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38—PALPATION OF THE HEART
LR
SIZE AND POSITION OF PALPABLE APICAL IMPULSE
Apical beat lateral to MCL, detecting
cardiothoracic ratio >0.5
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EBM BOX 38.1 Size and Position of Palpable Apical Impulse*
315
Likelihood Ratio‡ if Finding Is
Present Absent
Finding (Reference)
†
Sensitivity
(%)
Specificity
(%)
Position of Apical Beat
Supine apical impulse lateral to MCL
Detecting cardiothoracic ratio
19,22,25
>0.5
Detecting low ejection fraction
Detecting increased left ventricular
end-diastolic volume
21,30
Detecting pulmonary capillary
wedge pressure >12 mm Hg
39–60 76–93 3.4 0.6
26–29
5–66 93–99 10.3 0.7
33–34 92–96 5.1 0.7
42 93 5.8 NS
30
Supine apical impulse >10 cm from midsternal line
Detecting cardiothoracic ratio
17,22,25
>0.5
61–80 28–97 NS 0.5
Size of Apical Beat
Apical beat diameter ≥4 cm in left lateral decubitus position at 45 degrees
Detecting increased left ventricular
end-diastolic volume
Diagnostic standard: for cardiothoracic ratio, maximal transverse diameter of heart on chest radiography
divided by maximal transverse diameter of thoracic cage; for low ejection fraction, LV ejection fraction
<0.50 or <0.53 by scintigraphy,
echocardiography28; for increased LV end-diastolic volume:30 >90 ml/M2 or >138 mL (echocardiography,31
>109.2 ml/M2 (computed tomography),21 or upper 5th percentile of normal (echocardiography).
†
Definition of findings: except for “apical beat diameter,” these data apply to all patients, whether or not
an apical beat is palpable (i.e., nonpalpable apical beat = test “negative”). The only exception is the data
for “apical beat diameter,” which applies only to patients who have a measurable apical beat in the left
lateral decubitus position (i.e., apical beat diameter ≥4 cm = test positive; <4 cm = test negative; unable
to measure diameter = unable to evaluate using these data).
‡
Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.
LV, Left ventricle; MCL, midclavicular line; NS, not significant.
20,31
48–85 79–96 4.7 NS
26,27
<0.5 by echocardiography,29 or LV fractional shortening <25% by
20
Decrease Increase
s
0.1 0.2 0.5 12510
Probability
+45%+30%+15%–15%–30%–45%
LRs
Apical beat lateral to MCL,
detecting low ejection fraction
pulmonary capillary wedge pressure
>12 mm Hg
Apical beat lateral to MCL,
detecting increased LV volume
Apical beat diameter ≥4 cm in left lateral
decubitus position, detecting increased
LV volume
Apical beat lateral to MCL, detecting
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8—THE HEART
reduced.34 erefore, if patients with the murmur of mitral stenosis also have a hyperkinetic apical
impulse, an abnormality other than isolated mitral stenosis must be present, such as mitral regurgitation or aortic regurgitation (LR = 11.2; see EBM Box 38.2).
b. Sustained Apical Movements
A sustained or double apical movement (double refers to the combination of palpable S4 and apical
movement, see Chapter 41) increases the probability of left ventricular hypertrophy (LR = 5.6).
In patients with aortic ow murmurs, the nding of a sustained apical impulse increases the probability of severe aortic stenosis (LR = 4.1; see EBM Box 38.2). In patients with the early diastolic
murmur of aortic regurgitation, the sustained impulse is less helpful (LR = 2.4 for signicant
regurgitation), although the nding of a normal or absent apical impulse (i.e., not sustained or
EBM BOX 38.2 Abnormal Palpable Movements*
Finding (Reference)
†
Sensitivity
(%)
Hyperkinetic apical movement
Detecting associated mitral
74 93 11.2 0.3
regurgitation or aortic valve
disease in patients with
mitral stenosis
34
Sustained or double apical movement
Detecting left ventricular
hypertrophy
21
57 90 5.6 0.5
Sustained apical movement
Detecting severe aortic
stenosis in patients with
aortic flow murmurs
Detecting moderate-to-
35
78 81 4.1 0.3
97 60 2.4 0.1
severe aortic regurgitation
in patients with basal early
diastolic murmurs
36
Lower sternal pulsations
Detecting moderate-to-severe
tricuspid regurgitation
37
17 99 12.5 0.8
Sustained left lower parasternal movement
Detecting right ventricular
peak pressure ≥50 mm
38
Hg
71 80 3.6 0.4
Right ventricular rock
Detecting moderate-to-severe
tricuspid regurgitation
37
5 100 31.4 NS
Pulsatile liver
Detecting moderate-to-severe
tricuspid regurgitation
Palpable P
Detecting pulmonary
2
hypertension in patients
with mitral stenosis
37,39
40
12–30 92–99 6.5 NS
96 73 3.6 0.05
Specificity
(%)
Likelihood Ratio‡ if Finding Is
Present Absent
continued
38—PALPATION OF THE HEART
ABNORMAL PALPABLE MOVEMENTS
hypertension if mitral stenosis
regurgitation if diastolic murmur
Sustained lower parasternal movement,
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Diagnostic standard: for LV hypertrophy, computed tomographic LV mass index >104 g/M2;21 for severe
aortic stenosis and moderate-to-severe aortic regurgitation, see EBM Boxes in Chapters 44 and 45;
for moderate-to-severe tricuspid regurgitation, 3+ or 4+ by angiography39 or as assessed visually from
echocardiography,37 and; for pulmonary hypertension, mean pulmonary artery pressure ≥50 mm Hg.
†
Definition of findings: for abnormal apical movement, “apical impulse heave or enlarged,”36 “sustained,”35
or “thrust”34; for sustained or double apical movement, apical movement extending beyond S2 or
combination of palpable S4 + LV apical movement21; for abnormal parasternal movement, “movement
extending to or past S2”38; for right ventricular rock, see text; for palpable P2 “palpable late systolic tap in
second left intercostal space next to sternum, which frequently followed parasternal lift.”
‡
Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.
LV, Left ventricle; NS, not significant.
40
Probability
Decrease Increase
+45%+30%+15%–15%–30%–45%
LRs
0.1 0.2 0.5 12510
LRs
317
40
Absence of palpable P2,
arguing against pulmonary
hypertension in mitral stenosis
Absence of sustained apical
movement, arguing against
moderate-to-severe aortic
hyperkinetic) in these patients decreases signicantly the probability of moderate-to-severe aortic
regurgitation (LR = 0.1; see EBM Box 38.2).
c. Retracting Apical Impulse
(1). Constrictive Pericarditis. In up to 90% of patients with constrictive pericarditis, the
apical impulse retracts during systole (sometimes accompanied by systolic retraction of the left
parasternal area).
systolic movement of the ventricles but allows rapid and prominent early diastolic lling of
the ventricle. e prominent diastolic lling causes a palpable diastolic outward movement,
which contributes to the overall impression that the apical impulse retracts during systole (see
Chapter 47).
e rst clinician to recognize the retracting apical impulse as a sign of “adhesive” pericarditis
was Skoda in 1852.
(2). Tricuspid Regurgitation. In severe tricuspid regurgitation, a dilated right ventricle,
occupying the apex, ejects blood into a dilated right atrium and liver, located nearer the
sternum.
8
This causes a characteristic rocking motion (or right ventricular rock), the apical area retracting inward during systole and the lower left or right parasternal area moving
outward during systole,
RV rock, detecting moderate-tosevere tricuspid regurgitation
Hyperkinetic apical movement,
detecting other valvular disease if
mitral stenosis
Sustained apical movement,
detecting severe aortic stenosis if
aortic murmur
detecting RV pressure ≥50 mm Hg
Palpable P
8,41
In these patients, the diseased pericardium prevents the normal outward
42
43
often accompanied by a pulsatile liver. All three findings increase
, detecting pulmonary
2
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8—THE HEART
the probability of moderate-to-severe tricuspid regurgitation (LR = 31.4 for right ventricular rock, LR = 12.5 for lower sternal pulsations, and LR = 6.5 for pulsatile liver, see
EBM Box 38.2).
B. LEFT LOWER PARASTERNAL MOVEMENTS
In normal persons, the clinician either palpates no movement or only a tiny inward one during
systole at this location. Abnormal movements at this location are classied as hyperkinetic or
sustained, depending on their relationship to S2.
1. Hyperkinetic Movements
Hyperkinetic movements of the left lower parasternal area occur in up to 50% of patients with
atrial septal defect, which causes volume overload of the right ventricle.44 Nonetheless, this nding
has limited diagnosis value without other ndings of atrial septal defect—exaggerated y descent
in the neck veins, wide and xed S2 splitting, and midsystolic murmur at the left second intercostal space (usually of grade 2 of 6)—because it is also sometimes found in patients without heart
disease, such as those with thin chests, pectus excavatum, fever, or other high output states.
38,44
2. Sustained Movements
Sustained movements of the left lower sternal area may represent either an abnormal right ventricle (e.g., pressure overload from pulmonary hypertension or pulmonic stenosis or volume overload from atrial septal defect) or an enlarged left atrium (e.g., severe mitral regurgitation). Both
right ventricular and left atrial parasternal movements are outward movements that begin to move
inward only at S2 or just after it and therefore are classied as sustained; they are distinguished by
when the outward movement begins.
a. Right Ventricle
Outward right ventricular movements begin at the rst heart sound. If the clinician can exclude
volume overload of the right ventricle and mitral regurgitation (both of which also cause parasternal movements), the nding of a sustained left parasternal movement is a modest sign of pulmonary hypertension (often accompanied by tricuspid regurgitation; see earlier). In patients with mitral
stenosis, the duration of the sustained lower parasternal movement correlates well with pulmonary
pressures.34 In patients with a wide variety of valvular and congenital heart lesions (excluding mitral
regurgitation), the sustained lower left parasternal movement is a modest discriminator between those
with peak right ventricular pressures >50 mm Hg and those with lower pressures (positive LR = 3.6,
negative LR 0.4; see EBM Box 38.2). In patients with chronic liver disease undergoing evaluation for
liver transplantation, the right ventricular heave increases probability of pulmonary hypertension (i.e.,
mean pulmonary artery pressures ≥25 mm Hg, LR = 8.8; see Chapter 8).45 Even so, in patients seeing
pulmonary hypertension specialists, the right ventricular heave was not an accurate sign of pulmonary
hypertension (dened as mean pulmonary artery pressure ≥25 mm Hg; sensitivity = 42%, specicity =
84%, LR not signicant).46 Up to 30% of patients with atrial septal defect, whether or not there is
associated pulmonary hypertension, also have sustained lower left parasternal movements.
44
b. Left Atrium and Mitral Regurgitation
In patients with severe mitral regurgitation, ventricular contraction forces blood backwards into
a dilated left atrium, which lies on the posterior surface of the heart and acts like an expanding
cushion to lift up the heart, including the left parasternal area. is sustained movement, most
easily palpated in the 4th or 5th intercostal space near the sternum,
47,48
diers from those caused
by the right ventricle, because outward movement begins in the second half of systole (it parallels
the V wave on the left atrial pressure tracing).
38—PALPATION OF THE HEART
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319
In patients with isolated mitral regurgitation, the degree of the late systolic outward movement
at the lower sternal edge correlates well with the severity of mitral regurgitation (r = 0.93, p <0.01;
the correlation is much worse if there is associated mitral stenosis, which may cause parasternal
movements from pulmonary hypertension).
defect, the parasternal movement has no relationship to right ventricular pressures.
47,48
In pure mitral regurgitation, as in atrial septal
49
C. ANEURYSMS
In one study of consecutive patients with ventricular aneurysms identied by angiography, 33%
had abnormal precordial movements.50 Typical ndings were (1) a double cardiac impulse, the
rst component representing the normal apical outward movement and second the bulging of
the aneurysm during peak ventricular pressures later in systole,
51,52
and (2) a sustained impulse
that extended superiorly or medially from the usual location of the apical impulse.50 If detectable
by palpation, the aneurysm originates in the anterior wall or apex of the left ventricle; aneurysms
originating from the inferior or lateral wall are too distant from the anterior chest wall to be
detectable by palpation.
50
D. DIFFUSE PRECORDIAL MOVEMENTS
Diuse outward movements of the entire precordium, from the apex to lower parasternal area,
may result from (1) right ventricular enlargement (which dilates to occupy the apical area), (2) left
ventricular enlargement (which rotates to occupy the lower parasternal area), or (3) biventricular enlargement.11 Palpation alone cannot distinguish these dierent etiologies—even sensitive
recordings from impulse cardiography or kinetocardiography could not do this—and the clinician must rely on other ndings to determine which chamber is most likely causing the diuse
movement.
E. RIGHT LOWER PARASTERNAL MOVEMENTS
Abnormal systolic outward movements appear in the right lower parasternal area from tricuspid
regurgitation (ejection of blood into the right atrium and liver that lies under the right side of the
sternum) or from mitral regurgitation (ejection of blood in a dilated left atrium).
F. PALPABLE P
2
A palpable P2 (i.e., the pulmonic component of second heart sound) is a sharp, brief snapping
sensation felt over the left base, coincident with S2. It is much briefer than other precordial movements. In patients with mitral stenosis, a palpable P2 increases the probability of pulmonary hypertension (LR = 3.6 for mean pulmonary pressure >50 mm Hg). More importantly, the absence of
a palpable P2 in these patients decreases the probability of a pulmonary pressure this high (LR =
0.05; see EBM Box 38.2). Nonetheless, in other settings, such as pulmonary hypertension clinics,
the palpable P2 did not accurately identify pulmonary hypertension (dened as mean pulmonary
artery pressure ≥25 mm Hg; LR not signicant).
G. PALPABLE THIRD AND FOURTH HEART SOUNDS
Some patients with rapid early ventricular lling (e.g., mitral regurgitation) have a palpable
early diastolic movement at the apex. Other patients with strong atrial contractions into sti
ventricles (e.g., hypertensive or ischemic heart disease) have palpable presystolic apical movements. ese movements have the same signicance as their audible counterparts, the third
11,43,53
46
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8—THE HEART
and fourth heart sound (i.e., S3 and S4, see Chapter 41). ey are usually called palpable S3 and
palpable S4.
e S4 is much more likely to be palpable than the S3, and both are more likely to be felt when
the patient is in the lateral decubitus position.
7,9,10
e palpable S4 causes either a double outward
impulse near S1 (a common analogy is the grace note in music, see double apical movement in EBM
Box 38.2) or single outward movement, consisting of the palpable S4 and apical beat together,
which is distinguished from the apical beat alone because the outward movement begins slightly
before S1.
of a wooden coee stirrer, appears in the reference by Phan.
10,11
An excellent video of a palpable S4 (double apical movement), made visible with use
13
References may be accessed online at Elsevier eBooks for Practicing Clinicians.
References
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estimation of right and left ventricular ejection fraction in acute myocardial infarction. Am J Cardiol.
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mining left ventricular function: correlation with left ventricular ejection fraction determined by radionuclide ventriculography. J Am Coll Cardiol. 1983;1(2 pt 1):417–420.
28. Davie AP, Francis CM, Caruana FL, Sutherland GR, McMurray JJV. Assessing diagnosis in heart fail-
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45. Pilatis ND, Jacobs LE, Rerkpattanapipat P, et al. Clinical predictors of pulmonary hypertension in
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CHAPTER
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39
Auscultation of the Heart: General
Principles
KEY TEACHING POINTS
• Careful auscultation of the heart requires a quiet examination room. The clinician should
systematically inch the stethoscope from apex to base (or in the opposite direction, from
base to apex). At each location, the clinician should focus sequentially on the different
elements of the cardiac cycle (i.e., S1, S2, systole, and diastole).
• The bell of the stethoscope is used to identify low-frequency sounds; the diaphragm is
used to listen to high-frequency sounds.
• The best way to distinguish systole from diastole is by the cadence of heart tones (systole
is shorter than diastole if the heart rate is normal) or by identifying S2 at the second left
parasternal space, where it is the louder, snappier heart sound.
I. Characteristics of Heart Sounds and Murmurs
Different heart sounds and murmurs are distinguished by four characteristics: (1) timing (i.e.,
systolic or diastolic), (2) intensity (i.e., loud or soft), (3) duration (i.e., long or short), and (4)
pitch (i.e., low or high frequency). A fifth characteristic, the sound’s quality, is also sometimes
included in descriptions of sounds (e.g., it may be described as “musical,” a “whoop,” or a “honk”).
Almost all heart sounds contain a mixture of frequencies (i.e., they are not musical in the acoustical sense, but instead are “noise,” like the static of a radio tuned between stations). erefore,
the descriptors low-frequency and high-frequency do not indicate that a sound has a pure musical
tone of a certain low or high pitch, but instead that the bulk of the sound’s energy is within the
low or high range.
Although the human ear can hear sounds with frequencies from 20 to 20,000 cycles per
second (Hz), the principal frequencies of heart sounds and murmurs are at the lower end of
this range, from 20 to 500 Hz.
nant frequencies are less than 100 Hz, such as third and fourth heart sounds and the diastolic
murmur of mitral stenosis. ese sounds are usually difficult to hear because the human ear
perceives lower frequencies relatively less well than higher frequencies. e murmur containing the highest frequency sound is aortic regurgitation, whose dominant frequencies
are about 400 Hz. e principal frequencies of other sounds and murmurs are between 100
and 400 Hz.
1,2
Low-frequency sounds, therefore, are those whose domi-
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8—THE HEART
II. The Stethoscope
A. BELL AND DIAPHRAGM
e traditional stethoscope has two different heads to receive sound, the bell and the diaphragm.
e bell is used to detect low-frequency sounds and the diaphragm to detect high-frequency
sounds.
e traditional explanation that the bell selectively transmits low-frequency sounds and the
diaphragm selectively filters out low-frequency sounds is probably incorrect. Actually, the bell
transmits all frequencies well, but in some patients with high-frequency murmurs (e.g., aortic
regurgitation), any additional low-frequency sound may mask high-frequency sound and make
high-frequency murmurs more difficult to detect.3 e diaphragm does not selectively filter out
low-frequency sounds, but instead attenuates all frequencies equally, thus dropping the barely
audible low-frequency ones below the threshold of human hearing.
B. PERFORMANCE OF DIFFERENT STETHOSCOPE MODELS
Many studies have examined the acoustics of stethoscopes, but the clinical relevance of this
research has never been formally tested. In general, these studies show that shallow bells transmit sound as well as deeper bells and that double tube stethoscopes are equivalent to single
tube models.3 e optimal internal bore of a stethoscope is somewhere between one-eighth and
three-sixteenths of an inch, because smaller bores diminish transmission of the higher frequency
1,4,5
sounds.
tion of high-frequency sounds.
ous models for single frequencies being very small.3 e most important source of poor acoustic
performance is an air leak, which typically results from poorly fitting ear pieces. Even a tiny air
leak with a diameter of only 0.015 inch will diminish transmission of sound by as much as 20 dB,*
particularly for those sounds less than 100 Hz.
Compared with shorter lengths of stethoscope tubing, longer tubes impair the conduc-
1
Most modern stethoscopes, however, transmit sound equally well, the differences among vari-
6
3
III. Use of the Stethoscope
Between the 1950s and late 1970s, cardiac auscultation was at its peak.† During this time cardiologists perfected their skills by routinely comparing bedside findings to the patient’s phonocardiogram, angiogram, and surgical findings, which allowed clinicians to make precise and accurate
diagnoses from bedside findings alone. e principles of bedside diagnosis used by these clinicians
are included elsewhere in this book. How these clinicians specifically used the stethoscope to
examine the patient is presented below.
A. EXAMINATION ROOM
Many faint heart sounds and murmurs are inaudible unless there is complete silence in the room.
e clinician should close the door to the examination room, turn off the television and radio, and
ask that all conversation stop.
†
Decibels describe relative intensity (or loudness) on a logarithmic scale.
†
In the late 1970s, two events initiated the decline of cardiac auscultation: the widespread introduction
of echocardiography and the decision by insurance companies to no longer make reimbursements for
phonocardiography.
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