Auscultation of cardiac murmurs

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

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information is published. The literature review for version 12.3 is current through August 200! this topic was last changed
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INTRODUCTION Cardiac auscultation is one of the most useful investigative tools that the physician can use at the
edside to detect alterations in cardiovascular anatomy and physiology! Further evaluation of the patient is ased upon the
characteristics of the murmur as "ell as the presence of symptoms #sho" figure $%! &his topic "ill revie" the auscultation
of cardiac murmurs! &he auscultation of other heart sounds is discussed separately! #'ee (Auscultation of heart sounds(%!
MURMUR DESCRIPTION &he character of a murmur may e descried y a numer of features!
Intensity/pitc &he intensity of a murmur is primarily determined y the )uantity and velocity of lood flo" at the site
of its origin, the transmission characteristic of the tissues et"een the site of origin, the site of auscultation or recording, and
the distance of transmission! *n general, the intensity declines in the presence of oesity, emphysema, and pericardial
effusion! Murmurs are usually louder in children and in thin individuals!
'i+ grades are used to classify the intensity of a murmur,
-rade * is the faintest murmur that can e heard #"ith difficulty%
-rade ** murmur is also a faint murmur ut can e identified immediately
-rade *** murmur is moderately loud
-rade *. murmur is loud
-rade . murmur is very loud ut cannot e heard "ithout the stethoscope!
-rade .* murmur is the loudest and can e heard "ithout a stethoscope
&he gradation of intensity is purely sujective! /o"ever, it allo"s recognition of changes in the intensity of the murmur,
"hich has diagnostic relevance!
&he fre)uency determines the pitch, "hich may e high or lo"!
Confi!uration A numer of configurations or shapes of murmurs are recogni0ed,
Crescendo #increasing%
1ecrescendo #diminishing%
Crescendo2decrescendo #increasing2decreasing or diamond shaped%
Plateau #unchanged in intensity%
"uality &he )uality of a murmur can e descried as harsh, rumling, scratchy, grunting, lo"ing, s)uea3y, and
musical! &he )uality of a murmur may also change and, if recogni0ed, can e helpful in the diagnosis of an anomaly!
Duration &he duration of a murmur is assessed y determining the length of systole or diastole that the murmur
occupies! &he murmur can e long #eg, it occupies most of systole or diastole%, or it can e rief!
Radiation &he direction of radiation of a murmur follo"s the direction of lood flo"! *t can provide information
regarding the origin of the murmur!
Timin! &he timing of the murmur in relation to the cardiac cycle is the initial step in identifying the cause and
significance of the murmur #sho" tale $%!
Systolic murmurs A systolic murmur starts "ith or after '$ and terminates efore or at '4 # sho" figure 4%! 'ystolic
murmurs are recogni0ed y identifying '$ and '4 and timing them "ith the carotid pulse! *n patients "ith mar3ed
tachycardia, a long diastolic murmur can e occasionally confused "ith a systolic murmur5 timing "ith the carotid pulse
upstro3e avoids an incorrect diagnosis!
'ystolic murmurs are further classified according to the time of onset and termination in systole,
An ejection systolic murmur #midsystolic% egins after the '$ and ends efore A4 #left sided% or P4 #right sided% #sho"
tale 4%
A holosystolic murmur starts "ith '$ and e+tends up to A4 #left sided% or P4 #right sided%
An early systolic murmur starts "ith '$ and e+tends for a variale length in systole ut does not +tend up to '4
A late systolic murmur starts after '$ and e+tends to A4 #left sided% or P4 #right sided%
Diastolic murmurs A diastolic murmur starts "ith or after '4 and ends at or efore '$! 1iastolic murmurs are also
classified according to the time of onset and termination of the murmur in diastole,
An early diastolic murmur starts "ith A4 #left sided% or P4 #right sided% and e+tends into diastole for a variale duration
A mid2diastolic murmur starts after '4 and terminates efore '$
A late diastolic #presystolic% murmur starts "ell after '4 and e+tends up to the mitral component #left sided% or to the
tricuspid component #right sided% of '$
Continuous murmur A continuous murmur egins in systole and continues to diastole "ithout interruption,
encompassing the '4 #sho" figure 6 and sho" tale 6%!
MIDS#STO$IC E%ECTION MURMURS &he ejection or midsystolic murmur #'7M% is related to flo" of lood
across the semilunar valves5 onset of the '7M coincides "ith the eginning of ejection and termination occurs "ith the
cessation of for"ard flo"! '$ occurs at the onset of isovolumic systole "hen ventricular pressure rises5 ejection, and thus
the '7M egins at the end of isovolumic systole "hen the ventricular pressures e+ceed the semilunar valve opening
pressure! &he onset of a '7M is therefore separated from '$ and the interval et"een '$ and the onset of the murmur is
proportional to the duration of isovolumic systole #sho" figure 4%!
&he intensity of the '7M increases #crescendo% during the initial rapid ejection phase5 intensity declines #decrescendo% "ith
the later slo" ejection, resulting in a crescendo2decrescendo configuration! For"ard flo" from the ventricle stops "hen
ventricular pressure falls elo" the aortic or pulmonary artery pressures, efore the closure of the semilunar valves! &he
murmur terminates "ith cessation of flo", efore A4 or P4, depending upon "hether the murmur is left or right sided,
respectively! &he interval et"een the termination of the murmur and A4 or P4 is proportional to the aortic or pulmonary
hangout time, respectively!
*mportant causes of '7M include #sho" tale 4%,
Fi+ed or dynamic outflo" tract ostruction
*ncreased flo" across normal semilunar valves
1ilatation of the aortic root or pulmonary trun3
Anatomical changes in the semilunar valves "ithout ostruction
Aortic outflo& o'struction A '7M associated "ith fi+ed aortic ostruction due to valvular, suvalvular or
supravalvular stenosis or hypertrophic cardiomyopathy #/CM% is harsh and rough #sho" tale 8%! &he time the murmur
pea3s after its onset ears some correlation to the severity of the ostruction! *n patients "ith aortic stenosis #A'%, the longer
and later pea3ing murmur is usually associated "ith hemodynamically significant ostruction5 a rief and early pea3ing
murmur indicates less severe A' #sho" figure 4%!
&he intensity of the murmur is variale and may not correlate "ith the severity of stenosis! *n the presence of heart failure
and a reduced stro3e volume, the duration, configuration, and intensity ear a poor correlation to the degree of ostruction!
An ejection sound at the onset of the murmur suggests valvular A'! &he ejection sound is usually asent in severe A'!
&he site of ma+imum intensity and direction of radiation of the murmur are related to the site of ostruction and the
direction of the jet in the aortic root! 9evertheless, other noninvasive and invasive investigations are fre)uently re)uired for
accurate determination of the site of a fi+ed ostruction #valvular, supravalvular, or suvalvular%!
(al)ular aortic stenosis *n valvular A', the ma+imum intensity is appreciated over the right second interspace5 a thrill
may e palpale over the same area! &he murmur radiates up into the nec3 and over oth carotid arteries #sho" tale 8%!
*n older patients "ith calcific trileaflet A', a '7M "ith a musical )uality is fre)uently heard over the cardiac ape+ or along
the lo"er left sternal order, in addition to a harsh murmur over the right second interspace! A musical murmur appears to
originate from the viration of the valve and suvalvular structures and can e recorded in the left ventricular #:.% cavity
#-allavardin phenomenon%5 a harsh murmur originates in the aortic root and is related to the high2velocity ejection jet! #'ee
(Pathophysiology and clinical features of valvular aortic stenosis in adults(%!
A icuspid aortic valve is another fre)uent cause of a '7M5 this diagnosis should e entertained if the murmur is rief
#sho" tale 4%! &he murmur is est heard over the right second interspace "ith little or no radiation! &he diagnosis is
virtually confirmed if it is accompanied y an aortic ejection sound, a short early diastolic murmur, and normal carotid pulse
upstro3e and '4! #'ee (Causes and natural history of congenital aortic stenosis(%!
Supra)al)ular aortic stenosis *n supravalvular A', the murmur may e loudest at a slightly higher location than in
valvular aortic stenosis #sho" tale 8%! *n addition, the intensity of the radiated murmur over the right carotid may e greater
than over the left carotid artery! #'ee ('upravalvar aortic stenosis(%!
Su')al)ular outflo& o'struction *n suvalvular :. outflo" ostruction #/CM%, the ma+imum intensity of the
murmur is usually located along the lo"er left sternal order or over the cardiac ape+ #sho" tale 8%! *t radiates poorly to
the ase and nec3! &he site of the :. outflo" ostruction cannot e identified "ith certainty y the location, radiation, and
character of the '7M! #'ee (Clinical manifestations of hypertrophic cardiomyopathy( and see (7valuation of ostructive
hypertrophic cardiomyopathy(%!
*i+ed )ersus dynamic outflo& o'struction *t is usually not difficult to distinguish et"een fi+ed valvular A' and
dynamic #ostructive /CM% :. outflo" ostruction #sho" tale 8%! ;ith respect to the carotid pulse,
*n fi+ed valvular A', the initial upstro3e and the pea3 of the carotid pulse are delayed and the volume may e reduced!
*n ostructive /CM, the initial upstro3e of the carotid pulse is usually sharp and the volume is normal
&he change in intensity of the '7M in response to different maneuvers is also useful diagnostically!
Assuming a standing position increases the intensity of the murmur in /CM5 it decreases the murmur of valvular aortic
stenosis!
&he murmur of /CM increases in intensity "ith the straining phase of a .alsalva maneuver and the carotid pulse
decreases or is unchanged! Both the intensity of the murmur and the carotid pulse volume decline "ith .alsalva in A'!
&he murmur of /CM increases in intensity "ith amyl nitrate inhalation and the carotid pulse volume decreases or
remains unchanged! /eart rate increases and arterial lood pressure falls! *n A', oth the intensity of the murmur and
carotid pulse volume increase "ith amyl nitrate inhalation! *t is generally more difficult to interpret the responses to amyl
nitrite than to standing or .alsalva in distinguishing /CM from valvular A'!
&hese features can also e used to distinguish /CM from fi+ed suvalvular aortic stenosis #suaortic stenosis%, "hich is
seen primarily in children #sho" tale 8%! #'ee ('uvalvar aortic stenosis #suaortic stenosis%(%!
E,ection )ersus re!ur!itant systolic murmurs *t can e difficult to distinguish et"een a long '7M and a holosystolic
regurgitant murmur in certain situations! &he '7M transmitted to the cardiac ape+ in dynamic or fi+ed :. outflo"
ostruction may sound similar to the murmur of mitral regurgitation #MR% or ventricular septal defect #.'1%! *t is often
difficult to appreciate the onset of the murmur "hen '$ is soft, "hich can occur in A' or MR! ;hen A4 is soft, determining
the timing of murmur termination may also e difficult! *t has een suggested that echocardiography should e performed in
patients "ith systolic murmurs of un3no"n cause "ho are suspected of having heart disease < $=! /o"ever, a numer of
helpful distinguishing features can e elicited y auscultation #sho" figure 4%,
&he murmur is li3ely to e ejection or mid2systolic if A4 is clearly audile over the cardiac ape+! *f A4 is heard over the
right and left second interspaces ut not over the ape+, it is li3ely that A4 is (dro"ned( y the holosystolic murmur of MR!
&he intensity of a '7M increases "ith a longer RR cycle #eg, in patients "ith atrial firillation and varying RR cycles%
and "ith a post ectopic eat #in patients "ith premature eats%5 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 grip5 it increases the intensity of a n MR murmur
#increased afterload effect% and usually decreases the intensity of an A' murmur! &he physiologic responses to hand grip are
comple+5 in addition to an increase in systemic vascular tone and arterial pressure, a refle+ increase in contractility may
occur, "hich tends to increase the intensity of the stenotic murmur!
Amyl nitrite lo"ers systemic vascular resistance and arterial pressure, decreasing the severity of regurgitation and,
therefore the intensity of the regurgitant murmur! *n A', intensity of the '7M increases due to increased flo" across the
stenotic aortic valve! *n /CM, murmur intensity increases due to an accentuated :. outflo" ostruction!
Pulmonic outflo& o'struction &he murmur of valvular pulmonary stenosis is harsh and est heard over the left second
interspace! ;hen the murmur is loud it radiates to the left side of the nec3 and is fre)uently accompanied y a palpale
thrill! A pulmonary ejection sound at the onset of the murmur may e heard, and '4 is "idely split "ith a decreased
intensity of P4! #'ee (Clinical manifestations and diagnosis of pulmonic stenosis(%!
&he murmur duration correlates reasonaly "ell "ith the severity of stenosis! &he duration can e determined y timing the
termination of the murmur in relation to A4! A murmur terminating efore A4 #relatively short% is usually associated "ith
mild to moderate stenosis! 'tenosis is li3ely to e more severe if the murmur dro"ns A4 #terminating after A4% <4=!
>ccasionally, the long, harsh '7M of pulmonary stenosis can e confused "ith the holosystolic murmur of a ventricular
septal defect! &his is more li3ely to occur "ith infundiular than valvular stenosis ecause of the lo"er location of the
murmur! Careful attention to the ehavior of '4 helps in the differential diagnosis, '4 is usually normal in .'1, "hile in
pulmonary stenosis it is "idely split and the intensity of P4 is decreased! Amyl nitrite inhalation is sometimes helpful5 it
usually decreases the intensity of the .'1 murmur ut not that of the pulmonary stenosis #"hich may e accentuated%!
Dilation of te aortic root or pulmonary artery Aortic root dilatation or dilatation of the pro+imal pulmonary artery
may e associated "ith a '7M! &he usual findings of idiopathic dilatation of the pulmonary artery are a pulmonary ejection
sound, a short ejection systolic murmur, a relatively "idely split '4 "ith normal intensity of P4, and occasionally a short
pulmonary insufficiency murmur! &here is no hemodynamic anormality! &he auscultatory findings are very similar in
pulmonary hypertension, e+cept '4 is narro"ly split "ith P4 mar3edly accentuated, the pulmonary ejection sound is
relatively late, and hemodynamic anormalities are al"ays evident!
Increased semilunar 'lood flo& A '7M also occurs in the presence of normal valves "hen flo" across the semilunar
valve is significantly increased, as in anemia, pregnancy, or thyroto+icosis #sho" tale 4%! *n patients "ith pure aortic
regurgitation, an ejection systolic murmur may occur due to mar3edly increased flo" and should not e considered evidence
for A' in the asence of other findings! Atrial septal defect is an e+ample of an ejection systolic murmur resulting from
increased flo" across the pulmonary valve! &hese murmurs do not indicate associated pulmonary stenosis!
Aortic )al)e sclerosis &he murmur of aortic sclerosis is also a midsystolic ejection murmur #sho" figure 4%! *t is enign,
since it is not associated "ith hemodynamic conse)uences, ut it must e considered in the differential diagnosis of A' in
elderly patients! &he murmur results from stiffening and degenerative firous thic3ening of the roots of the aortic cusps at
the site of their insertions! &hese morphologic changes do not cause any impairment of moility of the valve and thus no
ostruction!
&he murmur is usually est heard over the right second interspace! *n some patients, a musical high2fre)uency murmur of
rief duration can e heard along the lo"er left sternal order and cardiac ape+! *n general, the murmur is rief and not very
loud! A normal carotid pulse and normal '4 confirm the asence of A'! &he clinical significance of the diagnosis of aortic
sclerosis is that aortic sclerosis is a ris3 factor of long term adverse outcome due to atherosclerotic heart disease!
Innocent midsystolic murmurs *nnocent murmurs are typically ejection type and midsystolic in timing #sho" tale 4%
<6=! &he (innocence( of an '7M should not depend upon the duration or intensity of the murmur, ut on the asence of
other anormal findings! 7ven a short grade *?.* ejection systolic murmur may not e innocent if there are coe+isting
findings such as an anormal '4!
A short, virating murmur #'till@s murmur% can e heard over the mid precordium in children that is not accompanied y any
other anormality! *t is thought to arise from virations of the attachments of the pulmonary valve leaflets!
Another innocent '7M can e heard in children and young adults that has a lo"ing )uality and is est heard over the left
second interspace! *t is thought to originate from virations of the pulmonary trun3!
*n patients "ith the straight ac3 syndrome "ho have a decreased anteroposterior diameter of the chest, a superficial '7M is
heard over the left second interspace <8=! &he mechanism of the murmur remains unclear!
-O$OS#STO$IC .PANS#STO$IC/ MURMURS /olosystolic, or pansystolic, murmurs are usually regurgitant
murmurs and occur "hen lood flo"s from a chamer "hose pressure throughout systole is higher than pressure in the
chamer receiving the flo"! &here are three causes of holosystolic murmurs #sho" tale $%,
MR
&ricuspid regurgitation
.'1
&he timing and duration of holosystolic murmurs are est e+plained y the hemodynamic changes of MR! *n
hemodynamically significant MR, regurgitant flo" from the left ventricle to the left atrium egins "ith the onset of
isovolumic systole "hen pressure in the left ventricle just e+ceeds pressure in the left atrium! &his pressure crossover point
also mar3s '$, e+plaining the onset of the holosystolic murmur "ith '$! &hroughout systole and e+tending to the early part
of the isovolumic rela+ation phase, the left ventricular pressure remains higher than the left atrial pressure! &hus, the
regurgitant flo" continues throughout systole, and even after aortic valve closure, e+plaining the holosystolic character of
the regurgitant murmur! &his also e+plains "hy A4 is often dro"ned y the murmur over the cardiac ape+!
Mitral re!ur!itation &he holosystolic murmur of MR is high pitched and est heard "ith the diaphragm of the
stethoscope and the patient in the left lateral decuitus position! Radiation depends upon the murmur intensity, "hich may
e variale! &he direction of radiation follo"s the direction of the regurgitant jet into the left atrium!
;hen the jet is directed posterolaterally, the apical holosystolic murmur radiates to"ard the left a+illa, inferior angle of
the left scapula, and over the thoracic spine <A=! *n some patients, a loud murmur may radiate to the top of the head!
&he murmur radiates to"ard the ase and root of the nec3 if the regurgitant stream is directed anteromedially against the
interatrial septum near the ase of the aorta! &hus, it can e confused "ith the murmur of A' or ostructive /CM! &he
character of the carotid pulse and the ehavior of '4 provide important clues to the diagnosis!
&he asence of an '6 and cardiac enlargement suggest hemodynamically insignificant chronic MR! *n contrast, clinical
evidence of pulmonary hypertension #accentuated P4, right ventricular systolic hypertension% and right2sided heart failure
are almost al"ays associated "ith significant MR, provided no other cause of pulmonary hypertension coe+ists!
:eft ventricular function should e assessed y 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 "ith a decreased left ventricular ejection fraction, "hich can
result from long2standing, severe MR, or may indicate secondary MR due to dilated cardiomyopathy! #'ee (7+amination of
the precordial pulsation(%!
*n dilated cardiomyopathy, '6 and findings of pulmonary hypertension may e present "ithout significant MR! &hus, the
differentiation et"een primary and secondary mitral regurgitation cannot e made at the edside in the presence of
depressed left ventricular systolic function! #'ee (Clinical features of chronic mitral regurgitation(%!
Tricuspid re!ur!itation &he holosystolic murmur of tricuspid regurgitation is est heard "ith the diaphragm of the
stethoscope over the left second and third interspaces and along the left sternal order! &he location of ma+imum intensity
may e shifted to"ard the cardiac ape+ "hen the right ventricle is dilated and the murmur can e misdiagnosed as MR!
Radiation and respiratory changes in the intensity of the murmur are t"o important distinguishing features!
;ith tricuspid regurgitation, the murmur is heard along the right sternal order or over the epigastrium!
1uring 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! &he increase in intensity does not occur immediately "ith the onset of
inspiration, ut after one or t"o cardiac cycles! &he mechanism for the increase in intensity appears to e augmented
regurgitant flo" follo"ing the inspiratory increase in right ventricular volume! A right ventricular '6 gallop and a mid2
diastolic flo" murmur, "hich also increase in intensity "ith inspiration, suggest more severe tricuspid regurgitation!
Murmur intensity does not change in the presence of severe right ventricular failure "hen right ventricular volume may not
change apprecialy! ;ith severe right2sided heart failure, the murmur can e asent, or only an early systolic murmur may
e recogni0ed! *n these circumstances, the edside diagnosis of tricuspid regurgitation relies upon the presence of other
physical findings, such as a prominent v "ave in the jugular venous pulse and systolic hepatic pulsation!
&ricuspid regurgitation is most often secondary to pulmonary arterial hypertension! &hus, a prominent left parasternal
impulse and narro" splitting of '4 "ith an accentuated P4 suggest secondary tricuspid regurgitation! &heoretically, severe
tricuspid regurgitation may produce reversed splitting of '4 due to shortened right ventricular ejection time5 ho"ever, this is
a rare finding!
Primary tricuspid regurgitation is much less common ut can occur follo"ing acterial endocarditis #eg, "ith intravenous
drug ause% or in patients "ith 7stein@s anomaly, carcinoid heart disease, or prior right ventricular infarction! A
hyperdynamic left parasternal impulse and normal or only slightly accentuated P4 suggest primary tricuspid regurgitation,
ut its diagnosis primarily depends upon the elimination of pulmonary hypertension and left2sided disorders such as mitral
and aortic valve disease and cardiomyopathy! *n primary tricuspid regurgitation, the murmur may e early systolic rather
than holosystolic, and have a decrescendo shape! #'ee (Pathophysiology and clinical features of tricuspid regurgitation(%!
(entricular septal defect .'1s cause a holosystolic murmur if pressure in the right ventricle is lo"er than the left
ventricle throughout systole, resulting in a continuous left2to2right shunt <B,C=! &his hemodynamic profile is present in small
.'1s and is associated "ith normal pulmonary artery pressure and pulmonary vascular resistance! &hus, '4 is normal and
pulmonary hypertension is asent!
&he murmur is usually loud and may e accompanied y a thrill! &he left2to2right shunt is directed to"ard the right
ventricular cavity! &he murmur is ma+imal over the third and fourth interspaces along the sternal order "hen the .'1 is
elo" the crista supraventricularis! ;hen the defect is aove the crista, the shunt is directed to"ard the pulmonary trun35
the ma+imal intensity of the murmur may e in the left second interspace in this case, and it can e confused "ith the
murmur of pulmonary valve stenosis <4=!
Changes in '4 help in the differential diagnosis! A "ide splitting of '4 "ith reduced intensity of P4 is present in pulmonary
stenosis5 a normal '4 favors .'1!
&he character and timing of the systolic murmur change "ith large .'1s due to increased right ventricular and pulmonary
artery pressure and an elevated pulmonary vascular resistance! *nstead of eing holosystolic, it ecomes early systolic and
the pea3 of the murmur occurs earlier! &he physical findings of pulmonary arterial hypertension and right ventricular
hypertrophy are present!
;hen the shunt is reversed in 7isenmenger comple+, the murmur may e asent and an ejection systolic murmur due to
dilatation of the pulmonary trun3 appears! '4 is mar3edly accentuated and single <D=! Murmurs of tricuspid pulmonary
regurgitation may also e present!
&hus, a holosystolic murmur in a patient "ith a .'1 usually indicates favorale hemodynamics #eg, relatively normal right2
sided pressures%! #'ee (Pathophysiology and clinical features of ventricular septal defects(%!
EAR$# S#STO$IC MURMURS 7arly systolic murmurs egin "ith '$, do not e+tend to '4, and generally have a
decrescendo configuration! 7arly systolic murmurs may result from MR, tricuspid regurgitation, or .'1 #sho" tale $%!
Mitral re!ur!itation 7ither acute severe or mild chronic MR can e associated "ith an early systolic murmur! Acute
severe mitral regurgitation causes a rapid increase in left atrial pressure and a giant regurgitant "ave #v "ave% during the
latter part of ventricular systole! An e)uali0ation of left atrial and left ventricular pressure may occur, preventing the
regurgitant flo" during this part of systole! &hus, the regurgitant murmur terminates efore A4! 'ince the regurgitant flo" is
ma+imal at the eginning of systole and decreases "ith increasing left atrial pressure, a decrescendo configuration of this
early systolic murmur is common <E2$$=! Associated clinical findings include pulmonary hypertension, hyperdynamic apical
impulse, a late systolic left parasternal impulse, and atrial and ventricular gallops! #'ee (Pathophysiology and clinical
features of acute mitral regurgitation(%
*n some patients "ith mitral stenosis, an early systolic murmur is heard and proaly represents mild mitral regurgitation!
'econdary mitral regurgitation in dilated cardiomyopathy is usually mild and may e early systolic in timing! Mitral annular
calcification can e associated "ith an early systolic murmur and suggests trivial MR! *neffective reduction of the
circumference of the annulus at the eginning of systole, due to calcification, is proaly the underlying mechanism for
mild MR and the early systolic murmur <$F=!
Tricuspid re!ur!itation Primary tricuspid regurgitation "ith normal right ventricular systolic pressure, as seen "ith
infective endocarditis in drug addicts, may e associated "ith an early systolic murmur "ith a decrescendo configuration!
&he mechanism is similar to that in acute, severe MR! A rapid increase in right atrial pressure and an accentuated v "ave in
the later part of systole decreases the regurgitant flo"! &he fre)uency of these murmurs is usually lo"er than the murmurs
associated "ith an elevated right ventricular systolic pressure, presumaly due to a lo"er rate of regurgitation! *n addition to
a relatively normal '4, palpating and recording the left parasternal impulse may reveal a systolic in"ard movement and a
diastolic out"ard movement reflecting right ventricular volume changes!
(entricular septal defect *n a large .'1 "ith pulmonary hypertension, the murmur may e early systolic in timing,
since the increasing right ventricular pressure during late systole decreases the left2to2right shunt! Findings of pulmonary
hypertension are al"ays present! An early systolic murmur may also occur in some patients "ith a .'1 in the asence of
pulmonary hypertension or increased pulmonary vascular resistance5 these murmurs are more fre)uently locali0ed and of
shorter duration! &hey tend to occur "ith .'1s that later close spontaneously <$4=!
'mall muscular .'1s may also cause an early systolic murmur, since the defect closes soon after the onset of systole!
7vidence of pulmonary hypertension is asent!
$ATE S#STO$IC MURMURS A late systolic murmur starts after '$ and, if left2sided, e+tends to A4, usually in a
crescendo manner #sho" figure 6%!
Mitral )al)e prolapse Mitral valve prolapse is the most common cause of a late systolic murmur! *t is est heard "ith
the diaphragm of the stethoscope, over or just medial to the cardiac ape+! *t is usually preceded y single or multiple clic3s
<$6=! Mitral valve prolapse can occur from disorders of the mitral annulus, redundancy of the leaflets, anormalities of the
chordae, or contraction anormalities of the left ventricular "all! Mitral regurgitation occurs "hen prolapse is sufficient to
cause a lac3 of apposition of the leaflets! #'ee (1efinition and diagnosis of mitral valve prolapse(%!
&he most common etiology for mitral valve prolapse is redundancy of valve tissue "ith respect to the valve ring #(floppy(
valve or Barlo"@s syndrome%! &his disparity increases "ith a decreased left ventricular volume, "hich is associated "ith an
earlier onset of prolapse and, therefore, the late systolic murmur occupies a relatively greater portion of systole! 'tanding,
sitting, .alsalva@s maneuver #phase 4%, and amyl nitrite inhalation, all decrease left ventricular volume and cause an earlier
onset of the clic3s and murmurs, "hich also appear long #sho" tale A! &he intensity, ho"ever, ecomes softer! Conversely,
s)uatting, elevation of the legs, isometric e+ercise #hand grip%, and infusion of phenylephrine, "hich increases left
ventricular volume, delay the onset of the clic3s and murmurs, the intensity of "hich may increase! A ("hoop( or (hon3,(
"hich is a high2fre)uency, musical, loud, and "idely transmitted murmur, can appear intermittently in some patients "ith
mitral valve prolapse and may e precipitated y a change of posture!
*n general, mitral valve prolapse "ith a late systolic murmur is associated "ith mild mitral regurgitation and is not
accompanied y an '6 or signs of pulmonary hypertension! :eft ventricular function is normal!
*n patients "ith pseudohypertrophic muscular dystrophy, mitral valve prolapse and a late systolic murmur are
manifestations of cardiac involvement! &hese may or may not e associated "ith midsystolic clic3s! &he electrocardiogram
almost al"ays demonstrates a relatively tall R "ave in leads .$, and .4, simulating true posterior myocardial infarction!
&he mechanism of mitral valve prolapse and its electrocardiographic changes is firosis of the posterior left ventricular "all!
Tricuspid )al)e prolapse &ricuspid valve prolapse is uncommon in the asence of mitral valve prolapse! *t causes a late
systolic murmur that e+tends up to P4! *t is est heard over the left lo"er sternal order! >nset of the murmur may e
delayed during inspiration due to an increase in right ventricular volume!
Papillary muscle dysfunction A late systolic murmur may occur "ith mild mitral regurgitation due to papillary muscle
dysfunction in acute myocardial infarction! *t can also occur in patients "ith chronic coronary artery disease during an
episode of myocardial ischemia, presumaly due to ischemic papillary muscle dysfunction! *n these patients, isometric
e+ercise or maneuvers that increase ventricular volume may precipitate mitral regurgitation and a late systolic murmur
ecause of increased myocardial o+ygen re)uirements, "hich may induce myocardial ischemia! #'ee (Role of
echocardiography in acute myocardial infarction(%!
EAR$# DIASTO$IC MURMURS 7arly diastolic murmurs, most often due to aortic or pulmonary regurgitation,
typically start at the time of semilunar valve closure and their onset coincides "ith '4! An aortic regurgitation murmur
egins "ith A45 pulmonary regurgitation egins "ith P4!
Aortic re!ur!itation 1iscovery of a diastolic murmur is essential for the diagnosis of aortic regurgitation! *n a revie" of
the literature, the presence of an early diastolic murmur "as the most useful finding for estalishing the presence of aortic
regurgitation #positive li3elihood ratio D!D <ie, the odds of aortic regurgitation are increased D!D2fold=% and its asence the
most useful finding for eliminating the presence of aortic regurgitation #negative li3elihood ratio F!4 to F!6 <ie, the odds of
disease are reduced y a factor of F!4 to F!6=% <$8=! Among patients "ith end2stage renal disease, a transient murmur of
aortic regurgitation may e induced y the effects of volume overload5 thus, such patients should e ree+amined after
dialysis, "hen the e+cess fluid has een removed <$8=!
&he murmur of aortic regurgitation is est heard "ith the diaphragm of the stethoscope! :o"2intensity, high2pitched aortic
regurgitation murmurs may not e heard unless firm pressure is applied "ith the diaphragm of the stethoscope over the left
sternal order or over the right second interspace, "hile the patient sits and leans for"ard "ith the reath held in full
e+piration!
&he radiation of an aortic regurgitation murmur is to"ard the cardiac ape+ and the location of ma+imum intensity may vary
consideraly! *t can e est heard in some patients over the mid precordium, along the lo"er left sternal order, or even over
the cardiac ape+! Radiation of the murmur to the right sternal order is more common in aortic regurgitation caused y
aortic root or aortic cusp anomalies <$A=!
&he configuration of the aortic regurgitation murmur is usually decrescendo ecause the magnitude of regurgitation
progressively declines! &he murmur is high2fre)uency and has a (lo"ing( character! >ccasionally the murmur can e
musical in )uality #diastolic "hoop%5 this has een attriuted to a flail everted aortic cusp! &he ("hoop( can e mid, late, or
pansystolic <$B=!
&he duration of the murmur is variale ut usually terminates efore '$! &he duration of the murmur does not al"ays
correlate "ith the severity of aortic regurgitation, although mild aortic regurgitation is usually associated "ith a murmur of
rief duration! &he murmur may also e short "ith acute severe aortic regurgitation ecause of a rapid increase in left
ventricular diastolic pressure, "hich e)uali0es "ith aortic diastolic pressure soon after the onset of diastole! *f the aortic
pressure remains higher than left ventricular pressure throughout diastole, a pandiastolic murmur may e present, even "hen
the severity of aortic regurgitation is only moderate! Bedside evaluation of the severity of aortic regurgitation should e
primarily ased upon a determination of the hemodynamic conse)uences! #'ee (7+amination of the arterial pulse(%!
An Austin Flint murmur is usually associated "ith significant aortic regurgitation #see (Austin Flint murmur( elo"%! A
decreased intensity of '4 does not necessarily suggest significant aortic regurgitation5 ho"ever, reversed splitting of '4,
"hich in the asence of left undle ranch loc3 results from increased left ventricular for"ard stro3e volume, indirectly
suggests significant aortic regurgitation! Changes in the intensity of '$ should e noted, since a reduced intensity is usually
associated "ith an elevated left ventricular end2diastolic pressure, "hich is more li3ely to occur in severe aortic
regurgitation! Physical findings of pulmonary venous and arterial hypertension and right2sided heart failure indicate
hemodynamically significant aortic regurgitation! #'ee (Pathophysiology and clinical features of chronic aortic regurgitation
in adults(%!
Assessment of left ventricular function is important, particularly "ith respect to the timing of surgery! A hyperdynamic left
ventricular impulse is associated "ith a relatively normal ejection fraction! >n the other hand, a sustained impulse and '6
gallop may indicate a reduced ejection fraction5 further evaluation to assess left ventricular function is indicated in this
circumstance!
&he onset of heart failure can modify many of the physical findings that suggest significant aortic regurgitation! &he pulse
pressure that "as initially high may decrease, and the arterial diastolic pressure that "as lo" may increase! &he duration of
the regurgitant murmur may decrease as the left ventricular diastolic pressure increases!
&he hemodynamic conse)uences of acute, severe aortic regurgitation differ consideraly from those of chronic aortic
regurgitation, e+plaining the differences in physical findings! #'ee (Pathophysiology and clinical features of acute aortic
regurgitation in adults(%!
'udden severe volume overload in a nondilated left ventricle causes a rapid increase in diastolic pressure and often
e)uali0ation of left ventricular and aortic root pressures in mid2diastole! &hus, the regurgitant murmur can e of short
duration!
'$ is soft or asent due to a reduced intensity of the mitral component of '$ and premature closure of the mitral valve
<$C=!
&he P4 of '4 is fre)uently accentuated due to postcapillary pulmonary hypertension!
A mar3ed increase in left ventricular end2diastolic pressure may prevent effective left ventricular filling during left atrial
systole5 an atrial gallop may therefore e asent!
&he carotid pulse can appear small since left ventricular for"ard stro3e volume may not increase or may even decrease,
although the character remains normal!
&he pulse pressure may ecome narro" as the systemic vascular resistance either increases or remains normal and the
arterial diastolic pressure does not fall, if the for"ard stro3e volume declines concomitantly!
A lac3 of left ventricular dilation and hypertrophy is recogni0ed y the relatively normal position of the left ventricular
impulse!
$eft anterior descendin! artery stenosis 1iastolic murmurs similar to those of aortic regurgitation can e heard in
some patients "ith left anterior descending coronary artery stenosis #1oc3@s murmur%! <$D=! &he murmur is not "idespread
li3e that of aortic regurgitation and usually is est heard over the left second or third interspace, a little lateral to the left
sternal order! &he murmur may e long or short! *t is caused y turulent flo" across the coronary artery stenosis and
usually indicates moderately severe stenosis! Coronary artery ypass surgery aolishes the murmur!
Pulmonary re!ur!itation Pulmonary regurgitation is most fre)uently a result of pulmonary hypertension #-raham2
'teell murmur% in adults <$E=! &he murmur is high2pitched and (lo"ing!( *t egins "ith an accentuated P4 of '4 and can e
of variale duration! *t may occupy all of diastole if there is a pandiastolic gradient et"een the pulmonary artery and the
right ventricular diastolic pressure! &he murmur has a decrescendo configuration li3e that of aortic regurgitation5
differentiation is difficult if not impossile y auscultation alone! &he murmur may increase in intensity during inspiration
and can e more locali0ed! *t is est heard over the left second and third interspaces!
Pulmonary regurgitation is suspected "hen other findings of pulmonary hypertension are present and peripheral signs of
aortic regurgitation are asent! /o"ever, it can occur in the asence of pulmonary hypertension, as in patients "ith
idiopathic dilatation of the pulmonary artery, after pulmonary valvulotomy, "ith right2sided endocarditis, and "ith
congenital asence of the pulmonary valve! *n these conditions, the pulmonary artery diastolic pressure is normal or lo" and
there is a lo"er rate of regurgitant flo"5 the regurgitant murmur is of lo" to medium pitch! &he murmur usually egins after
rather than "ith P4! 1elayed onset of the murmur is related to the minimal pulmonary artery2right ventricular pressure
gradient at the time of pulmonary valve closure! Regurgitation increases as the right ventricular pressure declines rapidly
after pulmonary valve closure, increasing the pressure gradient! &he murmur does not e+tend to '$ ecause the relatively
lo" pulmonary artery pressure e)uilirates "ith that of right ventricular pressure at the latter part of diastole!
*n congenital asence of the pulmonary valve, P4 is asent and there is a silent interval et"een A4 and the onset of the
regurgitant murmur! A loud to2and2fro murmur may e heard in these patients!
MID0DIASTO$IC MURMURS Mid2diastolic murmurs result from turulent flo" across the atrioventricular valves
during the rapid filling phase ecause of mitral or tricuspid valve stenosis and an anormal pattern of flo" across these
valves!
Mitral stenosis &he mid2diastolic murmur of mitral stenosis has a rumling character and is est heard "ith the ell of
the stethoscope over the left ventricular impulse "ith the patient in the left lateral decuitus position! &he murmur originates
in the left ventricular cavity e+plaining its location of ma+imum intensity!
&he murmur is present oth in sinus rhythm and in atrial firillation! *t characteristically starts "ith an opening snap! *ts
duration, "hich correlates "ith the duration of the diastolic pressure gradient across the mitral valve, is a reasonaly good
guide to assess the severity of mitral stenosis <4F=! &he longer the duration of the murmur, the more severe is the mitral
stenosis, provided the diastolic interval is not too short #asence of tachycardia%! *f the murmur e+tends up to '$ during a
longer diastolic interval, it can e assumed that the pressure gradient is still present at end2diastole, "hich implies severe
mitral stenosis!
;hen the flo" across the mitral valve is mar3edly reduced, "hich may result from associated right2sided heart failure and
pulmonary hypertension, the murmur may e of very rief duration or even asent #so2called silent mitral stenosis%, even in
the presence of severe mitral stenosis! Conversely, "ith enhanced flo" across the valve, as in the high2output state of
pregnancy, the intensity and duration of the murmur increase even "ith less severe stenosis! *n these circumstances, one
cannot rely on the duration of the murmur to assess the severity of mitral stenosis5 other ancillary investigations, particularly
echocardiographic studies, are necessary! #'ee (Pathophysiology and clinical features of mitral stenosis(%!
Tricuspid stenosis &ricuspid stenosis may e associated "ith a mid2diastolic rumle that is est heard along the left
sternal order! &he most characteristic feature is the increase in intensity of the murmur "ith inspiration #Carvallo@s sign%
<4$=! &he mid2diastolic rumle may e associated "ith a tricuspid opening snap and "ide splitting of '$ due to delayed
closure of the tricuspid valve! Most patients "ith tricuspid stenosis are in atrial firillation and the murmur is mid2diastolic
"hen the transvalvular pressure gradient is ma+imum! *n sinus rhythm, the murmur may occur only in late diastole,
resulting from an increased flo" due to right atrial systole!
&ricuspid stenosis most fre)uently occurs in association "ith mitral stenosis! *solated tricuspid stenosis is uncommon5 "hen
suspected, carcinoid heart disease and right atrial my+oma should e investigated as possile etiologies! A prominent a
"ave and a relatively slo" y descent in the jugular venous pulse, presystolic hepatic pulsation, and the asence of a right
atrial gallop should strengthen the suspicion of tricuspid stenosis!
Atrial my+oma Atrial my+oma may cause ostruction of the atrioventricular valves and a mid2diastolic murmur! *n left
atrial my+oma, the auscultatory findings can e similar to those of mitral stenosis! &he murmur is fre)uently presystolic and
crescendo in configuration5 it appears to occur "ith the onset of ventricular systole "hen the tumor is moved to"ard the left
atrium through the mitral orifice, and "hen the flo" across the valve is still continuing!
*t is difficult to distinguish et"een a left atrial my+oma and mitral stenosis at the edside! /o"ever, the character and
intensity of the murmur due to an atrial my+oma may change "ith alterations of position <44=! 'inus rhythm, changing
intensity and character of the murmur, and a (tumor plop( sound favor the diagnosis of left atrial my+oma! 9evertheless,
echocardiographic evaluation is necessary and is al"ays recommended in a patient "ith suspected mitral stenosis!
Right atrial my+oma is far less common than left atrial my+oma! Auscultatory findings may e similar to those of tricuspid
stenosis! #'ee (Cardiac tumors(%!
Increased flo& across te atrio)entricular )al)e Mid2diastolic murmurs may occur in the presence of normal
atrioventricular valves "hen the flo" across the valve is mar3edly increased in mid2diastole #flo" murmurs%! *n pure severe
mitral regurgitation, a larger volume of lood #due to the regurgitant volume% moves from the left atrium to the left ventricle
during diastole5 the etiology is a partial closing movement of the mitral valve "hich occurs after it opens "idely at the
eginning of diastole! &he rapid flo" to the left ventricle continues, and thus (functional mitral stenosis( occurs, e+plaining
the mid2diastolic rumle! *n some patients a mid2diastolic pressure gradient has een demonstrated <4624A=!
*n a left2to2right shunt, antegrade lood flo" across the mitral valve increases during diastole, "hich may e associated "ith
a mid2diastolic murmur! &he mechanism may e similar to that seen in mitral regurgitation! ;hen the etiology is an atrial
septal defect or anomalous pulmonary venous drainage, a tricuspid flo" murmur can also e heard along the lo"er left
sternal order5 this is due to a partial closing movement of the tricuspid valve after its full opening in early diastole and
functional tricuspid stenosis at mid2diastole <4B=! &he intensity of the tricuspid flo" murmur tends to increase during
inspiration!
Austin *lint murmur An apical diastolic rumling murmur has een descried in patients "ith pure aortic regurgitation
<4C,4D=! 'everal mechanisms have een proposed to e+plain the genesis of this murmur, including fluttering of the mitral
valve from the impingement y the aortic regurgitant jet, relative #functional% mitral stenosis, and regurgitant jets directed
against the left ventricular free "all <4C24E=!
Mitral fluttering is not the mechanism of the Austin Flint murmur, since fluttering occurs in early diastole "ith the onset of
regurgitation, "hile the rumle occurs in mid or late diastole! A second proposed mechanism "as premature partial closing
movement of the mitral valve at mid2diastole due to the regurgitant flo", leading to functional mitral stenosis! /o"ever, use
of M2mode and t"o2dimensional echocardiography, color flo" 1oppler, and cine magnetic resonance imaging has sho"n
that the murmur arises from the regurgitant jets that are directed at the left ventricular free "all, not functional mitral
stenosis <4E=!
*f the Austin Flint murmur is not recogni0ed, a mista3en diagnosis of organic mitral stenosis can occur! &he 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 "ith decreased
left ventricular afterload! *n contrast, the murmur of mitral stenosis increases in intensity and duration "ith an increased
heart rate and increased antegrade flo" across the mitral valve!
Carey0Coom's murmur *n acute rheumatic fever, a mid2diastolic murmur over the left ventricular impulse, a Carey2
Cooms murmur, has een attriuted to acute mitral valvulitis! /o"ever, first2degree atrioventricular loc3 #prolonged PR
interval% is common in rheumatic carditis and an increased flo" due to earlier atrial systole coinciding "ith the rapid filling
phase may contriute to a Carey2Cooms murmur!
$ATE DIASTO$IC .PRES#STO$IC/ MURMURS Presystolic murmurs occur in late diastole and e+tend up to '$!
&hey usually have a crescendo configuration! &he murmurs result from increased flo" across the mitral or tricuspid valve
and are most fre)uently oserved in the presence of normal sinus rhythm! /o"ever, crescendo presystolic murmurs can
occur in the presence of atrial firillation in the asence of atrial systole5 mitral valve closure, resulting in a reduction of an
effective mitral orifice, egins efore the onset of isovolumic systole and '$ and during this period antegrade flo" across
the mitral valve continues <6F=!
Mitral stenosis Atrial contraction increases the pressure gradient and flo" at end2diastole "hen mitral stenosis is
present, generating the presystolic murmur! ;hen a mid2diastolic rumle accompanies a presystolic murmur, the intensity
of the mid2diastolic murmur fre)uently decreases efore the onset of the presystolic murmur! &he presence of only a
presystolic murmur associated "ith increased intensity of '$ suggests mild mitral stenosis!
Tricuspid stenosis *n tricuspid stenosis "ith sinus rhythm, the murmur is usually presystolic ecause the transvalvular
gradient is ma+imum during this period <4$=! &he intensity of the presystolic murmur of tricuspid stenosis also increases
during inspiration, "hich is associated "ith an increased venous return to the right atrium! *ncreased right atrial volume is
associated "ith more forceful right atrial contraction and, therefore, an increased pressure gradient during this interval and
accentuation of the murmur!
My+oma Presystolic murmurs may occur "ith left or right atrial my+omas! &his is due to ostruction of the
atrioventricular valves!
$eft0to0ri!t sunts Flo" murmurs due to a large left2to2right shunt are usually mid2diastolic in location! >ccasionally
they can e+tend to late diastole!
Complete eart 'loc1 *n complete atrioventricular loc3 "ith a slo" idioventricular rhythm, a short late diastolic
murmur can occasionally e heard and recorded #Rytand@s murmur%! &he precise mechanism of Rytand@s murmur has not
een elucidated5 diastolic mitral regurgitation has een postulated <6$,64=! 1iastolic mitral regurgitation appears to depend
upon the position of the P "ave and atrial systole in ventricular diastole! #'ee (&hird degree #complete% atrioventricular
loc3(%!
CONTINUOUS MURMURS Continuous murmurs are defined as murmurs that egin in systole and e+tend up to
diastole "ithout interruption! &hey do not necessarily need to occupy the total duration of systole and diastole! Continuous
murmurs result from lood flo" from a higher pressure chamer or vessel to a lo"er system associated "ith a persistent
pressure gradient et"een these areas during systole and diastole! &hese murmurs may occur due to aortopulmonary
connections, arteriovenous communication, and disturances in the flo" patterns in the arteries or veins #sho" figure 6 and
sho" tale 6% <6626B=!
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 oth systole and diastole5 lood flo" from the high pressure
descending thoracic aorta to the lo" pressure pulmonary artery causes the continuous murmur #-ison@s murmur or
machinery murmur%!
&he ma+imum intensity of the murmur usually occurs at '4! &he duration of the murmur depends upon the pressure
difference et"een aorta and pulmonary artery! ;ith pulmonary hypertension, pulmonary artery diastolic pressure
increases5 "hen it approaches systemic level, the diastolic portion of the continuous murmur ecomes shorter and ultimately
asent <6C=! ;ith more severe pulmonary hypertension, pulmonary artery systolic pressure can e)uali0e "ith aortic systolic
pressure and the systolic component of the murmur may also e asent #silent ductus%! 1ifferential cyanosis due to the
reversal of the shunt and signs of pulmonary hypertension "ith or "ithout evidence of right2sided heart failure are the only
physical findings that are recogni0ale at the edside in these circumstances!
Aortopulmonary &indo& Continuous murmurs may e present "ith an aortopulmonary "indo"! /o"ever, ecause of
the large si0e of the communication, pulmonary vascular resistance and pulmonary artery diastolic pressure tend to e
higher, "hich is associated "ith a shorter duration of the diastolic component of the continuous murmur!
Sunts A left2to2right shunt through a small atrial septal defect in the presence of mitral valve ostruction, 3no"n as
:utemacher@s syndrome, may occasionally cause a continuous murmur <6D=! &otal anomalous pulmonary venous drainage,
a small atrial septal defect "ithout mitral valve ostruction, and mitral stenosis "ith a persistent left superior vena cava are
very rare causes of continuous murmurs!
Arterio)enous fistulas Congenital or ac)uired arteriovenous fistulas also cause continuous murmurs!
Coronary artery venous fistulas may produce a continuous murmur5 the location, duration, and character of the murmur
depend upon the anatomical type of fistulas! As an e+ample, the right coronary and right atrial, or coronary sinus,
communication produces continuous murmurs that are usually located along the parasternal areas! &he murmur of a
circumfle+ coronary artery and coronary sinus communication are usually located in the left a+illa! &he configuration of the
murmur and the intensity of the systolic and diastolic components are variale! Mar3ed systolic compression of the
anormal vessels reduces the systolic flo"5 thus, the systolic component of the murmur may e very soft! >n the other hand,
an increased systolic gradient may result from the partial compression of the intramural communication, "hich "ill tend to
increase the intensity of the systolic portion of the murmur!
A communication et"een the sinus of .alsalva and the right atrium or right ventricle produces continuous murmurs that
may appear as to2and2fro murmurs due to the increased intensity of oth the systolic and diastolic components and a softer
intensity around '4!
'ystemic and pulmonary arteriovenous fistulas are also associated "ith continuous murmurs! Although a systemic
arteriovenous communication usually produces a loud murmur, the murmur of pulmonary arteriovenous fistulas are softer
and may e primarily systolic! &he major pressure gradient occurs in systole, and the diastolic gradient is usually very
small! Pulmonary arteriovenous fistulas usually involve the lo"er left or right middle loe5 the location of the murmurs is
also over these areas!
Oter Constriction in the systemic or pulmonary arteries can e associated "ith continuous murmurs due to a persistent
pressure gradient across the narro"ed segment of the vessel! *n coarctation of the aorta, a continuous murmur can e heard
in the ac3 overlying the area of constriction! Continuous murmurs may originate in large tortuous collateral arteries in
coarctation of the aorta, "hich are also heard in the ac3 over the interscapular regions! 'ometimes large, tortuous
intercostal vessels are visile "hen the shoulders are rotated medially and for"ard to separate the scapulas #'u0man@s sign%
<6E=! Pulmonary artery ranch stenosis and a partial occlusion of the pulmonary artery due to pulmonary emolism may also
cause continuous murmurs!
Rapid flo" 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
"ith ventricular septal defect% and loud continuous murmurs may e heard along the parasternal area!
&he (mammary souffle( associated "ith pregnancy may e systolic or continuous! &hese innocent murmurs are usually of
higher fre)uency #high pitched% and louder in systole!
A venous hum, "hich results from altered flo" in the veins, can also cause an innocent continuous murmur! &he venous
hum is heard "ith the patient in the sitting position #usually in the supraclavicular fossa% and fre)uently disappears "hen the
patient moves to the supine position! &he hum tends to e louder in diastole and can e completely aolished y
compression of the ipsilateral internal jugular vein! A loud, left2sided venous hum transmitted elo" the clavicle should not
e mista3en for the murmur of patent ductus arteriosus! .enous hum is not heard in the supine position, and pressure on the
internal jugular vein aolishes the venous hum! *n contrast, the murmur of patent ductus arteriosus persists in the supine
position and despite pressure on the internal jugular vein!
Gse of UpToDate is suject to the 'uscription and :icense Agreement!
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4E! :and0erg, H', Pflugfelder, P;, Cassidy, MM, et al! 7tiology of the Austin Flint murmur! H Am Coll Cardiol $EE45
4F,8FD!
6F! Criley, HM, /ermer, AH! Crescendo presystolic murmur of mitral stenosis "ith atrial firillation! 9 7ngl H Med $EC$5
4DA,$4D8!
6$! Rutishauser, ;, ;ir0, P, -ander, M, et al! Atriogenic diastolic influ+ in patients "ith atrioventricular heart loc3!
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66! Craige, 7, Mil"ard, 1K! 1iastolic and continuous murmurs! Prog Cardiovasc 1is $EC$5 $8,6D!
68! 9ell, C, Mounsey, P! Auscultation in patent ductus arteriosus "ith a description of t"o fistulae simulating patent
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6A! -asul, BM, Arcilia, RA, Fell, 7/, et al! Congenital coronary arteriovenous fistula! Pediatrics $EBF5 4A,A6$!
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