Auscultation of Heart Sounds: S1, S2, S3, S4 Explained

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Auscultation of heart sounds
Author: Theo E Meyer, MD, PhD
Section Editor: Bernard J Gersh, MB, ChB, DPhil, FRCP, MACC
Deputy Editor: Susan B Yeon, MD, JD, FACC
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Mar 2019. | This topic last updated: Dec 12, 2018.
INTRODUCTION
The cardiovascular physical examination includes auscultation and palpation of the heart, as well as
examination of the arterial and venous pulses. The purpose of auscultation of the heart is to
characterize heart sounds and murmurs. (See "Examination of the precordial pulsation" and
"Examination of the arterial pulse" and "Examination of the jugular venous pulse".)
This topic will review the auscultation of heart sounds. The auscultation of cardiac murmurs is
discussed separately. (See "Auscultation of cardiac murmurs in adults".)
STETHOSCOPES
A variety of stethoscopes are available for auscultation of heart sounds. Many stethoscopes have a
separate bell and diaphragm. The bell is most effective at transmitting lower frequency sounds, while
the diaphragm is most effective at transmitting higher frequency sounds. Some stethoscopes combine
these functions into a single surface such that the intensity of pressure of the stethoscope against the
skin determines whether the stethoscope functions as a bell or a diaphragm. In addition, pressing the
bell more firmly against the skin alters the frequencies that are loudest towards those of a diaphragm,
such that higher frequency sounds become louder and lower frequency sounds become softer.
Acoustic as well as electronic stethoscopes are used for cardiac auscultation. There is limited
evidence comparing these devices [1­3]. Electronic auscultatory devices utilize advanced acoustic
sensor­based digital signal processing with a wide range of frequency response modes to enhance
sound acquisition [4]. Electronic devices offer bell or diaphragm modes, similar to acoustic
stethoscopes, although the acoustic characteristics of these devices differ [5]. Since an electronic
stethoscope is sensitive to ambient and friction noise, various electronic stethoscope models offer
technology for noise reduction. An electronic device enables shared auscultation for teaching
purposes and also enables direct digital recording of heart sounds for review and analysis.
CLASSIFICATION OF HEART SOUNDS
Heart sounds are broadly classified into high­ and low­frequency sounds [6].
High­frequency sounds arise from closing or opening valves, including mitral and tricuspid valve
closing sounds (M1 and T1), non­ejection sounds, opening snaps, aortic and pulmonary valve closure
sounds (A2 and P2), and early valvular ejection sounds. Prosthetic valve sounds are also high
frequency. (See 'First heart sound (S1)' below and 'Second heart sound (S2)' below and 'Ejection
sounds' below and 'Non­ejection systolic sounds' below and 'Early diastolic high­frequency sounds'
below and 'Prosthetic valve sounds' below.)
Low­frequency sounds include the third heart sound (S3, which may be physiologic or pathologic),
associated with early ventricular filling, and the fourth heart sound (S4), associated with the atrial
contribution to ventricular filling in late diastole. (See 'Third (S3) and fourth (S4) heart sounds' below.)
FIRST HEART SOUND (S1)
Genesis, timing, and location of S1 — The classic hypothesis for the genesis of the first heart
sound (S1), for which there is much support, relates the high­frequency components of S1 to mitral
and tricuspid valve closure. The first component of S1 is attributed to mitral valve closure (M1) and
the second to closure of the tricuspid valve (T1) [7­10]. More detailed examination of closure sounds
also suggest that the peak tension on the chordae tendineae and leaflets themselves appear to
contribute to the production of M1 and T1 [11,12]. A second hypothesis suggests that the principal
high­frequency elements of S1 are related to movement and acceleration of blood in early systole,
and are influenced by the peak rate of rise of left ventricular (LV) systolic pressure (dP/dt), which is a
measure of contractility and ejection of blood into the root of the aorta [13].
S1 occurs just before or is coincident with the upstroke of the carotid pulse. M1 precedes the upstroke
of the carotid pulse because it occurs before LV ejection begins. However, the delay between M1 and
the upstroke of the carotid pulse normally is too short to be appreciated at the bedside. T1 normally
coincides with the upstroke of the carotid pulse.
S1 normally is louder than the second heart sound (S2) over the apex and along the lower left sternal
border; intensity is reduced if S1 is softer than S2 over these areas. S1 intensity is likely to be
accentuated if S1 is much louder than S2 over the left or right second interspace. The M1 sound is
much louder than the T1 sound due to higher pressures in the left side of the heart; thus, M1 radiates
to all precordial areas (loudest at the apex), and T1 is usually only heard at the left lower sternal
border. This makes the M1 sound the main component of S1, and is best heard with the diaphragm of
the stethoscope.
Intensity of S1 — The following factors influence the intensity of S1:
● Mitral valve position at the onset of systole (wide versus partially open).
● Rate of M1 and T1.
● Mobility and structural integrity of the atrioventricular (AV) valves (eg, fibrosis, commissural fusion
of the leaflets, tethering of the posterior mitral leaflet, etc).
● The PR interval, the timing of atrial contraction (a determinant of mitral valve position) as it
relates to the onset of LV contraction.
● Force of ventricular systolic contraction.
Some of these factors, such as the rate of M1 and the strength of ventricular systole, are interrelated;
more than one factor may contribute to altered S1 intensity.
● Increased intensity of S1 – The following factors contribute to the position of mitral valve
(distance to closure) and velocity of closure (table 1):
• Increased transvalvular gradient, especially at end­diastole (mitral or tricuspid valve
obstruction as in mitral stenosis (movie 1), tricuspid stenosis, or atrial myxoma).
• Increased transvalvular flow (left­to­right shunt in patent ductus arteriosus, ventricular septal
defect, and high output state).
• Short diastole (tachycardia).
• Short PR intervals (preexcitation syndrome)
The relative contribution of the distance of travel and the velocity of M1 to increased S1 intensity
is difficult to determine; both factors are likely to play a role. When M1 occurs on the steeper part
of the LV pressure development, the intensity of S1 increases; this phenomenon may also
contribute to an accentuated S1 observed in patients with extremely short PR intervals, mitral
stenosis, and left atrial myxoma (figure 1)[14].
Similarly, S1 is normal or even accentuated in patients with mitral valve prolapse with late systolic
regurgitation. Increased intensity of S1 in some patients with mitral valve prolapse syndrome may
be caused by an increased strength of ventricular systole (hyperkinetic).
The increased intensity of T1 in atrial septal defect and tricuspid valve obstruction (eg, tricuspid
stenosis, right atrial myxoma) can also be explained by the same phenomenon. The tricuspid
valve is held open by increased transvalvular flow and the transvalvular gradient until final
closure with increased velocity occurs with right ventricular (RV) systole.
● Decreased intensity of S1 – A soft S1 is mostly related to decreased mobility or due to a semi­
closed position of the leaflets prior to systole. Thus, S1 is soft when the mitral valve is immobile
due to calcification and fibrosis, despite a significant transvalvular gradient. S1 may also be
reduced when the leaflets are semi­closed prior to the onset of systole or when the velocity of
closure is reduced, as can occur with LV dysfunction. These situations are illustrated by the
following examples (table 1):
• S1 is very soft or absent when mitral regurgitation (MR) results from fibrosis and destruction
of the valve leaflets (as in patients with rheumatic valve disease), which prevent effective M1.
In contrast, MR due to perforation of the valve leaflets from bacterial endocarditis may not be
associated with a reduced intensity of S1.
• Reduced S1 intensity occurs when the mitral valve remains in the semi­closed position
before the onset of ventricular systole, and the velocity of valve closure is decreased. S1 is
usually soft when the PR interval is prolonged (exceeding 0.2 seconds) since semi­closure of
the mitral valve occurs following atrial systole and before ventricular systole begins.
Premature closure of the mitral valve can occur in patients with severe acute aortic
regurgitation due to a rapid rise in LV diastolic pressure; the mitral valve may be virtually
closed at the onset of systole, resulting in a markedly decreased intensity of or even absent
S1 [15]. (See "Acute aortic regurgitation in adults", section on 'Cardiac auscultation'.)
• S1 is soft in some patients with left bundle branch block without any other obvious
abnormality; the mechanism is unclear. Decreased valve closure velocity due to myocardial
dysfunction is possible.
• Hemodynamically significant aortic stenosis may be associated with a soft S1; this can occur
in the absence of spreading calcification to the mitral valve and in the presence of a normal
PR interval [14]. Semi­closure of the mitral valve due to a powerful atrial contraction and an
abnormally elevated LV diastolic pressure before the onset of ventricular systole is the most
likely explanation.
• S1 is frequently soft in patients with dilated cardiomyopathy, even in the absence of a
prolonged PR interval or bundle branch block. The decreased S1 is almost invariably
associated with a significantly reduced LV ejection fraction (LVEF) and elevated pulmonary
capillary wedge pressure. The mechanism for a soft S1 in these patients remains unclear;
semi­closure of the mitral valve due to an elevated LV diastolic pressure and decreased
velocity of valve closure due to myocardial dysfunction may contribute.
• Decreased conduction of sounds through the chest wall reduces the intensity of S1 in
patients with chronic obstructive pulmonary disease, obesity, and pericardial effusion.
● Variation in the intensity of S1 may be evident in the following situations:
• It is a common feature of atrial fibrillation; the mechanism appears to be a variation in the
velocity of valve closure related to changes in the RR cycle length.
• The intensity of S1 varies in the presence of premature beats.
• Changing intensity of S1 occurs in AV dissociation, whether the heart rate is slow or fast (eg,
in complete heart block or ventricular tachycardia). The changing intensity is due to random
variation of the PR interval; the short PR interval is associated with an increased intensity
and the long PR interval with a decreased intensity. The pulse is regular in AV dissociation;
thus, the varying intensity of S1 in a patient with a regular pulse almost always suggests AV
dissociation.
• Auscultatory alternans, in which S1 is soft and loud with alternate beats, is a rare finding in
severe cardiac tamponade; it is almost always associated with electrical alternans and
pulsus paradoxus. Although the pulse is regular, changes in the intensity of S1 occur
regularly with the alternate beats and not randomly as in AV dissociation.
Splitting of S1 — There are normally two components of S1: The mitral component precedes the
carotid pulse upstroke, and the tricuspid component occurs later. The interval between M1 and T1 is
0.02 to 0.03 seconds, and can be appreciated with the diaphragm of the stethoscope along the lower
left sternal border [7]. The mitral component is much louder than the tricuspid component and is
normally heard more widely across the precordium; the tricuspid component is of low intensity and is
best heard over the left third and fourth interspaces close to the sternal border. Abnormal splitting of
S1 can result from conduction disturbances (eg, complete right bundle branch block), and/or
hemodynamic causes (eg, atrial septal defect with large left to right shunt).
Wide splitting of S1 is a feature of Ebstein anomaly which is associated with right bundle branch block
[16]. The extra early systolic sound around S1 is also referred to as the "sail sound." This auscultatory
finding in patients with Ebstein anomaly appears not simply as a closing sound of the tricuspid valve,
but as a complex closing sound that includes a sudden stopping sound after the anterior and/or other
tricuspid leaflets balloon out in systole [17]. (See "Clinical manifestations and diagnosis of Ebstein
anomaly".)
SECOND HEART SOUND (S2)
Genesis, timing, and location — The S2 consists of two components: aortic and pulmonary valve
closure sounds, traditionally designated as A2 and P2, respectively [7]. Simultaneous M­mode
echocardiograms and external phonocardiograms in healthy subjects showed that the onset of A2
was synchronous with the coaptation of the aortic valve cusps and a sharp vibration on the aortic wall.
The closed valve oscillated for 30 to 45 ms after the coaptation of the cusps. Magnified
echocardiographic studies of the interventricular septum revealed a consistent, momentary quiver
across the septal myocardium a mean of 4 ms after the onset of S2 [18]. The same mechanism can
be inferred for the P2 component of S2.
The onset of A2 occurs with the dicrotic notch of the aortic root pressure pulse [19,20]. S2 occurs
after the peak of the carotid pulse and coincides with its downslope.
The two components of S2 are best heard with the diaphragm of the stethoscope and over the left
second interspace, close to the sternal border. A2 is widely transmitted to the right second interspace,
along the left and right sternal border, and to the cardiac apex. P2 is normally best heard and
recorded over the upper left sternal border and is poorly transmitted. S2 is best heard when patients
are semi­recumbent (30 to 40 degrees upright) with quiet inspiration.
Factors determining the intensity of S2 — The major determinants of A2 intensity (and therefore
the major determinants of S2) include (table 2):
●
●
●
●
Aortic pressure, a major determinant of the velocity of valve closure
Relative proximity of the aorta to the chest wall
Size of the aortic root
Mobility and structural integrity of the aortic valve
The intensity of P2 is determined by:
● Pulmonary arterial pressure, particularly the diastolic pressure
● Size of the pulmonary artery
● Mobility and structural integrity of the pulmonary valve
The intensity of P2 is determined by comparing its intensity with A2. An increased P2 intensity is
suggested when it is louder over the left second interspace or when there is transmission to the
cardiac apex.
● Increased intensity of A2 often occurs in:
• Systemic hypertension.
• Coarctation of the aorta.
• Ascending aortic aneurysm; a "tambour" quality of A2 is commonly heard (table 2).
• When the aortic root is relatively anterior and closer to the anterior chest wall, as in tetralogy
of Fallot and transposition of the great arteries.
● Increased intensity of P2 often occurs in:
• Pulmonary arterial hypertension of any etiology (most common, even with pulmonary
regurgitation) [21].
• Idiopathic pulmonary artery dilation.
• Atrial septal defect (ASD); P2 is increased considerably and frequently greater than A2 over
the left second interspace.
A2 is soft in patients with mitral regurgitation (MR), and P2 may appear to be increased. In these
circumstances, one cannot rely on the relative intensity of P2 for the diagnosis of pulmonary
hypertension (PH).
● Decreased intensity of A2 occurs in:
• Conditions that affect the mobility and integrity of the aortic valve
• Severe aortic regurgitation (AR) or stenosis
• Hypotension
● Decreased intensity of P2 occurs in:
• Conditions that affect the mobility and integrity of the pulmonary valve.
• Pulmonary stenosis and regurgitation.
• Significant RV outflow obstruction associated with a soft and delayed P2. The low pulmonary
artery pressures also play a role in attenuating P2.
Splitting of S2 — Under normal physiologic conditions, the A2 and P2 components of S2 vary with
inspiration. A2 and P2 are usually fused during the expiratory phase of continuous respiration, but
during the inspiratory phase, separation of A2 and P2 occurs; the degree of splitting varies from 0.02
to 0.06 seconds (movie 2) [22]. The underlying mechanism for the normal splitting of S2 during
inspiration relates to longer RV ejection during inspiration compared with the LV, which is correlated
with increased right­sided and decreased left­sided filling. The width and order of splitting of S2 are
altered in a variety of clinical settings.
● Wide splitting of S2 occurs in the following conditions:
• Electromechanical delay of the RV (table 2 and figure 2):
-
Right bundle branch block (RBBB) (movie 3), artificial pacing from the LV, and Wolff­
Parkinson­White (WPW) syndrome with LV preexcitation.
-
Premature beats and an idioventricular rhythm of LV origin (QRS complex of RBBB
morphology) are also associated with wide splitting.
• Hemodynamic causes:
-
Increased resistance to RV ejection and prolongation of RV ejection time are other
important causes of wide expiratory splitting of S2 as seen in pulmonary valve,
infundibular, supravalvular, or pulmonary branch stenosis, and pulmonary arterial
hypertension.
In patients with pulmonary valve and infundibular stenosis, wide splitting of S2 is
associated with reduced intensity of P2, while P2 is accentuated in PH and pulmonary
branch stenosis.
In pulmonary valve stenosis, the degree of expiratory splitting of S2 (the A2­P2 interval)
is directly related to the severity of stenosis and RV systolic hypertension [23]. Further
splitting of S2 during inspiration usually occurs in these conditions, but wide splitting of
S1 is not observed.
-
Isolated reduction of the LV ejection time may also cause wide splitting of S2, due to the
early occurrence of A2. Examples of this hemodynamic abnormality include severe MR
when forward stroke volume decreases with increases in regurgitant volume [24]. In
constrictive pericarditis, differential filling of the ventricles occurs during inspiration,
resulting in a lower LV stroke volume [25].
● Wide and fixed splitting of S2 – Fixed splitting of S2 has been defined as ≤20 ms of variation in
the A2­P2 interval between the inspiratory and expiratory phases of respiration [26]. However,
such limitation in variation of splitting may be difficult to discern clinically, so wide and variable
splitting may be difficult to distinguish from wide and fixed splitting.
One common cause of wide and fixed splitting of S2 is a large interatrial communication (ASD,
common atrium) and left­to­right or bidirectional shunt; abnormally wide splitting of S2 occurs,
and respiratory variations of the A2­P2 intervals are minimal or absent (movie 4). (See "Clinical
manifestations and diagnosis of atrial septal defects in adults", section on 'Heart sounds'.)
The mechanism of wide expiratory splitting of S2 in ASD appears to result from two physiological
mechanisms. First, P2 is delayed due to a marked increase in RV stroke volume (left­to­right
shunt), which prolongs right­sided ejection. Second, when the right and left atria become a near
common chamber, differential filling that normally occurs between the RV and LV during
inspiration no longer exists (table 2) [26,27].
The other cause of fixed splitting of S2 is RV failure, when the RV is unable to vary its stroke
volume during inspiration, and inspiratory prolongation of its ejection time and delay of P2 does
not occur. Therefore, any condition that induces severe RV failure, such as RV outflow
obstruction, PH, and primary RV dysfunction, can be associated with fixed splitting (table 2).
● Reversed (paradoxical) splitting of S2 – Paradoxical splitting occurs when A2 follows P2
during the expiratory phase of respiration. The splitting of S2 is then maximal during expiration,
and the splitting is less or S2 becomes single during inspiration with the normal inspiratory delay
of P2 [7,28].
Reversed splitting of S2 may result from either conduction disturbances or hemodynamic causes
(table 2).
• Electromechanical delay Left bundle branch block, artificial RV pacing, preexcitation of the
RV (WPW syndrome), and premature beats of RV origin are examples of conduction
disturbances associated with delayed activation of the LV, and consequently delayed
completion of LV ejection causes a delayed A2 and reversed splitting of S2.
• Hemodynamic factors:
-
A markedly prolonged LV ejection time may delay A2 sufficiently to cause reversed
splitting of S2. With fixed LV outflow tract obstruction, as in patients with aortic valve
stenosis, LV ejection time is lengthened, and reversed splitting of S2 usually indicates
hemodynamically significant outflow obstruction (movie 5). However, P2 may be
inaudible due to the long ejection systolic murmur of aortic stenosis, making it difficult to
recognize the reversed splitting.
-
A prolonged LV ejection time and reversed splitting of S2 can occur with myocardial
dysfunction, as in myocardial ischemia, or in patients with long­standing severe AR [29].
However, reversed splitting is rarely observed with severe heart failure (HF) because of
the concomitant decrease in stroke volume, which is an important determinant of LV
ejection time.
The distinction between hypertrophic cardiomyopathy (HCM) and MR or ventricular septal defect
(VSD), conditions in which the character and locations of the systolic murmur may appear similar on
auscultation, is facilitated by recognizing the character of S2 splitting. Reversed splitting suggests
HCM, while physiologic splitting favors MR or VSD.
Single S2 — A single S2 may result from the absence of either of the two components of S2 or from
the fusion of A2 and P2 without inspiratory splitting (table 2).
● Absence of A2 is occasionally observed in severe calcific aortic stenosis with an immobile aortic
valve. A2 may be absent in some patients with severe AR due to destruction of the valve leaflets.
(See "Clinical manifestations and diagnosis of aortic stenosis in adults", section on 'Cardiac
auscultation' and "Clinical manifestations and diagnosis of chronic aortic regurgitation in adults",
section on 'Cardiac auscultation'.)
● P2 is absent with congenital absence of the pulmonary valve, pulmonary atresia, or truncus
arteriosus. In severe pulmonary valve stenosis or in tetralogy of Fallot, P2 may be markedly
attenuated and escape recognition by auscultation. (See "Clinical manifestations and diagnosis of
pulmonic stenosis in adults", section on 'Clinical manifestations' and "Pathophysiology, clinical
features, and diagnosis of tetralogy of Fallot", section on 'Cardiac auscultation'.)
● A2 is delayed and may be fused with P2 with aortic stenosis (movie 6). Fusion of A2 and P2
without inspiratory splitting occurs in Eisenmenger syndrome with VSD and in patients with a
single ventricle. (See "Clinical manifestations and diagnosis of aortic stenosis in adults", section
on 'Cardiac auscultation' and "Evaluation and prognosis of Eisenmenger syndrome", section on
'Physical examination'.)
However, a truly single S2 is rare. An apparently single S2 usually results from the inability to hear or
record P2 due to emphysema, obesity, or pericardial effusion.
THIRD (S3) AND FOURTH (S4) HEART SOUNDS
Genesis, timing, and location of S3 and S4 — S3 and S4 are low­frequency diastolic sounds that
appear to originate in the ventricles. The precise mechanism of the genesis of S3 and S4 has not
been identified with certainty [30]. It is generally agreed that both sounds, occasionally termed
"ventricular filling sounds," are associated with ventricular filling and an increase in ventricular
dimensions. They are heard during the rapid filling and atrial filling phases of ventricular diastole,
respectively.
● S3 occurs as the rapid filling phase of diastole is completed [31]. It appears to be related to a
sudden limitation of the movement during ventricular filling along its long axis [32], and it
coincides with the y descent of the atrial pressure pulse, occurring usually 0.14 to 0.16 seconds
after the second heart sound (S2).
● S4 occurs during the atrial filling phase after the P wave on the electrocardiogram (ECG) and
coincides with atrial systole and a waves of the atrial pressure pulse, and with the apical impulse.
S3 and S4 are best heard with the bell of the stethoscope. Auscultation over the cardiac apex in the
left lateral decubitus position is preferable for identification of LV S3 and S4. RV S3 and S4 are best
heard along the lower left sternal border; occasionally, right­sided filling sounds are also heard over
the lower right sternal border and over the epigastrium. The intensity of S3 and S4 of RV origin
usually increases during inspiration, while that of LV origin remains unchanged. S3 is closer to S2,
and S4 occurs prior to the first heart sound (S1).
An abnormal S3 or S4 tends to be louder and of higher pitch (sharper) and is frequently referred to as
a "gallop." S3 is the ventricular gallop, and S4 is the atrial gallop. S3 and S4 can be fused during
tachycardia to produce a loud diastolic filling sound, termed a "summation gallop" [33]. At the bedside,
carotid massage can cause separation of S3 and S4 as the heart rate slows. S3 and S4 may
occasionally be intensified or precipitated by exercise or by sustained hand grip. Gallops can
sometimes be seen and palpated. (See "Examination of the precordial pulsation".)
It is often difficult to distinguish between gallop sounds of RV and LV origin at the bedside when they
are present in the same patient. However, if one follows the "inching" method of auscultation (eg,
auscultation starting over the cardiac apex and then gradually moving the stethoscope inch by inch to
the left lower sternal border), the decreasing intensity of gallops of LV origin and the increasing
intensity of gallops of RV origin can be appreciated. Furthermore, the intensity of the right­sided gallop
sound increases during inspiration.
LV gallops
Clinical significance of S3 — Although an S3 can be heard in healthy young children and adults
(movie 7), it is usually abnormal in patients over the age of 40 years, suggesting an enlarged
ventricular chamber.
An S3 gallop is an important and common early finding of HF associated with dilated cardiomyopathy
and may also be heard in patients with diastolic HF (although less frequently than with systolic HF),
aortic valve disease, and coronary artery disease (CAD) (movie 8) [34]. In such patients, an S3 gallop
is usually associated with left atrial pressures exceeding 20 mmHg, increased LV end­diastolic
pressures (>15 mmHg), and elevated serum brain natriuretic peptide (BNP) concentrations [35­37].
(See "Evaluation of the patient with suspected heart failure", section on 'Heart sounds'.)
An S3 gallop is almost always present in patients with hemodynamically significant chronic mitral
regurgitation (MR); the absence of S3 is an important finding to exclude severe chronic MR. An S3
gallop in patients with chronic aortic regurgitation (AR) is frequently associated with a decreased
LVEF and increased diastolic volume; its recognition should prompt further evaluation [38].
The diagnostic test characteristics of the S3 and S4 for detection of LV dysfunction were evaluated in
a phonocardiographic study of patients who were undergoing cardiac catheterization [37]. These
sounds were not very sensitive (40 to 50 percent) for the detection of an elevated LV end­diastolic
pressure or a reduced LVEF; however, the S3 was highly specific (90 percent) for these parameters
and for an elevated serum BNP concentration. An additional problem is appreciable interobserver
variability in the ability to detect an S3 on cardiac auscultation that cannot be solely explained by the
experience of the observer [39,40].
The presence of an S3 gallop also has prognostic significance, being associated with a higher risk of
progression to symptomatic HF in those with asymptomatic LV dysfunction, and a higher risk of
hospitalization for HF or death from pump failure in patients with overt HF [41,42]. One limitation to
these observations is the operator dependence for the detection of this physical finding.
An S3 often occurs in high­output states such as thyrotoxicosis or pregnancy. It can also be
appreciated in athletes with slow heart rates and increased filling volumes [43]. In these settings, it
does not necessarily indicate LV dysfunction [44].
Clinical significance of S4 — An audible S4 is generally abnormal in young adults and children.
Effective atrial contraction and ventricular filling are both required for production of atrial gallop
sounds. Thus, this sound is usually absent in atrial fibrillation and in significant AV valve stenosis.
S4 can be heard in many healthy older adults without any other cardiac abnormality, due to decreased
ventricular compliance with age. An S4 is always abnormal when it is palpable, regardless of patient
age.
S4 may become audible in otherwise healthy subjects with a prolonged PR interval due to the
separation of S4 from S1. In patients with complete AV block, S4 is heard at a faster rate than S1 and
S2 and may not indicate any hemodynamic abnormality.
An abnormal S4 is most frequently observed in patients with decreased LV distensibility (movie 9)
[45]. Thus, S4 is common in hypertensive heart disease, aortic stenosis, and HCM. LV hypertrophy,
which is present in all these conditions, contributes to decreased LV distensibility.
In aortic stenosis, the presence of an S4 has been reported to indicate hemodynamically significant
LV outflow obstruction, with a peak transvalvular gradient ≥70 mmHg and an elevated LV end­diastolic
pressure [46]. However, in patients over 40 years of age, S4 can occur due to myocardial disease in
the absence of significant aortic stenosis. Thus, in elderly patients, the presence of an S4 cannot be
used to assess the severity of aortic stenosis. Associated CAD may also cause an S4 in patients with
mild to moderate aortic stenosis.
An S4 is heard in the vast majority of patients during the acute phase of myocardial infarction (MI)
[47]. Although pulmonary venous pressure may also be elevated, there is a poor correlation between
the presence and absence of an S4 and hemodynamic abnormalities. Thus, S4 is a poor guide to
assess the severity of LV dysfunction in patients with acute MI.
Audible and/or palpable atrial gallops are a frequent finding in chronic LV aneurysm and are usually
found with LV dyskinesia associated with elevated end­diastolic pressures. In patients with chronic
CAD, the transient appearance of an S4, particularly during chest pain, is a strong indication of
transient myocardial ischemia.
A loud S4 that is also usually palpable is a frequent finding in patients with acute and severe MR or
AR. It is almost always associated with an increased LV end­diastolic pressure (>15 mmHg) [48]. The
predictive value is increased in the presence of both S3 and S4 gallops [35]. (See "Examination of the
precordial pulsation".)
Right ventricular gallops — An S3 gallop of RV origin frequently occurs in patients with significant
tricuspid regurgitation, whether it is primary or secondary to pulmonary hypertension and RV failure.
An S3 gallop is also heard in RV failure in the absence of tricuspid regurgitation.
An S4 of RV origin is most commonly heard in patients with RV outflow obstruction (pulmonary valve
stenosis) and pulmonary arterial hypertension [49]. It likely denotes decreased RV distensibility due to
hypertrophy.
Differential diagnosis — An S3 and S4 may be confused with a split S2 and split S1, respectively.
When split, the two parts of S1 or S2 typically have a similar pitch, while S3 and S4 are lower pitched
sounds than S2 and S1.
This difference in pitch can be brought out by listening with the bell and the diaphragm of the
stethoscope. The lower­pitched S3 and S4 will be more pronounced when listening gently with the
bell, while the higher­pitched split S1 and S2 will be more pronounced when listening with the
diaphragm or when applying the bell more firmly to the skin. (See 'Stethoscopes' above.)
Auscultation to distinguish S3 and S4 from a splitting of S2 and S1 is best performed in the 45­degree
left lateral decubitus position (ie, with the chest rotated toward the examination table). The location of
the sound is useful in distinguishing an S4 from a split S1. The LV S4 is usually localized over the
cardiac apex, and becomes softer as the bell of the stethoscope is moved gradually to the left sternal
border.
PERICARDIAL KNOCK
Ventricular filling is confined to early diastole in constrictive pericarditis and terminates with a sharp
S3; this is termed a "pericardial knock." Its timing is earlier than a normal S3 and typically occurs 0.10
to 0.12 seconds after an S2. It is a common finding in constrictive pericarditis and can occur with or
without pericardial calcification [50]. It is occasionally heard only during inspiration and along the
lower right sternal border, suggesting an early manifestation of RV constriction. (See "Constrictive
pericarditis".)
EJECTION SOUNDS
An ejection sound is a high­frequency "clicky," early systolic sound. When aortic or pulmonary ejection
sounds occur in the presence of normal semilunar valves, the origin may be the proximal aortic or
pulmonary artery segments. Thus, the term "vascular ejection sound" has been suggested. These
sounds generally tend to occur later and are not associated with "doming" of the semilunar valves,
which is characteristic of a valvular ejection sound. The mechanism of the vascular ejection sound
remains unclear.
Aortic ejection sound — The aortic ejection sound is usually recorded 0.12 to 0.14 seconds after the
Q wave on the ECG. It is best heard with the diaphragm of the stethoscope and is widely transmitted,
heard at the cardiac apex and also over the right second interspace. Its intensity does not vary with
respiration. Aortic ejection sounds occur in association with a deformed but mobile aortic valve and
with aortic root dilation. Thus, it is present in aortic valve stenosis, bicuspid aortic valve, aortic
regurgitation, and with aneurysm of the ascending aorta. An aortic ejection sound is also heard in
some patients with systemic hypertension, probably due to associated aortic root dilation.
Aortic ejection sounds are heard frequently in patients with mild to moderate aortic valve stenosis;
they may be absent in severe calcific aortic stenosis, presumably due to the loss of valve mobility
[51]. Since ejection sounds are usually absent in subvalvular and supravalvular aortic stenosis, the
presence of an ejection sound helps to identify the site of obstruction at the level of the aortic valve.
An ejection sound also does not favor the diagnosis of HCM.
Identification of the aortic ejection sound is the most important and consistent bedside clue for the
diagnosis of an uncomplicated bicuspid aortic valve [52]. In patients with coarctation of the aorta, an
aortic ejection sound usually signifies the presence of an associated bicuspid aortic valve.
Pulmonary ejection sound — A pulmonary ejection sound occurs earlier than an aortic ejection
sound and is recorded 0.09 to 0.11 seconds after the Q wave on the ECG, beginning at the time of
maximal opening of the pulmonary valve. It is also a "clicky" sound of high frequency and is best
heard with the diaphragm of the stethoscope. In contrast to the aortic ejection sound, it is not widely
transmitted and is usually best heard at the left second interspace and along the left sternal border; it
is not usually heard over the cardiac apex or right second interspace.
The most helpful distinguishing feature of a pulmonary ejection sound is its decreased intensity, or
even its disappearance during the inspiratory phase of respiration. During expiration, the valve opens
rapidly from its fully closed position; sudden "halting" of this rapid opening movement is associated
with a maximal intensity of the ejection sound. With inspiration, the increased venous return to the RV
augments the effect of right atrial systole and causes partial opening of the pulmonary valve prior to
ventricular systole. The lack of a sharp opening movement of the pulmonary valve explains the
decreased intensity of the pulmonary ejection sound during inspiration.
The tricuspid closure sound should not be confused with the pulmonary ejection sound. The intensity
of tricuspid closure sound tends to increase rather than decrease during inspiration.
Pulmonary ejection sounds tend to be present in clinical conditions associated with a deformed
pulmonary valve and pulmonary artery dilation, including pulmonary valve stenosis, idiopathic dilation
of the pulmonary artery, and chronic pulmonary arterial hypertension of any etiology [53­56]. The
interval between the S1 and the pulmonary ejection sound is directly related to the RV isovolumic
contraction time, which usually is prolonged in PH, explaining a relatively late occurrence of the
ejection sound in these patients. With increasing severity of pulmonary valve stenosis, the isovolumic
systolic interval shortens, and the pulmonary ejection sound therefore tends to occur soon after the
S1. In patients with very severe pulmonary valve stenosis, the ejection sound can fuse with the S1
and may not be recognized.
NON­EJECTION SYSTOLIC SOUNDS
The non­ejection systolic sounds are also high­frequency sounds that occur much later after the first
heart sound (S1) and are best heard with the diaphragm of the stethoscope. These sounds are not
widely transmitted and not usually heard over the right or left second interspace.
Midsystolic click — Prolapse of the mitral valve is the most common cause for a non­ejection
midsystolic click; the timing coincides with maximal prolapse of the mitral valve into the left atrium. It
may or may not be associated with a late systolic murmur (movie 10 and movie 11) [57­60]. (See
"Definition and diagnosis of mitral valve prolapse".)
When the click occurs early in systole, it can be confused with the ejection sound or the second
component of a widely split S1. A number of bedside maneuvers can be performed to confirm the
presence of a midsystolic click. These maneuvers are based upon the fact that the systolic dimension
or volume at which mitral valve prolapse and the click occur tend to remain fixed in the same patient
[61]. Thus, whenever the "click" volume or dimension is reached following the onset of ventricular
ejection (corresponding roughly to the S1), a midsystolic click occurs. The S1­click interval, then, can
vary according to the preejection (end­diastolic) ventricular volume and the rate of ejection.
● The S1­click interval will increase, producing a late mid­systolic click whenever there is an
increase in end­diastolic volume (eg, supine position, squatting, hand grip) (movie 11).
● The S1­click interval usually shortens, and the click tends to occur earlier when there is a
reduction in end­diastolic volume (eg, standing, phase 2 Valsalva maneuver, amyl nitrite) or when
there is an increased rate of ejection, as occurs after an ectopic beat as a result of post­ectopic
potentiation (movie 10).
It is important to identify the other cardiovascular anomalies that may accompany mitral valve
prolapse, including Marfan syndrome, atrial septal defect (secundum or primum), musculoskeletal
abnormalities, systemic lupus erythematosus, and HCM. When there is no associated anomaly,
isolated mitral valve prolapse is identified [57]. (See "Definition and diagnosis of mitral valve
prolapse", section on 'Clinical manifestations'.)
Tricuspid valve prolapse also produces high­frequency midsystolic, "clicky" sounds; these are best
heard with the diaphragm of the stethoscope over the lower left sternal border and occasionally over
the lower right sternal border. The interval between S1 and the tricuspid valve click tends to increase
following inspiration and after raising the legs and other maneuvers that increase RV volume. Isolated
tricuspid valve prolapse occurs only rarely, and in most instances it accompanies mitral valve
prolapse. Tricuspid valve prolapse, however, may occur in the absence of mitral valve prolapse in
patients with Ebstein anomaly.
Precordial honk — The systolic "whoop" or "precordial honk" are short musical systolic murmurs
often preceded by a click and occurring in mid or late systole. These sounds can be transient, occur
only in certain positions, or may be precipitated by exercise. Mitral valve prolapse is the cause for the
"whoop" or "honk" in most cases [62,63].
Pseudo­ejection sound — A nonejection sound has been observed in some patients with HCM
associated with systolic anterior motion of the anterior mitral leaflet. This sound has been termed a
"pseudo­ejection sound" [64]. Unlike the ejection click of aortic stenosis, this sound begins
considerably after the upstroke of the carotid pulse. The precise mechanism of the pseudo­ejection
sound in HCM remains unclear. It may either result from contact of the anterior leaflet with the septum
or from the deceleration of blood flow in the LV outflow tract.
EARLY DIASTOLIC HIGH­FREQUENCY SOUNDS
The most common causes for sounds occurring in diastole include the opening snap of the mitral or
tricuspid valve or a tumor plop associated with an atrial myxoma (table 3).
Opening snap — The opening snap is a high­frequency, early diastolic sound associated with mitral
or tricuspid valve opening (movie 1). This opening of the AV valves, which is normally silent, becomes
audible in the presence of pathologic conditions.
The opening snap results from rapid opening of the mitral valve to its maximal open position; thus,
mobility of the valve contributes to its genesis. It is absent when the mitral valve is heavily calcified
and immobile. However, the opening snap is heard in the vast majority of patients with mitral stenosis,
and along with an accentuated first heart sound (S1), frequently provides the first clue to the
diagnosis.
Mitral valve — Mitral stenosis is the most frequent and important cause of an opening snap. It can
occur rarely in patients with pure mitral regurgitation (MR) [48,65].
The opening snap is best heard with the diaphragm of the stethoscope, medial to the cardiac apex. It
is usually widely transmitted and can be easily heard over the left second interspace and along the
left sternal border. The opening snap coincides with the full opening of the mitral valve and occurs
0.04 to 0.12 seconds after the second heart sound (S2) (movie 1) [66].
The opening snap can easily be confused with a split S2 since it is frequently transmitted to the left
second interspace. However, careful auscultation over the left second interspace in the supine
position and during both phases of respiration reveals three high­frequency sounds in close proximity
to each other during inspiration; the initial two are the two components of S2, and the third is the
opening snap. The recognition of these three sounds during inspiration helps to differentiate mitral
stenosis, as seen in mitral valve obstruction, from atrial septal defect (ASD), which may also be
associated with a mid­diastolic rumble. In ASD, only the two components of the S2 are heard during
expiration and inspiration.
The severity of mitral stenosis can be assessed at the bedside by noting the interval between the
aortic component of S2 and the opening snap. The S2­opening snap interval is related to the
difference in pressures at the time of aortic valve closure and the opening of the mitral valve, which
occurs during the isovolumic relaxation phase when the LV pressure falls below the left atrial
pressure. When mitral stenosis is severe, left atrial pressure is higher, and the pressure crossover
point between the LV and left atrium is closer to S2, which reduces the S2­opening snap interval. At
the bedside, the shorter S2­opening snap interval sounds like a widely split S2. However, the S2­
opening snap interval is not only related to the height of the left atrial pressure, but also to aortic valve
closing pressure. Thus, with a higher aortic valve closing pressure (systemic hypertension) and earlier
closure of the aortic valve, the S2­opening snap interval may be longer with the same degree of
elevation of left atrial pressure. Similarly, when the aortic valve closing pressure is lower (aortic
regurgitation and aortic stenosis), aortic valve closure is later, and the S2­opening snap interval
becomes shorter with the same degree of mitral stenosis. The S2­opening snap interval also
becomes shorter when mitral stenosis is associated with MR with a large V wave. Furthermore,
tachycardia decreases the S2­opening snap interval as the left atrial pressure increases with
increasing heart rate in mitral stenosis. Thus, assessment of the severity of mitral stenosis by
estimating the S2­opening snap interval alone should be done with caution in the presence of
tachycardia, hypertension, MR, and aortic valve disease. (See "Clinical manifestations and diagnosis
of rheumatic mitral stenosis".)
Tricuspid valve — Tricuspid valve stenosis may be associated with a tricuspid valve opening snap
that is not widely transmitted and is heard best over the lower left sternal border. The tricuspid
opening snap can also be heard in some patients with an ASD and a large left­to­right shunt [26].
Tumor plop — Early diastolic sounds (tumor "plop") are occasionally heard in atrial myxoma. These
sounds appear to occur when tumors move into the ventricle and come to a sudden halt [67]. (See
"Cardiac tumors".)
Vegetation plop — Vegetation plop is an early diastolic sound that is occasionally heard in bacterial
endocarditis. It appears that this sound is produced when a large vegetation attached to the mitral
valve leaflet enters the LV during early diastole [68].
Other causes — A high­frequency, diastolic sound can be heard in other conditions and should be
differentiated from the opening snap or tumor plop.
● In some patients with mitral valve prolapse, a high­frequency sound is heard in early diastole that
appears to be related to the rapid inward movement of the prolapsed mitral valve toward the LV
cavity before the opening of the mitral valve [69]. This early diastolic sound should not be
confused with an opening snap due to mitral stenosis.
● In some patients with HCM who have a small LV cavity size, early diastolic high­frequency
sounds are heard coinciding with the time of contact of the anterior leaflet of the mitral valve to
the interventricular septum [70].
● High­frequency early diastolic sounds, similar to the opening snap, can be heard in some patients
with severe MR due to ruptured chordae.
PROSTHETIC VALVE SOUNDS
The various types of prosthetic and tissue valves that are in use for valve replacement may produce
both opening and closing sounds. The relative intensity of the opening and closing sounds vary
according to the type and design of the prosthetic valve used (table 4). The artificial valve sounds are
of high frequency, are much louder than normal valve sounds, and are of a "clicky" character. The
opening or closing sound may consist of multiple clicks, which do not necessarily indicate valve
malfunction.
● The closing sound is generally louder than the opening sound with a disk valve
● Both the opening and closing sounds are loud with the ball­and­cage type of valve
● The closing sounds of the porcine valve are much louder than the opening sounds
Valve malfunction — Changes in the normal sounds produced by the prosthetic valve may indicate
valve malfunction. However, malfunction of an artificial valve can exist despite a normal intensity or
character of the opening or closing sounds. Doppler echocardiography and cardiac catheterization are
usually necessary to establish this diagnosis. (See "Diagnosis of mechanical prosthetic valve
thrombosis or obstruction" and "Overview of the management of patients with prosthetic heart
valves".)
● The closing sound is usually louder than the opening sound, regardless of the type of prosthetic
valve used. A decreased intensity of the closing sound should raise the possibility of malfunction
of the artificial valve.
● The absence of an opening click has been found in dehiscence of a mitral valve prosthesis [71].
● Obstruction of a prosthetic valve in the mitral position may be associated with a markedly
decreased S2­opening sound interval. A marked variation in the S2­mitral prosthesis opening
sound may indicate malfunction of a mechanical mitral prosthesis. The variation in this interval
usually does not exceed 25 ms with a normally functioning prosthesis [72].
Ball variance — "Ball variance" is a term used to describe certain physical changes in a ball­and­
cage valve and is associated with changes in the intensity of opening and closing sounds [73]. Ball
variance is related to a specific model of the caged ball type of prosthetic valve, which is rarely used
at the present time.
PERICARDIAL FRICTION RUB AND OTHER ADVENTITIOUS SOUNDS
A pericardial rub is generated by the friction of two inflamed layers of the pericardium and occurs
during the maximal movement of the heart within its pericardial sac. Thus, the rub can be heard
during atrial systole, ventricular systole, and the rapid­filling phase of the ventricle (three­component
rub) (movie 12). However, the rub may be present only during one (one component) or two phases
(two components) of the cardiac cycle. In myopericarditis following transmural MI, a one­component
rub, usually during ventricular systole, is more frequent than two­ or three­component rubs.
Pericardial rubs are of scratching or grating quality and appear superficial. They are best heard with
the diaphragm of the stethoscope. The intensity frequently increases after application of firm pressure
with the diaphragm, during held inspiration, and with the patient leaning forward. The rub may be
localized or widespread, but usually is heard over the left sternal border. (See "Acute pericarditis:
Clinical presentation and diagnostic evaluation".)
Pericardial rubs should be distinguished from the other superficial "scratchy" sounds.
● In patients with thyrotoxicosis, a to­and­fro, high­pitched sound may be heard over the left
second interspace, known as a Means­Lerman scratch; it may simulate a pericardial friction rub.
(See "Overview of the clinical manifestations of hyperthyroidism in adults".)
● Acute mediastinal emphysema, usually a benign, relatively common complication of open heart
surgery, may be associated with a "crunching" noise over the precordium that is coincident with
ventricular systole (mediastinal crunch).
● In patients with Ebstein anomaly, the sail sound may be of a scratchy quality and simulate a
pericardial friction rub.
● The movement of the balloon flotation catheter or the transvenous pacing catheter across the
tricuspid valve can cause an early systolic superficial scratchy sound that may also simulate a
soft, one­component friction rub. These sounds frequently disappear with the alteration of patient
position.
● A pleuropericardial rub results from the friction between the inflamed pleura and the parietal
pericardium; it can be heard only during the inspiratory phase of respiration.
● Twitching of the intercostal muscles or of the diaphragm during artificial pacing may cause a
superficial, scratchy, and high­frequency sound unrelated to the cardiac cycle. This sound is
called "pacemaker heart sound." The twitching of the intercostal muscles results from stimulation
of the adjacent intercostal nerves by the pacemaker stimulus [74].
● Inadvertent entry of air into the RV cavity via the systemic venous system may occur during
placement of catheters or pacemakers in the right side of the heart or as a complication of needle
aspiration biopsy of the lungs. The movement of air in the right ventricular cavity with systole and
diastole may produce a peculiar "slushing" or crunching sound ("mill wheel" murmur) over the
entire precordium, which can occasionally resemble pericardial friction rub [75].
● Swallowing sounds – These sounds are produced during swallowing and can be confused with
heart sounds. It is postulated that these sounds are produced by vibrations of the vocal cords
during swallowing [76].
SUMMARY AND RECOMMENDATIONS
● Heart sounds are broadly classified into high­ and low­frequency sounds. (See 'Classification of
heart sounds' above.)
• High­frequency sounds arise from closing or opening valves including mitral and tricuspid
valve closing sounds (M1 and T1), and aortic and pulmonary valve closure sounds (A2 and
P2).
• Low­frequency sounds include the third heart sound (S3, which may be physiologic or
pathologic), associated with early ventricular filling and the fourth heart sound (S4),
associated with the atrial contribution to ventricular filling in late diastole. (See 'Classification
of heart sounds' above.)
● The intensity of the first heart sound (S1) can be helpful in assessing left ventricular (LV) function
and hemodynamics. (See 'Intensity of S1' above.)
• A loud S1 in the absence of a short PR interval indicates increased peak rate of rise of LV
systolic pressure (dP/dt), as seen in patients with increased transatrioventricular valve
gradients (mitral or tricuspid stenosis).
• A soft S1 in the absence of a prolonged PR interval usually indicates increased LV end­
diastolic pressure (LVEDP) and decreased peak dP/dt or reduced mobility of the
atrioventricular valves (calcified mitral stenosis).
● Fixed wide splitting of the second heart sound (S2) is highly suggestive of an atrial septal defect.
(See 'Splitting of S2' above.)
● Paradoxical splitting of S2 in the absence of left bundle branch block suggests LV outflow
obstruction or impaired contractile function. (See 'Splitting of S2' above.)
● An S3 gallop in adults in the absence of mitral regurgitation usually indicates elevated LVEDP
and increased brain natriuretic peptide levels. (See 'Clinical significance of S3' above and
"Evaluation of the patient with suspected heart failure", section on 'Heart sounds'.)
● An abnormal S4 is most frequently observed in patients with decreased LV distensibility (eg,
acute myocardial ischemia, LV hypertrophy). (See 'Clinical significance of S4' above.)
● Other early diastolic high­frequency sounds include an opening snap of the mitral or tricuspid
valve (appreciated in mitral or tricuspid stenosis) or a tumor plop associated with an atrial
myxoma. (See 'Early diastolic high­frequency sounds' above.)
● A pericardial rub is characteristically a scratching or grating sound that may have one, two, or
three components. (See 'Pericardial friction rub and other adventitious sounds' above.)
ACKNOWLEDGMENT
UpToDate wishes to acknowledge the past work of the late Kanu Chatterjee, MD, as an author for this
topic.
Use of UpToDate is subject to the Subscription and License Agreement.
Topic 1079 Version 14.0
GRAPHICS
Causes of first heart sound (S1) abnormalities
Abnormality
Causes
Increased intensity
Atrioventricular valve obstruction
Mitral
Mitral stenosis and left atrial myxoma
Tricuspid
Tricuspid stenosis and right atrial myxoma
Increased transvalvular flow
Mitral
Patent ductus arteriosus; ventricular septal defect; atrial septal defect
Tricuspid
Forceful ventricular systole
Hyperkinetic heart syndrome; tachycardia (eg, exercise); mitral valve prolapse
Short PR interval
Pre­excitation syndrome; Lown­Ganong­Levine syndrome
Decreased intensity
Immobility of mitral valve
Calcific mitral stenosis
Lack of apposition of the mitral
leaflets
Rheumatic mitral regurgitation
Presystolic semiclosure of the
atrioventricular valves
Long PR interval; acute aortic regurgitation; significant aortic stenosis; dilated
cardiomyopathy
Conduction anomaly
Left bundle branch block
Wide splitting of S1
Conduction abnormalities
Complete right bundle branch block; left ventricular pacing; pre­excitation
syndrome (left ventricular connection); Ebstein's anomaly
Mechanical
Tricuspid stenosis; atrial septal defect; Ebstein anomaly
Reversed splitting of S1
Arrhythmia
Premature beats (right ventricular origin)
Mechanical
Severe mitral stenosis and left atrial myxoma
Graphic 65274 Version 2.0
Cause of loud S1 with mitral stenosis
This schematic representation shows the transition between left atrial (LA) and left ventricular (LV) pressures at end­
diastole in the normal heart (A) and in a patient with mitral stenosis (B). In B, a significant pressure gradient remains
at end­diastole. Note that at low LA pressures, the rate of LV pressure development (dP/dt) is much slower than
when crossover occurs at higher LA pressures. Hence, the rate of mitral valve closure is increased in mitral stenosis,
the principal cause of a loud S1.
S1: first heart sound.
Courtesy of Theo Meyer, MD.
Graphic 119876 Version 1.0
Abnormalities of the second heart sound (S2) and their mechanisms
Wide splitting of S2 with maintained inspiratory delay of P2
Delayed activation and completion of right ventricular ejection
Complete right bundle branch block
Artificial left ventricular pacing
Pre­excitation of the left ventricle (Wolff­Parkinson­White syndrome)
Premature beats and idioventricular rhythm originating from the left ventricle
Prolonged right ventricular ejection time
Pulmonary hypertension with right heart failure
Right ventricular outflow obstruction (eg, pulmonic stenosis, acute massive pulmonary embolus)
Increased pulmonary hangout time
Idiopathic dilatation of the pulmonary artery
Mild pulmonic stenosis
Postoperative atrial septal defect
Decreased left ventricular ejection time (early A2)
Mitral regurgitation
Ventricular septal defect with low pulmonary vascular resistance
Constrictive pericarditis
Fixed splitting of S2
Unchanged right ventricular stroke volume during respiration; severe right ventricular failure due to any cause
Interatrial communication; atrial septal defect; common atrium
Reversed splitting of S2
Delayed left ventricular activation and completion of ejection
Left bundle branch block
Artificial right ventricular pacing
Pre­excitation of the right ventricle (Wolff­Parkinson­White syndrome)
Premature beats of right ventricular origin
Prolonged left ventricular ejection time
Increased resistance to left ventricular ejection (aortic stenosis, obstructive hypertrophic cardiomyopathy,
hypertension)
Isolated increase in left ventricular forward stroke volume (aortic regurgitation, patent ductus arteriosus)
Myocardial dysfunction (mild to moderate left ventricular failure, myocardial ischemia or infarction)
Increased aortic hangout time (not the sole cause)
Aortic regurgitation
Patent ductus arteriosus
Aortic stenosis
Single S2
Apparent: obesity, emphysema, pericardial effusion
Absent A2: severe aortic stenosis, severe aortic regurgitation
Absent P2: absent pulmonary valve, pulmonary atresia, tetralogy of Fallot, truncus arteriosus
Fusion of A2 and P2: Eisenmenger ventricular septal defect, common ventricle
Graphic 77038 Version 3.0
Splitting of the second heart sound
Wide splitting of second heart sound (S2) may be due to delayed closure of pulmonic valve as in
right bundle branch block, pulmonic stenosis, and atrial septal defect, or to early closure of
aortic valve as in mitral regurgitation and ventricular septal defect. In atrial septal defect,
splitting is both wide and fixed.
S1: first heart sound; A2: aortic valve closure sound; P2: pulmonic valve closure sound; T1: tricuspid
valve closure sound; M1: mitral valve closure sound.
Reprinted with permission from: Shaver JA, Leonard JJ, Leon DF. Auscultation of the Heart.
Examination of the Heart, Part 4. American Heart Association, Dallas 1990. Copyright ©1990,
American Heart Association, Inc.
Graphic 55198 Version 11.0
Causes of a high frequency sound in early diastole
Mitral opening snap
Organic mitral stenosis
Rarely, pure mitral regurgitation
Tricuspid opening snap
Organic tricuspid stenosis
Functional tricuspid stenosis (rare)
Atrial septal defect
"Tumor plop"
Left atrial myxoma
Right atrial myxoma
Opening clicks of mitral stenosis
Mitral valve prolapse
Graphic 73281 Version 1.0
Normal auscultatory findings of prosthetic valves according to type and location
Auscultatory Findings
Valve prosthesis
Mitral
Ball valves (eg, Starr­Edwards)
Tilting disc valves (eg, Medtronic­Hall)
Bioprosthetic valves
Bileaflet valves (eg, St. Jude)
Aortic
A2­MO interval 0.07 to 0.11 seconds
S1­AO interval 0.07 seconds
MO louder than MC
AO louder than AC
Soft systolic murmur
Soft, harsh systolic ejection murmur
No diastolic murmur
"Seating puff" ­ diastolic rumble
A2­MO interval 0.05 to 0.09 second
S1­AO interval 0.04 seconds
MO is soft or may not be audible
AC louder than AO
Soft systolic murmur
Soft systolic ejection murmur
Soft and short diastolic rumble
"Seating puff" ­ diastolic rumble
A2­MO interval 0.1 seconds
S1­AO interval 0.03 to 0.08 seconds
MC louder than MO
AC louder than AO
MO is audible in approximately 50%
AO may be absent
Soft apical systolic murmur
Soft systolic ejection murmur
Soft diastolic ramble
No diastolic rumble
Loud AO and AC
Soft systolic ejection murmur
A2: aortic valve closure sound; MO: mitral prosthesis opening sound; MC: mitral prosthesis closing sound; S1: first heart
sound; AO: aortic prosthesis opening sound; AC: aortic prosthesis closing sound.
Data from Smith ND, Ralzada V, Abrams J: Auscultation of the normally functioning prosthetic valve. Ann Intern Med 95:594,
1981.
Graphic 61951 Version 5.0