Cardiovascular Physical Examination

"Harvey Sessions"
M3 Medicine Clerkship

Section of Cardiology, University of Illinois at Chicago

http://www.uic.edu/com/dom/cardio/teaching_m3.html#i#i
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
Cardiovascular Examination - used to assess both cardiac pathology and physiology
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
total height of the JVP is not altered by the patient position
tangential lighting on the neck enhances visualization of the
jugular venous pulse
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
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
(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
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 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
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
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 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 end-diastolic 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, 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)
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 midsternal 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

(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 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
(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
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 endorgan 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 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
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

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 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 end-diastolic
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, 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)
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

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.