HEART SOUNDS

1. First Heart Sound

The first heart sound (S1) is produced by vibrations generated by closure of the mitral (M 1) and tricuspid valves (T1).[3] It
corresponds to the end of diastole and beginning of ventricular systole and precedes the upstroke of carotid pulsation. Refer
to the audio example below.
The normal heart sound demonstrating S1 followed by an S2, best audible at the apex. Audio courtesy of 3M Littmann
Stethoscopes. (MP3)
M1 is best heard over the apex of the heart, and T1 is best heard over the fourth ICS at the left sternal border.
Typically, S1 is a high-pitched sound best heard with the diaphragm of the stethoscope. The intensity of S 1 depends on the
integrity and pliability of valvular cusps, the length of the PR interval (which governs the velocity of valve closure), the
strength of ventricular contraction, the presence or absence of valvular stenosis or regurgitation, the position of the valve
leaflets at end-diastole, and the amount of tissue between the heart and the stethoscope. The role of these factors is
discussed as below.[1, 4, 5]
The pliability of the valve cusps governs the ease of valvular apposition and closure. With an increased degree of
calcification and fibrosis, pliability is lost, leading to diminished valvular mobility and diminished S 1. This can happen in
advanced rheumatic mitral stenosis (MS) and postradiation MS.
S1 is influenced by ventricular contractility. Positive inotropic forces lead to a rapid rise in ventricular pressure and a loud S 1.
A sharp rise in ventricular pressure causes more rapid increase in ventricular pressure relative to atrial pressure and a faster
closure of atrioventricular (AV) valves, leading to louder S1. Similarly, negative inotropic forces lead to a diminished rate of
rise in ventricular pressure and a diminished S1.
The PR interval governs the time that atria have to empty their contents into the ventricle. With a short PR interval, the atria
have less time to empty into the ventricle, which leads to more forceful atrial contraction and maximal separation of the AV
valves, leading to louder S1 upon valvular closure. In addition, the tachycardia associated with a short PR interval leads to a
faster rise of ventricular systolic pressure relative to atrial pressure, with forceful closure of the AV valves and a loud S 1.
Similarly if the PR interval is prolonged, the atria have time to slowly empty into the ventricles, and the AV valves are less
separated by the end of atrial contraction, leading to less forceful closure of AV valves and a lower intensity S 1.
The valvular position at the end of ventricular diastole also determines the intensity of S 1. The farther apart the leaflets are at
the beginning of systole, the more rapid is their closure and the louder is S 1. Similarly, the closer the leaflets are to each
other at the beginning of the systole, the shorter the distance of travel required for valvular apposition and the softer the S 1.
The leaflets are far apart with increased transvalvular gradient (ie, MS or tricuspid stenosis [TS]), increased transvalvular
flow (ie, with left-to-right intracardiac shunts at the level of the ductus or ventricle), tachycardia, and preexcitation
syndromes.
With AV valvular regurgitation, the leaflets are not able to appose properly, leading to a muffled S 1. In acute aortic
regurgitation (AR), left ventricular (LV) end-diastolic pressure rapidly rises; thus, there is faster equilibration of ventricular
and atrial pressures, leading to early closure of mitral valve and a muffled S 1.
The S1 is muffled when there is an increased amount of tissue between the heart and the stethoscope, as occurs with
pleural effusion, pericardial effusion, emphysema, pneumothorax, and obesity. Similarly, in thin-walled individuals, the heart
is closer to the chest wall, and the sounds are better transmitted to the stethoscope, leading to a louder S 1.
Conditions associated with a loud S1 include the following:

Increased transvalvular gradient (MS, TS, atrial myxoma)

Increased force of ventricular contraction (tachycardia, hyperdynamic states [ie, anemia, fever, thyrotoxicosis,
exercise, inotropic agents])

Shortened PR interval - Tachycardia, preexcitation syndromes (ie, Wolff-Parkinson-White [WPW] syndrome)

Mitral valve prolapse (MVP), thin individuals

S1 can have a variable intensity in conditions that produce variable PR interval or variable ventricular contractility. This can
happen in Mobitz type I heart block, digitalis toxicity, atrial fibrillation, and ventricular tachycardia with AV dissociation.
Conditions associated with diminished intensity of S1 include the following:

Inappropriate apposition of the AV valves (ie, mitral regurgitation [MR], tricuspid regurgitation [TR], dilated
cardiomyopathy)
Prolonged PR interval (ie, bradycardia, heart block, digitalis toxicity)

Decreased force of ventricular contraction (ie, cardiomyopathy, myocarditis, myxedema, myocardial infarction [MI])
Increased calcification of the AV valve (ie, calcific MS, postirradiation)
Increased distance from the heart (ie, obesity, emphysema, pleural effusion, pericardial effusion)
Split S1
Normally, the mitral valve closes just prior to the tricuspid valve. Thus, M 1is audible before T1 (a difference that is often not
detectable).
Splitting of S1 is more prominent when the time difference between the closure of the mitral and the tricuspid valves is
increased. This can happen with early closure of the mitral valve or a delayed closure of the tricuspid valve relative to the
mitral valve.
Some of the conditions associated with a split S1 include the following:

Premature ventricular contractions (PVCs) of LV origin

Right bundle branch block
LV pacing
Ebstein anomaly
Atrial septal defect (ASD)
Additionally, in severe TS, the tricuspid valve closes after the mitral valve; this difference can be perceived on auscultation.
Reverse splitting of S1 occurs when M1 follows the closure of T1. This happens when the closure of mitral valve is delayed as
can happen with left bundle branch block, right ventricular (RV) pacing, severe MS, and left atrial myxoma.

2. Second Heart Sound

The second heart sound (S2) is produced by the closure of the aortic (A2) and the pulmonary valves (P2) at the end of
systole.[6] Refer to the audio example below.
The normal heart sound demonstrating S1 followed by an S2, best audible at the apex. Audio courtesy of 3M Littmann
Stethoscopes. (MP3)
A2 is best heard at the aortic area (second right intercostal space); P 2 is best heard at the pulmonary area. S2 is a highpitched sound heard best with the diaphragm of the stethoscope. The intensity depends on valvular factors, the
transvalvular gradient, mechanical factors, and size of the great vessels.
Intensity of aortic component
The intensity of A2 is increased with systemic hypertension, in coarctation of the aorta, in aortic aneurysm, in thin individuals,
and when the aorta is closer to the anterior chest wall as may occur with tetralogy of Fallot and transposition of the great
arteries (TGA).
Theintensity of A2 is decreased with decreased aortic diastolic pressure (as in AR), with improper valvular apposition (as can
occur with AR or aortic dissection), calcific immobile valves (as may occur with calcific aortic stenosis [AS]), and decreased
systemic arterial pressure.
Intensity of pulmonic component
The intensity of P2 is increased with pulmonary arterial hypertension[7]from any etiology. A loud P2 is also audible with ASD,
[8]
although the exact mechanism in this condition remains unclear.
Split S2
Normally, the aortic valve closes slightly before the pulmonary valve. This difference is more pronounced with inspiration
due to increased RV stroke volume. Refer to the audio example below.
The S2 splitting sound (MP3)

S2 splitting results from the aortic valve closing slightly before the pulmonary valve, and this is more prominent with
inspiration. The pulmonary and the aortic valves remain open briefly after the end of systole and after the LV and RV
pressures have been lowered compared to aortic pressures. This interval between the actual valve closure and pressure
crossover between ventricles and great vessels has been called the hangout time. [1] , which is inversely proportional to the
resistance to blood flow in the great vessels. The pulmonary vascular resistance is less than the systemic vascular
resistance. Thus, the hangout time is longer for the pulmonic valve than for the aortic valve. This accounts for delayed
closure of pulmonary valve relative to the aortic valve.
With inspiration, pulmonary arterial resistance further declines, leading to further delay in pulmonary valve closure and a
more pronounced split.[9]Another factor contributing to the delayed closure of pulmonary valve with inspiration is prolonged
RV emptying time due to increased stroke volume as a result of increased preload with inspiration.
Wide S2 splitting
Normally, with expiration, S2 is single, as the aortic and the pulmonary valve closures occur almost simultaneously. If, at
expiration, the two different components of S2 can still be appreciated separately, then S2 is said to be widely split.
The wide split can result from delayed closure of the pulmonary valve or early closure of the aortic valve during expiration.
Delayed closure of pulmonary valve can result from conduction or hemodynamic abnormalities. Delayed electrical activation
of the RV accounts for a delayed onset of systole, with delayed completion of RV emptying and thus delayed closure of the
pulmonary valve. This can happen with right bundle branch block, LV pacing, PVCs arising from the left ventricle, and WPW
with preexcitation of the left ventricle. Hemodynamic reasons for delayed closure of the pulmonary valve include RV outflow
obstruction (pulmonary valvular, supravalvular, or subvalvular stenosis), pulmonary hypertension, and pulmonary artery
branch stenosis.
Early closure of the aortic valve occurs with early emptying of the left ventricle, as can happen with MR or with ventricular
septal defect (VSD) with leftto-right shunting.
With widening of the S2 split, the respiratory variability is preserved (ie, with inspiration, the split becomes wider compared to
expiration).
Wide fixed splitting
The split S2 is said to be widely fixed when the respiratory variability in the relation of A2 -P2 is lost and the time interval
between A2 and P2 remains relatively constant, with P2 following A2. This occurs most commonly ASD with left-to-right
shunting but can also occur with right ventricular failure.
The exact mechanism of the fixed-split S2 in ASD is unknown, but it is postulated that the RV systolic time remains relatively
constant (ie, there is a loss of respiratory variability in RV stroke volume). In the presence of ASD with left-to-right shunt, the
RV stroke volume is composed of contributions from the superior vena cava (SVC) and the left atrium. During inspiration,
the contribution from the SVC is increased owing to increased blood flow from the body to the heart. During expiration, there
is a greater flow across the atrial shunt. Thus, the net RV stroke volume remains constant throughout the respiratory cycle.
Conditions associated with RV failure may also cause fixed splitting of S 2by compromising the ability of RV to alter its stroke
volume with respiration. This can occur with primary RV failure, pulmonary hypertension, and RV outflow tract obstruction.
Reverse splitting
When the A2 is audible after P2 during expiration, S2 is said to be paradoxically split. This can happen when the RV
contraction is completed before LV contraction. This can result from conduction or hemodynamic reasons.
Reverse splitting due to conductive disturbance occurs in conditions that cause delayed activation (and thus delayed
emptying) of the left ventricle, such as left bundle branch block, RV pacing, PVCs of RV origin, and preexcitation of the RV
in WPW syndrome.
Reverse splitting due to hemodynamic reasons may occur with delayed emptying of the LV, as can occur with LV outflow
tract obstruction caused by AS.

3. Third Heart Sound

The third heart sound (S3) is a low-pitched, early diastolic sound audible during the rapid entry of blood from the atrium to
the ventricle. When arising from the LV, it is best audible at the apex with the patient in left lateral decubitus position with
breath held at end expiration. When it is of RV origin, S 3 is best audible at the left lower sternal border or the xiphoid with the
patient in supine position. These are best heard with the bell of the stethoscope. Refer to the audio example below.
The low-pitched third heart sound as audible at the apex. Audio Courtesy of 3M Littmann Stethoscopes. (MP3)
The exact mechanism of genesis of S3 is debatable. Some of the proposed mechanisms are listed below.[10, 11, 12]
S3 occurs when rapidly rushing blood flow from the atria is suddenly decelerated by the ventricle when it reaches its elastic
limit. In a normal ventricle, this can happen with excessive volume of incoming blood, as can happen in hyperdynamic states
or volume-loaded conditions. Similarly, in a ventricle that is already stretched and overfilled owing to systolic dysfunction,
even a relatively normal (or less than normal) amount of blood entry can stretch the ventricle enough for it to reach its elastic
limit. With decreased compliance of the ventricle, as can happen with hypertrophy and diastolic dysfunction, a normal
amount of blood entry during diastole can challenge ventricular elasticity and generate the S 3.
Movement of ventricle closer to the chest wall (the so-called impact theory): When the ventricle is dilated, it moves closer
to the chest wall. This close proximity of the ventricle to the chest wall leads to a more forceful impact with entry of blood
during diastole.
S3 can be physiologically present in patients younger than 40 years. These patients often have a thin chest wall to permit
the easy transmission of S3. In the presence of heart failure, S3 is a bad prognostic sign.[13]Conditions associated with
pathological S3 include the following:

Systolic and/or diastolic ventricular dysfunction

Ischemic heart disease
Hyperkinetic states - Anemia, fever, pregnancy, thyrotoxicosis, AV fistula
MR or TR
Chronic AR with systolic dysfunction
Systemic and pulmonary hypertension
Acute aortic regurgitation
Volume overload - Renal failure
4. Fourth Heart Sound
The fourth heart sound (S4) is a late diastolic sound that corresponds to late ventricular filling through active atrial
contraction. It is a low-intensity sound heard best with the bell of the stethoscope. When of LV origin, S 4 is best heard at the
apex with the patient in the left lateral decubitus position at end expiration. When of RV origin, it is heard best at the left
lower sternal border. Maneuvers that increase the preload increase the intensity of S 4 by increasing the separation of
S4 from S1. Left-sided S4 is also augmented by increased afterload as can happen with hand grip. Refer to the audio
example below.
The low-pitched diastolic heart sound audible just before S1 in the cardiac cycle. Audio courtesy of 3M Littmann
Stethoscopes. (MP3)
The exact mechanism of S4 generation is debatable. The ventricular theory proposes that S 4 is generated by sudden
deceleration of the jet of blood as it enters a ventricle with decreased compliance. The impact theory proposes the
movement and impact of the ventricle on the chest wall as the jet of blood from atrial systole strikes the ventricle. In either
case, active atrial contraction is necessary for the generation of S 4. Thus, S4 is not audible with atrial fibrillation or flutter.
Some of the conditions associated with S4 include the following:

Ventricular hypertrophy - LV hypertrophy (systemic hypertension, hypertrophic cardiomyopathy, AS)

hypertrophy (pulmonary hypertension, pulmonary stenosis [PS])
Ischemic heart disease - Acute MI, [15] angina
Ventricular aneurysm
Hyperkinetic states that cause forceful atrial contraction

[14]

; RV

Both S3 and S4 need to be differentiated from splitting of the normal heart sounds. With splitting, the heart sounds are high
pitched and best audible with the diaphragm, whereas the S 3 or S4 are low-pitched sounds best audible with the bell of the
stethoscope.

5. Opening Snap
The opening snap (OS) is a high-pitched diastolic sound produced by rapid opening of the mitral valve in MS or tricuspid
valve in TS.[16] When mitral in origin, it is best heard at the apex following the aortic sound A2, with the patient in left lateral
decubitus position.
The time difference between the A2 and OS has a diagnostic implication. The closer the OS is to A2, the more severe the
stenosis. The OS signifies the time moment when the left atrial pressure exceeds the LV diastolic pressure and marks the
beginning of blood entry into the LV from the LA. The more severe the stenosis, the greater the LA pressure and the lesser
the LA-LV early diastolic pressure gradient, leading to an early opening of the respective valve. In general, the relation
between A2 and the OS depends on LV pressure at A2 closure, LA pressure at A2 closure, and the rate of LV pressure
decline.[17]
The A2 -OS interval can be increased despite severe MS in patients who have systemic hypertension with an early closure
of AV.
TS usually occurs in association with MS, and, as such, the findings are generally obscured by the findings of MS.

6. Ejection Systolic Sounds

The ejection systolic sounds are heard during the early part of ventricular systole. These sounds are generally high pitched
and best audible with the diaphragm of the stethoscope. They can be valvular or vascular in origin.
Valvular ejection sounds
These are the systolic sounds that are audible in patients with defects in aortic or pulmonary valves. They are present in
early systole after the S1. The aortic ejection sound is best audible at the apex or the aortic area. The pulmonary valve
ejection sound is best audible at the pulmonary area.
The aortic valvular ejection sound is associated with bicuspid aortic valves and aortic regurgitation. Pliable valves generate
a higher-intensity ejection click. The intensity of the ejection click decreases with increased valvular calcification. Thus, the
aortic ejection click may be absent in severe calcific AS.[18] The ejection click is also absent in supravalvular or subvalvular
AS. The presence of an aortic ejection sound, in the absence of other signs of AS, strongly suggests the presence of a
bicuspid aortic valve.[19]
The pulmonary valvular ejection sound is predominantly associated with pulmonary valvular stenosis. [20] Unlike most rightsided sounds, the ejection click of PS is decreased in intensity with inspiration. One of the proposed mechanisms is a rapid
opening of the valve from the closed position with expiration, giving rise to the high-intensity sound. With inspiration, the
rapid jet from the right atrium can partially open the pulmonary valve during diastole; thus, the opening of pulmonary valve
with the onset of RV systole is more gradual, leading to decreased intensity of the sound.
Vascular ejection sounds
These sounds are produced at the aorta or pulmonary artery.
The aortic vascular ejection sounds are associated with aortic sclerosis with tortuous aortic root, systemic hypertension,
ascending aortic aneurysm, and aortic root dilatation. This sound is usually audible at the aortic area and is not well
transmitted to the apex.

The pulmonary vascular ejection sound is associated with pulmonary hypertension and pulmonary arterial dilatation. It is
best audible at the left second and third intercostal area.
Nonejection systolic click
This is associated with mitral or tricuspid valve prolapse. Of the two entities, MVP is more common. Refer to the audio
example below.
The mid-systolic click from mitral valve prolapse. Audio courtesy of 3M Littmann Stethoscopes. (MP3)
The nonejection systolic click is a high-pitched systolic sound that follows S 1 and is heard best at the apex (MVP) or the
tricuspid area (tricuspid valve prolapse) with the diaphragm of the stethoscope. The interval between S 1 and the prolapse
click may vary depending on the volume status of the respective ventricles, as the prolapse occurs at a specific ventricular
volume.[21] . Thus, if the end-diastolic volume of the ventricle is increased, as can happen with bradycardia, in the supine
position, or during hand grip or squatting, the S1 -prolapse interval is increased.
Similarly, if the end-diastolic volume is decreased, as can occur in tachycardia, upon standing up, and during the Valsalva
maneuver, the S1 -click interval decreases. This time-based variation can help identify the click of mitral or tricuspid prolapse
from other heart sounds.

7. Murmurs
The production of murmurs results from turbulent flow across valves. Three main factors have been attributed to cause a
murmur: (1) high flow rate through normal or abnormal orifices, (2) forward flow through a constricted or irregular orifice or
into a dilated vessel or chamber, and (3) backward or regurgitant flow through an incompetent valve. [22, 1, 23]
When evaluating a heart murmur, it is important to know the timing of the murmur in the cardiac cycle, the location, the
duration, character, configuration, radiation, aggravating maneuvers, and diminishing maneuvers.
Recognizing the periodicity of murmur helps to narrow the differential diagnoses and often guides further diagnostic
evaluation. For example, all diastolic murmurs and any systolic murmur above grade 2 in severity requires further evaluation
with echocardiography.[22] The timing of the murmur is determined by palpating the carotid pulse while listening to the
murmur. The carotid upstroke corresponds to the onset of systole.
The factors to focus on while evaluating a murmur are discussed briefly below.
Intensity: The intensity of the murmur depends on the volume of blood flow across the valve and the pressure gradient
across which the blood flow occurs. The intensity is graded into 6 different grades, as follows:

Grade I - Heard in a quiet room by an expert examiner

Grade II - Heard by most examiners
Grade III - Loud murmur without thrill
Grade IV - Loud murmur with a thrill
Grade V - Thrill with a very loud murmur audible with stethoscope placed lightly over the chest
Grade VI - Thrill with a very loud murmur audible even with the stethoscope slightly away from the chest
The grade of the murmur is important, as any diastolic murmur and a systolic murmur above grade II/VI in severity warrants
echocardiographic evaluation as per ACC/AHA guidelines.
Timing: Depending on when they are best heard in the cardiac cycle, the murmurs can be systolic (holosystolic,
early/middle/late systolic), diastolic (early/middle/late) or continuous (ie, present in both systole and diastole).
Location: This is the area of the heart where the murmur is heard the loudest. While auscultating, one should concentrate
on the apex, pulmonary area, tricuspid, and aortic areas, in addition to the axilla, base of the heart, and left fourth ICS for
evidence of radiation of murmur.
As shown in Table 3, the location and timing help in determining whether the murmur is arising from the right or the left side
of the heart. In addition, the position can help in locating the involved valves.
Quality/character: Different murmurs have different qualities, such as harsh, blowing, rumbling, musical, or cooing. See
Table 3.

Pitch: This can be high or low pitched depending on the frequency of the murmur. The high-pitched sounds are best audible
with a diaphragm and the low-pitched sounds with the bell.
Radiation: Murmurs tend to radiate to certain specific areas that are often characteristic of a particular murmur. The murmur
of MR radiates to the axilla or base of the heart, depending on which leaflet is involved. In the case of AS, the murmur
radiates in the direction of the jet of turbulent blood (ie, radiates to the carotids). Similarly, the aortic regurgitant murmur
tends to radiate along the left sternal border.
Configuration: This corresponds to the shape of murmur intensity over time. It can be a plateau, decrescendo, crescendodecrescendo, or crescendo murmur.
Dynamic auscultation
Dynamic auscultation involves certain specific maneuvers that affect the blood flow through the valves and can aid in
recognition and differentiation of heart murmurs.
Inspiration: Inspiration leads to a decrease in the intrathoracic pressure with an increase in venous return to the right side
of the heart. The murmurs generated from the right side of the heart increase in intensity with inspiration.
Expiration: Expiration has the opposite effect as inspiration. There is an increase in the intrathoracic pressure and a
decrease in venous return to the right side of the heart. Blood in the lung is forced into the left heart. Hence, murmurs
arising from the left side of the heart become more prominent with expiration.
Standing up: This causes a peripheral pooling of blood and a net decrease in venous return. Most murmurs are thus
decreased in intensity upon standing, except that of hypertrophic obstructive cardiomyopathy (HOCM) and MVP, which
become more prominent.
Squatting: Squatting causes an increase in the afterload and venous return (ie, preload). The net effect is an increase in
intensity of all the murmurs, except those associated with MVP and HOCM, which become less prominent with squatting.
Straight leg raising: Passive straight leg raising increases venous return (ie, preload) and has an effect similar to brisk
squatting. All murmurs increase in intensity except those of HOCM and MVP, which decrease in intensity with this
maneuver.
Hand grip: Hand grip is a form of isometric exercise and increases the afterload, arterial pressure, LV volume, and LV
pressure. The net effect of these changes is complex and variable. Murmurs of MR, AR, and VSD worsen with hand grip,
while those of HOCM and MVP become less prominent.
Valsalva maneuver: Valsalva maneuver involves asking the patient to strain, which increases the intrathoracic pressure,
thus causing a net decrease in preload. Most heart murmurs decrease in intensity with Valsalva, except those of HOCM and
MVP, which become more prominent.
Amyl nitrate inhalation: Amyl nitrate is an arteriolar vasodilator and initially causes decreased afterload followed by reflex
tachycardia. During the initial phase, because of reduced afterload, the murmurs of AR, MR, and VSD diminish, while those
of AS are accentuated. Later on, during the tachycardic phase, the murmur of MS is accentuated.

Table 1. Effect of Different Maneuvers on Some Common Murmurs

Murmur
Type

Inspiration

Expiration

Passive Leg
Raising

Squatting

Standing

Hand
Grip

Valsalva

Amyl Nitrate
Inhalation

TS

MS

MR

MVP

AS

AR

HOCM

VSD

--

With squatting, there is an increase in afterload and preload. Initially, the MVP click is delayed and murmur shortened,
but, as the regurgitation worsens, the murmur may increase in intensity.

The murmur and the click of MVP occurs earlier with amyl nitrate inhalation.

TS: tricuspid stenosis; MS: mitral stenosis; MR: mitral regurgitation; MVP: mitral valve prolapse; AS: aortic stenosis; AR:
aortic regurgitation; HOCM: hypertrophic obstructive cardiomyopathy; VSD: ventricular septal defect

Table 2. Differential Diagnoses of Cardiac Murmur [29]

Systolic Murmurs
Early systolic murmur

Mitral - Acute MR

Tricuspid - TR

VSD Muscular or non-restrictive with pulmonary hypertension

Mid-systolic/mid-to-late systolic murmurs

Aortic

Obstructive

Supravalvular - Supravalvular AS, aortic coarctation

Valvular - AS, aortic sclerosis

Subvalvular - HOCM

Increased flow, hyperkinetic states, aortic regurgitation, complete heart block

Dilatation of the ascending aorta, aortitis, atheroma

Pulmonary

Obstructive

Supravalvular - Pulmonary artery stenosis

Valvular - Pulmonary valve stenosis

Subvalvular - Infundibular stenosis

Increased flow, hyperkinetic states, left-to-right shunt

Dilation of the pulmonary artery

Late systolic murmurs

Mitral - MVP

Tricuspid - Tricuspid valve prolapse

Holosystolic murmurs

AV valve regurgitation - MR, TR

VSD with left-to-right shunt

Diastolic Murmurs
Early diastolic murmur

Aortic regurgitation

Valvular - Congenital (bicuspid valve), rheumatic, endocarditis, prolapse, trauma, postvalvulotomy

Dilatation of the valve annulus - Aortic dissection, annuloaortic ectasia, cystic medial degeneration,
hypertension, ankylosing spondylitis, syphilis, Takayasu

Pulmonary regurgitation

Valvular - Postvalvulotomy, endocarditis, rheumatic fever, carcinoid

Dilatation of the valve annulus - Pulmonary hypertension, Marfan syndrome, Takayasu

Congenital - Isolated or associated with tetralogy of Fallot, VSD, pulmonic stenosis

Mid-diastolic murmur

Mitral

Mitral stenosis

Carey Coombs murmur (mid-diastolic apical murmur in acute rheumatic fever due to mitral valvulitis)

Increased flow across nonstenotic mitral valve (eg, MR, VSD, PDA, high-output state, complete heart
block)

Tricuspid

TS

Increased flow across nonstenotic tricuspid valve (eg, TR, ASD, anomalous pulmonary venous return)

Left and right atrial tumors - Myxoma

Severe or eccentric AR (Austin Flint murmur)

Late diastolic murmur

Presystolic accentuation of MS murmur

Austin Flint murmur of severe or eccentric AR

Continuous Murmurs

PDA
Coronary arteriovenous fistula
Ruptured sinus of Valsalva aneurysm
Aortopulmonary window
Cervical venous hum
Anomalous left coronary artery from the pulmonary artery
Mammary souffle of pregnancy
Bronchial collateral circulation
Intercostal or pulmonary arteriovenous fistula

Systolic Murmurs

Systolic murmurs occur during the ventricular contraction. They can result from (1) leakage across the abnormal
atrioventricular valves (tricuspid or mitral) or interventricular septal defects or (2) ventricular outflow tract obstruction, which
can be valvular, supravalvular, or subvalvular. In some cases, the systolic murmurs can be audible owing to an abnormal
amount of blood flow across normal valves, as can occur in hyperdynamic states.
Systolic murmurs can be holosystolic, early systolic, late systolic, or mid-systolic in their timing. As per the ACC/AHA
guidelines, any patient with a holosystolic, early systolic, late systolic, or a mid-systolic murmur greater than II/VI in severity
or with evidence of cardiac compromise due to valvular disease should be further evaluated with echocardiography.[22]
Early systolic murmurs
Early systolic murmurs are produced by acute MR or TR or in VSD with pulmonary hypertension. They are blowing in nature
and decrescendo in character. Blood flows rapidly from the ventricle into an unprepared atrium, leading to rapid equalization
of the pressures and early systolic murmur.
Acute MR can occur in the setting of an acute MI, infective endocarditis, chordal rupture in patients with MVP, or blunt chest
wall trauma. In the acute setting, the LA does not have sufficient time to dilate in response to the high-volume regurgitant jet.
Thus, the LA and LV pressures equalize in the early part of systole, confining the murmur to early systole. When acute, the
murmur of MR is accompanied by an S4. MI can damage the papillary muscles, resulting in acute MR. This usually occurs
on day 2-7 postacute MI, and the posteromedial muscle is involved more often than the anterolateral muscle.
The murmur of acute MR must be differentiated from a murmur of ventricular septal rupture, which is usually holosystolic
and associated with a palpable systolic thrill. Nevertheless, any newly onset systolic murmur following MI should be
evaluated with echocardiography.
Infective endocarditis can directly damage the valve leaflets, the chordae, or both, producing MR. Blunt chest wall trauma
can damage the papillary muscle and/or cause chordal rupture or valvular leaflet avulsion, leading to acute MR. Chordal
rupture due to myxomatous degeneration caused by MVP or other associated connective tissue disease worsens the
severity of a pre-existing murmur.
A small muscular VSD alone and a large VSD with pulmonary hypertension can also produce an early systolic murmur.
These murmurs are soft and blowing and audible at the left lower sternal border. In case of a muscular VSD, the septal
defect closes during septal contraction in systole, thus limiting the murmur to the early part of systole. In the presence of
pulmonary hypertension with VSD, the pressure gradient is maintained between the left and the right ventricle only in the
early part of systole. This confines the murmur to early systole.

Acute TR can occur in the setting of infective endocarditis. The murmur is usually soft, blowing, and decrescendo and is not
associated with signs of right heart failure. It is often accompanied by a right-sided S 4 and a diastolic flow rumble.
Mid to late systolic murmurs
These murmurs are usually associated with ventricular outflow tract obstruction (which can be valvular, supravalvular, or
subvalvular) or an abnormal amount of blood flow across normal valves as can happen in hyperdynamic states
(hyperthyroidism, fever, pregnancy, anemia, renal failure).
The murmur associated with valvular stenosis (AS or PS) is usually a harsh murmur which is crescendo- decrescendo in
configuration and high pitched.
AS-associated murmurs are most audible at the right upper sternal border/right third ICS with the patient in the upright
position and breath held at end expiration. In some cases, it is audible at the apex, in which case it can be confused with the
murmur of MR. Some of the findings that help delineate the murmur of MR from that of AS include an audible S 1, forceful
apex, radiation to carotids, changes with atrial fibrillation, and post-PVC accentuation. The AS murmur usually radiates to
the carotid arteries.
An S4 is audible with severe AS. The time to peak of murmur often depends on the severity of valvular obstruction. The later
the murmur peak, the more severe the obstruction. The exact location of the murmur varies depending on whether the
murmur is valvular, subvalvular, or supravalvular. A valvular murmur is most prominent at the right second ICS, while a
supravalvular stenosis produces a murmur that is located slightly higher than the valvular murmur. Refer to the audio
example below.
The mid-systolic harsh crescendo-decrescendo murmur of aortic stenosis best audible at the right upper sternal border.
Audio courtesy of 3M Littmann Stethoscopes. (MP3)
The murmur of PS is best audible at the left second ICS just to the left of sternum. It is late peaking, is crescendodecrescendo in configuration, and may be associated with a systolic click that becomes softer with inspiration. The P 2 is
usually soft and S2 usually split, with the split directly proportional to the degree of stenosis. The split depends on the
severity of the murmur. As the severity increases, the P2 component of the S2 is delayed to the extent that a severe stenotic
murmur can overshadow the sound generated by aortic valve closure. In severe PS, a right-sided S 4 is often audible.
The murmur of HOCM is most audible at the left lower sternal border, left fourth ICS. It is harsh and crescendo-decrescendo
in character. The murmur of HOCM is dynamic, and its intensity varies with the changes in left ventricular outflow tract
(LVOT). An increase in LV volume leads to a decrease in the severity of outflow tract obstruction, thus leading to a decrease
in the intensity of HOCM murmur. This can happen during leg raising, during squatting, or with handgrip. Similarly, any
decrease in the LV volume leads to an increase in outflow tract obstruction, increasing the intensity of HOCM murmur. This
can be seen with Valsalva maneuver and sudden standing.
MVP produces a mid- to late systolic murmur that is preceded by a nonejection click. [24] The murmur is blowing and high
pitched in nature. The murmur is increased in intensity upon sudden standing and Valsalva. Squatting, hand grip, and
bradycardia decrease the intensity of MVP murmur.
Holosystolic murmurs
These murmurs last throughout ventricular systole. They usually start at S 1and proceed through S2; the intensity of the
murmur may overshadow both valve closure sounds.
These murmurs are typically produced by emptying of the high-pressure ventricle during systole into chambers that have
lower pressure at that time (the atria with MR or TR or the right ventricle in the case of VSD).
At the start of isovolumetric ventricular contraction, the ventricular pressure rapidly exceeds the atrial pressure. The
abnormal AV valves cannot prevent the regurgitation of blood from ventricle to atrium. As a result, the high-pressure
ventricle empties into the low pressure atria. This marks the beginning of the holosystolic murmur, in which the sound of
murmur onset often muffles S1. The regurgitant murmur can also muffle S2, as the ventricular pressure continues to exceed
atrial pressure for a short period after closure of the aortic/pulmonary valve.

The murmur of MR is blowing and high pitched and is best heard at the apex with radiation to the axilla or the base of the
heart. It is usually plateau in configuration. The MR murmur is increased during expiration, passive leg raising, squatting,
and handgrip and decreased in intensity with inspiration, Valsalva, and standing. The radiation of the murmur depends on
which leaflet is involved. A murmur generated by the deformity of anterior leaflet radiates more toward the axilla, thoracic
spine, and scapula, while a murmur arising from posterior leaflet involvement radiates to the base of the heart. [25]
The presence of S3 with valvular MR indicates a more severe and hemodynamically significant lesion. The association of
signs of pulmonary hypertension and right heart failure also indicate hemodynamically significant MR. Refer to the audio
example below.
The holosystolic, blowing murmur from mitral regurgitation audible best at the apex. Audio courtesy of 3M Littmann
Stethoscopes. (MP3)
The murmur of TR is best heard at the left lower sternal border. It is a blowing high-pitched murmur heard that increases in
intensity with inspiration (Carvallo sign). It can result primarily from involvement of the tricuspid valve or secondarily from
pulmonary hypertension. When due to pulmonary hypertension, it is associated with a loud P 2.
In VSD with normal pulmonary arterial pressures, a holosystolic murmur can be heard over the left lower sternal border at
the level of the third and fourth ICSs. This murmur depends on the orifice size of the septal defect. The smaller the defect,
the greater the intensity of the murmur.
With a larger orifice size, RV and pulmonary pressure increase, confining the murmur to early systole. Subsequently, once
pressure equalization occurs, blood flow is absent. This is associated with pulmonary hypertension and is a bad prognostic
sign, as it indicates progression of disease. Thus, the presence of holosystolic murmur in VSD indicates early disease and,
depending on clinical setting, carries a better prognosis than the absence of a murmur in the presence of VSD. Refer to the
audio example below.
The murmur from ventricular septal defect, best audible at the left lower sternal border. Audio courtesy of 3M Littmann
Stethoscopes. (MP3)
Innocent murmurs and functional systolic ejection murmurs
Innocent murmurs are mid- to late-systolic, medium- to high-pitched ejection murmurs audible at the left lower sternal border
or the left second ICS, depending on origin from the LV or RV outflow tract. These murmurs are usually blowing in character
and grade I or II/VI in intensity. They can vary in intensity with the bodys positioning and always end before the closure of
the semilunar valves. Murmurs are categorized as innocent only if examination of the cardiovascular system reveals normal
findings.
Functional systolic ejection murmurs are associated with increased blood flow across the semilunar valves
(aortic/pulmonary). Some of the conditions associated with functional murmurs include anemia, thyrotoxicosis, pregnancy,
fever, exercise, arteriovenous fistula, and complete heart block. With complete heart block, there is beat-to-beat variation in
the murmur intensity.

Diastolic Murmurs

Diastolic murmurs are audible during ventricular diastole and caused by either (1) regurgitation across the aortic or
pulmonary valve or (2) stenotic AV valves.
Early diastolic murmurs
Early diastolic murmurs are produced by either AR or pulmonary regurgitation.
The AR murmur is a soft high-pitched sound, is decrescendo in configuration, and is most audible at the left sternal border
or the right second ICS just to the right of sternum, with the patient leaning forward at end expiration. The murmur radiates
to the left lower sternal border if it is due to primary valve disease. In patients with aortic root disease, the murmur may
radiate to the right sternal border. The murmur increases in intensity during expiration and decreases in intensity with hand
grip, squatting, Valsalva, and amyl nitrate inhalation. The S 2 is usually muffled with AR, and there is an audible wide
physiologic split. Refer to the audio example below.

The early diastolic decrescendo murmur from aortic regurgitation. Audio courtesy of 3M Littmann Stethoscopes. (MP3)
The murmur of pulmonary regurgitation is best audible at the pulmonary area. The character, quality, and pitch of the
murmur vary depending on the presence or absence of pulmonary hypertension. In the presence of pulmonary
hypertension, it is a high-pitched, decrescendo murmur also known as a Graham Steell murmur. S 2 is usually loud in
association with pulmonary regurgitation. In the absence of pulmonary hypertension, it is a low-pitched crescendodecrescendo murmur.
Mid- to late diastolic murmurs
These murmurs are produced by the blood flow across stenotic AV valves.
MS produces a low-pitched, mid-diastolic, rumbling murmur with presystolic accentuation, best heard with the bell of the
stethoscope placed over the cardiac apex with the patient in the left lateral position. S 1is loud. The murmur usually follows
an OS, and the interval between the A2 and OS is inversely proportional to the severity of obstruction.
The murmur of MS is increased in intensity with expiration and maneuvers that increase cardiac output, such as exercise.
The presystolic accentuation results from atrial contraction in late diastole and is absent in patients with atrial fibrillation. The
duration of murmur corresponds to the period in which the LA-LV diastolic pressure gradient is maintained. This duration
correlates with the severity of obstruction; the longer the murmur duration, the more severe the MS (provided the diastolic
filling time is not shortened, as may happen in tachycardia).
The duration of murmur does not correlate to the severity of MS in high-output states, such as pregnancy, as the murmur is
long-lasting owing to increased blood flow. Similarly, in the presence of pulmonary hypertension or right heart failure, the
flow across the mitral valve is decreased, and, even in severe MS, the duration of murmur may be shortened. Refer to the
audio example below.
The mid to late diastolic, low-pitched, rumbling murmur from mitral stenosis. Murmur is best audible at the apex with the bell
of the stethoscope. Audio courtesy of 3M Littmann Stethoscopes. (MP3)
TS produces a low-pitched, mid-systolic rumbling murmur best audible at the left third ICS/left sternal border and xiphoid
process. The murmur increases in intensity with inspiration (Carvallo sign) and decreases in intensity during expiration and
with Valsalva maneuver.
Atrial myxoma can produce a diastolic murmur that is very similar to that associated with MS or TS. This murmur is also low
pitched, mid-diastolic, and rumbling with presystolic accentuation. An OS is absent and is replaced by a tumor plop. It is
difficult to clinically differentiate the murmur of atrial myxoma from that of MS, but the murmur of atrial tumors changes in
intensity as the patient changes positions.
Austin Flint murmur: This is an early diastolic rumbling murmur associated with valvular AR. This murmur arises from aortic
regurgitant jets abutting the LV free wall and causing premature closure of the MV.[26] The Austin Flint murmur decreases in
intensity with maneuvers that would decrease the intensity of AR, such as afterload reduction with amyl nitrate. On the other
hand, amyl nitrate inhalation would increase the intensity of MS. This can potentially differentiate Austin Flint murmur from
MS murmur.
Carey Coombs murmur: This is a mid-diastolic murmur audible during acute rheumatic fever over the apical impulse. It is
attributed to acute mitral valvulitis due to rheumatic fever.
States of increased flow across AV valves can also produce diastolic rumbling murmurs. Patients with MR have an
increased amount of diastolic blood flow across the mitral valve. There is a partial closure of the mitral valve in mid diastole
after wide opening of the valve leaflets during early diastole. This, combined with increased blood flow, causes a functional
MS murmur.[27] Similarly, ASD with left-to-right shunt can produce a mid-diastolic rumbling murmur over the tricuspid area.

Continuous murmurs

These murmurs are audible in systole and diastole, although their intensity usually varies during systole and diastole. They
result from a communication between a high-pressure arterial and low-pressure venous chamber or vessel. Some of the
causes of continuous murmurs are listed in Table 2.

The continuous murmurs produced by patent ductus arteriosus (PDA) result from an abnormal communication between the
aorta and the pulmonary artery. The aortic pressure is always higher than that of the pulmonary artery and results in a
continuous murmur, with peak flow occurring during the end of systole (ie, at S 2). The murmur is blowing, high pitched, and
best audible at the left upper sternal border near the left second ICS.
If the communication is large, pulmonary arterial pressure eventually rises, leading to pulmonary hypertension. This may
cause the diastolic component of the murmur to become muffled; in severe pulmonary hypertension, it may lead to reversal
of flow during diastole and differential cyanosis. The continuous murmur of PDA may be confused with the murmur
associated with AS with coexisting AR. In the case of AS with AR, the murmur is least intense around S 2, while, in PDA, the
murmur is most pronounced at S2.
The continuous murmur from anomalous origin of left coronary artery from the pulmonary artery (so called Bland-GarlandWhite syndrome) can produce a continuous murmur best audible around the left sternal border. In this case, the collateral
vessels from the right coronary artery to the left coronary artery give rise to the continuous murmur. Rupture of a sinus of
Valsalva into the RA or RV can produce a continuous murmur best audible over the lower left sternal border and the xiphoid.
These murmurs are more pronounced during diastole, a fact that differentiates them from the murmur of PDA.
Coronary artery fistulas emptying in the RA can produce a continuous murmur audible at the right or left sternal area. These
murmurs are more prominent in diastole, as the flow in the coronary arteries occurs during diastole.
A continuous murmur due to coarctation of aorta is best audible at the level of coarctation, usually between the shoulder
blades.

Table 3. Summary of Characteristics of Some Common Murmurs

Murmu
r Type

Location

Quality

Periodicity Configuration

Radiation

S1

S2

Pitch

Loud

Initially normal;
later, loud
P2with
pulmonary
hypertension,
ultimately
single S2

Low

Muffled

Widely split

High

MS

Apex

Rumblin
g

Diastolic

Mid to late diastolic with

-presystolic accentuation

MR

Apex

Blowing

Systolic

Plateau

AS

Apex/right
upper
sternal
border

Systolic

Crescendodecrescendo

Carotids

Normal

Delayed aortic
valve closure
High
causing narrow
split or single S2

AR

Right
upper
sternal
Blowing
border/left
third/fourth
ICS

Diastolic

Decrescendo

Apex

Normal/sof
t

Soft A2, P2 may

be obscured by
murmur

TR

PS

Left fourth
ICS

Left
second
ICS

Harsh

Blowing

Diastolic

Plateau

Blowing

Systolic

Crescendo/decrescend
o

Axilla/base
of heart

Left sternal
border/over Muffled
xiphoid

--

Normal

When TR is
due to
pulmonary
hypertension,
P2 is
accentuated
with delayed
split

High

Loud P2 with
High
prominent split,
which becomes
fixed with
increasing

severity
VSD

Left lower
sternal
border

Harsh

Systolic

PDA

Left upper
sternal
border

Harsh

CrescendoContinuous decrescendo with peak

around S2

Plateau

None

--

Split

High

None

Normal

Widely split
S2 due to
delayed P2

High

--

High

Diastolic
click
MVP

Apex

Blowing

Mid-late
systolic

Plateau

Axilla/base
After S1

HOCM

Left lower
sternal
border

Harsh

Mid-late
systolic

Similar to valvular AS
murmur

None

Normal

Normal initially,
with increased
severity;
High
S2 paradoxically
split

Erbs point pada sela

iga III

pada sela iga V

pada sela iga IV dan V

Surface anatomy
The aortic area, pulmonic area, tricuspid area and mitral area are areas on the surface of the chest
where the heart is auscultated. Heart sounds result from reverberation within the blood associated with
the sudden block of flow reversal by the valves closing. Because of this, auscultation to determine
function of a valve is usually not performed at the position of the valve, but at the position to where the
sound waves reverberate.

Aortic valve (to aorta)

right second intercostal space

upper right sternal border

Pulmonary valve (to pulmonary trunk)

left second intercostal space

upper left sternal border

Erb's point

Left third intercostal space

left sternal border

Tricuspid valve (to right ventricle)

left fourth, fifth intercostal spaces

lower left sternal border

Mitral valve (to left ventricle)

left fifth intercostal space

left midclavicular line

Murmurs
Heart murmurs are produced as a result of turbulent flow of blood strong enough to produce audible noise. They are usually
heard as a whooshing sound. The term murmur only refers to a sound believed to originate within blood flow through or near
the heart; rapid blood velocity is necessary to produce a murmur. It should be noted that most heart problems do not
produce any murmur and most valve problems also do not produce an audible murmur.
Murmurs can be heard in many situations in adults without major congenital heart abnormalities:

Regurgitation through the mitral valve is by far the most commonly heard murmur, producing a
pansystolic/holosystolic murmur which is sometimes fairly loud to a practiced ear, even though the volume of regurgitant
blood flow may be quite small. Yet, though obvious using echocardiography visualization, probably about 20% of cases
of mitral regurgitation do not produce an audible murmur.

Stenosis of the aortic valve is typically the next most common heart murmur, a systolic ejection murmur. This is
more common in older adults or in those individuals having a two, not a three leaflet aortic valve.

Regurgitation through the aortic valve, if marked, is sometimes audible to a practiced ear with a high quality,
especially electronically amplified, stethoscope. Generally, this is a very rarely heard murmur, even though aortic valve
regurgitation is not so rare. Aortic regurgitation, though obvious using echocardiography visualization, usually does not
produce an audible murmur.

Stenosis of the mitral valve, if severe, also rarely produces an audible, low frequency soft rumbling murmur, best
recognized by a practiced ear using a high quality, especially electronically amplified, stethoscope.

Other audible murmurs are associated with abnormal openings between the left ventricle and right heart or from the
aortic or pulmonary arteries back into a lower pressure heart chamber.
Gradations of

(Defined based on use of an acoustic, not a high-fidelity amplified electronic stethoscope)

Murmurs[1]
Grade

Description

Grade 1

Very faint, heard only after listener has "tuned in"; may not be heard in all positions. Only heard if
the patient "bears down" or performs the Valsalva maneuver.

Grade 2

Quiet, but heard immediately after placing the stethoscope on the chest.

Grade 3

Moderately loud.

Grade 4

Loud, with palpable thrill (a tremor or vibration felt on palpation) [1]

Grade 5

Very loud, with thrill. May be heard when stethoscope is partly off the chest.

Grade 6

Very loud, with thrill. May be heard with stethoscope entirely off the chest.

Though several different cardiac conditions can cause heart murmurs, the murmurs can change markedly with the severity
of the cardiac disease. An astute physician can sometimes diagnose cardiac conditions with some accuracy based largely
on the murmur, related physical examination, and experience with the relative frequency of different heart conditions.
However, with the advent of better quality and wider availability of echocardiography and other techniques, heart status can
be recognized and quantified much more accurately than formerly possible with only a stethoscope, examination, and
experience.

Effects of inhalation/expiration[edit]

Inhalation pressure causes an increase in the venous blood

return to the right side of the heart by decreasing intrathoracic
negative pressure making it more negative (pulling blood into
the right side of the heart via a vacuum-like effect). Therefore,
right-sided murmurs generally increase in intensity with
inspiration. The increased (more negative) intrathoracic
pressure has an opposite effect on the left side of the heart,
making it harder for the blood to exit into circulation.
Therefore, left-sided murmurs generally decrease in intensity
during inspiration.
With expiration, the opposite haemodynamic changes occur:
left-sided murmurs generally increase in intensity with
expiration. If a patient lies supine with his legs up at a 45degree angle, venous return to the right side of the heart
produces effects similar to inhalation-increased blood flow.

Interventions that change murmurs[edit]

Main article: Heart murmur
There are a number of interventions that can be performed that alter the intensity and characteristics of abnormal heart
sounds. These interventions can differentiate the different heart sounds to more effectively obtain a diagnosis of the cardiac
anomaly that causes the heart sound.

Other abnormal sounds

Clicks Heart clicks are short, high-pitched sounds that can be appreciated with modern non-invasive imaging techniques.
Rubs The pericardial friction rub can be heard in pericarditis, an inflammation of the pericardium, the sac surrounding the
heart. This is a characteristic scratching, creaking, high-pitched sound emanating from the rubbing of both layers of inflamed
pericardium. It is the loudest in systole, but can often be heard at the beginning and at the end of diastole. It is very
dependent on body position and breathing, and changes from hour to hour.