform intensity typical of atrioventricular valve
regurgitation. It is usually possible to distinguish the systolic murmurs of
organic disease from those of little signicance occurring only in early systole
or mid-systole [Etchells E, Bell C, Robb K. The rational clinical examination.
Does this patient have an abnormal systolic murmur? JAMA. 1997;277:564–
571]. Echocardiography is an important adjunct for evaluating pathological
systolic murmurs since some lesions are misdiagnosed even by experienced
observers. Common errors are underestimating the severity of aortic stenosis
because of decreased LV function, failing to identify combined mitral and
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FIG. 8-39 Common Pathologic Heart Murmurs. The diagrams are drawn to represent intensity of the heart sounds
and murmurs on the vertical axis and duration on the horizontal axis. Pitch is depicted by the spacing of the shading: wider
spacing lower pitch. “A” and “P” refer to the aortic and pulmonic components of the S2. “OS” indicates the opening snap of
the mitral valve in mitral stenosis. Note that the systolic ejection murmurs are inaudible at either end of systole and attain
maximum intensity at mid-systole (in this diagram they form the upper halves of diamond-shaped figures of the phonocardiogram). Systolic regurgitant murmurs are pansystolic. The configuration of the diastolic ejection murmur of mitral stenosis
terminates in a crescendo caused by superimposition of atrial contraction. Although the diastolic regurgitant murmurs are
pandiastolic, in aortic and pulmonic regurgitation, the late diastolic part is seldom heard.
aortic murmurs, and missing aortic insufciency in association with aortic
systolic murmurs.
Benign, innocent, physiologic, functional, nonpathologic basal systolic
murmurs. These murmurs can be produced by increased ow velocity and
decreased blood viscosity. Most commonly heard in the second left interspace, they have medium pitch and a reusually grade I-II/VI. They are best
heard when supine and tend to disappear with sitting or standing. They are
infrequently transmitted to the neck. Functional murmurs occur in normal
adults with anemia, fever, anxiety, exercise, hyperthyroidism, or pregnancy.
Approximately 50% of normal children have functional systolic murmurs.
Aortic valve stenosis.
Progressive commissural fusion and leaet brosis
result in a small valve orice impeding LV ejection (Fig. 8-40C). The Murmur:
Classically the murmur is heard in the second right interspace, but almost as
often it is audible along the left sternal border in the third and fourth interspaces and at the apex. In ~15% of cases, it is loudest at the apex. Regardless
of the site of maximal intensity, it transmits to the carotid arteries. Loud murmurs can be accompanied by systolic thrills at the base and in the carotids.
Onset is very shortly after S1, when intraventricular pressure rst exceeds
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A. Normal ventricular
systole
D. Aortic
regurgitation
Blood flow in
normal direction
Blood flow in
abnormal direction
Zigzag indicates
murmur associated
with flow of blood
Normal thickness
of myocardium
Hypertrophy of
myocardium
Region of increased
blood pressure
B. Normal ventricular
diastole
E. Pulmonic
stenosis
FIG. 8-40 Anatomic Bases for Cardiac Murmurs I.
C. Aortic
stenosis
F. Pulmonic
regurgitation
SymbolsSymbols
Ventricular systole
Ventricular diastole
Heart sound S
Heart sound S
Ejection murmur
Regurgitant murmur
1
2
aortic pressure. It ceases at or before S2. It is diamond shaped, initially rising
(crescendo) then falling (decrescendo) in intensity (Fig. 8-39). As stenosis worsens the murmur’s peak moves later in systole, i.e., late peaking. The murmur
is usually harsh, medium pitched, and audible with the bell and diaphragm.
Occasionally it sounds like gull’s call or a dove cooing. With decreased LV
contractility, it decreases in intensity and duration. Heart Sounds: In moderate
and severe aortic stenosis accompanied by signicant valve leaet calcication,
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