cardiovascular physical examination

Cardiovascular Physical Examination "Harvey Sessions"

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, MDAssociate Professor of MedicineAssociate Chief, Cardiology SectionDirector, Clinical CardiologyUniversity of Illinois at Chicago

Mondays, 7:00-8:30 AMCardiovascular Teaching CenterSection of Cardiology840 S. Wood StreetRoom 903 CSB

Cardiovascular Physical ExaminationTable 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 ICardiovascular 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 muscle2) Differentiation from the arterial pulsation

(1) location(2) positional variation(3) respiratory variation3) 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 vein2. 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


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


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


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


4. Left ventricular apical area

(1) S1 louder than S2 - normal


(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


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


(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


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


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


4. Pulmonic area

(1) location - second left intercostal space


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


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


(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. Left ventricular apical area

(1) S1 louder than S2 - normal


(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


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.

cardiovascular physical examination

Documents

jugular venous pulses

jugular venous pulse1

internal jugular vein2

jvp waveforms

villing wave

total right atrial pressure

right atrium3

auscultation session