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39—AUSCULTATION OF THE HEART: GENERAL PRINCIPLES
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323
B. BELL PRESSURE
To detect low-frequency sounds, the stethoscope bell should be applied to the body wall with
only enough pressure to create an air seal and exclude ambient noise. Excessive pressure with the
bell stretches the skin, which then acts like a diaphragm and makes low-frequency sounds more
difficult to hear. By selectively varying the pressure on the stethoscope bell, the clinician can easily
distinguish low- from high-frequency sounds: if a sound is audible with the bell using light pressure but disappears with firm pressure, it is a low-frequency sound. is technique is f requently
used to confirm that an early diastolic sound is indeed a third heart sound (i.e., third heart sounds
are low-frequency sounds, whereas other early diastolic sounds like the pericardial knock are
high-frequency sounds) and to distinguish the combined fourth and first heart sounds (S4-S1)
from the split S1 (the S4 is a low-frequency sound but the S1 is not; firm pressure renders the S4-S1
into a single sound but does not affect the double sound of the split S1).
C. PATIENT POSITION
e clinician should listen to the patient’s heart with the patient in three positions: supine, left lateral
decubitus, and seated upright. e lateral decubitus position is best for detection of the third and
fourth heart sounds and the diastolic murmur of mitral stenosis (to detect these sounds, the clinician places the bell lightly over the apical impulse or just medial to the apical impulse).7 e seated
upright position is necessary to further evaluate audible expiratory splitting of S2 (see Chapter 40)
and to detect some pericardial rubs and murmurs of aortic regurgitation (see Chapters 45 and 47).
D. ORDER OF EXAMINATION
Routine auscultation of the heart should include the right upper sternal area, the entire left sternal
border, and the apex. Some cardiologists recommend proceeding from base to apex2; others from apex
to base.8 e diaphragm of the stethoscope should be applied to all areas, especially at the upper left
sternal area to detect S2 splitting and at all areas to detect other murmurs and sounds. After using the
diaphragm to listen to the lower left sternal area and apex, the bell should also be applied to these areas
to detect diastolic filling sounds (S3 and S4) and diastolic rumbling murmurs (e.g., mitral stenosis).
In selected patients, the clinician should also listen over the carotid arteries and axilla (in patients
with systolic murmurs, to clarify radiation of the murmur), the lower right sternal area (in patients with
diastolic murmur of aortic regurgitation, to detect aortic root disease), the back (in young patients
with hypertension, to detect the continuous murmur of coarctation), or other thoracic sites
(in patients with central cyanosis, to detect the continuous murmur of pulmonary arteriovenous fistulas).
E. DESCRIBING THE LOCATION OF SOUNDS
When describing heart sounds and murmurs, the clinician should identify where on the chest wall
the sound is loudest. Traditionally, the second right intercostal space next to the sternum is called
the aortic area or right base; the second left intercostal space next to the sternum, the pulmonary
area or left base; the fourth or fifth left parasternal space, the tricuspid area or left lower sternal
border; and the most lateral point of the palpable cardiac impulse, the mitral area or apex (see
Fig. 38.1 in Chapter 38 ).
Even so, the terms aortic area, pulmonary area, tricuspid area, and mitral area are ambiguous and
are best avoided. Many patients with aortic stenosis have murmurs loudest in the mitral area, and
some with mitral regurgitation have murmurs in the pulmonary or aortic area. A more precise way
to describe the location of sounds is to use the apex and the parasternal areas as reference points,
the parasternal location being further specified by the intercostal space (first, second, or third
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intercostal space; or lower sternal border) and whether it is the right or left edge of the sternum. For
example, a sound might be loudest at the “apex,” the “second left intercostal space” (i.e., next to the
left sternal edge in the 2nd intercostal space), or “between the apex and left lower sternal border.”
8—THE HEART
F. TECHNIQUE OF FOCUSING
e human brain has an uncanny ability to isolate and focus on one type of sensory information
by repressing awareness of all other sensations. A common example of this phenomenon is the
person reading a book in a room in which a clock is ticking: the person may read long passages
of the book without even hearing the clock but hears the ticking clock immediately after putting
the book down. When listening to the heart, the clinician’s attention is quickly drawn to the most
prominent sounds, but this occurs at the expense of detecting the fainter sounds. erefore, to
avoid missing these fainter sounds or subtle splitting, the clinician should concentrate sequentially
on each part of the cardiac cycle, asking the following questions at each location: (1) Is S1 soft or
loud? (2) Is S2 split and, if so, how is it split? (3) Are there are any extra sounds or murmurs during
systole? and (4) Are there are any extra sounds or murmurs during diastole?
G. IDENTIFYING SYSTOLE AND DIASTOLE
Because all auscultatory findings are characterized by their timing, distinguishing systole from
diastole accurately is essential. ree principles help the clinician distinguish these events.
1. Systole is Shorter than Diastole
If the heart rate is normal or slow, systole can be easily distinguished from diastole because systole
is much shorter. e normal cadence of the heart tones, therefore, is
lub dup duplub duplub duplub
(lub is S1 and dup is S2). When the heart rate accelerates, however, diastole shortens and, at a
rate of 100 or more, the cadence of S1 and S2 resembles the following “tic toc” rhythm:
lub dup duplub duplub duplub duplub duplub
In these patients, other techniques are necessary to distinguish systole from diastole.
2. Characteristics of the First and Second Heart Sounds
At the second left intercostal space, S2 is generally louder, shorter, and sharper than S1 (S2 has more
high-frequency energy than S1, which is why dup, a snappier sound than lub, is used to characterize S2). If the timing of extra heart sounds and murmurs is confusing at the lower sternal edge or
apex (as it often is in patients with fast heart rhythms), the clinician can return the stethoscope to
the second left intercostal space, identify S2 by its louder and sharper sound, and then inch slowly
back to the area of interest, keeping track of S2 along the way.
3. Carotid Impulse
e palpable impulse from the carotid usually occurs just after S1, which the clinician detects by
simultaneously listening to the heart tones and palpating the carotid artery. In elderly patients
with tachycardia, however, this rule is sometimes misleading because the carotid impulse seems to
fall closer to S2, although even in these patients the carotid impulse still falls between S1 and S2.
References may be accessed online at Elsevier eBooks for Practicing Clinicians.
References
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1. Ongley PA, Sprague HB, Rappaport MB, Nadas AS. Heart Sounds and Murmurs: A Clinical and
Phonocardiographic Study. Grune & Stratton; 1960.
2. Leatham A. Auscultation of the Heart and Phonocardiography. 2nd ed. Churchill Livingstone; 1975.
3. Kindig JR, Beeson TP, Campbell RW, Andries F, Tavel ME. Acoustical performance of the stethoscope:
a comparative analysis. Am Heart J. 1982;104(2 Pt 1):269–275.
4. Rappaport MB, Sprague HB. e effects of tubing bore on stethoscope efficiency. Am Heart J.
1951;42(4):605–609.
5. Ravin A, Craddock LD, Wolf PS, Shander D. Auscultation of the Heart. 3rd ed. Year Book Medical
Publishers, Inc.; 1977.
6. Rappaport MB, Sprague HB. e effects of improper fitting of stethoscope to ears on auscultatory effi-�
ciency. Am Heart J. 1952;43(5):713–715.
7. Bethell HJN, Nixon PGF. Examination of the heart in supine and left lateral positions. Br Heart J.
1973;35(9):902–907.
8. Perloff JK. Physical Examination of the Heart and Circulation. 1st ed. W. B. Saunders; 1982.
324.e1
CHAPTER
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40
The First and Second Heart
Sounds
KEY TEACHING POINTS
• The most important characteristic of S1 is its intensity. A loud S1 indicates a vigorous
ventricular contraction, short PR interval, or both. A soft S1 indicates a feeble ventricular
contraction, long PR interval, or both.
• If the pulse is regular and S1 intensity varies from beat to beat, the only possible diagnosis
is atrioventricular dissociation (e.g., complete heart block).
• The most important characteristic of S2 is splitting, which may be normal (single or
physiologic) or abnormal (wide physiologic, fixed, or paradoxic). The most common
causes of wide physiologic or paradoxic splitting are bundle branch blocks.
e rst and second heart sounds (S1 and S2) dene systole and diastole and therefore form the
framework for analyzing all other auscultatory physical signs, including the third and fourth heart
sounds, clicks and ejection sounds, knocks and opening snaps, and systolic and diastolic murmurs.
In his classic treatise describing the discovery of the circulatory system, written in 1628, Harvey
described both S1 and S2, comparing them to the gulping sound made by a horse drinking water.1
e rst person to state that S1 and S2 were the sounds of closing heart valves was Rouanet of
France, who wrote in his 1832 MD thesis that S1 occurred when the atrioventricular (i.e., mitral
and tricuspid) valves closed, and S2 occurred when the semilunar (i.e., aortic and pulmonic) valves
2
closed.
THE FIRST HEART SOUND (S1)
I. The Finding
S1 is heard well across the entire precordium, both with the bell and diaphragm of the stethoscope.
It is usually loudest at or near the apex and contains more low frequency energy than does S2,
which explains why, when mimicking the sound, the term lub is used for S1 and the sharper term
dup for S2.
*
It was Williams in 1840 who invented the lub dup onomatopoeia.
*
3
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II. Pathogenesis
8—THE HEART
A. CAUSE OF S
1
e precise cause of S1 has been debated for decades. Although its two recordable components
coincide with closure of the mitral and tricuspid valves, the force of valve closure itself is insufcient to generate sound.4 Instead, their closure probably causes moving columns of blood to
abruptly decelerate, which sets up vibrations in the chordae tendineae, ventricles, and blood as a
unit (i.e., cardiohemic system).
B. INTENSITY OF S
4,5
1
e most important abnormalities of S1 relate to its intensity: e sound can be abnormally loud,
abnormally faint, or vary in intensity abnormally from beat to beat. e primary variables governing intensity of S1 are strength of ventricular contraction and the position of the atrioventricular
leaets at the onset of ventricular systole.
1. Ventricular Contractility
e stronger the ventricular contraction, the louder the S1. Strong contractions, which have a high
dP/dT (i.e., large increase in pressure with respect to time), intensify S1 because the valves close
with more force and generate more vibrations in the cardiohemic system.
6–8
2. Position of the Valve Leaflets at Onset of Ventricular Systole
If the mitral valve is wide open at the onset of ventricular systole, it will take longer to close completely
than if it had been barely open. Even this small delay in closure intensies S1, because closure occurs
on a later and steeper portion of the left ventricular (LV) pressure curve (i.e., dP/dT is greater).
9
e PR interval is the main variable determining the position of the valves at the beginning of
ventricular systole. If the PR interval is short, ventricular systole immediately follows atrial systole
(i.e., the R wave immediately follows the P wave). Because atrial systole kicks the valve open, a
short PR guarantees that the valve will be wide open at the onset of ventricular systole. In contrast,
a long PR interval allows time for the cusps of the atrioventricular valves to oat back together
before ventricular systole occurs. Studies show that, with PR intervals less than 0.20 seconds, the
intensity of S1 varies inversely with the PR interval (the shorter the PR interval, the louder the
sound). With PR intervals greater than 0.20 seconds, S1 is faint or absent.
8–10
III. Clinical Significance
A. LOUD S
S1 may be abnormally loud because of unusually vigorous ventricular contractions or because of
delayed closure of the mitral valve.
1. Vigorous Ventricular Contractions
Vigorous contractions, such as those occurring from fever and sympathetic stimulation (e.g., betaadrenergic inhalers, thyrotoxicosis), increase dP/dT and intensify S1.
2. Delayed Closure of the Mitral Valve
a. Prolapsed Mitral Valve
In patients with the murmur of mitral regurgitation, a loud S1 is a clue to the diagnosis of early
prolapse of the mitral valve (many patients with mitral regurgitation have a normal or soft S1).
1
6
11,12
40—THE FIRST AND SECOND HEART SOUNDS
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327
S1 is loud in these patients because the prolapsing leaets stop moving and tense later than nor-
mal, when dP/dT in the ventricle is greater.
11
b. Mitral Stenosis
Ninety percent of patients with pure uncomplicated mitral stenosis have a loud S1.13 Because the
murmur of mitral stenosis is often dicult to hear, a traditional teaching is that clinicians should
suspect mitral stenosis in any patient with an unexplained loud S1 and listen carefully for the
murmur with the patient lying on the left side.
Mitral stenosis delays closure of the mitral valve because the pressure gradient between the
left atrium and left ventricle keeps the leaets open until the moment of ventricular systole. After
successful valvuloplasty, the loud S1 becomes softer.
13
c. Left Atrial Myxoma
Many patients with left atrial myxoma (7 of 9 in one series) also have a loud S1 because the tumor
falling into the mitral orice during diastole delays closure of the valve.
B. FAINT OR ABSENT S
1
14
S1 is unusually faint if ventricular contractions are weak or if the mitral valve is already closed
when ventricular systole occurs.
1. Weak Ventricular Contractions (Low dP/dT)
Common examples of weak contractions causing a faint S1 are myocardial infarction and left
bundle branch block.
15
2. Early Closure of the Mitral Valve
Common causes of early mitral closure causing the faint S1 include the following:
a. Long PR Interval (>0.20 seconds)
See the section on intensity of S1.
b. Acute Aortic Regurgitation
In patients with the murmur of aortic regurgitation, the faint or absent S1 is an important clue that
the regurgitation is acute (e.g., endocarditis) and not chronic. Patients with acute aortic regurgitation have much higher LV end diastolic pressures than those with chronic regurgitation, because
the acutely failing valve has not allowed time for the ventricle to enlarge, as it does to compensate
for chronic regurgitation. e high pressures in the ventricle eventually exceed diastolic left atrial
pressures, closing the mitral valve before ventricular systole and thus making S1 faint or absent.
C. VARYING INTENSITY OF S
If the arterial pulse rhythm is regular but S1 varies in intensity, the only possible explanation is that the
PR interval is changing from beat to beat, which means the patient has atrioventricular dissociation.
In contrast, in patients with irregular rhythms, changing intensity of S1 has no diagnostic signicance,
because ventricular lling and dP/dT—and therefore S1 intensity—depend completely on cycle length.
In patients with pacer-induced regular rhythms, an S1 that varies in intensity is compelling
evidence for atrioventricular dissociation (likelihood ratio [LR] = 24.4; see EBM Box 40.1).
Presumably, the nding is also as accurate in patients with native rhythms. In patients with complete heart block, S1 intensity is predictable, varying inversely with the PR interval for intervals
16
1
328
),567$1'6(&21'+($576281'6
, detecting
atrial septal defect
hypertension if mitral stenosis
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8—THE HEART
EBM BOX 40.1 The First and Second Heart Sounds*
Likelihood Ratio‡ if
Finding Is
Present Absent
20,21
or ≥25 mm Hg.
Finding (Reference)
†
Sensitivity
(%)
Specificity
(%)
First heart sound
Varying intensity S
Detecting atrioventricular
dissociation
1
17
58 98 24.4 0.4
Second heart sound
Fixed wide splitting
Detecting atrial septal defect
18
92 65 2.6 0.1
Paradoxic splitting
Detecting significant aortic stenosis1950 79 NS NS
Loud P
Detecting pulmonary hypertension in
patients with mitral stenosis
Detecting pulmonary hypertension in
patients with cirrhosis
Palpable P
Detecting pulmonary hypertension in
2
mitral stenosis
20
Absent or diminished S
Detecting significant aortic stenosis
in patients with aortic flow
19,23–27
murmurs
*
Diagnostic standard: for atrioventricular dissociation, ventricles were paced independently of atria; for
atrial septal defect, right heart catheterization; for severe aortic stenosis, aortic valve area <0.75 cm2,
<0.8 cm2;
for pulmonary hypertension, mean pulmonary arterial pressure ≥50 mm Hg
†
second interspace than right second interspace21; the figures for fixed splitting of S2 apply only to patients
having audible expiratory splitting.
‡
22,25
peak gradient >50 mm Hg;
Definition of findings: for loud P2, splitting heard with loud second component20 or S2 louder at left
Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.
AV, Atrioventricular; NS, not significant.
20,21
22
2
58–96 19–46 NS NS
38 98 17.6 NS
96 73 3.6 0.05
44–90 63–98 3.8 0.4
19,25
or peak velocity of aortic flow >3.6 m/sec24 or ≥4 m/sec;26
22
LRs
0.1 0.2 0.5 12510
0QbT]RT of palpable P2,
PaVdX]VPVPX]bc pulmonary
0QbT]RT of fixed wide S
splitting, PaVdX]VPVPX]bcatrial
septal defect
Probability
3TRaTPbT 8]RaTPbT
Varying intensity S
AV dissociation if tachycardia
Loud P2, detecting pulmonary
2
hypertension if cirrhosis of liver
Palpable P
hypertension if mitral stenosis
Fixed wide S
+45%+30%+15%–15%–30%–45%
, detecting pulmonary
2
splitting, detecting
2
LRs
1
40—THE FIRST AND SECOND HEART SOUNDS
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329
less than 0.2 seconds, becoming inaudible for intervals 0.2 to 0.5 seconds, and becoming louder
again with intervals more than 0.5 seconds (because the mitral valve reopens).
D. PROMINENT SPLITTING OF S
1
10
Any delay in the closure of the tricuspid valve, the second component of S1, accentuates splitting
of S1. is nding therefore occurs in patients with right bundle branch block (RBBB) or in LV
ectopic or paced beats, all of which delay the onset of right ventricular (RV) systole and also cause
wide physiologic splitting of S2 (see later).
5,28
How to distinguish the split S1 from other double sounds occurring around S1, such as S4 + S1
and S1 + ejection sound, is discussed in Chapter 41.
THE SECOND HEART SOUND (S2)
I. Introduction
e most important diagnostic feature of S2 is its “splitting,” which refers to how the aortic and
pulmonic components of S2 vary in timing during the respiratory cycle. e intensity of S2 has
less diagnostic importance. (is contrasts with S1, in which intensity is more important than
splitting.) Splitting of S2 was rst recognized by Potain in 1865, and its importance to cardiac
auscultation was described by Leatham in the 1950s, who called S2 the “key to auscultation of the
29,30
heart.”
circulation—was discovered in the 1970s.
II. Normal Splitting of S
A. THE FINDING
e correct explanation for normal splitting—increased “hangout” in the pulmonary
31,32
2
In normal persons, the rst component of S2 is caused by closure of the aortic valve (A2); the second, by closure of the pulmonic valve (P2). During inspiration the interval separating A2 and P2
increases by about 20 to 30 milliseconds (ms) (Fig. 40.1).
Although the phonocardiogram almost always records both components of S2, the human ear perceives them as a single sound during expiration in over 90% of normal persons.33 In normal persons
during inspiration, the human ear either perceives two components (physiologic splitting, heard in 65%
to 75% of normal adults; see Fig. 40.1)† or still perceives a single component (single S2, heard in 25% to
35% of normal adults). e older the person, the more likely S2 will be single instead of physiologic.
In a minority of normal persons, expiratory splitting is heard in the supine position, although
S2 becomes single during expiration in these patients when they sit up.
B. LOCATION OF SOUND
S2 splitting is usually heard only in the second or third intercostal space, next to the left sternum.34
It is sometimes heard at a slightly lower location, especially in patients with chronic pulmonary
disease, and at a slightly higher location in those who are obese.34 Splitting is not normally heard
at other locations because P2 is too faint.
†
ese two components are very close together, bordering the threshold of being perceived as a single sound.
Harvey suggests mimicking the normal expiratory sound by striking a single knuckle against a tabletop and
mimicking inspiratory physiologic splitting by striking two knuckles almost simultaneously.
suggests mimicking inspiratory splitting by rolling the tongue as in a Spanish dr or tr or by saying pa-da as
quickly and sharply as possible.
18,30,32
33, 34
37
35
36
Constant
330
2
Single
Ph
Wid
ph
Wide fix
Pa
Expiration:
Inspiration:
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8—THE HEART
ysiologic
e
S
1
S
1
S
1
A
2
P
2
A
2
P
2
A
2
P
2
S
1
S
1
S
1
A
2
P
2
A
2
P
2
A
2
P
2
ysiologic
ed
S
1
S
1
A
2
P
2
A
2
P
2
S
1
S
1
A
2
P
A
2
P
2
radoxic
Fig. 40.1 S2 splitting. Splitting refers to the separation of the aortic component (A2) and the pulmonic compo-
nent (P2) during expiration (left column) and inspiration (right column). There are two normal patterns (single and
physiologic) and three abnormal patterns (wide physiologic, wide fixed, and paradoxic). The dotted lines indicate that all three abnormal forms of splitting are distinguished by having audible expiratory splitting. See text.
C.
TECHNIQUE
It is important that the patient breathe regularly in and out when evaluating S
held inspiration or held expiration tends to make the two components drift apart, thus making it
impossible to interpret the sound.
D.
PHYSIOLOGY OF SPLITTING
e normal delay in P
results from a long “hangout” interval in the normal pulmonary circulation.
2
(It is not because RV systole ends later than LV systole; they actually end at the same moment, see
Fig. 40.2.) Hangout means that the pulmonary circulation oers so little resistance to blood ow
that ow continues for a short period even after completion of RV mechanical systole.
aortic valve, there is little hangout, causing ow to cease and the valve to close immediately after
completion of LV contraction.
A
and P
2
move apart during inspiration, primarily because inspiration delays P
2
About half of the inspiratory augmentation of the A2-P
hangout interval in the pulmonary circulation. About 25% of inspiratory augmentation is due to
lengthening of RV systole (from increased lling of the right side of the heart during inspiration),
and the remaining 25% is due to shortening of LV systole (from a reduction of lling of the left
side of the heart during inspiration).
splitting, because
2
18
31,32
At the
even more.
interval is due to a further increase in the
2
32
2
40—THE FIRST AND SECOND HEART SOUNDS
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331
Heart tones
Aorta
Left ventricle
Pulmonary
artery
Right ventricle
Mechanical systole
S
1
A
2
P
2
A
interval = 50 ms
2-P2
Hangout = 10 ms
Hangout = 60 ms
Fig. 40.2 Mechanism of S2 splitting. The timing of heart tones (top) is correlated with pressure tracings from
the left side of the heart (i.e., aorta and left ventricle, top pressure tracings) and right side of the heart (i.e.,
pulmonary artery and right ventricle, bottom pressure tracings). The solid rectangle at the bottom of the figure
depicts the duration of mechanical systole, which is the same for the right and left ventricles. A2 coincides with
the incisura (i.e., notch) on the aorta tracing, P2 coincides with the incisura on the pulmonary artery tracing,
and both sounds occur a short interval after completion of mechanical systole (the interval between the end
of mechanical systole and valve closure is called hangout). On the left side of the heart, hangout is very short
(10 ms, i.e., the aortic valve closes almost immediately after completion of mechanical systole). On the right
side of the heart, however, hangout is longer (60 ms) because the compliant pulmonary circulation offers so
little resistance to continued forward flow. The difference between these numbers explains why P2 normally
occurs after A2 (i.e., A2-P2 interval in this patient = 60 − 10 = 50 ms). Changes in hangout also explain in part
why splitting normally increases during inspiration, and why most patients with pulmonary hypertension have
a single S2. See the text.
III. Abnormal Splitting of S
A. THE FINDING
ere are three abnormalities of S2 splitting (Fig. 40.1):
1. Wide Physiologic Splitting
Wide physiologic splitting means that splitting occurs during inspiration and expiration, though
the A2P2 interval widens further during inspiration.
2
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