5.10 Cardiac Auscultation

5.
10 Cardiac Auscultation
5.10 CARDIAC AUSCULTATION
ACCSAP
Copyright © 2019 American College of Cardiology 0

5.10 Cardiac Auscultation
Table of Contents
5.10 Cardiac Auscultation ...........................................................................................................................1
Cardiac Auscultation .......................................................................................................................................... 2
Background ........................................................................................................................................................ 3
Normal Heart Sounds and Their Hemodynamic Correlates............................................................................... 6
Abnormalities in the Heart Sounds .................................................................................................................... 8
Aortic Valve Murmurs ...................................................................................................................................... 20
Mitral Valve Murmurs ...................................................................................................................................... 27
Pulmonary Valve Murmurs .............................................................................................................................. 34
Tricuspid Valve Murmurs ................................................................................................................................. 39
References ....................................................................................................................................................... 43
1
Cardiac Auscultation
Cardiac Auscultation
Author
Thomas M. Bashore, MD
Disclosures
This author has nothing to disclose.
Learner Objectives
Upon completion of this module, the reader will be able to:
1. Name the normal heart sounds and their origins.
2. Describe disease states that result in abnormalities in the first heart sound (S1) and second heart
sound (S2).
3. Describe the cause of extraneous heart sounds in both systole and diastole, as well as their timing
relative to S1 and S2.
4. Assess auscultatory valve lesion severity in aortic stenosis (AS) and aortic regurgitation (AR), as well
as how it may be distinguished from other systolic murmurs.
5. Discuss the difference between acute and chronic AR on physical examination.
6. Assess auscultatory valve lesion severity in mitral stenosis (MS) and mitral regurgitation (MR).
7. Discuss the differences between acute and chronic MR.
8. Describe the difference between pulmonary regurgitation (PR) in the setting of low pulmonary
pressures compared with high pulmonary pressures.
9. Identify tricuspid stenosis (TS) and tricuspid regurgitation (TR) by physical examination.

Background
Background
Direct, or immediate, auscultation (employed by placing the ear on the chest wall and listening for lung and
heart sounds) has been practiced at least since the time of Hippocrates, and possibly as early as the Ebers
Papyrus in 1500 BCE. This changed with the invention of the stethoscope.
Rene Theophile Hyacinthe Laënnec was born in 1781 in France, where his uncle was dean of the faculty of
medicine in Nantes. Laënnec went on to study medicine in Paris and completed his qualifications in 1804. He
suffered from tuberculosis, a disease that eventually took his life at 45 years of age. Laënnec had a profound
interest in chest disease, correlating physical findings with postmortem anatomy on autopsies he performed
himself. He was influenced by the work of Leopold Tunaburger, who described percussion as a means of
detecting lung consolidation and pleural effusion. The Austrian’s percussion work was later translated from
its original Latin to French by Jean Nicolas Corvisart, who eventually became a mentor to Laënnec.
The story goes that, one day in 1816, Laënnec was watching a couple of children playing in the park, who
were scratching a beam of wood at one end and listening to the sounds coming from the other end, giving
him the fundamental concept for mediate auscultation. Soon after that incident, he was consulted to see a
young overweight female, for whom direct or immediate auscultation was not possible physically. By rolling
multiple sheets of paper into a cylinder and placing one end on the patient’s chest and the other end to his
ear, he was delighted that the heart sounds were much louder and clearer than he had ever heard.
An accomplished woodworker, Laënnec set about the task of creating a better cylinder, using paper, wood,
and/or Indian cane. After several trials and errors, his description of his original design revealed that it
“consists simply of a cylinder of wood, perforated at its centre longitudinally, by a bore three times in
diameter and formed so as to come apart in the middle for the benefit of being more easily carried.” A
removable funnel-shaped plug that could fit into one end was also designed to be “used in exploring the
signs obtained through the medium of the voice and action of the heart; the other modification, or with the
stopper removed, is for examining the sounds communicated by respiration. This instrument I commonly
designate simply the Cylinder, sometimes the Stethoscope.” Figure 1 is a plate from the original treatise. He
chose the word stethoscope from the Greek for “chest” and “to inspect.”
Laënnec then labored to complete his classic work, De l ’Auscultation mediate, even though his tuberculosis
continued to progress. He sold his initial book for 12 Francs, and a hand-carved wooden stethoscope was
included for an additional 2.5 Francs. In this work, he also defined terms such as rales, bruits, pectoriloquism
(egophony), murmurs, and friction rubs. In his second edition, completed just prior to his death in 1826, he
also described atrophic scarring of the liver, which subsequently became known as Laënnec’s cirrhosis. The
stethoscope subsequently went through many iterations over the next 200 years, emerging from the original
tubular monaural form to the more familiar binaural shape used now.
3
Interest in what creates the heart sounds and murmurs and in recording them for direct observation
(phonocardiography) grew throughout the first half of the 1900s, spurred on by the development of the
string galvanometer electrocardiograph, which allowed for simultaneous, and graphic, recordings of the
electrocardiogram and the heart sounds or heart pulsations. The development of the heart catheterization
laboratory and eventually echocardiography further allowed for more accurate interpretation of the origin
and relevance of cardiac auscultatory events.
Auscultatory skills, however, have declined considerably over the last few decades, given the emergence of
ever-more-sophisticated cardiac imaging that better defines abnormal cardiac structures and performance
than cardiac auscultation. Auscultation, however, remains a vital component of the cardiac physical
examination. Indeed, the stethoscope continues to be a universal symbol of a physician.
This module is designed to provide a schematic of the most commonly encountered heart sounds and
murmurs, as well as a brief discussion of their origins. The text is purposely kept to a minimum on the
assumption that this information should be simply a reminder for the average reader. Examples and clinical
pearls will be provided when appropriate to help put the changes into clinical context.

Figure 1
The schematic for the first hollow cylindrical stethoscope. The ear was placed against the end without the
cone, while the other end was placed over the heart. The end cone was removed for listening to the lungs.
5
Normal Heart Sounds and Their Hemodynamic

Correlates
Normal Heart Sounds and Their Hemodynamic Correlates
The first heart sound is derived from the

closure of the tricuspid valve (TV) and Key Point
mitral valve (MV) with the onset of
• The splitting of the second heart sound is a
ventricular systole. The second heart function of the lower resistance in the pulmonary
sound reflects the closure of the aortic circuit compared with the systemic circulation. This
and pulmonary valves and the onset of results in the right ventricular ejection time being
ventricular diastole. These sounds longer than the left ventricular ejection time.
establish the framework for
auscultation. Higher-pitched sounds are
heard best with the diaphragm or while putting pressure on the bell; lower-pitched sounds with the bell
itself.
As shown in Figure 2, panel A, right ventricular ejection time (RVET) starts earlier than the left ventricular
ejection time (LVET) and finishes later. The right ventricular end-diastolic pressure (RVEDP) is lower than the
left ventricular end-diastolic pressure (LVEDP). The onset of systole closes the TV before the left ventricle
(LV) pressure rises enough to close the MV; thus, TV closure precedes MV closure.
The difference in the resistance of the pulmonary and systemic vascular beds allows for forward blood flow
into the pulmonary circuit, even as the right ventricle (RV) goes into its diastole. This results in the RVET
being longer than the LVET (Figure 2, panel B). The RV in effect acts much like a “fall-away jump shot.” This
difference in the pulmonary and aortic vascular resistance creates the splitting of the second heart sound.
With inspiration, the negative intrapleural pressures “pull” systemic venous blood into the lung through the
RV, and the RVET gets even longer, while there is a reduction in return to the LV and the LVET shortens. The
result is a widening in the splitting of the second sound with inspiration, with the reverse with expiration
(Figure 2, panel C), as the increased pleural pressure drains the pulmonary bed of the blood that
accumulated with inspiration and reduces the input coming in from the right heart.
The following is not intended to be comprehensive, but rather a review of the most common abnormalities
in heart sounds and in murmurs that the adult cardiologist is likely to encounter. Only valvular lesions are
discussed.

Figure 2
Normally the right ventricular (RV) ejection begins before the left ventricular (LV) ejection, as the pressure
needed to open the pulmonary valve is much lower than the pressure needed to open the aortic valve (panel
A). Because of the low resistance presented by the pulmonary circuit (panel B), blood continues to flow
forward, even as the RV goes into its diastole. This results in the pulmonary valve closing later than the aortic
valve (this interval is called “hangout”). The changes in the RV and LV ejection times during inspiration and
expiration (panel C). With inspiration the RV stroke volume increases and the LV stroke volume decreases;
the reverse occurs with expiration.
LV = left ventricular; LVET = left ventricular ejection time; RV = right ventricular; RVET = right ventricular
ejection time.
7
Abnormalities in the Heart Sounds

Figure 3 outlines the timing of the normal and abnormal heart sounds relative to S1 and S2.

Figure 3
Figure 3
This schematic outlines the approximate time when cardiac sounds occur during systole and diastole.
Ejection sounds from semilunar valves occur early in systole and nonejection sounds occur from mitral
prolapse in mid systole. The mitral opening snap occurs early in diastole, followed by the timing of a
pericardial knock and S3. An S4 occurs prior to the next systole.
Abnormalities in the First Heart Sound
Abnormalities in the First Heart Sound
Key Points
9
Increased S1
• The only right-sided auscultatory event that
Increased S1 is due to maximal opening diminishes with inspiration is the pulmonary
ejection click associated with pulmonary valve
of the MV and TV leaflets at the onset of
stenosis.
ventricular systole.
Examples: • The midsystolic click in Ebstein’s anomaly is
referred to as the “sail sound.”
 Short P-R interval
 Rapid heart rate (anemia,
thyrotoxicosis, etc.)
 Short cycles in atrial fibrillation
 MS
 Mitral valve prolapse (MVP)
Clinical pearls. A loud closure sound requires a mobile valve and at least moderate valvular excursion.
Decreased S1
Decreased S1 is due to reduced mobility of the MV or TV, or to early partial closure.

Examples:
 Worsening MS
 Acute AR with preclosure of the MV
 Long P-R interval
 Left bundle branch block (LBBB)
 Body habitus issues (obesity, large breasts, etc.)
Early Systolic Sounds
Early systolic sounds generally emanate from the semilunar valves (aortic or pulmonic), occur commonly,
and are due to the sudden abrupt cessation of a doming valve.
Examples:
 Bicuspid aortic valve
 Pulmonary valve stenosis
 Dilated aorta
 Abnormal (or stiff) aortic valve from systemic hypertension
 Abnormal (or stiff) pulmonary valve from pulmonary hypertension
Clinical pearls. The opening sound in a bicuspid aortic valve implies the valve is stiff and remains mobile. This
sound diminishes as the valve lesion worsens. The ejection or opening sound of pulmonary valve stenosis is
the only right-sided event that decreases with inspiration. This is because of the inspiratory increase in the
atrial contractile force into the RV, which prematurely opens the pulmonary valve, resulting in a reduction in
the distance the valve travels and a softer ejection sound as more blood enters the right heart with
inspiration. Recall that the RV is hypertrophied and the pulmonary artery (PA) pressure is normal in
pulmonary valve stenosis.

Mid-Late Systolic Sounds
Mid-late systolic sounds generally emanate from the MV (most commonly) or the TV. These clicks coincide
with the maximal MV excursion into the left atrium (LA), and are thought to be due to abrupt tensing of the
redundant leaflets or chordae. At times, multiple clicks are audible.
Examples:
 MVP
 Ebstein’s anomaly
 Pericardial rub
Clinical pearls. In MVP, timing of the click is dependent on the LV volume and the point at which the
maximal valve excursion occurs. This can be altered with positional maneuvers. When supine, the heart is
“full” and the sound occurs late in systole. With sitting or standing, the heart volume is less, the prolapse
greater, and the sound or sounds appear earlier in systole. Squatting increases the LV afterload and preload,
and the sound appears late again (as discussed later). The ejection sound in Ebstein’s anomaly has been
likened to the unfurling of a sail on a sailboat; hence, the “sail sound.” Pericardial friction rubs are often very
localized. There are generally two components (in diastole and systole), with a third component coming at
the time of atrial contraction and often heard in late diastole.
Abnormalities in the Second Heart Sound
Abnormalities in the Second Heart Sound

The normal splitting of the second heart
sound depends on the differences in the Key Points
capacitance of the pulmonary and
• A single S2 may be present in severe pulmonary
systemic vascular beds, as noted earlier. stenosis or aortic stenosis, transposition of the
When pulmonary hypertension occurs, great arteries, or pulmonary hypertension.
this difference between the two circuits
is reduced and the splitting becomes • Fixed splitting of the second heart sound is
narrower. classic for a patient with an atrial septal defect and
is due to a fixed right ventricular stroke volume
because of reduced shunting that occurs with
Single S2
inspiration and increased shunting with expiration.
A single S2 implies there is loss of one of • Examples of early diastolic sounds include the
the components (aortic or pulmonary mitral stenosis opening snap, tricuspid stenosis
closure sound), or the sounds are opening snap, a pericardial knock, an S3, and an
simultaneous. atrial myxoma plop.
Examples:
 Transposition of the great
arteries
 Pulmonary hypertension with RV dysfunction
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 Severe pulmonary stenosis (PS)

 Severe AS
Clinical pearls. In transposition of the great arteries, the P2 is often inaudible because the PA is displaced
posteriorly and away from the chest wall. Loss of the second heart sound component in severe PS or AS
implies the valve is immobile. In pulmonary hypertension, the RVET may be shortened if RV dysfunction
occurs; this shortening of the RVET may result in a merger of A2 and P2.
Wide or Fixed Splitting of S2
Wide or fixed splitting of S2 occurs when there is an increase in the RVET compared with the LVET or when
the RVET begins late.
Examples:
 Right bundle branch block (RBBB)
 Atrial septal defect (ASD)
 Acute pulmonary embolus
 Pulmonary valve stenosis
 MR
 Ventricular septal defect (VSD)
Clinical pearls. In RBBB, the RV ejects later than the LV, widening splitting. Fixed splitting of the second heart
sound is a hallmark finding in an ASD. The low pulmonary vascular resistance and high RV stroke volume
increase the splitting of S2 by increasing the RVET. With inspiration, the increase in right atrial (RA) pressure
reduces the left-to-right shunt. The balance between the inspiratory increase in RV flow and the inspiratory
decrease in the shunt flow results in a fixed RV stroke volume and ejection time, resulting in fixed splitting.
In PS with preserved RV function and in acute pulmonary embolism (PE), the increased resistance to the RV
may increase the RVET and widen splitting. In MR and VSD, there may be a reduction in the LVET across the
aortic valve so that A2 appears earlier.
Paradoxical Splitting of S2
Paradoxical splitting of S2 occurs when the LV is depolarized later than the RV.
Examples:
 LBBB
 RV pacing
 Severe AS
 Right-sided Wolff-Parkinson-White (WPW) syndrome
Clinical pearls. Anything that delays the onset of LV contraction (pacing, LBBB, right-sided WPW) compared
with LV contraction allows for A2 to occur late, and A2 may even occur after P2. In severe AS with preserved
LV function, the LVET may be quite prolonged.
Increased Intensity of A2 or P2

Increased intensity of A2 or P2 occurs when there is either systemic or pulmonary hypertension or when the
aorta or PA is closer to the chest wall. This is also evident in patients with a thin or shallow chest dimension.
Examples:
 Pulmonary hypertension
 Systemic hypertension
 Transposition of the great arteries
 Dilated aorta
 Dilated PA
Clinical pearls. A louder A2 or P2 would be expected if there were systemic or pulmonary hypertension. In
transposition of the great arteries, the aortic valve is anterior to the pulmonary valve; with higher aortic
pressure, the second sound is louder than would be expected. Dilated great vessels also result in louder
closure sounds.
Early Diastolic Sounds
Early diastolic sounds reflect the “popping open” of a stenotic MV or TV, or the rapid early filling of the
ventricles.
Examples:
 MS
 TS
 Constrictive pericarditis (pericardial knock)
 Severe MR (associated S3)
 Atrial myxoma
Clinical pearls. In MS, the higher the LA pressure rises with worsening stenosis severity, the earlier the time
interval from the aortic closure (A2) to the opening of the MV (and the opening snap). Therefore, a wide
interval from the A2 to opening snap suggests less severe disease, as the LA pressure is lower. A similar
phenomenon occurs in TS. In constrictive pericarditis, the heart is only able to fill during early diastole and
the atrial pressures are elevated. Thus, the resultant early rapid filling often creates a loud filling sound or
pericardial knock that occurs slightly earlier than the traditional S3. In severe MR, the rapid flow back into
the LV from the LA may also create an early diastolic filling sound at the timing of an S3. An atrial myxoma
“plop” is at times a loud early diastolic sound, often variable in intensity beat to beat. It results from the LA
tumor moving in and out of the MV orifice in diastole.
Mid-Late Diastolic Sounds
Diastolic filling of the ventricles occurs both actively (early) and passively (later). A sound generated during
the active filling phase when more than one-half of the LV is filled is an S3 sound related to rapid filling. A
late diastolic sound related to atrial contraction into the LV is an S4 (Figure 3). These can be normal filling
sounds, especially the S3, but in older patients they imply a noncompliant ventricle. At times, both sounds
13
may be present, or the two sounds may merge (summation gallop), especially at higher heart rates. These
sounds tend be of low intensity and are best heard with the bell of the stethoscope.
Examples:
 Normal S3 (especially in younger patients)
 Noncompliant LV or RV
 Pacemaker sound
Clinical pearls. Although normal in younger patients (<40 years of age), an S3 is pathologic in older patients,
where it implies a noncompliant ventricle. It is thought to be due to a sudden intrinsic limitation of
longitudinal expansion of the ventricular wall during early diastole. An S4 requires atrial contraction and is
commonly associated with systemic hypertension, LV hypertrophy, or ischemic heart disease. It is lost during
atrial fibrillation. In patients with a pacemaker, an early filling sound from the wire across the TV may be
audible. A right-sided gallop may sometimes be distinguished from left-sided gallop by noting its presence in
the right subclavicular area (away from the LV) or by the increased intensity with inspiration.

Figure 3
Figure 3
This schematic outlines the approximate time when cardiac sounds occur during systole and diastole.
Ejection sounds from semilunar valves occur early in systole and nonejection sounds occur from mitral
prolapse in mid systole. The mitral opening snap occurs early in diastole, followed by the timing of a
pericardial knock and S3. An S4 occurs prior to the next systole.
15
Cardiac Murmurs
Cardiac Murmurs
Murmurs are defined based on their shapes (crescendo, decrescendo, both, or continuous), timing in systole
or diastole (early, mid, late, holosystolic, holodiastolic, or continuous), their location and pitch, and their
audible intensity. They can sometimes be varied using maneuvers that alter afterload and preload. The
intensity grading system, originally proposed in 1933, is still in use. Table 1 outlines the grading of systolic
murmurs on a scale of 1 to 6 and diastolic murmurs on a scale of 1 to 4.

Table 1
Table 1
Note that it is presumed that no diastolic murmurs would be loud enough to create a thrill. This may not
actually be the case in rare instances.
“Normal” Heart Murmurs
“Normal” Heart Murmurs

Not all murmurs are pathologic. Many
systolic murmurs are considered Key Point
innocent. Some normal-flow murmurs
• The murmur of aortic stenosis can often be
occur in the supraclavicular region distinguished from mitral regurgitation by noting a
(especially in children) and are likely due gap between the murmur and S1 and S2.
to branch turbulence in the
brachiocephalic arteries. These can be
mitigated at times by simply bringing the elbows back behind the back. A “mammary souffle” may be heard
in pregnant or lactating females.
17
Pulmonary flow murmurs are occasionally present and are audible simply because the PA is located near the
chest wall. A continuous murmur in the neck is occasionally heard in children and young adults, and is
related to flow in the jugular vein (the venous hum). This is usually related to stretch in the vein when the
patients turn their heads and necks to the opposite side or lift their chins upward. Pressure on the vein
obliterates the murmur. Diastolic murmurs, however, should always be considered pathologic.
Murmurs should also be described based on their location and radiation. Systolic aortic murmurs radiate
from the left sternal border (LSB) toward the right and to the neck, whereas systolic pulmonary murmurs
radiate to the left and are often more localized. AR and PR are best heard along either side of the sternum,
often in the fourth intercostal space. MR tends to radiate to the axilla. MS is best heard in the left lateral
position. MS and TS are both difficult to hear, as they are low pitched and the diastolic gradients, even if
significant, are low. TR is notoriously hard to hear at times and is usually best appreciated by examining the
neck vessels for a positive systolic wave during ventricular systole.
The timing of the murmur relative to the first and second heart sounds may also help distinguish the systolic
murmur from a semilunar valve (AS or PS) from that originating from an AV regurgitant (MR or TR) valve. As
shown in Figure 4, the murmur of AS can be distinguished from MR by noting the S1, then a gap before the
murmur, the murmur, then a gap following the murmur, and then S2. In MR, there is no gap from S1 to the
onset of the murmur, and the holosystolic murmur extends through S2 until the MV reopens.

Figure 4
Figure 4
The murmurs of AS and MR can have similar qualities and both may be well heard at the apex. One way to
differentiate the two is to appreciate that MR starts with the first heart sound and travels through the
second, whereas in AS there is a gap between the murmur and both the first and second heart sounds.
Ao = aorta; AS = aortic stenosis; LA = left atrium; LV = left ventricle; MO = mitral opening; MR = mitral
regurgitation.
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Aortic Valve Murmurs
Aortic Stenosis
Aortic Stenosis
The AS murmur is due to turbulence
across the stenotic aortic valve. It Key Point
radiates from the valve to the right
• As the murmur of aortic stenosis (AS) worsens,
sternal border and often to the carotids. the ejection sound and the intensity of A2 diminish;
In calcific AS, this murmur may be the murmur peaks later in systole. The AS murmur
coarse and impure along the aortic increases after a premature ventricular
outflow, but more musical and purer at contraction.
the LV apex. This dissociation was
described by Louis Gallavardin in 1925.
The Gallavardin murmur of AS can be differentiated from MR by noting the timing of the murmur with the
first and second heart sounds, as suggested in Figure 4.
Mild AS may include an ejection sound, a crescendo-decrescendo murmur that peaks early, and a preserved
A2. As the stenosis worsens and the valve mobility declines, the ejection sound becomes lost, A2 becomes
less audible, and the murmur peaks later in systole. The murmur increases following premature ventricular
contractions (PVCs), as the stroke volume after the PVC is greater than before the PVC. Figure 5 outlines the
progression of the murmur and S2 changes with worsening AS.

Figure 4
Figure 4
The murmurs of AS and MR can have similar qualities and both may be well heard at the apex. One way to
differentiate the two is to appreciate that MR starts with the first heart sound and travels through the
second, whereas in AS there is a gap between the murmur and both the first and second heart sounds.
Ao = aorta; AS = aortic stenosis; LA = left atrium; LV = left ventricle; MO = mitral opening; MR = mitral
regurgitation.
21
Figure 5
Figure 5
The top panel reveals the typical AS murmur when mild. The valve is mobile and an ejection click may be
present. The murmur peaks in early systole. As the lesion progresses, the ejection click becomes less audible,
the murmur peaks later, and A2 gets softer. With severe aortic stenosis, there is no ejection click, the murmur
peaks later, and A2 may no longer be heard or is much diminished. In severe AS with preserved LV function
and preserved A2, the second sound may be paradoxically split with respiration (not shown).
AS = aortic stenosis; ES = ejection sound; LV = left ventricular.
Aortic Regurgitation
Aortic Regurgitation
Key Points

The diastolic murmur of AR is a high-

pitched diastolic decrescendo murmur • The murmur in aortic regurgitation (AR) differs
that begins with A2. Its duration in depending on whether it is acute or chronic in
nature. Due to the rapid rise in left ventricular
diastole may depend on the acuity, as
diastolic pressures in acute AR, the diastolic
well as the severity, of the regurgitation murmur may be short, the mitral valve might close
(Figures 6a, b). In acute severe AR, the prematurely (S1 softens), and a mid-diastolic
murmur may be short, given the rapid rumble of relative mitral stenosis (the Austin-Flint
rise in the LV diastolic pressure. An S3 murmur) may occur. In chronic AR, the murmur
may accompany. In chronic AR, the tends to be throughout diastole.
murmur will extend longer within
• A Duroziez sign is elicited by compressing the
diastole. femoral artery with the diaphragm of the
stethoscope, creating a systolic murmur. If severe
Other findings may also be present in aortic regurgitation is present, a diastolic murmur
chronic AR and can help with the from retrograde flow will also then be heard.
bedside determination of severity.
Figure 7 reflects the proper
performance of the Duroziez maneuver. The femoral artery is compressed by the diaphragm of the
stethoscope to create a systolic bruit. Once the systolic bruit is audible, if there is an associated diastolic
murmur, then there is presumed retrograde aortic flow back to the heart and severe AR present. In the
normal situation, the systolic pressure in the legs should be higher than in the arms (particularly in younger
patients). This increased systolic pressure is due to the reflected waves from the peripheral bouncing back
and becoming additive to the pressure wave traveling toward the periphery. In the normal situation, the
femoral artery systolic may be about 20 mm Hg higher than the central aortic pressure. If there is a high
stroke volume, such as in chronic AR, then this difference is magnified. When the difference between the
arm systolic blood pressure (BP) and the leg systolic BP by palpation is >40 mm Hg, then Hill’s sign is present,
and it represents severe AR. Other causes of a positive Hill’s sign include hyperthyroidism and anemia.
A murmur due to a perforation in the aortic valve may present with a high-pitched “cooing dove” sound. At
times, a mid-diastolic rumble may occur due to premature closure of the MV and a relative MS being
created. This rumble was first described by Austin Flint.
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Figure 6a
Figure 6a
The hemodynamics of acute and chronic AR are sketched. In acute AR, the LV has not adapted to the
increased volume and diastolic pressures are high. There may be premature closure of the mitral valve and S1
is soft. P2 may be increased in intensity if pulmonary hypertension is present. Early equilibration of the left
ventricular and aortic diastolic pressures results in the AR diastolic murmur being abbreviated in duration. In
chronic AR, the LV is enlarged and diastolic pressures tend to be normal for a prolonged period of time. The
murmur is holodiastolic in nature, as there is a substantial gradient between the aorta and LV throughout
diastole.
Ao = aorta; AR = aortic regurgitation; LV = left ventricle.

Figure 6b
Figure 6b
The murmurs from Figure 6a are shown again.
25
Figure 7
Figure 7
With compression of the femoral artery using the edge of the stethoscope diaphragm to create a systolic
murmur, the presence of a diastolic murmur suggests retrograde aortic flow and is consistent with severe AR.
AR = aortic regurgitation.

Mitral Valve Murmurs
Mitral Stenosis
Mitral Stenosis
In rheumatic MS, the first sound is loud,
but declines as valve mobility becomes Key Points
reduced with disease progression. The
• With worsening of the stenosis in mitral stenosis
opening snap in early diastole reflects (MS), the A2-opening snap interval in MS shortens
preservation of the valve mobility. As as the left atrium pressure rises and approaches
MS severity worsens, the LA pressure that of the aortic early diastolic pressure.
rises and the A2-opening snap interval
declines (Figure 8a). This auscultatory • In acute rheumatic mitral valvulitis, a mitral
gap between A2 and the opening sound stenosis rumble may occur transiently, the so-
called Carey Coombs murmur.
can also be applied to the prosthetic MV
sounds, and provides an estimate of LA
pressure in that setting.
The diastolic rumble is best heard in the left lateral position and initially involves only early diastole,
although a presystolic component also may be present. As the severity of the MS worsens, the gradient
occurs throughout all of diastole, which is reflected by the murmur (Figure 8b). A loud P2 implies pulmonary
hypertension. In acute rheumatic valvulitis, a transient mitral rumble may be heard during the acute phase
of the disease (the Carey Coombs murmur).
27
Figure 8a
Figure 8a
The hemodynamics of mild and severe MS are shown. As the severity of the MS worsens, the interval
between when the aortic valve closes, A2, and the mitral OS occurs shortens.
Ao = aorta; LA = left atrium; LV = left atrium; MS = mitral stenosis; OS = opening snap.

Figure 8b
Figure 8b
The resultant murmurs and changes in heart sounds are sketched. The top image reveals mild mitral stenosis.
S1 is usually loud and the interval between A2 and the OS of the valve is long, as the LA pressure is only mildly
elevated. The rumble is soft and does not extend throughout diastole. Presystolic accentuation is common,
due to the valve closure and the atrial kick. The lower image reveals severe mitral stenosis. The immobile
valve results in a softer S1, the higher LA pressure shortens the time when the mitral valve opens following A2
(short A2-OS interval), and the gradient persists throughout diastole.
LA = left atrial; OS = opening snap.
Mitral Regurgitation
Mitral Regurgitation
Key Points
29
The murmur of MR is high pitched due

to the large gradient between the LV • In severe chronic mitral regurgitation, there may
and LA during ventricular systole. In be an accompanying S3.
MVP, it may begin in midsystole, and
• The murmur of acute mitral regurgitation (MR)
often following the mitral click. At times, differs from that of chronic MR because of the
the late systolic murmur is very high rapid rise in left atrium pressures in the acute
pitched, creating a “whoop” sound. In setting. The acute MR murmur may be short.
severe MVP, and in other conditions
with MR, the murmur is holosystolic, • The timing of the click and murmur in mitral
valve prolapse occur earlier in systole with any
beginning at S1 and extending through
maneuver that reduces the left ventricular volume
S2 to the time of the MV opening in (e.g., sitting, standing) and later in systole with
diastole. squatting.
Following a PVC, there is little change in

the intensity of the murmur, as the LV to LA gradients are high during sinus rhythm and after PVCs. When
the MR is moderate to severe, an accompanying S3 may be present (Figure 9). In patients with anterior
leaflet prolapse, the murmur may radiate predominately toward the back and even up the spine to the
head. In posterior prolapse, the murmur may radiate anteriorly and along the aortic outflow.
MR can usually be differentiated from AS (described earlier) by noting that there is no gap from the first
sound to the beginning of the murmur and the murmur extends through S2. Acute MR may differ from
chronic MR, however (Figure 10). In acute MR, often from chordal rupture or myocardial infarction and
papillary muscle rupture, the MR murmur may be much softer due to the rapid equilibration of the LA and
LV pressures during systole. As described earlier, the MR timing in MVP may be altered by positional
changes (Figure 11).

Figure 9
Figure 9
The top panel reveals mild chronic mitral regurgitation (MR). The murmur begins with S1 and extends
through the second heart sound. As the MR worsens, the murmur generally becomes louder, and in severe
MR the presence of pulmonary hypertension may be noted by an increase in the intensity of P2. Flow back
into the left ventricle often produces an S3 in severe MR.
31
Figure 10
Figure 10
LV to LA gradients and the associated murmurs in acute and chronic mitral regurgitation. In acute MR, the
murmur is shortened due to the high V wave markedly increasing the LA pressure in late systole. In chronic
MR, it is holosystolic.
LA = left atrium; LV = left ventricle; MR = mitral regurgitation.

Figure 11
Figure 11
In the top panel, with the patient supine, the LV chamber is full and the murmur and nonejection sound (NES)
appears late in systole. In the middle panel, with standing, the left ventricular chamber is smaller, the
prolapse greater, and both the NES and murmur come earlier. With squatting, as shown in the lower panel,
afterload and preload are increased, and the NES and murmur move to later in systole.
33
Pulmonary Valve Murmurs
Pulmonary Valve Stenosis
Pulmonary Valve Stenosis

In general, the longer RVET in patients with PS results in wider splitting of the second heart sound. This
splitting becomes even wider as the PS worsens, but if RV dysfunction becomes evident, the RV stroke
volume will decline and with it the RVET and the width of the splitting. P2 may soften as the valve becomes
less mobile. Whereas the murmur increases with inspiration, the ejection sound decreases (the only right-
sided event that goes down with inspiration). Also, as the PS lesion worsens, the murmur peaks later in
systole and the P2 component of the second sound diminishes, much like in AS. Figure 12 outlines the
auscultatory changes with progressive pulmonary valve stenosis.

Figure 12
Figure 12
The ES in PS is the only right-sided event that is softer with inspiration. (Top) In mild PS, the click is evident
and the murmur (which increases with inspiration) peaks in early systole. (Middle) As the PS worsens, the
right ventricular ejection time increases, and there is increased splitting of the second sound. The murmur
peaks in mid-late systole. (Bottom) In severe PS, the ES may be diminished, the splitting of the second sound
wider, and the murmur harsher with later peaking in systole.
ES = ejection sound; PS = pulmonary stenosis.
Pulmonary Regulation
Pulmonary Regulation
Key Point
35
There is a marked difference in the

murmur of PR, depending on the • The murmur of pulmonary regurgitation differs
presence or absence of pulmonary greatly, depending on whether the pulmonary
pressure is low or high. In low-pressure pulmonary
hypertension. In low-pressure PR (such
regurgitation, there may be little diastolic gradient
as that observed following a between the pulmonary artery and right ventricle,
transannular patch in the RV outflow of and the murmur may be terminating early and be
patients with tetralogy of Fallot), there quite soft, despite severe regurgitation. The
may be very little gradient between the murmur is higher pitched and often holodiastolic in
PA diastolic pressure and the RV severe pulmonary regurgitation with pulmonary
hypertension. Secondary acute pulmonary
diastolic pressure despite severe PR.
regurgitation due to pulmonary hypertension is
This results in equalization of the PA occasionally referred to as the Graham Steell
diastolic and RV diastolic pressures early murmur.
in diastole and no murmur is then heard
once that happens. In high-pressure PR,
the murmur is obvious and continues throughout diastole, as there remains a gradient during all of diastole.
The PR murmur increases in intensity with inspiration. The PR associated with acute pulmonary
hypertension is sometimes referred to as the Graham Steell murmur. The difference between low-pressure
and high-pressure PR is outlined in Figures 13a and b.

Figures 13a
Figures 13a
The hemodynamics of high and low pressure PR are shown. In low pressure PR, there may be little murmur
despite wide open PR. This is due to rapid equilibration between the diastolic PA pressure and the RV
diastolic pressures. In high pressure PR, the murmur is evident throughout diastole.
PA = pulmonary artery; PR = pulmonary regurgitation; RV = right ventricle.
37
Figures 13b
Figures 13b
The schematic outlines low pressure and high pressure PR. In both instances, there is usually an
accompanying systolic flow murmur. In high pressure PR, P2 would be expected to be accentuated.
PR = pulmonary regurgitation.

Tricuspid Valve Murmurs
Tricuspid Stenosis
Tricuspid Stenosis
TS is usually due to rheumatic disease, a stenotic bioprosthetic valve, or carcinoid syndrome. The diastolic
murmur is similar to that of MS, but it is audible along the LSB and usually the rumble increases with
inspiration. An opening snap is less often present in TS than in MS, but the sound is common when there is a
bioprosthetic TV. A giant A wave is present during the jugular venous pulse (JVP), if the patient is in sinus
rhythm, and there is loss of the Y descent (Figure 14).
39
Figure 14
Figure 14
The murmurs of tricuspid stenosis and regurgitation may not always be evident. Therefore, careful
examination of the JVP is important to clinically observe these lesions. Timing of the JVP waveforms with the
opposite carotid waveform helps to differentiate the two lesions. A normal JVP is shown. The X descent
occurs during ventricular systole. In tricuspid stenosis, there is often a giant A wave, and the V wave is ill
defined, as the Y descent is blunted. There is a systolic wave that occurs in the JVP, confirming tricuspid
regurgitation.
Note: blue is systole; grey is diastole.
JVP = jugular venous pulse.

Tricuspid Regurgitation
Tricuspid Regurgitation
TR is common in many cardiac
conditions. It is usually functional in Key Point
nature. The TR murmurs may not be
• The murmurs of tricuspid stenosis and
very audible and often the best bedside regurgitation are often soft, and the jugular venous
diagnostic tool is to note a positive pulse contour should be examined closely for the
systolic (C-V) wave in the JVP. The diagnosis. Both murmurs increase with inspiration.
murmur is often pansystolic and The increase in systolic murmur in tricuspid
increases with inspiration (Carvallo’s regurgitation is sometimes called Carvallo’s sign.
sign). In patients with Ebstein’s
anomaly, a “sail sound” may be present.
Associated RBBB often results in wider splitting of the second heart sound. In severe TR, a diastolic flow
murmur may be present across the TV related to flow back across the TV during diastole. In general, TS and
TR are better diagnosed at bedside by carefully observing the JVP waveforms rather than relying on
auscultation (Figure 14).
41
Figure 14
Figure 14
The murmurs of tricuspid stenosis and regurgitation may not always be evident. Therefore, careful
examination of the JVP is important to clinically observe these lesions. Timing of the JVP waveforms with the
opposite carotid waveform helps to differentiate the two lesions. A normal JVP is shown. The X descent
occurs during ventricular systole. In tricuspid stenosis, there is often a giant A wave, and the V wave is ill
defined, as the Y descent is blunted. There is a systolic wave that occurs in the JVP, confirming tricuspid
regurgitation.
Note: blue is systole; grey is diastole.
JVP = jugular venous pulse.

References
References
1. Blaufox MD. An Ear to the Chest. An Illustrated History of the Evolution of the Stethoscope. New
York: The Parthenon Publishing Group Inc.: 2002.
2. Sakula A. R T H Laënnec 1781-1826 his life and work: a bicentenary appreciation. Thorax 1981;36:81-
90.
3. Tavel ME. Clinical Phonocardiography and External Pulse Recording. 2nd ed. Chicago: Year Book
Medical Publishers: 1972.
4. Perloff JK. Physical Examination of the Heart and Circulation. 2nd ed. Philadelphia: W.B. Saunders;
1990.
5. Sapira JD. The Art & Science of Bedside Diagnosis. Baltimore: Urban and Schwarzenberg; 1990.
6. Sprague HB, Ongley PA. The clinical value of phonocardiography. Circulation 1954;9:127-34.
43

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5.10 CARDIAC AUSCULTATION

Copyright © 2019 American College of Cardiology 0

5.10 Cardiac Auscultation

Copyright © 2019 American College of Cardiology 2

Copyright © 2019 American College of Cardiology 4

Normal Heart Sounds and Their Hemodynamic

Normal Heart Sounds and Their Hemodynamic Correlates

The first heart sound is derived from the

Copyright © 2019 American College of Cardiology 6

Abnormalities in the Heart Sounds

Abnormalities in the Heart Sounds

Abnormalities in the Heart Sounds

Copyright © 2019 American College of Cardiology 8

Abnormalities in the First Heart Sound

Abnormalities in the First Heart Sound

Decreased S1 is due to reduced mobility of the MV or TV, or to early partial closure.

Copyright © 2019 American College of Cardiology 10

Mid-Late Systolic Sounds

Abnormalities in the Second Heart Sound

Abnormalities in the Second Heart Sound

 Severe pulmonary stenosis (PS)

Wide or Fixed Splitting of S2

Copyright © 2019 American College of Cardiology 12

Early Diastolic Sounds

Mid-Late Diastolic Sounds

Copyright © 2019 American College of Cardiology 14

Copyright © 2019 American College of Cardiology 16

“Normal” Heart Murmurs

“Normal” Heart Murmurs

Copyright © 2019 American College of Cardiology 18

Aortic Valve Murmurs

Copyright © 2019 American College of Cardiology 20

AS = aortic stenosis; ES = ejection sound; LV = left ventricular.

Copyright © 2019 American College of Cardiology 22

The diastolic murmur of AR is a high-

Ao = aorta; AR = aortic regurgitation; LV = left ventricle.

Copyright © 2019 American College of Cardiology 24

The murmurs from Figure 6a are shown again.

Copyright © 2019 American College of Cardiology 26

Mitral Valve Murmurs

Ao = aorta; LA = left atrium; LV = left atrium; MS = mitral stenosis; OS = opening snap.

Copyright © 2019 American College of Cardiology 28

LA = left atrial; OS = opening snap.

The murmur of MR is high pitched due

Following a PVC, there is little change in

Copyright © 2019 American College of Cardiology 30

LA = left atrium; LV = left ventricle; MR = mitral regurgitation.

Copyright © 2019 American College of Cardiology 32

Pulmonary Valve Murmurs

Pulmonary Valve Stenosis

Pulmonary Valve Stenosis

Copyright © 2019 American College of Cardiology 34

ES = ejection sound; PS = pulmonary stenosis.

There is a marked difference in the

Copyright © 2019 American College of Cardiology 36

PA = pulmonary artery; PR = pulmonary regurgitation; RV = right ventricle.

Copyright © 2019 American College of Cardiology 38

Tricuspid Valve Murmurs