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Cardiovascular Physical Examination "Harvey

Sessions"
M3 Medicine Clerkship

George T. Kondos, MD
Associate Professor of Medicine
Associate Chief, Cardiology Section
Director, Clinical Cardiology
University of Illinois at Chicago
Mondays, 7:00-8:30 AM
Cardiovascular Teaching Center
Section of Cardiology
840 S. Wood Street
Room 903 CSB
Cardiovascular Physical Examination
Table of Contents
Session I .......................................Introduction, Jugular Venous Pulse, Carotid and Arterial Pulses
Session II ......................................Precordial evaluation, Auscultation
Session III ....................................Auscultation, Innocent murmurs, Patient Presentations
Session IV .....................................Patient presentations, Cardiovascular Physical Examination Review
Graphics
The Cardiac Cycle
Diagraming Heart Sounds and Murmurs
Measurement of the JVP, JVP Waveforms, Carotid Waveforms
Precordial Palpation
Parting Remarks
Harvey Session I
1. Cardiovascular Examination - used to assess both cardiac pathology and physiology

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1. Jugular Venous Pulse - Physiology

1. Identification of the internal jugular vein
1. Location
(1) lateral to the carotid artery
(2) beneath the sternocleidomastoid muscle
2. Differentiation from the arterial pulsation
(1) location
(2) positional variation
(3) respiratory variation
3. External jugular vein - may be used if the internal jugular vein is not readily
apparent. Problems with using the external jugular vein include:
(1) anatomic variation
(2) not a direct communication with the right atrium
(3) affected by sympathetic tone more than the internal jugular vein
2. Evaluation of the jugular venous pulse (remember JVP not JVD)
1. Estimation of central venous pressure - this is the most important part of the
jugular venous pulse examination.
(1) measured as a vertical distance above the sternal angle
(2) the mid-right atrium is 5 cm beneath the sternal angle of Louis (this
represents an arbitrary zero point)
(3) elevated JVP - the total right atrial pressure is greater than 8 cm of water
(note - NOT mmHG)
(4) position the patient so as to best see the JVP
(1) total height of the JVP is not altered by the patient position
(2) tangential lighting on the neck enhances visualization of the jugular
venous pulse
(3) relax the sternocleidomastoid muscle
2. Contour of the jugular venous pulse
(1) Why do jugular venous pulses occur - they result from the repeated interference
with the relatively steady flow of venous return by the contraction and relaxation of
the right atrium and ventricle
(2) Normal JVP contours
(1) A-wave
1) results from ATRIAL contraction
2) Timing - PRESYSTOLIC
3) Peak of the a-wave near S1
(2) V-wave
1) results from PASSIVE filling of the right atrium while the tricuspid valve
is closed during ventricular systole (Remember the V-wave is a "V"ILLING
WAVE)
2) Large V-waves on the left side of the heart may be seen with mitral
regurgitation, atrial septal defect, ventricular septal defect. The v-wave in
the jugular venous pulse reflects right atrial events. To see the v-wave on the
left side of the heart Swan-Ganz monitoring is needed
3) timing - peaks just after S2
(3) X-descent
1) results from ATRIAL RELAXATION
2) timing - occurs during ventricular systole, at the same time as the carotid
pulse occurs
(4) Y-descent
1) results from a FALL in right atrial pressure associated with opening of

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the tricuspid valve

2) timing - occurs during ventricular diastole
(5) Generalizations
1) the A-wave in a normal individual is always larger than the V-wave
2) the X-descent is MORE PROMINENT than the Y-descent
(6) Detailed analysis of the jugular venous pulse is indicated when one of the
following occurs
1) absence of the X-descent
2) presence of prominent systolic waves
3) easily appreciable A and V waves
4) prominent diastolic collapse of the venous pulse (remember - systolic
collapse of the X-descent is generally more prominent than the Y-descent
3. Abdominal jugular reflex (AJR) previously known as the hepatojugular reflex or
HJR)
(1) apply pressure to the abdomen while the patient is breathing normally for
about 20 seconds
(2) normal AJR - there is either an increase or no change in the height of the
jugular venous pulse
(3) abnormal AJR - the JVP increases 2-3 cm during abdominal compression
above baseline and remains elevated until abdominal compression is released
(4) physiology of the AJR - abdominal compression increases venous return to
the right ventricle. This is why it is very important that the patient breath quietly
during compression. If the patient bears down, like a valsalva maneuver venous
return is decreased to the heart therefore there are two opposing forces. In the
normal individual the increased venous return causes an increased right
ventricular contraction to accommodate the increased venous return. In abnormal
hearts IE., with right or left heart failure the increase venous return cannot be
accommodate by the right ventricle which is then transmitted to the jugular
venous pulse
(5) the AJR has NO value in a patient with an already elevated JVP
(1) use in patients with normal to questionably elevated JVP
(2) avoid compressing over the liver to avoid patient discomfort in patients
with heart failure and hepatic congestion
(3) make sure the patient is breathing quietly during abdominal compression
3. Abnormalities of the jugular venous pulse
1. A-wave
(1) prominent a waves occur when the force of atrial contraction increases in
response to an increased resistance to atrial emptying
(1) decreased right ventricular compliance - diastolic dysfunction (IE.,
heart failure)
(2) tricuspid stenosis
(3) pulmonary hypertension
1) left heart failure
2) cor pulmonale
3) primary pulmonary hypertension
(4) right ventricular outflow tract obstruction
1) pulmonic stenosis
2) hypertrophic cardiomyopathy
(5) clots or tumors in the right ventricle
(2) Cannon a-waves - the right atrium is contracting against a closed
tricuspid valve this is different than a giant or prominent wave in timing

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(1) cannon a wave: occurs during right ventricular systole, the

prominent a-wave is a presystolic event
(2) cannon a waves have a more rapid rate of rise or flickering motion
than prominent a waves
(3) causes
1) intermittent
1) premature ventricular or nodal contractions
2) complete heart block
3) right ventricular pacemakers
2) regular
1) paroxysmal supraventricular or junctional tachycardia
2) ventricular pacemakers and normal AV nodal retrograde
conduction
2. X-descent
(1) prominent X-descent: cardiac tamponade
(2) decreased X-descent: atrial fibrillation/flutter
3. V-wave
(1) prominent V-wave
(1) tricuspid regurgitation
(2) atrial septal defect (left sided v-wave seen with Swan-Ganz
monitoring
(2) A-wave equal in height to V-wave - think atrial septal defect
4. Y-descent
(1) prominent Y-descent: constrictive or restrictive heart disease
(2) decreased Y-descent: tricuspid stenosis
2. Carotid Arterial Pulsations
1. Evaluation
1. Upstroke - rate of rise: normal, rapid, delayed
(1) rapid
(1) hyperdynamic contractions
1) anxiety
2) hypertrophic cardiomyopathy
3) anemia
4) thyrotoxicosis
(2) increased aortic runoff - aortic insufficiency
(2) delayed - think FIXED LEFT VENTRICULAR OUTFLOW
TRACT OBSTRUCTION - aortic stenosis
2. Volume - normal, increased, decreased
(1) increased - aortic insufficiency
(2) decreased - mitral insufficiency, cardiomyopathy, aortic stenosis
3. Contour - single beating or twice beating carotid pulse
(1) double carotid impulse
(1) occurrence at the PEAK of the carotid
1) aortic regurgitation
2) hypertrophic cardiomyopathy
3) combined aortic stenosis/regurgitation
(2) occurrence at the DOWNSTROKE of the carotid - this
represents an exaggeration of the normal dicrotic pulse seen in
association with
1) dilated cardiomyopathy
2) low cardiac output states

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3) increased peripheral vascular resistance

Harvey Session II - III
3. Examination of the Precordium
1. The art of palpation of the precordium
1. Palpation is an important part of the cardiovascular physical examination.
The cardiovascular examination is incomplete if careful palpation is not
done
2. Importance of palpation
(1) at times heart sounds and extra heart sounds can be better palpated
than auscultated
(2) by palpating sounds you can "tune in" and actually hear them when
you auscultate
(3) at times the presence of an extra sound may only be palpated and
never heard
(4) palpation can give the examiner a clue as to end-organ damage IE.,
a sustained left ventricular impulse in a patient with systemic
hypertension
(5) palpation can give the examiner an idea of the severity of the
underlying condition IE., palpation of a carotid shudder in patients with
valvular aortic stenisis indicates a severely obstructed aortic valve
(6) palpation of the left ventricular apex tells you where to place the
bell of your stethoscope to ensure you will hear subtle S4 and S3 heart
sounds
3. Technique of palpation
(1) initially palpate with the base of your fingers NOT your finger tips
(1) the base of the fingers is more sensitive than the finger tips
(2) once the are of the impulse is localized use the finger tips to
examine in a more precise manner
(3) alter the pressure you place on the base of the fingers or finger tips
1) light pressure - HIGH pitched sounds IE., ejection sounds,
opening snaps, clicks
2) heavy pressure - LOW pitched sounds IE., third and fourth heart
sounds
(2) the following areas should be systematically palpated with light and
heavy pressure
(1) aortic area - second right intercostal space at the base of the heart
(2) pulmonic area - second left intercostal space at the base of the heart
(3) right ventricular area - along the left parasternal border
(4) ectopic area - between the right ventricle and the cardiac apex
(5) apical area
2. Normal precordial activity
1. Left ventricular apical beat or apical impulse
(1) etiology - produced by the anterior movement of the left ventricle during
early systole
(1) the heart rotates in a counterclockwise direction when viewed from
beneath IE., as if you were looking form the cardiac apex
(2) occurs during isovolumetric contraction of the left ventricle
(3) part of the palpated left ventricular apical impulse may be related to
a recoil force produced by the ejection of blood into the aorta in a
upward, rightward, and posterior direction which thrusts the left

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ventricle against the chest wall

(2) terminology - the point of maximal impulse (PMI) and left ventricular
apical beat are generally used interchangeably. PMI should be avoided
because the PMI may not be the left ventricular apical beat in certain disease
states IE., in rheumatic mitral valve stenosis the PMI may be the right
ventricle
(3) normal characteristics of the left ventricular apical impulse
(1) location - no more than 10 cm from the midsternal line (other
examiners may prefer to measure the left ventricular apical beat in
relation to the midclavicular line)
1) in the supine position the apical beat can be located in 20% of
patients over 40 years old
2) in the left lateral decubitus position the apical impulse may be
felt in 80% of patients over 40 years old
3) the apical impulse can be felt in about 90% of young children
and teenagers
4) the apical impulse may be absent ID., you just can't find it in
some older individuals
5) identification of the apical beat - when multiple impulses are
present if often confusing. USE THE CAROTID as a timer. The
impulse coincident with the carotid is the apical beat
6) there are two situations when the apical impulse may be more
than 10 cm from the midsternal line and the heart is not enlarged
1) pectus excavatum
2) massive pneumothorax - in both cases examination of the
X-ray would indicate the cardiothoracic ratio was normal
(2) size - detectable in only one intercostal space, palpable area less
than 2-2.5 cm. If the precordial impulse is larger it is described as
DIFFUSE and indicates left ventricular dysfunction IE., more of the left
ventricle is striking the chest wall
(3) the apical impulse should be felt as a GENTLE NONSUSTAINED
TAP - sustained means the impulse lasts longer than 2/3 of systole. By
simultaneously feeling the carotids the LV impulse should last as long
as the carotid upstroke. If the apical impulse lasts longer and you have
the perception that you finger tips are being held up longer than normal
the apical impulse is described as being SUSTAINED. A sustained
apical impulse indicates a pressure overloaded left ventricle such as in
hypertension or aortic stenosis. A volume overloaded left ventricle such
as in mitral regurgitation can also be associated with a sustained left
ventricular impulse
2. right ventricular apical impulse
(1) location - palpated along the left parasternal border
(2) technique
(1) use the palm of the left hand
(2) use light pressure over the left parasternal area
(3) normally the right venticular impulse cannot be felt. Sometimes the
RV impulse may be palpated in young children because of a
hyperdynamic circulation.
3. Aortic area
(1) location - second right intercostal space
(2) normally no impulses are felt in this area

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4. Pulmonic area
(1) location - second left intercostal space
(2) normally no impulses are felt in this area
3. Precordial abnormalities
1. Systolic events
(1) left ventricle
(1) hyperdynamic states - the apical impulse displays an increased
force and amplitude
(2) volume overloaded left ventricles, as in mitral insufficiency or
aortic insufficiency
1) early volume overload - hyperdynamic impulse
2) late volume overload - enlarged inferolaterally displaced
apical impulse. This impulse may be sustained because the
ventricle has hypertrophied IE., thickened to help maintain
wall stress and tension
(3) pressure overloaded left ventricle - as in systemic hypertension
or aortic stenosis - SUSTAINED LEFT VENTRICULAR APICAL
IMPULSE
(4) abnormal left ventricular systolic function IE., decreased
ejection fraction - DIFFUSE APICAL IMPULSE IE., larger than a
rib space or larger than 2-2.5 cm (2) right ventricle - the same
events palpated with respect to the left ventricle can be palpated
for the right ventricle
(1) volume overload IE., tricuspid regurgitation or pulmonic
insufficiency may have a hyperdynamic RV impulse
(2) pressure overload IE., pulmonic stenosis may have a
sustained RV impulse
(3) NOTE SOMETIMES SYSTOLIC EXPANSION OF THE
LEFT ATRIUM MAY BE FELT IN SEVERE MITRAL
REGURGITATION - this may be confused with an RV
impulse
1) location - lower left parasternal border
2) location of the left atrium - the left atrium is a posterior
structure IE., the right atrium and right ventricle are
anterior cardiac structures. The left atrium and left
ventricle are posterior cardiac structures (interestingly not
really right and left)
3) identification of the left atrium versus the right
ventricular impulse
1) the right ventricular apical impulse is in
synchrony with the left ventricular apical impulse IE., palpate the LV apex and the RV apex. The
impulses should occur simultaneously
2) when sever mitral regurgitation occurs use
simultaneous palpation over the left ventricular
apical area and right lower left parasternal area - the
lower left parasternal area is out of synchrony with
the earlier LV apical beat.
(3) palpable systolic heart sounds
(1) ejection clicks - occur as a result of
1) aortic valvular stenosis

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2) pulmonic valvular stenosis

3) dilated aorta or pulmonary artery
(2) clicks of mitral valve prolapse
(4) diastolic events - to determine diastole always use carotid
vessels as a timing mechanism. Normally you can tell when systole
and diastole occur because diastole is longer than systole. In
tachycardiac patients diastole shortens more than systole;
therefore, systole and diastole may be equal in length making it
confusing if an abnormal event occurs during systole or diastole.
By using the carotids as a timing mechanism this mistake is less
likely to occur
(1) palpable S4
(2) palpable S3
(3) palpable opening snap in mitral stenosis
(5) other palpable precordial events - THRILLS are palpable
murmurs because of increased turbulence
(1) palpable murmur of at least GRADE IV intensity or higher
(2) location or where thrills can be best appreciated
1) left ventricular apex
2) lower left sternal border
3) cardiac base - pulmonic or aortic areas
4. Cardiac auscultation
1. Cardiac auscultation pearls
1. Your eyes and ears hear what your mind know
2. You must know what you expect to hear in each of the four primary
auscultatory areas prior to auscultating in these areas
3. Know what normal heart sounds sound like
4. Use a GOOD stethoscope
(1) optimal stethoscope tubing length is twelve inches
(2) make sure the earpieces fit snugly. If you experience pain in
your auditory canals while auscultating the earpieces are too far in
the auditory canals
(3) make sure no air leaks occur between the chest wall and the
stethoscope earpiece
2. Primary auscultatory areas
1. Aortic area - second intercostal space
(1) the aortic valve is not exactly located in this area. It actually is
located slightly to the right of the sternum slightly below the
second right intercostal space
(2) sounds from the aortic valve tend to radiate in a sash like
contour toward the left ventricular apical area
(3) heart sounds
(1) S1 softer than S2 in the aortic area
(2) S4 is not typically heard in the aortic area
(3) aortic ejection sounds are typically heard in the aortic area
and at the left ventricular apex
1) aortic ejection sounds are caused by the sudden tensing
of the aortic valve leaflets early during systole
2) aortic ejection sounds can also be caused by a dilated
aortic root which causes the aortic valve to be stretched
and tensed when the aortic valve opens in systole. Aortic

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ejection sounds are high pitched in character, remember

an S4 is a low pitch sound
3) aortic ejection sounds do not vary with respiration,
they are not affected by decreasing volume IE., by having
the patient stand
4) remember aortic ejection sounds occur before the
upstroke of the carotid
5) aortic ejection sounds may also be heard in patients
with a stenotic aortic valve. Their presence indicates a
mobile valve. As aortic stenosis becomes more severe the
ejection sound disappears
(4) abnormal auscultatory findings in the aortic area
(1) A2 soft
1) critical aortic stenosis IE., calcified aortic valve which
does not move well therefore not creating a closing sound
2) acute aortic insufficiency - the aortic valve drifts close
because of the markedly elevated left ventricular enddiastolic pressure
(2) A2 louder than normal
1) hypertension - because of an elevated systemic
vascular resistance the aortic valve closes under a higher
pressure causing a louder A2
2) aortic stenosis non-critical - the aortic valve is calcified
but moves normally thus because of a mobile valve and
calcification the A2 is louder (think of this as the closing
of a screen door vs the closing of a lead door - which
closes louder?)
2. Pulmonary area - second left intercostal space
(1) S2 louder than S1
(2) S2 is physiologically split
(1) A2-P2 split during inspiration (remember increasing
splitting during Inspiration)
(2) A2-P2 single during expiration
(3) A2 is louder than P2 in the second left intercostal space
(4) mechanism of physiological splitting
1) as a result of increased venous return to the right heart
during inspiration the pulmonic valve stays open longer
and therefore closes later resulting in a delayed P2
2) as a result of decreasing venous return to the left heart
during inspiration because of blood pooling in the lungs
the aortic valve closes sooner
3) both of these changes result in increase splitting of S2
during inspiration
(3) abnormal auscultatory findings
(1) P2 is louder than S2 the patient has pulmonary
hypertension. The etiology of the pulmonary hypertension has
to be then determined
(2) abnormal A2-P2 splitting
1) A2-P2 fixed split during inspiration and expiration think ATRIAL SEPTAL DEFECT
2) A2-P2 paradoxically split IE., split during expiration,

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single sound during inspiration - think anything which

prolongs left ventricular ejection such as: CRITICAL
AORTIC STENOSIS, HYPERTROPHIC
CARDIOMYOPATHY, LEFT BUNDLE BRANCH
BLOCK, DILATED CARDIOMYOPATHY
3) A2-P2 split during inspiration and expiration but
moving physiologically IE., wider splitting during
inspiration than expiration - think RIGHT BUNDLE
BRANCH BLOCK. L
3. Lower left sternal border
(1) M1-T1: asynchronous closure of the mitral and tricuspid
valves. Generally T1 unless accentuated is not heard anywhere else
other than the lower left sternal border
(2) S1(M1-T1) louder than S2
(3) Abnormal auscultatory findings
(1) S1 loud - think calcified mitral or tricuspid valves, IE.,
mitral or tricuspid stenosis where the valve leaflets are mobile
causing a loud first heart sound
(2) S1 soft - think calcified mitral or tricuspid valve IE., mitral
or tricuspid stenosis where the valve does not move well
(3) S1 variable intensity - think atrial fibrillation
(4) S4 - right ventricular in origin, which may vary with
respiration IE., increase with inspiration decrease in intensity
or absent with expiration
(5) S3 - right ventricular in origin, which may vary with
respiration IE., increase with inspiration decrease in intensity
or absent with expiration
4. Left ventricular apical area
(1) S1 louder than S2 - normal
(2) Abnormal auscultatory findings
(1) S4 left ventricular in origin - low pitch
1) an S4 should always be considered abnormal. S4 is a
filling sound and occurs as a result of atrial contraction.
Blood entering the ventricle rapidly halts as a result of a
stiff non-compliant left ventricle thus generating an S4
2) As S4 is low pitch and should not be confused with a
split S1 which is high pitch. An S4 should also not be
confused with an ejection sound. Remember ejection
sounds are very high pitch
3) Because an S4 is very volume dependent standing the
patient will decrease venous return to the right ventricle
and also the left ventricle, an S4 will disappear or become
softer
(2) S3 left ventricular in origin - low pitch, fading away sound
1) physiological S3 - occurs as a result of turbulence of
blood flow as blood enters the ventricle during rapid
passive filling
2) pathological S3 - occurs as a result of rapid cessation
of blood flow as blood enters the ventricle during rapid
passive filling
(3) Mitral valve opening snap (OS)

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1) high pitch sound after S2, heard best in the left lateral
decubitus position with the diaphragm of the stethoscope
2) the opening snap is heard because of the calcified
mitral leaflets. Normally opening valve sounds are not
heard.
Harvey Session IV
2. Cardiovascular Physical Examination Review
1. Be organized
1. Examine the patient the same way every time look for the
1. Jugular venous pulse
(1) height
(2) contours - a and v waves, X and Y descents
(3) abdominojugular reflex
2. Carotids - the timing mechanism
(1) volume - normal, increased, decreased
(2) upstroke - normal, delayed, brisk
(3) contour - single beating or twice beating
3. Precordium
(1) apical area
(1) location of the left ventricular impulse - no more than 10
cm from mid-sternal line
(2) contour - diffuse or sustained
(3) palpable sounds - S4, S3
(2) lower left sternal border
(1) right ventricular lift - indicating pulmonary hypertension
(2) other palpable sounds and murmurs
(3) second left intercostal space - palpable pulmonary artery,
palpable P2
(4) second right intercostal space - palpable sounds and murmurs
2. Cardiac auscultation
1. The previous parts of the cardiovascular examination guide your
subsequent auscultation. It is very possible to palpate heart sounds
before hearing them. Once sounds are palpated they may then be
carefully listened for
2. Listen in a QUIET room
3. Always try to think PHYSIOLOGICALLY IE., what's causing the
heart sound or murmur
4. DIAGRAM the heart sounds and murmurs - (aside - I have never
seen a student who diagrams not improve their physical exam skills)
5. Listen to as many normal and abnormal hearts during your training.
Experience is definitely the best teacher

Graphics

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Parting Remarks:
Remember the stethoscope is a very powerful instrument. It is only as good as the person listening to the
patient. After completing the cardiovascular examination the physician should know the diagnoses and
the severity of the patients cardiac condition. Other tests which are ordered like the echocardiogram,
EKG, etc., only serve to confirm the astute clinicians physical examination.
Everybody has the potential of doing an excellent cardiovascular examination. Be patient, compulsive,
and above all think while you are doing the cardiac examination.
Good listening, and above all be good detectives and have fun doing the cardiovascular examination.

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