Heart Murmurs

By Eric Strong

Learning Objectives
To understand the basic physiology behind the generation of murmurs.
To be able to describe the specific characteristics of murmurs using
standardized terminology.
To be able to identify the most likely cardiac pathology based upon the
characteristics of a heart murmur.

Physiology of Murmurs

Murmurs are acoustical phenomenon produced

by turbulent blood flow. They can occur in a wide
variety of locations in the body and in a variety of dv
clinical settings. When a murmur occurs outside NR =
of the heart, for example in an abdominal aortic
aneurysm or narrowing of a carotid artery, this
sound is usually referred to as a bruit. Despite the
different names, murmurs and bruits represent density of the fluid
the same type of phenomenon. d diameter of the vessel
V velocity of flow
The chance that blood flow will be turbulent in viscosity of fluid
any given situation, and thus produce a murmur,
can be predicted from its Reynolds number (NR)1,
Figure 1: Mathematical definition of the
mathematically defined in Figure 1. Turbulence is Reynolds number.

1. In physics literature, Reynolds number is often denoted as Re.

more likely in situations with higher Reynolds numbers. Within the heart, the most important factors
determining the Reynolds number (and thus chance of a murmur), are the viscosity and velocity.
Additionally, when blood is squeezed through a pathologically narrowed structure, its velocity is
increased exponentially as the diameter is decreased linearly1. In other words, forcing blood through a
pathologically narrowed structure will result in an increased Reynolds number and higher likelihood of
producing a murmur. Figure 2 categorizes murmur etiologies based on the mechanism by which they
impact the Reynolds number. Additionally listed here, valvular regurgitation due to abnormal valve
morphology creates eddies in the flow of blood which cant be easily accounted for by Reynolds
number.

Mechanism Examples

Decreased blood viscosity Anemia

Valvular stenosis
Decreased diameter of vessel,
Coarctation of the aorta
valve, or orifice
Ventricular septal defect

Increased velocity of blood Hyperdynamic states

through normal structures (e.g. sepsis, hyperthyroidism)

Regurgitation across an incompetent valve Valvular regurgitation

Figure 2: Etiologies of heart murmurs listed by general physical mechanism.

Characteristics of Murmurs

Although the cardiac portion of a patients physical exam may often read something like systolic
murmur present, such a vague statement is of little diagnostic help. A systolic murmur could be due
something as benign as mild pregnancy-related anemia, or as something as dangerous as acute
tricuspid valve bacterial endocarditis. As a consequence, murmurs can and should be described based
on a number of specific characteristics. Thus systolic murmur present might be transformed into A
harsh, grade III, early peaking crescendo-decrescendo systolic murmur loudest at the right upper
sternal border and radiating to the carotids. Any experienced clinician hearing this second description
will immediately become concerned about severe aortic stenosis. Several extra words transform a
near-meaningless statement into something of important diagnostic value.

1. The relationship between velocity and diameter and/or radius is governed by the continuity equation, which in
its most simple form states: Cross Sectional Area1 x Velocity1 = Cross Sectional Area2 x Velocity2.
Timing

The timing of a murmur specifically refers to its timing relative to the cardiac cycle: Is the murmur
present in systole, diastole, or both? The timing is the single most important characteristic that will aid
in the diagnosis of an associated abnormality. The overwhelming majority of murmurs are present
only during systole (i.e. systolic murmurs). However, recognition of diastolic murmurs is important
because, while uncommon, they always represent significant pathology. Continuous murmurs have
components present during both systole and diastole, and this is the rarest form timing, generally
observed only in infancy in children with congenital heart disease, with the exception of a cervical
venous hum caused by turbulent flow in the internal jugular and/or subclavian veins, and which is
usually non-pathologic. Figure 3 lists common murmur etiologies by their timing.

Timing Examples

Flow murmurs
Aortic and pulmonic stenosis
Systolic Mitral and tricuspid regurgitation
Ventricular septal defect
Aortic outflow tract obstruction

Aortic and pulmonic regurgitation

Diastolic
Mitral and tricuspid stenosis

Continuous Patent ductus arteriosus

Cervical venous hum

Figure 3: Etiologies of common heart murmurs listed by timing.

There are two circumstances of which one should be aware when the identification of the timing of a
murmur can lead to an erroneous conclusion as to possible etiologies. First, in patients with mild to
modest, chronic aortic regurgitation, sometimes the classic diastolic component from regurgitating
blood will be inaudible while a systolic flow murmur will be present from excess blood ejected with
each contraction. Second, occasionally, a patient may have two related murmurs, one systolic and one
diastolic, which may give the impression of a continuous murmur; this is most commonly encountered
with concurrent aortic stenosis and aortic regurgitation.

Location

When the word location is used to describe a murmur, unless otherwise specified, it is referring to the
location on the chest wall where the murmur is the loudest or most easily heard. Traditionally, four
distinct and specific points on the chest wall were identified where murmurs caused by specific valves
would typically be the loudest. For example, murmurs caused by a problem with the aortic valve
would typically sound loudest at the 2nd right intercostal space just adjacent to the sternum. Thus, this
location was known as the aortic area. Unfortunately, as shown in Figure 4, the acoustical
localization of valve-based murmurs is not as neat and specific, particularly for aortic valve murmurs,
which can be heard basically anywhere in the chest. As a consequence, while a murmurs location is
helpful, it should never be used as the sole factor in determining the likely etiology.

Figure 4: Acoustical localization of murmurs separated by valve of origin.

Radiation

The radiation of a murmur describes a location where the murmur is audible, despite it not lying
directly over the heart. Murmurs generally radiate in the same direction as the turbulent blood is
flowing. For example, a murmur from aortic stenosis can radiate into the carotid arteries, a murmur
from tricuspid regurgitation can radiate to the anterior right thorax, and a murmur from mitral
regurgitation can radiate to the left axilla.

Shape

The shape of a murmur describes how its intensity changes from onset to completion. There are three
basic shapes heard: crescendo-decrescendo, decrescendo, and uniform (also called holosystolic, when
occurring during systole). In general, crescendo-decrescendo and uniform murmurs are heard during
systole, and decrescendo murmurs are heard during diastole. The shape of a murmur is generally
determined by the pattern of the pressure gradient driving the turbulent flow, with the loudest
segment occurring at the time of the greatest gradient (since this will be the moment of highest
velocity.) The following are some example of murmur shapes caused by common valvular pathologies.
 Aortic Stenosis (Crescendo-Decrescendo)
The timing of the peak of an AS murmur may be
related to the severity of the AS. An early peaking
murmur suggests mild AS, while a leak peaking
murmur suggests severe AS.
Mitral Regurgitation (Uniform, Holosystolic)
As discussed below under Pitch, higher pitched
MR murmurs suggest higher gradients. Lower
pitched murmurs, or those sounding more harsh,
suggest higher amounts of flow. (i.e. severe MR
creates moderately pitched, harsh murmurs which
may be hard to distinguish from AS.)
Figure 5: The shape of the murmur reflects the pattern of the pressure gradient during turbulent blood flow.
Aortic Regurgitation (Decrescendo)
In mild to moderate AR, there may be a very brief,
initial crescendo segment to the diastolic murmur
that corresponds to the dicrotic notch in arterial
pressure tracings.
Mitral Stenosis (Uniform or slight decrescendo
with presystolic accentuation).
Predictably, the presystolic accentuation is
usually (though not always) absent during atrial
fibrillation and flutter. This murmur is frequently
preceded by an opening snap from the mitral
valve in very early diastole.
Pitch

There are two factors which affect the pitch of a murmur. First, high pressure gradients (such as those
from mitral regurgitation and a ventricular septal defect) tend to produce high pitched murmurs.
Second, large volumes of blood flow across low pressure gradients (such as those from mitral stenosis)
tend to produce low pitched murmurs. In the situation where there exists both a high pressure
gradient and high flow (e.g. severe aortic stenosis), both high and low pitches are produced
simultaneously. The simultaneous production of sound across the acoustic spectrum produces a
subjectively unpleasant sounding murmur which is frequently termed harsh.

Intensity

The intensity of a murmur describes how loud the volume is. It depends upon many factors, including
the velocity of blood at the murmurs source, the acoustical properties of intervening tissue, the
hearing and experience of the examiner, the stethoscope used, and the presence of ambient noise. It
is usually graded on a largely subjective scale from I-VI.

I Barely audible
II Faint, but undoubtedly present
III Easily and immediately heard
IV Associated with a thrill (a palpable vibration over the involved heart valve)
V Can be heard with only the edge of the stethoscope touching the chest wall
VI Can be heard without a stethoscope at all (or alternatively, without the stethoscope
making any direct contact with the chest wall)

Quality
The quality of the murmur is the most Common Qualitative
Etiology
subjective and non-specific characteristic of Description(s)
murmurs, which attempts to capture the Mitral Regurgitation Blowing, musical
timbre of the murmur. With heart murmurs
(as with all sounds), the timbre is dependant Mitral Stenosis Rumbling
upon how many different base frequencies of Aortic Stenosis Harsh
sound are being generated, and the relative
amplitude of their various harmonics. Aortic Regurgitation Blowing
Historically, certain etiologies of murmurs Stills Murmur Musical, vibratory
have been associated with specific qualitative (a benign systolic
terms, although there may be little scientific murmur of childhood)
evidence supporting these characterizations.
PDA Machine-like

Figure 6: Common descriptive terms for select murmurs.

Response to Manuevers

Some murmurs will display characteristic changes in intensity and/or timing in response to physical
maneuvers, as a consequence of changes to a persons hemodynamics during the maneuvers.
Listening for these subtle changes during physical maneuvers is occasionally referred to as dynamic
auscultation. Increased intensity of a murmur during inspiration as compared to expiration identifies
right sided murmurs with very high sensitivity and specificty, particularly if auscultation is performed
with the patient in the seated or standing position, instead of supine. The subsequent table (Figure 7)
lists well-described auscultatory findings during specific diagnostic maneuvers.

Diagnostic Maneuver Resulting Hemodynamic Auscultatory Findings

Change(s)
Inspiration intrathoracic pressure Left sided murmurs instensity
pulmonary venous return to Right sided murmurs intensity
right side of heart and PVR
results in RV stroke volume.
pulmonary venous return to
left side of heart due to dilation
of the pulmonary vascular
system results in LV stroke
volume.
Expiration intrathoracic pressure Left sided murmurs intensity
pulmonary venous return to Right sided murmurs intensity
right side of heart and PVR
results in RV stroke volume.
pulmonary venous return to
left side of the heart results in
LV stroke volume.
Valsalva Manuever venous return HOCM and occasionally MVP
intensity
The patient attempts to LV volume
forcefully exhale against a closed All other systolic murmurs
glottis. Can be simulated by CO intensity
having the patient attempt to
blow open a fully depressed
syringe. (Should not be
continued for longer than 10
seconds due to risk of triggering
syncope.)
Isometric Handgrip venous return Murmurs from MR, AR, and a
VSD intensity
The patient squeezes two object sympathetic tone results in
such as a rolled towel or with HR and SVR Murmur from HOCM intensity
both hands. Examiner should
ensure patient does not Both of the above result in CO Murmur from AS is most
concurrently perform Valsalva commonly unchanged.
maneuver. In an unconscious
patient, this can be simulated by
transient arterial occlusion, in
which blood pressure cuffs are
applied to both upper arms and
inflated to 20-40mmHg above
SBP for 20 seconds.
Leg Elevation venous return Murmur from HOCM intensity
Both legs raised to 45 degrees LV volume Murmurs from AS and MR or
with patient in supine position. unchanged intensity
Mller Maneuver May venous return to both Murmur from HOCM or
With nares held closed, patient sides of the heart, but true unchanged intensity.
forcibly sucks on an incentive hemodynamic effects not well Other murmurs with
spirometer or air-filled syringe characterized. unpredictable responses.
for 10 seconds. Conceptually,
the oppositive of the Valsalva
maneuver.
Squatting to standing venous return Murmur from HOCM intensity
Patient abruptly assumes LV volume Murmur from AS or
standing position after 30 unchanged intensity.
seconds of squatting. SVR
Standing to squatting venous return Murmur from HOCM intensity
For patients unable to squat, the LV volume Murmur from AS or
examiner can passively bend the unchanged intensity
knees up towards the abdomen SVR
to mimic the maneuver. Murmur from AR intensity

Figure 7: Table of common physical maneuvers used in cardiac physical diagnosis. RV=right ventricle, LV=left ventricle,
PVR=pulmonary vascular resistance, CO=cardiac output, HOCM=hypertrophic obstructive cardiomyopathy, MVP=mitral
valve prolapse, SBP=systolic blood pressure, HR=heart rate, SVR=systemic vascular resistance, MR=mitral regurgitation,
AR=aortic regurgitation, VSD=ventricular septal defect, AS=aortic stenosis.

Terms to Avoid

Ejection Murmur A murmur produced by blood flowing forward through the aortic or
pulmonic valves during systole.
 Flow Murmur A murmur produced by blood flowing forward through a morphologically
normal valve, usually the consequence of blood flowing through the
aortic valve during hemodynamic states, or in the presence of anemia.

These terms are best avoided during description of the physical exam because there definitions imply
an etiology, while the reporting of the exam should be purely objective. In addition, they are
frequently used inappropriately by trainees.

Eponymous Murmurs

Description Eponym
A mid to late, apical, diastolic rumble heard in aortic regurgitation Austin Flint murmur
which can mimic mitral stenosis.
Situation when the highest frequency components of an aortic Gallavardin phenomenon
stenosis murmur radiate to the apex, mimicking mitral regurgitation.
A murmur of pulmonic regurgitation occuring in the setting of Graham Steell murmur
pulmonary hypertension.
A mid diastolic murmur heard at the apex during acute rheumatic Carrey Coombs murmur
fever.
A diastolic murmur heard in stenosis of the LAD. Docks murmur
Figure 8: Eponymous murmurs

Additional Reading
Constant, J. (1999). Bedside Cardiology. 5th ed. Lippincott, Williams, and Wilkins. ISBN: 0781721687.
Grewe K, Crawford MH. Differentiation of cardiac murmurs by dynamic auscultation. Curr Probl Cardiol. 1988;
13:669-721. PMID: 3069335.
Lembo NJ, et al. Bedside diagnosis of systolic murmurs. NEJM. 1988; 318:1572-8. PMID: 2897627.
McGee S. Etiology and diagnosis of systolic murmurs in adults. Am J Med. 2010; 123:913-21. PMID: 20920693.
Orient, J. (2009). Sapiras Art and Science of Bedside Diagnosis. 4th ed. Lippincott, Williams, and Wilkins. ISBN:
1605474118.

Copyright 2012 by Eric Strong

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