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
Contributor Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Mar 2020. | This topic last updated: May 01, 2019.

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 [1-3]. Electronic auscultatory devices utilize
advanced acoustic sensor-based 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 low-frequency sounds [6].

High-frequency sounds arise from closing or opening valves, including mitral and
tricuspid valve closing sounds (M1 and T1), non-ejection 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 'Non-ejection
systolic sounds' below and 'Early diastolic high-frequency sounds' below and 'Prosthetic
valve sounds' below.)

Low-frequency 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 high-frequency
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) [7-10]. 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 high-
frequency 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).
●Cardiac cycle length.
●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 end-diastole (mitral or tricuspid
valve obstruction as in mitral stenosis (movie 1), tricuspid stenosis, or atrial
myxoma).
•Increased transvalvular flow (left-to-right 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 semi-closed
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 semi-closed
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 semi-closure 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]. Semi-closure 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; semi-closure 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 M-mode 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 semi-recumbent (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
right-sided and decreased left-sided 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-Parkinson-White (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
A2-P2 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 A2-P2 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 left-to-right or bidirectional shunt;
abnormally wide splitting of S2 occurs, and respiratory variations of the A2-P2
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 (left-to-right shunt), which prolongs right-sided 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
long-standing 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 low-frequency 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, right-
sided 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 right-sided 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 end-diastolic pressures (>15 mmHg), and
elevated serum brain natriuretic peptide (BNP) concentrations [35-37]. (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 should raise questions about the
severity of 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 end-diastolic 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 high-output 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 end-diastolic 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 end-diastolic 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 end-diastolic
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 lower-pitched S3 and S4 will be more pronounced when
listening gently with the bell, while the higher-pitched 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 45-degree 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 by experienced auscultators, suggesting an early
manifestation of RV constriction. (See "Constrictive pericarditis".)

EJECTION SOUNDS An ejection sound is a high-frequency "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. The ejection click is often described by auscultators as a split S1. 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 [53-56]. 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.

NON-EJECTION SYSTOLIC SOUNDS The non-ejection systolic sounds

are also high-frequency 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 non-
ejection 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) [57-60]. (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 S1-click interval, then,
can vary according to the preejection (end-diastolic) ventricular volume and the rate of
ejection.

●The S1-click interval will increase, producing a late mid-systolic click whenever
there is an increase in end-diastolic volume (eg, supine position, squatting, hand
grip) (movie 11).
●The S1-click interval usually shortens, and the click tends to occur earlier when
there is a reduction in end-diastolic volume (eg, standing, phase 2 Valsalva
maneuver) or when there is an increased rate of ejection, as occurs after an ectopic
beat as a result of post-ectopic 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 high-frequency 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].

Pseudo-ejection 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 "pseudo-ejection 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 pseudo-ejection 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 HIGH-FREQUENCY 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 high-frequency, 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 many
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 often widely transmitted and can be 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 high-frequency 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 mid-diastolic rumble. In ASD, only the two components of the S2 are
heard during expiration and inspiration.
Experienced clinicians with advanced ausculatory skills may estimate the severity of
mitral stenosis at the bedside by noting the interval between the aortic component of S2
and the opening snap. The S2-opening 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 S2-opening snap interval. At the bedside, the shorter S2-opening 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 S2-opening 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 S2-
opening snap interval becomes shorter with the same degree of mitral stenosis. The S2-
opening snap interval also becomes shorter when mitral stenosis is associated with MR
with a large V wave. Furthermore, tachycardia decreases the S2-opening 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 S2-opening 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 left-to-right 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 high-frequency, 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 high-frequency 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 high-
frequency sounds are heard coinciding with the time of contact of the anterior
leaflet of the mitral valve to the interventricular septum [70].
 ●High-frequency 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 ball-and-cage 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 S2-opening sound interval. A marked variation in the S2-mitral
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 ball-and-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 rapid-filling phase of the ventricle (three-component 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 one-component rub,
usually during ventricular systole, is more frequent than two- or three-component 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 to-and-fro, high-pitched sound may be heard over
the left second interspace, known as a Means-Lerman 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, one-component 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 high-frequency 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 low-frequency sounds.
(See 'Classification of heart sounds' above.)
•High-frequency 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).
•Low-frequency 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 high-frequency 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 high-frequency
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.
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