MEDICINE 2

APPROACH TO THE PATIENT WITH CARDIAC MURMURS

HEART MURMURS INTENSITY (I)

 Caused by audible vibrations that are due to:  Diminished by any process that increases the distance
 Increased turbulence from accelerated blood flow between the intracardiac source and the stethoscope on
through normal or abnormal orifices the chest wall, such as obesity, obstructive lung disease,
 Flow through a narrowed or irregular orifice into a and a large PE.
dilated vessel or chamber  Intensity of a murmur may also be misleadingly soft
 Backward flow through an incompetent valve, when cardiac output is significantly reduced.
ventricular septal defect, or patent ductus arteriosus.
Grading Description
DURATION Grade 1 Very soft and is heard with great effort
 Depends on the length of time in the cardiac cycle over Grade 2 Easily heard, but not particularly loud
which a pressure difference exists between two cardiac Grade 3 Loud, but is not accompanied by a
chambers, the left ventricle and the aorta, the right palpable thrill over the site of maximal
ventricle and the pulmonary artery, or the great vessels intensity. (Safest to report, since Grade 1
 Diastolic murmur of chronic aortic regurgitation (AR): a & 2 are very difficult to hear except if
blowing, high-frequency event. you’re really a good Cardiologist)
 Mitral stenosis (MS): indicative of the left atrial–left Grade 4 Very loud and accompanied by a thrill
ventricular diastolic pressure gradient; of low frequency Grade 5 Loud enough to be heard with only the
and heard as a rumbling sound with the bell of the edge of the stethoscope touching the
stethoscope chest
FREQUENCY Grade 6 Loud enough to be heard with the
stethoscope slightly off the chest
 Gallavardin effect/Sash phenomenon: A phenomenon
that is a low-frequency event, heard as a rumbling sound LOCATION AND RADIATION (L)
coarse systolic murmur of aortic stenosis (AS) may
sound higher-pitched and more acoustically pure at the
apex.
***To verify AS, listen for carotid murmur and not a
bruit***
 "HONKING"/Bruiting sound appreciated in some patients
with mitral regurgitation (MR) due to (MVP).
CONFIGURATION
 Configuration of a heart murmur may be:
1. Crescendo
2. Decrescendo (chronic AR)- due to progressive
decline of diastolic pressure gradient between aorta
and left ventricle
3. Crescendo-decrescendo (AS)- due to changes in
systolic pressure gradient between left ventricle and
aorta as ejection occurs
4. Plateau (chronic rheumatic MR)- consistent with a
large and nearly constant pressure difference
between left ventricle and left atrium

LECTURE RECORDING BOOK OLD TRANS EMPHASIZED

GROUP 7 | YOU CAN DO IT, DOC! 1
 SYSTOLIC MURMURS
 Begin with or after the first heart sound (S1) and
terminate at or before the component (A2 or P2) of the
second heart sound (S2) that corresponds to their side of
origin.
LEGEND:
1. Presystolic murmur of mitral or tricuspid stenosis.
CRESCENDO
2. Holosystolic (Pansystolic)/ SYSTOLIC murmur: MR,
TR, VSD. PLATEAU
3. Still in Systolic: Aortic ejection murmur beginning with
ejection click and fading before the S2. CRESCENDO-
DECRESCENDO
4. Systolic murmur in pulmonic stenosis
5. Aortic or pulmonary diastolic
murmur. DECRESCENDO
6. Long diastolic murmur of mitral stenosis following the
opening snap
7. Short mid-diastolic inflow murmur following a third
heart sound
8. Continuous murmur of patent ductus arteriosus
EARLY SYSTOLIC MURMURS
ACUTE SEVERE MR
 Configuration: Decrescendo systolic murmur
 Location: Medial apical impulse
 Reflect the progressive attenuation of the pressure
gradient between the left ventricle and left atrium during
systole owing to the rapid rise in left atrial pressure
caused by sudden volume load into an unprepared,
noncompliant chamber (Left Atrium)
LECTURE RECORDING BOOK OLD TRANS EMPHASIZED
GROUP 7 | YOU CAN DO IT, DOC!
 Clinical settings in which acute, severe MR occur:
1. Papillary muscle rupture complicating acute
myocardial infarction (MI)- often signaled by chest
pain, hypotension, and pulmonary edema
2. Rupture of chordae tendineae in the setting of
myxomatous mitral valve disease
3. Infective endocarditis- there is destruction of leaflet
tissue, chordal rupture, or both
4. Blunt chest wall trauma- usually self-evident but may
be disarmingly trivial
 A new heart murmur after an MI is an indication for
transthoracic echocardiogram (TTE)
 TTE is indicated in all cases of suspected acute,
severe MR
CONGENITAL, SMALL MUSCULAR VSD
 Chronic MR: heart already decompensates.
 Defect closes progressively during septal contraction,
and thus, the murmur is confined to early systole
 Location: left sterna border
 Intensity: grade 4 or 5
 Signs of pulmonary hypertension or left ventricular
volume overload are absent
 Suspicion of a VSD is an indication for TTE
TRICUSPID REGURGITATION
 Present in IE (Infective endocarditis)
 Intensity: murmur is soft (grade 1 or 2)
 Location: lower left sterna border
 May increase in intensity with inspiration (Carvallo’s sign)
2
 MID SYSTOLIC MURMURS
 Short interval following S1, end before S2.
 Configuration: Crescendo-decrescendo usually
AORTIC STENOSIS
 Most common cause of mid-systolic murmur in an adult
 Location: Right of the sternum in the second intercostal
space, radiates into the carotids
 Transmission to the apex, where it becomes higher-
pitched (Gallavardin effect)
 AS murmur vs. MR murmur
 AS murmur: increase in intensity in the beat after a
premature beat
 MR murmur: have constant intensity form beat to
beat
 Intensity varies directly with cardiac output
 Severe AS: normal cardiac output, systolic thrill, and a
gradae 4 or higher murmur
 parvus et tardus – is a small and delayed upstroke
consistent with severe AS
 ECG: shows signs of left ventricular hypertrophy
 TTE is indicated
OBSTRUCTIVE FORM OF HYPERTROPHIC
CARDIOMYOPATHY (HOCM)
 Location: left sterna border or between the left sternal
border and apex
 Murmur is produced by both dynamic left ventricular
outflow tract obstruction and MR
 Configuration: hybrid between ejection and regurgitant
phenomena
 Intensity: vary from beat to beat, but usually does not
exceed grade 3
 Murmur classically increase in intensity with maneuvers
that increase degree of outflow tract obstruction, such as:
 In preload or afterload – valsalva, standing,
vasodilators
 in augmentation of contractility – inotropic stimulation
 Maneuvers that decrease the intensity of the murmur:
 Increase preload- squatting, passive leg raising,
volume administration
 Increase afterload – squatting, vasopressors
 Reduce contractility – β-blockers
 ECG: left ventricular hypertrophy
 Confirmation by TTE
 HOCM vs MVP
 HOCM: Presence of LVH
 MVP: Presence of non-ejection click
CONGENITAL PULMONIC STENOSIS
 Configuration: crescendo-decrescendo murmur
 Location: 2nd and 3rd left ICS
ATRIAL SEPTAL DEFECT
 Left-to-right intracardiac shunting.
 Leads to an increase in pulmonary blood flow
 Intensity: grade 2-3 mid-systolic murmur
 L: Middle to upper left sterna border
 Ostium secundum ASDs – most common cause of these
shunts in adults
PHYSIOLOGIC STATES
 Pregnancy, hyperthyroidism, or anemia
 Associated with accelerated blood flow.
STILL’S MURMUR
 Benign grade 2
 Vibratory or musical mid-systolic murmur at the lower left
sternal border in normal children and adolescents
 Best heard in the supine position
LATE SYSTOLIC MURMURS
MITRAL VALVE PROLAPSE
 L: left ventricular apex
 Often introduced by one or more nonejection clicks
 Incompetent valve (systolic)
 Flail – movement made by an unsupported portion of the
leaflet after loss of its chordal attachment(s)
 Posterior leaflet prolapse or flail: jet or MR is directed
anteriorly and medially; as a result, radiates to the
base of the heart and masquerades as AS.
 Anterior leaflet prolapse or flail: results in a
posteriorly directed MR jet that radiates to the axilla
or left infrascapular region.
 Leaflet flail- grade 3 or 4; heard throughout precordium
of thin-chested patients

LECTURE RECORDING BOOK OLD TRANS EMPHASIZED

GROUP 7 | YOU CAN DO IT, DOC! 3
 Bedside maneuvers that ↓ left ventricular preload:  Small, restrictive VSDs – exemplified by Maladie de
 Standing: Cause the click and murmur of MVP to Roger (very loud murmur due to the significant and
move closer to the first heart sound, as leaflet sustained systolic pressure gradient between the left and
prolapse occurs earlier in systole; murmur becomes right ventricles)
louder and longer
 Squatting: Left ventricular preload and afterload are
increased abruptly, leading to an increase in left
ventricular volume, and the click and murmur move
away from the first heart sound as leaflet prolapse is
delayed; the murmur becomes softer and shorter in
duration
 TTE is recommended for late systolic murmurs
HOLOSYSTOLIC MURMURS
 Begin with S1 and continue through systole to S2
 Usually indicative of Chronic mitral/ tricuspid valve
regurgitation or VSD
CHRONIC MITRAL REGURGITATION
 L: At left ventricular apex and radiates to the axilla
 C: High-pitched and plateau (d/t the wide difference
between left ventricular and left atrial pressure
throughout systole)
 Acute MR vs chronic MR:
 Acute MR: ↓ left atrial compliance
 Chronic MR: normal or ↑ left atrial compliance DIASTOLIC MURMURS
 “MR begets MR”: Because the mitral annulus is  Begin with or after the associated component of S2 and
contiguous with the left atrial endocardium, gradual end at or before the subsequent S1.
enlargement of the left atrium from chronic MR will result
in further stretching of the annulus and more MR
 Chronic and severe MR: enlargement and leftward
displacement of the left ventricular apex beat
TRICUSPID REGURGITATION
 Generally softer and MR
 L: Left lower sterna border
 Increases in intensity with inspiration (Carvallo's sign)
 Causes of primary TR:
 Myxomatous disease (prolapse)
 Endocarditis
 RHD
 Radiation
 Carcinoid
 Ebstein’s anomaly
 Chordal detachment as a complication of right
ventricular endomyocardial biopsy
 More commonly a passive process from annular
enlargement due to right ventricular dilatation in the face
of volume or pressure overload
VENTRICULAR SEPTAL DEFECT (VSD)
 L: Mid- to lowerleft sternal border and radiates widely
 A thrill is present at PMI in the majority of patients
 Large defects – ventricular pressures tend to equalize,
shunt flow is balanced, and a murmur is not appreciated

LECTURE RECORDING BOOK OLD TRANS EMPHASIZED

GROUP 7 | YOU CAN DO IT, DOC! 4
 CHRONIC ATRIAL REGURGITATION
 High-pitched, blowing, decrescendo, early to mid-
diastolic murmur that begins following the aortic
component of S2 (A2) and is best heard at the second
right interspace.
 Soft and difficult to hear unless auscultation is performed
with the patient leaning forward at end of expiration (this
maneuver brings the aortic root closer to the anterior
chest wall)
 Austin Flint murmur – a lower-pitched mid to late, grade 1
or 2 diastolic murmur at the apex produced by chronic,
severe AR
 Thought to reflect turbulence at the mitral inflow area
from the admixture of regurgitant (aortic) and forward
(mitral) blood flow
 Distinguished from that due to MS by the absence of
an opening snap and the response of the murmur to
a vasodilator challenge
 With amyl nitrate (afterload lowering agent): AF
murmur will become shorter and softer
 Accompanied by several peripheral signs of significant
diastolic run-off:
 Wide pulse pressure
 “Water-hammer” carotid upstroke (Corrigan’s pulse)
 Quincke’s pulsations of the nail beds
 Acute, severe AR
 Shorter, lower pitched
 Peripheral signs of significant diastolic run-off are not
present
PULMONIC REGURGITATION
 Results in a decrescendo, early to mid-diastolic
murmur (Graham Steele murmur)
 Begins after the pulmonic component of S2 (P2) is
best heard at the second left interspace, and radiates
along the left sternal border
 Intensity increases with respiration
 Most commonly due to dilation of the valve annulus
from chronic elevation of the pulmonary artery
pressure
 AR vs PR
 AR: presence of pulmonary hypertension, right
ventricular lift
 TTE is indicated for an early to mid-diastolic murmur
MID DIASTOLIC MURMURS
 From obstruction and/or augmented flow at the level of
the mitral or tricuspid valve
MITRAL STENOSIS
 Rheumatic fever – most common cause of MS
 S1 is loud and the murmur begins after an opening snap,
mid diastolic rumble.
 Murmur of MS is low-pitched (best heard using the bell)
LECTURE RECORDING BOOK OLD TRANS EMPHASIZED
GROUP 7 | YOU CAN DO IT, DOC!
 An increase in the intensity of the murmur just before S1,
a phenomenon known as presystolic accentuation,
occurs in patients in sinus rhythm and is due to a late
increase in transmitral flow with atrial contraction. It does
not occur in patients with atrial fibrillation.
 L: Left ventricular apex and often is appreciated only
when the patient is turned in the left lateral decubitus
position
 I : Grade 1 or 2
TRICUSPID STENOSIS (TS)
 L: lower left sternal border
 Increases in intensity with inspiration
 Very difficult to hear
LARGE LEFT ATRIAL MYXOMAS
 May prolapse across the mitral valve and cause variable
degrees of obstruction to left ventricular inflow
 An opening snap is not present, and there is no
presystolic accentuation
CAREY COOMBS MURMUR
 A short, mid-diastolic murmur is rarely heard during an
episode of Acute Rheumatic Fever
 Probably due to flow through an edematous mitral valve
 TTE is indicated for evaluation of a patient with a mid- to
late diastolic murmur
CONTINUOUS MURMURS
 Not confined to either phase of the cardiac cycle, but
rather begin in early systole and proceed through S2 into
all or part of diastole
 Their presence throughout the cardiac cycle implies a
pressure gradient between two chambers or vessels
during both systole and diastole
PATENT DUCTUS ARTERIOSUS
 Best heard at the upper left sternal border
 Large, uncorrected shunts may lead to pulmonary
hypertension, attenuation or obliteration of the diastolic
component of the murmur, reversal of shunt flow, and
differential cyanosis of the lower extremities
5
 RUPTURED SINUS OF VALSALVA ANEURYSM
(RSOV)
 More common
 Abrupt onset at the upper right sternal border
 Rupture typically occurs into a right heart chamber, and
the murmur is indicative of a continuous pressure
difference between the aorta and either the right ventricle
or the right atrium.
CORONARY ARTERIOVENOUS FISTULA
 At the site of an arteriovenous fistula used for
hemodialysis access
HIGH-GRADE CAROTID ARTERY STENOSIS
 A cervical bruit with both systolic and diastolic
components (to-fro murmur)
NON-PATHOLOGIC CONTINUOUS MURMURS
 Continuous venous hum can be heard in healthy children
and young adults, especially during pregnancy; it is best
appreciated in the right supraclavicular fossa and can be
obliterated by pressure over the right internal jugular vein
or by having the patient turn his or her head toward the
examiner
 Continuous mammary souffle of pregnancy is created by
enhanced arterial flow through engorged breasts and
usually appears during the late third trimester or early
puerperium
INTERVENTIONS USED TO ALTER THE INTENSITY
OF CARDIAC MURMURS
RESPIRATION
 Right-sided murmurs generally increase with inspiration.
(TR or PR murmurs)
 Left-sided murmurs usually are louder during expiration.
Intensity either remains constant or decreases with
inspiration. (murmur of AR)
VALSALVA MANEUVER
 Most murmurs decrease in length and intensity. Two
exceptions: are the systolic murmur of HOCM and MVP,
which usually becomes much louder and longer
 After release of the Valsalva maneuver, right-sided
murmurs tend to return to baseline intensity earlier than
left-sided murmurs.
EXERCISE
 Murmurs caused by blood flow across normal or
obstructed valves (e.g., PS and MS) become louder with
both isotonic and isometric (handgrip) exercise
 Murmurs of MR, VSD, and AR also increase with
handgrip exercise
POSITIONAL CHANGES
 With standing, most murmurs diminish; two exceptions
being the murmur of HOCM, which becomes louder, and
that of MVP, which lengthens and often is intensified.
LECTURE RECORDING BOOK OLD TRANS EMPHASIZED
GROUP 7 | YOU CAN DO IT, DOC!
 With squatting, most murmurs become louder, but those
of HCM and MVP usually soften and may disappear.
Passive leg raising usually produces the same results as
squatting.
POSTVENTRICULAR PREMATURE BEAT OR
ATRIAL FIBRILLATION
 Murmurs originating at normal or stenotic semilunar
valves increase in intensity during the cardiac cycle after
a VPB or in the beat after a long cycle length in AF.
 By contrast, systolic murmurs due to atrioventricular
valve regurgitation do not change, diminish (papillary
muscle dysfunction), or become shorter after a
premature beat (MVP).
TRANSIENT ARTERIAL OCCLUSION
 Transient external compression of both brachial arteries
by bilateral cuff inflation to 20 mm Hg greater than peak
systolic pressure augments the murmurs of MR, VSD, and
AR, but not murmurs due to other causes.
 Hemodynamic studies/Catheterization/Angiography is
done if you are suspecting of right to left shunt,
congenital heart disease.
 Cut off for catheterization: 35 years old
 Contraindication for preparation of TOF if there are
already pulmonary collaterals (body can adjust to
hypoxemic states) therefore an indication that the patient
is inoperable.
PHARMACOLOGICAL INTERVENTIONS
 During the initial relative hypotension after amyl nitrite
inhalation, murmurs of MR, VSD, and AR decrease in
intensity, whereas the murmur of AS increases in
intensity because of increased stroke volume.
 During the later tachycardia phase, murmurs of MS and
right-sided lesions also become louder. This intervention
may help distinguish the murmur of the Austin-Flint
phenomenon from that of MS. The response in MVP
often is biphasic (softer and then louder than control).
ADDITIONAL INFO
 There are some physiologic murmur in systolic murmur;
example is low grade murmur of anemia, pregnancy,
hyperthyroidism etc. (murmur of secondary problem) that
indicates echocardiography.
 Hemodynamic studies/ Catheterization/ Angiography is
done if you are suspecting of right to left shunt,
congenital heart disease.
 Cut off for catheterization: 35 years old
 Contraindication for preparation of TOF if there are
already pulmonary collaterals (body can adjust to
hypoxemic states) therefore an indication that the patient
is inoperable.
REFERENCES
 MD2021 Transcription
 Harrison’s Principles of Internal Medicine, 20th ed.
6
 PRETEST QUESTIONS
 Based on your physical exam, how can you tell if the patient has systolic murmur?
 What is 6/6 Grade murmur?
 Example of systolic murmur
 Example of diastolic murmur
 What is a Carvallo’s sign?

LECTURE RECORDING BOOK OLD TRANS EMPHASIZED

GROUP 7 | YOU CAN DO IT, DOC! 7