The Cardiac Physical Exam- Auscultation
There is no more important component to cardiac diagnosis than the cardiac physical
exam. A good exam requires only 4 items- your eyes, your hands, a stethoscope, and
knowledge of what is normal and abnormal. The following is a summary of possible
ausculatory findings on the cardiac physical exam. It is not intended to be exhaustive or
complete. Rather, its purpose is to provide a basic framework for the provider when
performing a cardiac physical exam. Throughout this paper, we will refer to the
Wigger’s diagram displayed in Figure 1, which is perhaps the most important diagram in
cardiology as it represents the physiology of what we see and hear in cardiology.
Figure 1
S1
S1 is the first and most basic finding of the cardiac physical exam, signifying the end of
diastole and onset of systole. The sound is created by the summation of the closure of the
tricuspid (TV) and mitral (MV) valves when ventricular pressure rises above atrial
pressure. See point “b” on the Figure 1.
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S1 is best heard at the left lower sternal border (LLSB) and apex using the diaphragm of
the stethoscope. S1 may be heard to “split” occasionally- this is usually a normal finding.
In those instances when splitting is appreciated, it is a result of the tricuspid valve closing
shortly after the mitral valve. Splitting of S1 can be easily appreciated in right bundle
branch block. Of note, when “splitting” of S1 is heard at the base of the heart, you
should suspect that you are actually hearing an S1 and then an ejection click, rather
than a split S1.
Abnormalities of S1
S1 is made louder by:
1) Short PR interval or tachycardia- this occurs due to the distance between the
valve leaflets at the onset of systole. The further the leaflets are from each
other before they are “slammed shut” by the rise in ventricular pressure, the
louder the sound. With a short PR or in tachycardia, the onset of systole
occurs immediately after the leaflets have been maximally opened by atrial
systole, thus the S1 is loud. It is analogous to slamming a door shut when it is
wide open compared to slamming it when it is mostly closed (as in a normal
PR interval).
2) Mitral stenosis- calcified or thickened valve leaflets create a louder sound
when they move against each other compared to pliable, noncalcified leaflets.
Listen carefully for other evidence of mitral stenosis when you hear an
unusually loud S1.
3) Hypertension- elevated systemic blood pressure leads to elevated ventricular
pressure (especially LV Pressure). Higher ventricular pressure leads to
greater force with which the atrioventricular valves are closed. This then
generates a louder sound.
S1 is made softer by:
1) Long PR interval- this mechanism is basically the opposite of the effect of a
short PR. When ventricular systole is delayed after atrial systole, the valve
leaflets have already moved closer to each other at the time when they forced
to closure. The effect is a softer sound.
2) Aortic insufficiency- in patients with significant AI, the volume of blood
returning to the ventricle during diastole raises LV pressure during diastole.
The elevated pressure partially closes the mitral valve even prior to ventricular
systole. The effect is a softer S1.
3) Insulation of the heart- air in COPD, fluid in pericardial effusions, and fat in
obesity all serve to diminish sound propagation, thus limiting the listener’s
ability to hear S1 (or many other heart sounds).
4) Mitral regurgitation- when the valve fails to fully close due an intrinsic defect,
S1 may be softer.
5) Low cardiac output or low EF- in cases of severe systolic dysfunction, the LV
cannot generate a sufficient force rapidly enough to create a “crisp” S1. The
effect is a soft S1.
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S2
S2 is the second, basic sound of the cardiac cycle and signifies the end of systole and
onset of diastole. S2 is created by the closure of the aortic and pulmonic valves and is
best heard at the left or right upper sternal borders with the diaphragm of the stethoscope.
See point “e” on the Figure 1.
It is important for any auscultator to understand the different forms of splitting of S2:
Normal- normally the aortic component of S2 (S2a) closes prior to the pulmonic
component of S2 (S2p). During expiration, S2a and S2p are so closely timed, no
splitting can be appreciated. However, when one inspires, the RV takes longer to eject
due to a decrease in the pulmonary artery pressure and an increase in RV preload due to
enhanced venous return. Thus, S2p moves away from S2a and one appreciates a splitting
of the sound. [WINE- widens inspiration, narrows expiration]
Expiration
S1
Inspiration
S2a&p
S1
S2a
S2p
Persistent splitting or Widely split- When the RV ejection is delayed
abnormally, splitting can be heard in expiration and inspiration. Delays in RV ejection
result from right bundle branch block, pulmonary embolism, pulmonary hypertension,
and pulmonic stenosis. In addition, persistent splitting can be heard when the LV
ejection is shortened due to a second low pressure outlet for LV ejection- most
commonly, this would result from severe mitral regurgitation or a ventricular septal
defect. Of note, when this type of splitting occurs, S2p still varies with respiration, but
the S2a and S2p never “come together”.
Expiration
S1
S2a
Inspiration
S2p
S1
S2a
S2p
Paradoxical- When the LV ejection is delayed, S2a occurs after S2p. Thus,
inspiration moves S2p closer to S2a. The result is splitting during expiration which goes
away with inspiration, hence “paradoxical”. The main causes include LBBB, paced
ventricular rhythm, severe AS, severe systolic dysfunction.
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Expiration
S1
S2p
Inspiration
S2a
S1
S2p&a
Fixed splitting- in patients with an atrial septal defect, changes in respiration
may not change RV preload. However, due to the left-to-right shunt, RV preload is
always greater than LV preload, and hence RV systole is prolonged but never changes
with inspiration or expiration. Hence, S2 splitting is audible and fixed.
Expiration
S1
S2a
Inspiration
S2p
S1
S2a
S2p
Abnormalities of S2
S2 is made louder by:
1) S2a: systemic hypertension- the pressure closing the valve is higher
2) S2p: pulmonary hypertension- same as above
S2 is made softer by:
1) S2a: aortic stenosis and systemic hypotension
2) S2p: pulmonic stenosis
Sounds in Diastole
Early: (occurring near point “f” in figure 1)
1) S3- a low pitched sound occurring 0.1-0.2 seconds after S2. It is best
heard with the bell of the stethoscope with the patient in the left lateral
decubitus position. S3 has numerous causes which can be divided
into 3 separate states:
a. Normal/athletic hearts- S3 occur in normal healthy individuals
under the age of 40. A “normal” S3 is easily heard when a
young patient is hyperdynamic- pregnancy, anemia, postexercise, or thyrotoxic.
b. Diastolic overload states- when a large amount of blood moves
from the atrium into the ventricle during early diastole, an S3
may be heard. Examples include severe mitral regurgitation
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and lesions leading to L-R shunting with RV volume overload
such as a ventricular septal defect or a patent ductus arteriosis.
c. LV dysfunction- classically an S3 signifies global systolic
dysfunction and usually an elevated BNP.
2) Opening Snap (OS) - the classic sound of mitral stenosis. It
typically is associated with a loud S1 (see above) and is created by the
opening of the calcified mitral cusps early in diastole. The timing of the
OS can be a clue as to the severity of the stenosis: the earlier the OS (the
shorter the S2-OS interval), the worse the stenosis. OS is usually heard
best between the apex and the left sternal border with the patient in the left
lateral decubitus position. It is higher pitched than an S3 and can be heard
with the diaphragm or bell.
3) Tumor Plop- this early diastolic sound is created by the movement
of a myxoma through the mitral valve. It is usually low pitched and heard
best with the bell of the stethoscope.
4) Pericardial Knock- in patients with constrictive pericarditis, the
initial movement of blood from the atrium into the ventricle in early
diastole causes the ventricular walls to suddenly abut the stiff pericardium.
The result is a medium-pitched sound which mimics an S3 or an opening
snap. This sound is best heard with the diaphragm of the stethoscope at
the apex with the patient in the left lateral decubitus position.
5) Intraaortic Balloon Pump Sound- patients who have had an
intraaortic balloon pump inserted will have a early diastolic sound created
by the inflation of the balloon pump after closure of the aortic valve.
Late: (occurring near point “a” in figure 1)
1) S4- a low-pitched sound which follows atrial systole by 0.1-0.2s. The
sound is created by the sudden movement of blood into a ventricle
with a higher than normal diastolic pressures. The sudden, further
increase in pressure created by the new influx of blood causes
stiffening of the ventricle and tensing of the mitral apparatus, which
then generates sound. An S4 is best heard with the bell of the
stethoscope at the apex with the patient in the left lateral decubitus
position. Causes of S4 include:
a) Aging- as patients age, it is normal to lose some of the
compliance of the left ventricle. Thus, many elderly patients
have an S4.
b) Ventricular hypertrophy- an increase in wall thickness leads to
elevated intraventricular pressure as per LaPlace’s Law (wall
tension= pressure x radius / wall thickness). Thus, any cause
of LVH can lead to an S4:
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i. HCM
ii. Systemic hypertension
iii. Aortic stenosis
iv. Athletic heart (controversial)
c) Ischemic heart disease- both chronic and acute ischemic
disease lead to stiffening of the ventricle and increased
intraventricular pressures.
2) Split S1- in some normal patients, splitting of S1 can be appreciated.
The timing of the split may mimic an S4-S1; however, the components of
S1 are higher pitched and heard best with the diaphragm of the
stethoscope at the lower left sternal border.
Sounds in Systole
1) Ejection click/sound (occurring near point “c” in figure 1) - this
high pitched sound occurring soon after S1 and is heard best at the right or left
upper sternal border. The interval between S1 and the ejection sound is
essentially the time of isovolumic contraction. The ejection sound is a result
of one of two possible etiologies:
a. Valvular- an abnormal aortic or pulmonic valve can abruptly “dome”
in early systole leading to an ejection sound. In adults, this
abnormality is usually a bicuspid aortic valve.
b. Arterial- the root of the aorta or pulmonary artery can abruptly tense
in some patients leading to an ejection sound.
2) Mitral Valve Prolapse (occurring near “d” in figure 1) - a
redundant mitral valve leaflet may tense in mid or late systole leading to a
high-pitched snapping sound, termed a “click”. This sound is best heard at
the lower left sternal border and apex. Any maneuver which decreases LV
preload, such as the Valsalva, will move the click closer to S1. On the other
hand, any maneuver which increases preload will move the click away from
S1.
Murmurs
In general, murmurs can be characterized by 8 different qualities:
1) Timing (systole, diastole, continuous)
2) Intensity or grade
I- heard with concentration only
II- soft, but easily heard during auscultation
III- moderate intensity
IV- loud with a palpable thrill
V- loud with the rim of the stethoscope barely on chest
VI- loud with stethoscope off of the chest
3) Frequency (high, low)
4) Configuration (flat, crescendo-decrescendo, decrescendo, crescendo, holosystolic)
5) Quality (harsh, blowing, musical, rumble)
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6) Duration (short, pansystolic)
7) Radiation (neck, axilla, back)
8) Maneuvers
In this review, we will classify murmurs by timing and then discuss the murmurs heard
best during those timing periods. The grade or intensity of each individual murmur
depends upon the disease severity and thus will not be discussed further.
1) Systolic
a. Aortic stenosis- the murmur of aortic stenosis arises from the
pressure gradient between the high pressure left ventricular chamber
and the low pressure aortic root due to obstruction to left ventricular
outflow from the immobile aortic valve leaflets. As seen in figure 2,
the LV pressure rises above aortic pressure; initially there is a small
pressure difference which soon rises to its maximum and then
decreases. This pattern of change in pressure gradient leads to the
crescendo-decrescendo nature of the murmur. This murmur is heard
best at the right upper sternal border with the diaphragm. It is
important to note the location of the peak given that typically, worse
stenosis peaks later in systole. Also important is the quality of S2, for
reasons described above.
i. Frequency- typically medium to high pitched
ii. Configuration- crescendo-decrescendo for reasons described
above
iii. Quality- harsh or coarse
iv. Duration- ends prior to or at S2
v. Radiation- the murmur of AS follows the direction of blood
flow leaving the aortic valve. Thus, the murmur radiates into the
upper chest and into the carotids. In most patients it can also be
heard in the left subclavian artery.
vi. Maneuvers- any maneuver which increases LV filling (and
hence LV stroke volume) will tend to increase the murmur
intensity. For example, a PVC will lead to a compensatory
pause, which increases diastolic LV filling. Based on the
Starling mechanism, the LV will then contract with a greater
force, hence a greater pressure and stroke volume will be
generated within the left ventricle. The aortic pressure will stay
the same so the absolute LV-Ao gradient will increase. This will
serve to increase the murmur.
vii. NB- Occasionally the murmur of severe aortic stenosis can be
heard as a musical murmur (not a harsh murmur) at the apex.
This is referred to as the Gallaverdin’s murmur or phenomenon.
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b. Mitral regurgitation- The murmur of MR derives from the
movement of blood from the high pressure LV chamber to the low
pressure left atrium. In contradistinction from aortic stenosis, the LV
and LA never reach an equal pressure, so the murmur of MR will last
throughout systole (“holosystolic”) and may even last past S2. This
murmur is best heard at the apex with the diaphragm.
i. Frequency- medium to high pitched
ii. Configuration- usually flat (the intensity does not change during
systole)
iii. Quality- blowing
iv. Duration- holosystolic
v. Radiation- classically, the MR murmur radiates to the axilla.
However, in patients with either a prolapsed leaflet, a flail leaflet,
or a restricted leaflet, the murmur will radiate in the direction of
the blood. For example, patients with a posterior leaflet which
prolapses have an anterior directed jet. Their murmur then is
directed towards the anterior chest wall and can mimic aortic
stenosis. Posteriorly-directed jets radiate to the back and can
even produce murmurs on the crown of the head through
radiation up the spine.
vi. Maneuvers- Any maneuver which increases afterload will
increase the amount of blood moving into the LA because LV
pressure correlates with aortic pressure. Thus, classically handgrip and squatting will increase the intensity of an MR murmur.
c. TR- TR has the same characteristics as MR, but the murmur is best
heard at the left sternal border or subdiaphragmatically. The murmur
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of TR should increase with inspiration secondary to increase in
systemic venous return.
d. VSD- Most VSDs found incidentally in adults are small and
restrictive. Thus, the murmur of a VSD is typically a loud, highpitched, holosystolic at the lower left sternal border.
i. Frequency- usually high pitched in adults
ii. Configuration- usually flat or decrescendo
iii. Quality- blowing or musical
iv. Duration- pansystolic
v. Radiation- the murmur of a VSD can radiate throughout the
precordium since it is such a loud murmur in most adults. Other
VSDs radiate to the right sternal border.
vi. Maneuvers -Any maneuver which increases LV pressure, such
as hand grip, will increase the intensity of the murmur.
e. Hypertrophic obstructive cardiomyopathy (HOCM)- Not all
patients with hypertrophic cardiomyopathy have a murmur because not
all hypertrophic cardiomypathies lead to outflow obstruction.
However, when there is outflow obstruction from septal hypertrophy, a
murmur is generated with its loudness dependent upon the degree of
obstruction and height of the pressure gradient. Like aortic stenosis,
the murmur of HOCM usually has a crescendo-decrescendo pattern,
but the murmur of HOCM is usually best heard along the left sternal
border, lower down the sternum that the murmur of aortic stenosis.
The murmur also does not typically radiate to the carotids which helps
distinguish it from aortic stenosis.
i. Frequency- medium to high
ii. Configuration- crescendo-decrescendo
iii. Quality- harsh
iv. Duration- usually begins after S1 and does not last throughout
systole
v. Radiation- as above, does not radiate to the neck
vi. Maneuvers- any maneuver which leads to either a reduction in
LV preload (e.g. Valsalva), decreases afterload (squat-stand), or
increases LV contractile force (post-PVC) will increase the
murmur of HOCM. The Valsalva maneuver helps distinguish
HOCM from the murmur it most closely resembles, aortic
stenosis. In HOCM, the decrease in preload and stoke volume
created by the strain phase of the Valsalva will increase the
murmur due to more obstruction from the hypertrophic
ventricular septum. However, in aortic stenosis, the decrease in
stroke volume created by the strain phase of Valsalva will lead to
a decrease in the left ventricular-aorta gradient, and hence a
reduction in the volume of the murmur.
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2) Diastolic
a. Aortic insufficiency- the murmur of aortic insufficiency is created
by the regurgitation of blood from the aortic root into the left ventricle
during diastole. The murmur thus begins early in diastole, as soon as
left ventricular pressure falls below aortic pressure. It is best heard
with the diaphragm of the stethoscope at the right or left upper sternal
border. The length of the murmur depends upon the severity of the
regurgitation and the compliance of the ventricle. For example, in
acute severe aortic regurgitation, the noncompliant left ventricle
equilibrates with aortic pressure very quickly; thus the murmur is
brief. In chronic severe AI, pressure in the more compliant, dilated
left ventricle rises more slowly. Thus the murmur may last throughout
diastole.
i. Frequency- variable, usually higher pitch indicates more
severe regurgitation
ii. Configuration- decrescendo (always)
iii. Quality- blowing
iv. Duration- depends on severity: very mild AI may be so short a
murmur that it only makes S2 seem long. More severe AI is
usually associated with longer, decrescendo murmur heard
throughout diastole. N.B. however that some very severe,
especially acute severe AI may lead to rapid equalization of
aortic and LV pressure which shortens the murmur.
v. Radiation- none
vi. Maneuvers- any maneuver which increases afterload
(handgrip) will increase the amount of regurgitation.
b. MS- the murmur of mitral stenosis is one of the more challenging
physical exam auscultation findings. It usually requires a quiet room
with the patient in the left lateral decubitus position with the
diaphragm or bell of the stethoscope at the apex. The murmur usually
begins after an opening snap and then has a decrescendo pattern; in
patients in normal sinus rhythm there may be a brief crescendo
immediately before S1 (when the atrial kick pushes blood through the
noncompliant mitral valve).
i. Frequency- low
ii. Configuration- decrescendo after S2, may crescendo prior to
S1 (presystolic accentuation in patients in sinus rhythm)
iii. Quality- rumbling
iv. Duration- brief
v. Radiation- none
vi. Maneuvers- any maneuver which increases cardiac output will
increase the murmur of MS. This is most easily accomplished by
having the patient exercise briefly (sit-ups or jogging in place) and
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then immediately examing the patient in the left lateral decubitus
position.
Pericardial Friction Rub
The pericardial friction rub is created by movement of the heart within an inflamed
pericardium. Classically, it has 3 components- two in diastole and one in systole. The
diastolic components occur when the left ventricle is stretched during diastole, namely
with early diastolic filling and later with the atrial kick. Each of these events, changes the
left ventricular volume which makes it more likely that the visceral and parietal
pericardial surfaces will contact each other. Ventricular systole causes motion of the
ventricle which then creates the 3rd component.
The pericardial friction rub may be transient and requires a prolonged auscultation. It is
best heard with the diaphragm, usually with at the lower left sternal border.
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Mitral Valve Prolapse
Pulmonary Stenosis
S1 normal
S2 normal splitting
Mid Systolic Click
Earlier-Standing, Valsalva
Later – Squatting, Handgrip
Mid to Late Systolic Murmur
Longer-Standing, Valsalva
Shorter-Squatting, Handgrip
S1 normal
S2 Wide Splitting
P2 Loud
S3 Often Present
Pansystolic Murmur
Filling Rumble
IHSS (HOCM)
A2 normal
Paradoxical Splitting S2
S4 Usually Present
Systolic Ejection Murmur
 Valsalva, Standing, post PVC
 Handgrip, Squatting
Bisferiens Carotid Pulse
Tricuspid Insufficiency
Mitral Insufficiency
Atrial Septal Defect
S1 normal
S2 Paradoxical Splitting
Pansystolic-Holosystolic Murmur
 With Inspiration, Squatting
 With Expiration, Standing
Giant GV Waves
S1 – Split
S2 Wide Fixed Splitting
Pulmonic SEM
Tricuspid Mid Diastolic Filling Murmur
Prominent JVP
Diminished S1
Wide Splitting S2
S3 (moderate to severe)
High Frequency Holosystolic Murmur
Occasional Diastolic Filling Rumble
Brisk-Low Amplitude Carotid Pulse
Aortic Stenosis
Ejection Sound (non-calc)
Diminished A2 (Immobile)
Paradoxical Splitting S2
S3 and S4 (severe)
Late Peaking Systolic Ejection Murmur
Delayed-Low Amplitude Carotid Pulse
(Parvus Tardes)
Delayed Brachial-Radial, ApicalCarotid Interval
Mitral Stenosis
Aortic Insufficiency
Ventricular Septal Defect
Loud S1
Narrow Splitting S2
Loud P2
Opening Snap
Narrow A2-OS Interval (severe)
Diastolic Rumble with
Presystolic Accentuation
Duration = Severity
S1 Diminished
Soft A2 and Narrow Splitting S2
S3 – Common
Diastolic Decrescendo Murmur
Early Peaking SEM
S1 normal
S2 Wide Splitting
P2 Loud
S3 Often Present
Pansystolic Murmur
Filling Rumble
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