Auscultation of cardiac murmurs

Kanu Chatterjee, MB, FRCP, FCCP, FACC, MACP

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INTRODUCTION Cardiac auscultation is one of the most useful investigative tools that the physician can use at the
bedside to detect alterations in cardiovascular anatomy and physiology. Further evaluation of the patient is based upon the
characteristics of the murmur as well as the presence of symptoms (show figure 1). This topic will review the auscultation
of cardiac murmurs. The auscultation of other heart sounds is discussed separately. (See "Auscultation of heart sounds").
MURMUR DESCRIPTION The character of a murmur may be described by a number of features.
Intensity/pitch The intensity of a murmur is primarily determined by the quantity and velocity of blood flow at the site
of its origin, the transmission characteristic of the tissues between the site of origin, the site of auscultation or recording, and
the distance of transmission. In general, the intensity declines in the presence of obesity, emphysema, and pericardial
effusion. Murmurs are usually louder in children and in thin individuals.
Six grades are used to classify the intensity of a murmur:
Grade I is the faintest murmur that can be heard (with difficulty)
Grade II murmur is also a faint murmur but can be identified immediately
Grade III murmur is moderately loud
Grade IV murmur is loud
Grade V murmur is very loud but cannot be heard without the stethoscope.
Grade VI murmur is the loudest and can be heard without a stethoscope
The gradation of intensity is purely subjective. However, it allows recognition of changes in the intensity of the murmur,
which has diagnostic relevance.
The frequency determines the pitch, which may be high or low.
Configuration A number of configurations or shapes of murmurs are recognized:
Crescendo (increasing)
Decrescendo (diminishing)
Crescendo-decrescendo (increasing-decreasing or diamond shaped)
Plateau (unchanged in intensity)
Quality The quality of a murmur can be described as harsh, rumbling, scratchy, grunting, blowing, squeaky, and musical.
The quality of a murmur may also change and, if recognized, can be helpful in the diagnosis of an anomaly.
Duration The duration of a murmur is assessed by determining the length of systole or diastole that the murmur
occupies. The murmur can be long (eg, it occupies most of systole or diastole), or it can be brief.
Radiation The direction of radiation of a murmur follows the direction of blood flow. It can provide information
regarding the origin of the murmur.
Timing The timing of the murmur in relation to the cardiac cycle is the initial step in identifying the cause and
significance of the murmur (show table 1).
Systolic murmurs A systolic murmur starts with or after S1 and terminates before or at S2 (show figure 2). Systolic
murmurs are recognized by identifying S1 and S2 and timing them with the carotid pulse. In patients with marked

tachycardia, a long diastolic murmur can be occasionally confused with a systolic murmur; timing with the carotid pulse
upstroke avoids an incorrect diagnosis.
Systolic murmurs are further classified according to the time of onset and termination in systole:
An ejection systolic murmur (midsystolic) begins after the S1 and ends before A2 (left sided) or P2 (right sided) (show
table 2)
A holosystolic murmur starts with S1 and extends up to A2 (left sided) or P2 (right sided)
An early systolic murmur starts with S1 and extends for a variable length in systole but does not xtend up to S2
A late systolic murmur starts after S1 and extends to A2 (left sided) or P2 (right sided)
Diastolic murmurs A diastolic murmur starts with or after S2 and ends at or before S1. Diastolic murmurs are also
classified according to the time of onset and termination of the murmur in diastole:
An early diastolic murmur starts with A2 (left sided) or P2 (right sided) and extends into diastole for a variable duration
A mid-diastolic murmur starts after S2 and terminates before S1
A late diastolic (presystolic) murmur starts well after S2 and extends up to the mitral component (left sided) or to the
tricuspid component (right sided) of S1
Continuous murmur A continuous murmur begins in systole and continues to diastole without interruption,
encompassing the S2 (show figure 3 and show table 3).
MIDSYSTOLIC EJECTION MURMURS The ejection or midsystolic murmur (SEM) is related to flow of blood
across the semilunar valves; onset of the SEM coincides with the beginning of ejection and termination occurs with the
cessation of forward flow. S1 occurs at the onset of isovolumic systole when ventricular pressure rises; ejection, and thus
the SEM begins at the end of isovolumic systole when the ventricular pressures exceed the semilunar valve opening
pressure. The onset of a SEM is therefore separated from S1 and the interval between S1 and the onset of the murmur is
proportional to the duration of isovolumic systole (show figure 2).
The intensity of the SEM increases (crescendo) during the initial rapid ejection phase; intensity declines (decrescendo) with
the later slow ejection, resulting in a crescendo-decrescendo configuration. Forward flow from the ventricle stops when
ventricular pressure falls below the aortic or pulmonary artery pressures, before the closure of the semilunar valves. The
murmur terminates with cessation of flow, before A2 or P2, depending upon whether the murmur is left or right sided,
respectively. The interval between the termination of the murmur and A2 or P2 is proportional to the aortic or pulmonary
hangout time, respectively.
Important causes of SEM include (show table 2):
Fixed or dynamic outflow tract obstruction
Increased flow across normal semilunar valves
Dilatation of the aortic root or pulmonary trunk
Anatomical changes in the semilunar valves without obstruction
Aortic outflow obstruction A SEM associated with fixed aortic obstruction due to valvular, subvalvular or supravalvular
stenosis or hypertrophic cardiomyopathy (HCM) is harsh and rough (show table 4). The time the murmur peaks after its
onset bears some correlation to the severity of the obstruction. In patients with aortic stenosis (AS), the longer and later
peaking murmur is usually associated with hemodynamically significant obstruction; a brief and early peaking murmur
indicates less severe AS (show figure 2).
The intensity of the murmur is variable and may not correlate with the severity of stenosis. In the presence of heart failure
and a reduced stroke volume, the duration, configuration, and intensity bear a poor correlation to the degree of obstruction.
An ejection sound at the onset of the murmur suggests valvular AS. The ejection sound is usually absent in severe AS.
The site of maximum intensity and direction of radiation of the murmur are related to the site of obstruction and the

direction of the jet in the aortic root. Nevertheless, other noninvasive and invasive investigations are frequently required for
accurate determination of the site of a fixed obstruction (valvular, supravalvular, or subvalvular).
Valvular aortic stenosis In valvular AS, the maximum intensity is appreciated over the right second interspace; a thrill
may be palpable over the same area. The murmur radiates up into the neck and over both carotid arteries (show table 4).
In older patients with calcific trileaflet AS, a SEM with a musical quality is frequently heard over the cardiac apex or along
the lower left sternal border, in addition to a harsh murmur over the right second interspace. A musical murmur appears to
originate from the vibration of the valve and subvalvular structures and can be recorded in the left ventricular (LV) cavity
(Gallavardin phenomenon); a harsh murmur originates in the aortic root and is related to the high-velocity ejection jet. (See
"Pathophysiology and clinical features of valvular aortic stenosis in adults").
A bicuspid aortic valve is another frequent cause of a SEM; this diagnosis should be entertained if the murmur is brief
(show table 2). The murmur is best heard over the right second interspace with little or no radiation. The diagnosis is
virtually confirmed if it is accompanied by an aortic ejection sound, a short early diastolic murmur, and normal carotid pulse
upstroke and S2. (See "Causes and natural history of congenital aortic stenosis").
Supravalvular aortic stenosis In supravalvular AS, the murmur may be loudest at a slightly higher location than in
valvular aortic stenosis (show table 4). In addition, the intensity of the radiated murmur over the right carotid may be greater
than over the left carotid artery. (See "Supravalvar aortic stenosis").
Subvalvular outflow obstruction In subvalvular LV outflow obstruction (HCM), the maximum intensity of the
murmur is usually located along the lower left sternal border or over the cardiac apex (show table 4). It radiates poorly to
the base and neck. The site of the LV outflow obstruction cannot be identified with certainty by the location, radiation, and
character of the SEM. (See "Clinical manifestations of hypertrophic cardiomyopathy" and see "Evaluation of obstructive
hypertrophic cardiomyopathy").
Fixed versus dynamic outflow obstruction It is usually not difficult to distinguish between fixed valvular AS and
dynamic (obstructive HCM) LV outflow obstruction (show table 4). With respect to the carotid pulse:
In fixed valvular AS, the initial upstroke and the peak of the carotid pulse are delayed and the volume may be reduced.
In obstructive HCM, the initial upstroke of the carotid pulse is usually sharp and the volume is normal
The change in intensity of the SEM in response to different maneuvers is also useful diagnostically.
Assuming a standing position increases the intensity of the murmur in HCM; it decreases the murmur of valvular aortic
stenosis.
The murmur of HCM increases in intensity with the straining phase of a Valsalva maneuver and the carotid pulse
decreases or is unchanged. Both the intensity of the murmur and the carotid pulse volume decline with Valsalva in AS.
The murmur of HCM increases in intensity with amyl nitrate inhalation and the carotid pulse volume decreases or
remains unchanged. Heart rate increases and arterial blood pressure falls. In AS, both the intensity of the murmur and
carotid pulse volume increase with amyl nitrate inhalation. It is generally more difficult to interpret the responses to amyl
nitrite than to standing or Valsalva in distinguishing HCM from valvular AS.
These features can also be used to distinguish HCM from fixed subvalvular aortic stenosis (subaortic stenosis), which is
seen primarily in children (show table 4). (See "Subvalvar aortic stenosis (subaortic stenosis)").
Ejection versus regurgitant systolic murmurs It can be difficult to distinguish between a long SEM and a holosystolic
regurgitant murmur in certain situations. The SEM transmitted to the cardiac apex in dynamic or fixed LV outflow
obstruction may sound similar to the murmur of mitral regurgitation (MR) or ventricular septal defect (VSD). It is often
difficult to appreciate the onset of the murmur when S1 is soft, which can occur in AS or MR. When A2 is soft, determining
the timing of murmur termination may also be difficult. It has been suggested that echocardiography should be performed in
patients with systolic murmurs of unknown cause who are suspected of having heart disease [1]. However, a number of
helpful distinguishing features can be elicited by auscultation (show figure 2):

The murmur is likely to be ejection or mid-systolic if A2 is clearly audible over the cardiac apex. If A2 is heard over the
right and left second interspaces but not over the apex, it is likely that A2 is "drowned" by the holosystolic murmur of MR.
The intensity of a SEM increases with a longer RR cycle (eg, in patients with atrial fibrillation and varying RR cycles)
and with a post ectopic beat (in patients with premature beats); the intensity of a regurgitant murmur usually remains
unchanged in these situations.
Changes in the intensity of the murmur may occur in response to hand grip; it increases the intensity of a n MR murmur
(increased afterload effect) and usually decreases the intensity of an AS murmur. The physiologic responses to hand grip are
complex; in addition to an increase in systemic vascular tone and arterial pressure, a reflex increase in contractility may
occur, which tends to increase the intensity of the stenotic murmur.
Amyl nitrite lowers systemic vascular resistance and arterial pressure, decreasing the severity of regurgitation and,
therefore the intensity of the regurgitant murmur. In AS, intensity of the SEM increases due to increased flow across the
stenotic aortic valve. In HCM, murmur intensity increases due to an accentuated LV outflow obstruction.
Pulmonic outflow obstruction The murmur of valvular pulmonary stenosis is harsh and best heard over the left second
interspace. When the murmur is loud it radiates to the left side of the neck and is frequently accompanied by a palpable
thrill. A pulmonary ejection sound at the onset of the murmur may be heard, and S2 is widely split with a decreased intensity
of P2. (See "Clinical manifestations and diagnosis of pulmonic stenosis").
The murmur duration correlates reasonably well with the severity of stenosis. The duration can be determined by timing the
termination of the murmur in relation to A2. A murmur terminating before A2 (relatively short) is usually associated with
mild to moderate stenosis. Stenosis is likely to be more severe if the murmur drowns A2 (terminating after A2) [2].
Occasionally, the long, harsh SEM of pulmonary stenosis can be confused with the holosystolic murmur of a ventricular
septal defect. This is more likely to occur with infundibular than valvular stenosis because of the lower location of the
murmur. Careful attention to the behavior of S2 helps in the differential diagnosis: S2 is usually normal in VSD, while in
pulmonary stenosis it is widely split and the intensity of P2 is decreased. Amyl nitrite inhalation is sometimes helpful; it
usually decreases the intensity of the VSD murmur but not that of the pulmonary stenosis (which may be accentuated).
Dilation of the aortic root or pulmonary artery Aortic root dilatation or dilatation of the proximal pulmonary artery
may be associated with a SEM. The usual findings of idiopathic dilatation of the pulmonary artery are a pulmonary ejection
sound, a short ejection systolic murmur, a relatively widely split S2 with normal intensity of P2, and occasionally a short
pulmonary insufficiency murmur. There is no hemodynamic abnormality. The auscultatory findings are very similar in
pulmonary hypertension, except S2 is narrowly split with P2 markedly accentuated, the pulmonary ejection sound is
relatively late, and hemodynamic abnormalities are always evident.
Increased semilunar blood flow A SEM also occurs in the presence of normal valves when flow across the semilunar
valve is significantly increased, as in anemia, pregnancy, or thyrotoxicosis (show table 2). In patients with pure aortic
regurgitation, an ejection systolic murmur may occur due to markedly increased flow and should not be considered evidence
for AS in the absence of other findings. Atrial septal defect is an example of an ejection systolic murmur resulting from
increased flow across the pulmonary valve. These murmurs do not indicate associated pulmonary stenosis.
Aortic valve sclerosis The murmur of aortic sclerosis is also a midsystolic ejection murmur (show figure 2). It is benign,
since it is not associated with hemodynamic consequences, but it must be considered in the differential diagnosis of AS in
elderly patients. The murmur results from stiffening and degenerative fibrous thickening of the roots of the aortic cusps at
the site of their insertions. These morphologic changes do not cause any impairment of mobility of the valve and thus no
obstruction.
The murmur is usually best heard over the right second interspace. In some patients, a musical high-frequency murmur of
brief duration can be heard along the lower left sternal border and cardiac apex. In general, the murmur is brief and not very
loud. A normal carotid pulse and normal S2 confirm the absence of AS. The clinical significance of the diagnosis of aortic
sclerosis is that aortic sclerosis is a risk factor of long term adverse outcome due to atherosclerotic heart disease.
Innocent midsystolic murmurs Innocent murmurs are typically ejection type and midsystolic in timing (show table 2)
[3]. The "innocence" of an SEM should not depend upon the duration or intensity of the murmur, but on the absence of other
abnormal findings. Even a short grade I/VI ejection systolic murmur may not be innocent if there are coexisting findings

such as an abnormal S2.

A short, vibrating murmur (Still's murmur) can be heard over the mid precordium in children that is not accompanied by any
other abnormality. It is thought to arise from vibrations of the attachments of the pulmonary valve leaflets.
Another innocent SEM can be heard in children and young adults that has a blowing quality and is best heard over the left
second interspace. It is thought to originate from vibrations of the pulmonary trunk.
In patients with the straight back syndrome who have a decreased anteroposterior diameter of the chest, a superficial SEM is
heard over the left second interspace [4]. The mechanism of the murmur remains unclear.
HOLOSYSTOLIC (PANSYSTOLIC) MURMURS Holosystolic, or pansystolic, murmurs are usually regurgitant
murmurs and occur when blood flows from a chamber whose pressure throughout systole is higher than pressure in the
chamber receiving the flow. There are three causes of holosystolic murmurs (show table 1):
MR
Tricuspid regurgitation
VSD
The timing and duration of holosystolic murmurs are best explained by the hemodynamic changes of MR. In
hemodynamically significant MR, regurgitant flow from the left ventricle to the left atrium begins with the onset of
isovolumic systole when pressure in the left ventricle just exceeds pressure in the left atrium. This pressure crossover point
also marks S1, explaining the onset of the holosystolic murmur with S1. Throughout systole and extending to the early part
of the isovolumic relaxation phase, the left ventricular pressure remains higher than the left atrial pressure. Thus, the
regurgitant flow continues throughout systole, and even after aortic valve closure, explaining the holosystolic character of
the regurgitant murmur. This also explains why A2 is often drowned by the murmur over the cardiac apex.
Mitral regurgitation The holosystolic murmur of MR is high pitched and best heard with the diaphragm of the
stethoscope and the patient in the left lateral decubitus position. Radiation depends upon the murmur intensity, which may
be variable. The direction of radiation follows the direction of the regurgitant jet into the left atrium.
When the jet is directed posterolaterally, the apical holosystolic murmur radiates toward the left axilla, inferior angle of
the left scapula, and over the thoracic spine [5]. In some patients, a loud murmur may radiate to the top of the head.
The murmur radiates toward the base and root of the neck if the regurgitant stream is directed anteromedially against the
interatrial septum near the base of the aorta. Thus, it can be confused with the murmur of AS or obstructive HCM. The
character of the carotid pulse and the behavior of S2 provide important clues to the diagnosis.
The absence of an S3 and cardiac enlargement suggest hemodynamically insignificant chronic MR. In contrast, clinical
evidence of pulmonary hypertension (accentuated P2, right ventricular systolic hypertension) and right-sided heart failure
are almost always associated with significant MR, provided no other cause of pulmonary hypertension coexists.
Left ventricular function should be assessed by determining the character of the left ventricular apical impulse. A normal or
hyperdynamic apical impulse suggests a normal left ventricular ejection fraction and primary mitral regurgitation. A
displaced and sustained apical impulse is usually associated with a decreased left ventricular ejection fraction, which can
result from long-standing, severe MR, or may indicate secondary MR due to dilated cardiomyopathy. (See "Examination of
the precordial pulsation").
In dilated cardiomyopathy, S3 and findings of pulmonary hypertension may be present without significant MR. Thus, the
differentiation between primary and secondary mitral regurgitation cannot be made at the bedside in the presence of
depressed left ventricular systolic function. (See "Clinical features of chronic mitral regurgitation").
Tricuspid regurgitation The holosystolic murmur of tricuspid regurgitation is best heard with the diaphragm of the
stethoscope over the left second and third interspaces and along the left sternal border. The location of maximum intensity
may be shifted toward the cardiac apex when the right ventricle is dilated and the murmur can be misdiagnosed as MR.

Radiation and respiratory changes in the intensity of the murmur are two important distinguishing features.
With tricuspid regurgitation, the murmur is heard along the right sternal border or over the epigastrium.
During the inspiratory phase of respiration, the intensity of the murmur of tricuspid regurgitation increases (Carvello's
sign) if severe right ventricular failure is not present. The increase in intensity does not occur immediately with the onset of
inspiration, but after one or two cardiac cycles. The mechanism for the increase in intensity appears to be augmented
regurgitant flow following the inspiratory increase in right ventricular volume. A right ventricular S3 gallop and a middiastolic flow murmur, which also increase in intensity with inspiration, suggest more severe tricuspid regurgitation.
Murmur intensity does not change in the presence of severe right ventricular failure when right ventricular volume may not
change appreciably. With severe right-sided heart failure, the murmur can be absent, or only an early systolic murmur may
be recognized. In these circumstances, the bedside diagnosis of tricuspid regurgitation relies upon the presence of other
physical findings, such as a prominent v wave in the jugular venous pulse and systolic hepatic pulsation.
Tricuspid regurgitation is most often secondary to pulmonary arterial hypertension. Thus, a prominent left parasternal
impulse and narrow splitting of S2 with an accentuated P2 suggest secondary tricuspid regurgitation. Theoretically, severe
tricuspid regurgitation may produce reversed splitting of S2 due to shortened right ventricular ejection time; however, this is
a rare finding.
Primary tricuspid regurgitation is much less common but can occur following bacterial endocarditis (eg, with intravenous
drug abuse) or in patients with Ebstein's anomaly, carcinoid heart disease, or prior right ventricular infarction. A
hyperdynamic left parasternal impulse and normal or only slightly accentuated P2 suggest primary tricuspid regurgitation,
but its diagnosis primarily depends upon the elimination of pulmonary hypertension and left-sided disorders such as mitral
and aortic valve disease and cardiomyopathy. In primary tricuspid regurgitation, the murmur may be early systolic rather
than holosystolic, and have a decrescendo shape. (See "Pathophysiology and clinical features of tricuspid regurgitation").
Ventricular septal defect VSDs cause a holosystolic murmur if pressure in the right ventricle is lower than the left
ventricle throughout systole, resulting in a continuous left-to-right shunt [6,7]. This hemodynamic profile is present in small
VSDs and is associated with normal pulmonary artery pressure and pulmonary vascular resistance. Thus, S2 is normal and
pulmonary hypertension is absent.
The murmur is usually loud and may be accompanied by a thrill. The left-to-right shunt is directed toward the right
ventricular cavity. The murmur is maximal over the third and fourth interspaces along the sternal border when the VSD is
below the crista supraventricularis. When the defect is above the crista, the shunt is directed toward the pulmonary trunk;
the maximal intensity of the murmur may be in the left second interspace in this case, and it can be confused with the
murmur of pulmonary valve stenosis [2].
Changes in S2 help in the differential diagnosis. A wide splitting of S2 with reduced intensity of P2 is present in pulmonary
stenosis; a normal S2 favors VSD.
The character and timing of the systolic murmur change with large VSDs due to increased right ventricular and pulmonary
artery pressure and an elevated pulmonary vascular resistance. Instead of being holosystolic, it becomes early systolic and
the peak of the murmur occurs earlier. The physical findings of pulmonary arterial hypertension and right ventricular
hypertrophy are present.
When the shunt is reversed in Eisenmenger complex, the murmur may be absent and an ejection systolic murmur due to
dilatation of the pulmonary trunk appears. S2 is markedly accentuated and single [8]. Murmurs of tricuspid pulmonary
regurgitation may also be present.
Thus, a holosystolic murmur in a patient with a VSD usually indicates favorable hemodynamics (eg, relatively normal rightsided pressures). (See "Pathophysiology and clinical features of ventricular septal defects").
EARLY SYSTOLIC MURMURS Early systolic murmurs begin with S1, do not extend to S2, and generally have a
decrescendo configuration. Early systolic murmurs may result from MR, tricuspid regurgitation, or VSD (show table 1).

Mitral regurgitation Either acute severe or mild chronic MR can be associated with an early systolic murmur. Acute
severe mitral regurgitation causes a rapid increase in left atrial pressure and a giant regurgitant wave (v wave) during the
latter part of ventricular systole. An equalization of left atrial and left ventricular pressure may occur, preventing the
regurgitant flow during this part of systole. Thus, the regurgitant murmur terminates before A2. Since the regurgitant flow is
maximal at the beginning of systole and decreases with increasing left atrial pressure, a decrescendo configuration of this
early systolic murmur is common [9-11]. Associated clinical findings include pulmonary hypertension, hyperdynamic apical
impulse, a late systolic left parasternal impulse, and atrial and ventricular gallops. (See "Pathophysiology and clinical
features of acute mitral regurgitation")
In some patients with mitral stenosis, an early systolic murmur is heard and probably represents mild mitral regurgitation.
Secondary mitral regurgitation in dilated cardiomyopathy is usually mild and may be early systolic in timing. Mitral annular
calcification can be associated with an early systolic murmur and suggests trivial MR. Ineffective reduction of the
circumference of the annulus at the beginning of systole, due to calcification, is probably the underlying mechanism for
mild MR and the early systolic murmur [10].
Tricuspid regurgitation Primary tricuspid regurgitation with normal right ventricular systolic pressure, as seen with
infective endocarditis in drug addicts, may be associated with an early systolic murmur with a decrescendo configuration.
The mechanism is similar to that in acute, severe MR. A rapid increase in right atrial pressure and an accentuated v wave in
the later part of systole decreases the regurgitant flow. The frequency of these murmurs is usually lower than the murmurs
associated with an elevated right ventricular systolic pressure, presumably due to a lower rate of regurgitation. In addition to
a relatively normal S2, palpating and recording the left parasternal impulse may reveal a systolic inward movement and a
diastolic outward movement reflecting right ventricular volume changes.
Ventricular septal defect In a large VSD with pulmonary hypertension, the murmur may be early systolic in timing,
since the increasing right ventricular pressure during late systole decreases the left-to-right shunt. Findings of pulmonary
hypertension are always present. An early systolic murmur may also occur in some patients with a VSD in the absence of
pulmonary hypertension or increased pulmonary vascular resistance; these murmurs are more frequently localized and of
shorter duration. They tend to occur with VSDs that later close spontaneously [12].
Small muscular VSDs may also cause an early systolic murmur, since the defect closes soon after the onset of systole.
Evidence of pulmonary hypertension is absent.
LATE SYSTOLIC MURMURS A late systolic murmur starts after S1 and, if left-sided, extends to A2, usually in a
crescendo manner (show figure 3).
Mitral valve prolapse Mitral valve prolapse is the most common cause of a late systolic murmur. It is best heard with
the diaphragm of the stethoscope, over or just medial to the cardiac apex. It is usually preceded by single or multiple clicks
[13]. Mitral valve prolapse can occur from disorders of the mitral annulus, redundancy of the leaflets, abnormalities of the
chordae, or contraction abnormalities of the left ventricular wall. Mitral regurgitation occurs when prolapse is sufficient to
cause a lack of apposition of the leaflets. (See "Definition and diagnosis of mitral valve prolapse").
The most common etiology for mitral valve prolapse is redundancy of valve tissue with respect to the valve ring ("floppy"
valve or Barlow's syndrome). This disparity increases with a decreased left ventricular volume, which is associated with an
earlier onset of prolapse and, therefore, the late systolic murmur occupies a relatively greater portion of systole. Standing,
sitting, Valsalva's maneuver (phase 2), and amyl nitrite inhalation, all decrease left ventricular volume and cause an earlier
onset of the clicks and murmurs, which also appear long (show table 5. The intensity, however, becomes softer. Conversely,
squatting, elevation of the legs, isometric exercise (hand grip), and infusion of phenylephrine, which increases left
ventricular volume, delay the onset of the clicks and murmurs, the intensity of which may increase. A "whoop" or "honk,"
which is a high-frequency, musical, loud, and widely transmitted murmur, can appear intermittently in some patients with
mitral valve prolapse and may be precipitated by a change of posture.
In general, mitral valve prolapse with a late systolic murmur is associated with mild mitral regurgitation and is not
accompanied by an S3 or signs of pulmonary hypertension. Left ventricular function is normal.
In patients with pseudohypertrophic muscular dystrophy, mitral valve prolapse and a late systolic murmur are manifestations

of cardiac involvement. These may or may not be associated with midsystolic clicks. The electrocardiogram almost always
demonstrates a relatively tall R wave in leads V1, and V2, simulating true posterior myocardial infarction. The mechanism
of mitral valve prolapse and its electrocardiographic changes is fibrosis of the posterior left ventricular wall.
Tricuspid valve prolapse Tricuspid valve prolapse is uncommon in the absence of mitral valve prolapse. It causes a late
systolic murmur that extends up to P2. It is best heard over the left lower sternal border. Onset of the murmur may be
delayed during inspiration due to an increase in right ventricular volume.
Papillary muscle dysfunction A late systolic murmur may occur with mild mitral regurgitation due to papillary muscle
dysfunction in acute myocardial infarction. It can also occur in patients with chronic coronary artery disease during an
episode of myocardial ischemia, presumably due to ischemic papillary muscle dysfunction. In these patients, isometric
exercise or maneuvers that increase ventricular volume may precipitate mitral regurgitation and a late systolic murmur
because of increased myocardial oxygen requirements, which may induce myocardial ischemia. (See "Role of
echocardiography in acute myocardial infarction").
EARLY DIASTOLIC MURMURS Early diastolic murmurs, most often due to aortic or pulmonary regurgitation,
typically start at the time of semilunar valve closure and their onset coincides with S2. An aortic regurgitation murmur
begins with A2; pulmonary regurgitation begins with P2.
Aortic regurgitation Discovery of a diastolic murmur is essential for the diagnosis of aortic regurgitation. In a review of
the literature, the presence of an early diastolic murmur was the most useful finding for establishing the presence of aortic
regurgitation (positive likelihood ratio 8.8 [ie, the odds of aortic regurgitation are increased 8.8-fold]) and its absence the
most useful finding for eliminating the presence of aortic regurgitation (negative likelihood ratio 0.2 to 0.3 [ie, the odds of
disease are reduced by a factor of 0.2 to 0.3]) [14]. Among patients with end-stage renal disease, a transient murmur of
aortic regurgitation may be induced by the effects of volume overload; thus, such patients should be reexamined after
dialysis, when the excess fluid has been removed [14].
The murmur of aortic regurgitation is best heard with the diaphragm of the stethoscope. Low-intensity, high-pitched aortic
regurgitation murmurs may not be heard unless firm pressure is applied with the diaphragm of the stethoscope over the left
sternal border or over the right second interspace, while the patient sits and leans forward with the breath held in full
expiration.
The radiation of an aortic regurgitation murmur is toward the cardiac apex and the location of maximum intensity may vary
considerably. It can be best heard in some patients over the mid precordium, along the lower left sternal border, or even over
the cardiac apex. Radiation of the murmur to the right sternal border is more common in aortic regurgitation caused by
aortic root or aortic cusp anomalies [15].
The configuration of the aortic regurgitation murmur is usually decrescendo because the magnitude of regurgitation
progressively declines. The murmur is high-frequency and has a "blowing" character. Occasionally the murmur can be
musical in quality (diastolic whoop); this has been attributed to a flail everted aortic cusp. The "whoop" can be mid, late, or
pansystolic [16].
The duration of the murmur is variable but usually terminates before S1. The duration of the murmur does not always
correlate with the severity of aortic regurgitation, although mild aortic regurgitation is usually associated with a murmur of
brief duration. The murmur may also be short with acute severe aortic regurgitation because of a rapid increase in left
ventricular diastolic pressure, which equalizes with aortic diastolic pressure soon after the onset of diastole. If the aortic
pressure remains higher than left ventricular pressure throughout diastole, a pandiastolic murmur may be present, even when
the severity of aortic regurgitation is only moderate. Bedside evaluation of the severity of aortic regurgitation should be
primarily based upon a determination of the hemodynamic consequences. (See "Examination of the arterial pulse").
An Austin Flint murmur is usually associated with significant aortic regurgitation (see "Austin Flint murmur" below). A
decreased intensity of S2 does not necessarily suggest significant aortic regurgitation; however, reversed splitting of S2,
which in the absence of left bundle branch block results from increased left ventricular forward stroke volume, indirectly
suggests significant aortic regurgitation. Changes in the intensity of S1 should be noted, since a reduced intensity is usually
associated with an elevated left ventricular end-diastolic pressure, which is more likely to occur in severe aortic

regurgitation. Physical findings of pulmonary venous and arterial hypertension and right-sided heart failure indicate
hemodynamically significant aortic regurgitation. (See "Pathophysiology and clinical features of chronic aortic regurgitation
in adults").
Assessment of left ventricular function is important, particularly with respect to the timing of surgery. A hyperdynamic left
ventricular impulse is associated with a relatively normal ejection fraction. On the other hand, a sustained impulse and S3
gallop may indicate a reduced ejection fraction; further evaluation to assess left ventricular function is indicated in this
circumstance.
The onset of heart failure can modify many of the physical findings that suggest significant aortic regurgitation. The pulse
pressure that was initially high may decrease, and the arterial diastolic pressure that was low may increase. The duration of
the regurgitant murmur may decrease as the left ventricular diastolic pressure increases.
The hemodynamic consequences of acute, severe aortic regurgitation differ considerably from those of chronic aortic
regurgitation, explaining the differences in physical findings. (See "Pathophysiology and clinical features of acute aortic
regurgitation in adults").
Sudden severe volume overload in a nondilated left ventricle causes a rapid increase in diastolic pressure and often
equalization of left ventricular and aortic root pressures in mid-diastole. Thus, the regurgitant murmur can be of short
duration.
S1 is soft or absent due to a reduced intensity of the mitral component of S1 and premature closure of the mitral valve
[17].
The P2 of S2 is frequently accentuated due to postcapillary pulmonary hypertension.
A marked increase in left ventricular end-diastolic pressure may prevent effective left ventricular filling during left atrial
systole; an atrial gallop may therefore be absent.
The carotid pulse can appear small since left ventricular forward stroke volume may not increase or may even decrease,
although the character remains normal.
The pulse pressure may become narrow as the systemic vascular resistance either increases or remains normal and the
arterial diastolic pressure does not fall, if the forward stroke volume declines concomitantly.
A lack of left ventricular dilation and hypertrophy is recognized by the relatively normal position of the left ventricular
impulse.
Left anterior descending artery stenosis Diastolic murmurs similar to those of aortic regurgitation can be heard in
some patients with left anterior descending coronary artery stenosis (Dock's murmur). [18]. The murmur is not widespread
like that of aortic regurgitation and usually is best heard over the left second or third interspace, a little lateral to the left
sternal border. The murmur may be long or short. It is caused by turbulent flow across the coronary artery stenosis and
usually indicates moderately severe stenosis. Coronary artery bypass surgery abolishes the murmur.
Pulmonary regurgitation Pulmonary regurgitation is most frequently a result of pulmonary hypertension (GrahamSteell murmur) in adults [19]. The murmur is high-pitched and "blowing." It begins with an accentuated P2 of S2 and can be
of variable duration. It may occupy all of diastole if there is a pandiastolic gradient between the pulmonary artery and the
right ventricular diastolic pressure. The murmur has a decrescendo configuration like that of aortic regurgitation;
differentiation is difficult if not impossible by auscultation alone. The murmur may increase in intensity during inspiration
and can be more localized. It is best heard over the left second and third interspaces.
Pulmonary regurgitation is suspected when other findings of pulmonary hypertension are present and peripheral signs of
aortic regurgitation are absent. However, it can occur in the absence of pulmonary hypertension, as in patients with
idiopathic dilatation of the pulmonary artery, after pulmonary valvulotomy, with right-sided endocarditis, and with
congenital absence of the pulmonary valve. In these conditions, the pulmonary artery diastolic pressure is normal or low and
there is a lower rate of regurgitant flow; the regurgitant murmur is of low to medium pitch. The murmur usually begins after
rather than with P2. Delayed onset of the murmur is related to the minimal pulmonary artery-right ventricular pressure
gradient at the time of pulmonary valve closure. Regurgitation increases as the right ventricular pressure declines rapidly
after pulmonary valve closure, increasing the pressure gradient. The murmur does not extend to S1 because the relatively
low pulmonary artery pressure equilibrates with that of right ventricular pressure at the latter part of diastole.

In congenital absence of the pulmonary valve, P2 is absent and there is a silent interval between A2 and the onset of the
regurgitant murmur. A loud to-and-fro murmur may be heard in these patients.
MID-DIASTOLIC MURMURS Mid-diastolic murmurs result from turbulent flow across the atrioventricular valves
during the rapid filling phase because of mitral or tricuspid valve stenosis and an abnormal pattern of flow across these
valves.
Mitral stenosis The mid-diastolic murmur of mitral stenosis has a rumbling character and is best heard with the bell of
the stethoscope over the left ventricular impulse with the patient in the left lateral decubitus position. The murmur originates
in the left ventricular cavity explaining its location of maximum intensity.
The murmur is present both in sinus rhythm and in atrial fibrillation. It characteristically starts with an opening snap. Its
duration, which correlates with the duration of the diastolic pressure gradient across the mitral valve, is a reasonably good
guide to assess the severity of mitral stenosis [20]. The longer the duration of the murmur, the more severe is the mitral
stenosis, provided the diastolic interval is not too short (absence of tachycardia). If the murmur extends up to S1 during a
longer diastolic interval, it can be assumed that the pressure gradient is still present at end-diastole, which implies severe
mitral stenosis.
When the flow across the mitral valve is markedly reduced, which may result from associated right-sided heart failure and
pulmonary hypertension, the murmur may be of very brief duration or even absent (so-called silent mitral stenosis), even in
the presence of severe mitral stenosis. Conversely, with enhanced flow across the valve, as in the high-output state of
pregnancy, the intensity and duration of the murmur increase even with less severe stenosis. In these circumstances, one
cannot rely on the duration of the murmur to assess the severity of mitral stenosis; other ancillary investigations, particularly
echocardiographic studies, are necessary. (See "Pathophysiology and clinical features of mitral stenosis").
Tricuspid stenosis Tricuspid stenosis may be associated with a mid-diastolic rumble that is best heard along the left
sternal border. The most characteristic feature is the increase in intensity of the murmur with inspiration (Carvallo's sign)
[21]. The mid-diastolic rumble may be associated with a tricuspid opening snap and wide splitting of S1 due to delayed
closure of the tricuspid valve. Most patients with tricuspid stenosis are in atrial fibrillation and the murmur is mid-diastolic
when the transvalvular pressure gradient is maximum. In sinus rhythm, the murmur may occur only in late diastole,
resulting from an increased flow due to right atrial systole.
Tricuspid stenosis most frequently occurs in association with mitral stenosis. Isolated tricuspid stenosis is uncommon; when
suspected, carcinoid heart disease and right atrial myxoma should be investigated as possible etiologies. A prominent a wave
and a relatively slow y descent in the jugular venous pulse, presystolic hepatic pulsation, and the absence of a right atrial
gallop should strengthen the suspicion of tricuspid stenosis.
Atrial myxoma Atrial myxoma may cause obstruction of the atrioventricular valves and a mid-diastolic murmur. In left
atrial myxoma, the auscultatory findings can be similar to those of mitral stenosis. The murmur is frequently presystolic and
crescendo in configuration; it appears to occur with the onset of ventricular systole when the tumor is moved toward the left
atrium through the mitral orifice, and when the flow across the valve is still continuing.
It is difficult to distinguish between a left atrial myxoma and mitral stenosis at the bedside. However, the character and
intensity of the murmur due to an atrial myxoma may change with alterations of position [22]. Sinus rhythm, changing
intensity and character of the murmur, and a "tumor plop" sound favor the diagnosis of left atrial myxoma. Nevertheless,
echocardiographic evaluation is necessary and is always recommended in a patient with suspected mitral stenosis.
Right atrial myxoma is far less common than left atrial myxoma. Auscultatory findings may be similar to those of tricuspid
stenosis. (See "Cardiac tumors").
Increased flow across the atrioventricular valve Mid-diastolic murmurs may occur in the presence of normal
atrioventricular valves when the flow across the valve is markedly increased in mid-diastole (flow murmurs). In pure severe
mitral regurgitation, a larger volume of blood (due to the regurgitant volume) moves from the left atrium to the left ventricle
during diastole; the etiology is a partial closing movement of the mitral valve which occurs after it opens widely at the
beginning of diastole. The rapid flow to the left ventricle continues, and thus "functional mitral stenosis" occurs, explaining

the mid-diastolic rumble. In some patients a mid-diastolic pressure gradient has been demonstrated [23-25].
In a left-to-right shunt, antegrade blood flow across the mitral valve increases during diastole, which may be associated with
a mid-diastolic murmur. The mechanism may be similar to that seen in mitral regurgitation. When the etiology is an atrial
septal defect or anomalous pulmonary venous drainage, a tricuspid flow murmur can also be heard along the lower left
sternal border; this is due to a partial closing movement of the tricuspid valve after its full opening in early diastole and
functional tricuspid stenosis at mid-diastole [26]. The intensity of the tricuspid flow murmur tends to increase during
inspiration.
Austin Flint murmur An apical diastolic rumbling murmur has been described in patients with pure aortic regurgitation
[27,28]. Several mechanisms have been proposed to explain the genesis of this murmur, including fluttering of the mitral
valve from the impingement by the aortic regurgitant jet, relative (functional) mitral stenosis, and regurgitant jets directed
against the left ventricular free wall [27-29].
Mitral fluttering is not the mechanism of the Austin Flint murmur, since fluttering occurs in early diastole with the onset of
regurgitation, while the rumble occurs in mid or late diastole. A second proposed mechanism was premature partial closing
movement of the mitral valve at mid-diastole due to the regurgitant flow, leading to functional mitral stenosis. However, use
of M-mode and two-dimensional echocardiography, color flow Doppler, and cine magnetic resonance imaging has shown
that the murmur arises from the regurgitant jets that are directed at the left ventricular free wall, not functional mitral
stenosis [29].
If the Austin Flint murmur is not recognized, a mistaken diagnosis of organic mitral stenosis can occur. The presence of an
opening snap suggests organic mitral stenosis. Amyl nitrite inhalation is also a helpful method of differentiation. An Austin
Flint murmur tends to decrease in intensity and duration as the severity of the aortic regurgitation decreases with decreased
left ventricular afterload. In contrast, the murmur of mitral stenosis increases in intensity and duration with an increased
heart rate and increased antegrade flow across the mitral valve.
Carey-Coombs murmur In acute rheumatic fever, a mid-diastolic murmur over the left ventricular impulse, a CareyCoombs murmur, has been attributed to acute mitral valvulitis. However, first-degree atrioventricular block (prolonged PR
interval) is common in rheumatic carditis and an increased flow due to earlier atrial systole coinciding with the rapid filling
phase may contribute to a Carey-Coombs murmur.
LATE DIASTOLIC (PRESYSTOLIC) MURMURS Presystolic murmurs occur in late diastole and extend up to S1.
They usually have a crescendo configuration. The murmurs result from increased flow across the mitral or tricuspid valve
and are most frequently observed in the presence of normal sinus rhythm. However, crescendo presystolic murmurs can
occur in the presence of atrial fibrillation in the absence of atrial systole; mitral valve closure, resulting in a reduction of an
effective mitral orifice, begins before the onset of isovolumic systole and S1 and during this period antegrade flow across
the mitral valve continues [30].
Mitral stenosis Atrial contraction increases the pressure gradient and flow at end-diastole when mitral stenosis is
present, generating the presystolic murmur. When a mid-diastolic rumble accompanies a presystolic murmur, the intensity of
the mid-diastolic murmur frequently decreases before the onset of the presystolic murmur. The presence of only a
presystolic murmur associated with increased intensity of S1 suggests mild mitral stenosis.
Tricuspid stenosis In tricuspid stenosis with sinus rhythm, the murmur is usually presystolic because the transvalvular
gradient is maximum during this period [21]. The intensity of the presystolic murmur of tricuspid stenosis also increases
during inspiration, which is associated with an increased venous return to the right atrium. Increased right atrial volume is
associated with more forceful right atrial contraction and, therefore, an increased pressure gradient during this interval and
accentuation of the murmur.
Myxoma Presystolic murmurs may occur with left or right atrial myxomas. This is due to obstruction of the
atrioventricular valves.
Left-to-right shunts Flow murmurs due to a large left-to-right shunt are usually mid-diastolic in location. Occasionally

they can extend to late diastole.

Complete heart block In complete atrioventricular block with a slow idioventricular rhythm, a short late diastolic
murmur can occasionally be heard and recorded (Rytand's murmur). The precise mechanism of Rytand's murmur has not
been elucidated; diastolic mitral regurgitation has been postulated [31,32]. Diastolic mitral regurgitation appears to depend
upon the position of the P wave and atrial systole in ventricular diastole. (See "Third degree (complete) atrioventricular
block").
CONTINUOUS MURMURS Continuous murmurs are defined as murmurs that begin in systole and extend up to
diastole without interruption. They do not necessarily need to occupy the total duration of systole and diastole. Continuous
murmurs result from blood flow from a higher pressure chamber or vessel to a lower system associated with a persistent
pressure gradient between these areas during systole and diastole. These murmurs may occur due to aortopulmonary
connections, arteriovenous communication, and disturbances in the flow patterns in the arteries or veins (show figure 3 and
show table 3) [33-36].
Patent ductus arteriosus Patent ductus arteriosus is a relatively common cause of a continuous murmur in adults. Aortic
pressure is higher than pulmonary artery pressure during both systole and diastole; blood flow from the high pressure
descending thoracic aorta to the low pressure pulmonary artery causes the continuous murmur (Gibson's murmur or
machinery murmur).
The maximum intensity of the murmur usually occurs at S2. The duration of the murmur depends upon the pressure
difference between aorta and pulmonary artery. With pulmonary hypertension, pulmonary artery diastolic pressure
increases; when it approaches systemic level, the diastolic portion of the continuous murmur becomes shorter and ultimately
absent [37]. With more severe pulmonary hypertension, pulmonary artery systolic pressure can equalize with aortic systolic
pressure and the systolic component of the murmur may also be absent (silent ductus). Differential cyanosis due to the
reversal of the shunt and signs of pulmonary hypertension with or without evidence of right-sided heart failure are the only
physical findings that are recognizable at the bedside in these circumstances.
Aortopulmonary window Continuous murmurs may be present with an aortopulmonary window. However, because of
the large size of the communication, pulmonary vascular resistance and pulmonary artery diastolic pressure tend to be
higher, which is associated with a shorter duration of the diastolic component of the continuous murmur.
Shunts A left-to-right shunt through a small atrial septal defect in the presence of mitral valve obstruction, known as
Lutembacher's syndrome, may occasionally cause a continuous murmur [38]. Total anomalous pulmonary venous drainage,
a small atrial septal defect without mitral valve obstruction, and mitral stenosis with a persistent left superior vena cava are
very rare causes of continuous murmurs.
Arteriovenous fistulas Congenital or acquired arteriovenous fistulas also cause continuous murmurs.
Coronary artery venous fistulas may produce a continuous murmur; the location, duration, and character of the murmur
depend upon the anatomical type of fistulas. As an example, the right coronary and right atrial, or coronary sinus,
communication produces continuous murmurs that are usually located along the parasternal areas. The murmur of a
circumflex coronary artery and coronary sinus communication are usually located in the left axilla. The configuration of the
murmur and the intensity of the systolic and diastolic components are variable. Marked systolic compression of the
abnormal vessels reduces the systolic flow; thus, the systolic component of the murmur may be very soft. On the other hand,
an increased systolic gradient may result from the partial compression of the intramural communication, which will tend to
increase the intensity of the systolic portion of the murmur.
A communication between the sinus of Valsalva and the right atrium or right ventricle produces continuous murmurs that
may appear as to-and-fro murmurs due to the increased intensity of both the systolic and diastolic components and a softer
intensity around S2.
Systemic and pulmonary arteriovenous fistulas are also associated with continuous murmurs. Although a systemic

arteriovenous communication usually produces a loud murmur, the murmur of pulmonary arteriovenous fistulas are softer
and may be primarily systolic. The major pressure gradient occurs in systole, and the diastolic gradient is usually very small.
Pulmonary arteriovenous fistulas usually involve the lower left or right middle lobe; the location of the murmurs is also over
these areas.
Other Constriction in the systemic or pulmonary arteries can be associated with continuous murmurs due to a persistent
pressure gradient across the narrowed segment of the vessel. In coarctation of the aorta, a continuous murmur can be heard
in the back overlying the area of constriction. Continuous murmurs may originate in large tortuous collateral arteries in
coarctation of the aorta, which are also heard in the back over the interscapular regions. Sometimes large, tortuous
intercostal vessels are visible when the shoulders are rotated medially and forward to separate the scapulas (Suzman's sign)
[39]. Pulmonary artery branch stenosis and a partial occlusion of the pulmonary artery due to pulmonary embolism may also
cause continuous murmurs.
Rapid flow through tortuous collateral vessels, as in coarctation of the aorta, may cause a continuous murmur. Bronchial
arterial collateral vessels develop in certain types of cyanotic congenital heart disease (tricuspid atresia, pulmonary atresia
with ventricular septal defect) and loud continuous murmurs may be heard along the parasternal area.
The "mammary souffle" associated with pregnancy may be systolic or continuous. These innocent murmurs are usually of
higher frequency (high pitched) and louder in systole.
A venous hum, which results from altered flow in the veins, can also cause an innocent continuous murmur. The venous
hum is heard with the patient in the sitting position (usually in the supraclavicular fossa) and frequently disappears when the
patient moves to the supine position. The hum tends to be louder in diastole and can be completely abolished by
compression of the ipsilateral internal jugular vein. A loud, left-sided venous hum transmitted below the clavicle should not
be mistaken for the murmur of patent ductus arteriosus. Venous hum is not heard in the supine position, and pressure on the
internal jugular vein abolishes the venous hum. In contrast, the murmur of patent ductus arteriosus persists in the supine
position and despite pressure on the internal jugular vein.
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