BY DR. MAGDI AWAD SASI
Detailed analysis of cardiovascular examination 2012
Cardiovascular History
Record the date and time the history was taken.
Name, Age, Occupation(s)
Presenting Problem/ Complaint
Remember the questions you need to ask about each symptom?
There are 4 main cardiovascular symptoms:
1. Chest pain (character, radiation)
2. Shortness of breath (exercise tolerance, orthopnoea, paroxysmal
nocturnal dyspnoea)
3. Presence and extent of oedema (ankle, leg or sacral)
4. Palpitations (tap out rhythm, any dizziness or blackouts)
Systemic Review
During the history consider (and ask about) the main risk factors for
Ischaemic Heart Disease:
1. Smoking
2. Hypertension
3. Diabetes mellitus
4. Hyperlipidaemia
5. Family history
Past Medical History (may ask under presenting complaint)
e.g. angina, myocardial infarction, bypass operation, rheumatic fever,
stroke, intermittent
claudication
Social History
Smoking (pack years), alcohol, stairs
Family History
At what age did the relative have illness?
Drug History
Allergies
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INTRODUCTION
W
- Wash your hands.
I
- Introduce yourself (full name and role). Greet the patient with
their title and surname.
P - Permission. Explain that you wish to examine their heart.
E
- Expose the necessary parts of the patient. Ideally the patient
should be undressed from the waist up taking care to ensure the
patient is not cold or unnecessarily embarrassed.
R
- Reposition the patient. In this examination the patient should
be supine and reclined at 45 degrees.
In the cardiovascular examination a lot of information can be obtained
by looking for peripheral signs of cardiovascular disease.
The examination is therefore split into a
A.peripheral examination and B. examination of the precordium.
Adequate exposure and a quiet environment are critical.
Peripheral Examination
End of the Bed
• Examine the patient for signs of breathlessness or distress.
• It is also important to look at the surrounding environment for oxygen,
fluid restriction signs or GTN spray.
Hands
• To assess warmth, sweating and whether there is peripheral cyanosis.
• Examine the nails for clubbing or signs of infective endocarditis (splinter
haemorrhages, Osler’s nodes and Janeway lesions).
• Palpate the radial pulse and assess the rate and rhythm.
Rate , rhythm , volume, special character, synchronicity, radiofemoral delay
Small volume = stenotic lesion mitral and aortic stenosis.
Large volume = regurgitation lesion mitral and aortic regurgitation.
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Types of pulses
Slow rising pulse (delayed up strokes / parvus et tardus) A
carotid arterial pulse that is reduced (parvus) and delayed (tardus) argues
for aortic valvular stenosis. Occasionally this also may be accompanied by
a palpable thrill. If ventricular function is good, a slower upstroke correlates
with a higher transvalvular gradient. In left ventricular failure, however,
parvus and tardus may occur even with mild aortic stenosis (AS).
Pulsus bisferience = AR + AS
Pulsus paradocsus = acute sever asthma or cardiac tamponade
Pulsus paradoxus is an exaggerated fall in systolic blood pressure during
quiet inspiration
Pulsus alternans = LVF
Pulsus alternans is the alternation of strong and weak arterial
pulses despite regular rate and rhythm.
Collapsing pulse= hyperdynamic circulation
A high volume pulse that hits the fingers suddenly and falls
away just as quickly. It is exaggerated by raising the arm well above
the level of the heart. This is a sign of aortic regurgitation. The pulse
is examined with the arm by the patient’s side; then briskly raise the arm
• Measure the blood pressure.
If the blood pressure is raised compare both arms.
Face
• Check eyes for corneal arcus and xanthelasma.
• Inspect the conjunctivae for anaemia.
• Check for mouth and tongue for central cyanosis.
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Check Jugular Venous Pressure (JVP)
o With the head resting back on the pillow ask the patient to turn the head to the
left while the head of bed is elevated to 45.
1 Think anatomically. The right IJ runs between the two heads (sternal and
clavicular) of the sternocleidomastoid muscle (SCM) and up in front of the ear.
2 Take your time. Look at the area in question for several minutes while
the patient's head is turned to the left. The carotid artery is adjacent to the
IJ, lying just medial to it . The carotid impulse coincides with the palpated
radial artery pulsation and is characterized by a single upstroke timed with
systole. The venous impulse (at least when the patient is in sinus rhythm
and there is no tricuspid regurgitation) has three components a, c and v
waves. When these are transmitted to the skin, they create a series of
flickers that are visible diffusely within the overlying skin. In contrast, the
carotid causes a single up and down pulsation. Furthermore, the carotid is
palpable. The IJ is not and can, in fact, be obliterated by applying pressure
in the area where it emerges above the clavicle.
3. Shine a pen light tangentially across the neck. This sometimes
helps to accentuate the pulsations.
4 . Hepatojugular reflux If you are still uncertain, apply gentle pressure
to the right upper quadrant of the abdomen for 5 to 10 seconds. This elicits
Hepato-Jugular Reflux which, in pathologic states, will cause blood that has
pooled in the liver to flow in a retrograde fashion and fill out the IJ, making
the transmitted pulsations more apparent. Make sure that you are looking
in the right area when you push as the best time to detect any change in
the height of this column of blood is immediately after you apply hepatic
pressure.
5 . The Angle of Louis
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The angle is the site of the joint which connects the manubrium with the rest
of the sternum.
First identify the supra-sternal notch, a concavity at the top of the
manubrium.
Then walk your fingers downward until you detect a subtle change in the
angle of the bone, which is approximately 4 to 5 cm below the notch. This is
roughly at the level of the 2nd intercostal space.
The vertical distance from the top of the column to this angle is added to 5cm,
the rough vertical distance from the angle to the right atrium with the patient
lying at a 45 degree angle.
The sum is an estimate of the CVP.Normal is 7-9 cm.
o Look for pulsation along the right internal jugular vein.
o The height of the pulsation is measured vertically in cm from the sternal angle.
Add 5cm to get the JVP.
o You should know how the JVP can be differentiated from carotid pulsation
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Explain what you're doing (& why) before doing it .
Expose the minimum amount of skin necessary - this requires "artful" use
of gown & drapes (males & females)
Examining heart & lungs of female patients:
Ask pt to remove bra prior (you can't hear the heart well thru fabric)
Enlist patient's assistance, asking them to raise their breast to a position
that enhances your ability to listen to and palpate the heart
Don't rush, act in a callous fashion, or cause pain
PLEASE... don't examine body parts thru gown as:
1. It reflects Poor technique
2. You'll miss things
3. You'll lose points on scored exams .
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INSPECTION
The examination should be conducted in a warm, quiet room. Place the patient in a supine position with
the upper body elevated 30 to 45 degrees after all clothing has been removed from the chest. Explain to
the patient that you are going to examine the heart. Warm your hands and stethoscope, but warn the
patient that your hands may be cool at first. The most comfortable and satisfactory position for most
examiners is on the patient's right side
The praecordium is the front of the chest overlying the heart.
A. Look for abnormal chest shape
Normal chest =anterior posterior diameter 1/3- 2/3 of side to side
Barrel shaped = anterior posterior equal to side to side
COPD, Bronchial asthma , Bronchiectasis
Pigeon chest = pectus incavatum= sternum protruded out
Funnel chest= pectus excavatum = sternum depressed
B. Look for skin , scar , pulsation ,Pacemaker
Midline – sternotomy scar – CABG/valve replacement.
Left – thoracotomy scar (diagonal from under left breast to left axilla) –
mitrial valvectomy for mitrial stenosis.
Pacemaker – under skin inferior to left clavicle.
Apical pulsation , parasternal pulsation , epigastric pulsation
C. Look for respiratory movement
Thoraco abdominal in female , Abdominothoracic in male
Any change gives a clue to pathological process.
D.Look for accessory muscles
Contracted sternomastoid , recession of intercostals muscles that
gives a clue that the patient is dyspneic or he had a chronic
respiratory disease with chronic dyspnea.
Note
This is the same even for chest inspection that for CVS concentrate
on pulsation and for chest lok for respiratory movement.
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PALPATION
1.Palpate trachea
2.Apex beat = Point of Maximum Impulse (PMI)
It is the lower most , outer most and most forceful pulsation.
LOCATE the apex beat accurately with the flat of and fingers of your right
hand. Try to pin down the precise location with the tip of your index finger.
The normal sized and functioning ventricle will generate a penny sized
impulse Count down the ribs from the sternal angle= 2ND intercostals
space. The normal apex beat should be in the 5th intercostal space in the
mid clavicular line. Decide if the apex beat is normal or displaced.
Locate
the line “axillary, midclavicular “ , space “ 5th,6th,7th “ and
character “ tapping,foreceful heaving or unsustained “.
.Apex beat not palpable
Normal cause Obesity , thick chest , behind rib
Pathological cause barrel chest ,pericardial effusion,dextocardia
.Rotating the patient to a left lateral decubitus position tips the
heart towards the chest wall and makes the apex beat easier to feel.
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1.Mitral stenosis
produces a particularly characteristic cardiac apical impulse. The
apical impulse often has a sharp tapping nature. This is because the
first heart sound is loud because of forceful closure of the mitral valve
and this forceful closure is transmitted to the chest wall as a ‘tap’.
Same line and same space “ tapping”
2.Aortic stenosis- pressure load “heaving”
A forceful or ‘thrusting’ apex, either in the normal position or slightly
displaced to 6th intercostals space. This is usually due to concentric
LV hypertrophy as a result of conditions such as aortic stenosis or
hypertension. same line and change space. “forceful sustained”
3. Mitral and aortic regurgitation- volume load
The apical impulse may be displaced to the left and have a more
diffuse heaving nature. This is usually when there is volume overload.
A similar type of apex beat is often seen when there is sever LV
dysfunction and the ventricle is enlarged. If the patien has an audible
gallop rhythm this can sometimes also be palpated with a hand
placed over the cardiac apex. Line and space changed.
“forceful unsustained”
D. Constrictive pericarditis , which is rare in many developed
countries, but common in the developing world, can produce indrawing of the intercostals spaces during systole because the LV is
tethered to the chest wall by the diseased pericardium.
Summary:
For apex beat , check line , space and character.
Palpation of the precordium of a female patient is best
done by placing the palm of your right hand directly
beneath the patient's left breast such that the edge of
your index finger rests against the inferior surface of the
breast. Tell that patient what you are about to do (and
why) before actually performing this maneuver.
Remember that with age tissue turgor often declines,
causing the breasts to hang below the level of the heart.
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Palpate the 2nd left intercostals space “pulmonary area” for
palpable 2nd heart sound which normally not felt.
In pulmonary hypertension , the pulmonary artery dilates and
produces an impulse in the second left intercostals space and
the loud pulmonary component of the S 2 may also be
appreciated as a sharp snapping feeling in this area.
3.THRILL
It is a palpable vibratory sensation, often compared to the purring of a cat,
and typical of murmurs caused by very high pressure gradients.
These, in turn, lead to great turbulence and loudness.
Hence, thrills are only present in pathologic murmurs whose intensity is
greater than 4/6. It should be checked in the four areas by palmer
surface of the right hand at the junction of metacarpophalangeal
surfaces.
The commonest cause of a thrill is aortic stenosis.
If present there should be an easily audible murmur present on
auscultation.
In mitral area= diastolic thrill , in aortic area= systolic thrill
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Figure 1 AREAS TO BE PALPATED FOR THRILL
1.Aortic area:
2.Pulmonary area
3.Tricuspid area
4. Mitral area
“AA”
2nd parasternal right intercostals space
“ PA”:2nd parasternal left intercostals space
“TA” : 4th paraeternal left intercostals space
“MA” : 5th left intercostals space-apex beat
4.HEAVE
Left parasternal (right ventricular) heave
A signifi cantly hypertrophied and/or dilated RV will produce
an abnormal impulse at the lower end of the sternum,
usually to the left side. In a patient with lung disease and
an abnormal RV this physical sign may be absent because
the over-infl ated lung acts as a cushion between the heart
and the chest wall and therefore prevents the impulse being
transmitted to the surface. Heaves represent ventricular hypertrophy
and feel as if your hand is being lifted of patient’s chest.
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Auscultation
. Don’t auscultate over clothes or gown.
. Warm your hands and stethoscope.
. The most satisfactory position for examiner is on the patient's right side.
. Become comfortable with your stethoscope.
. Learn how to use it correctly bell and diaphragm.
. The most important "part" is what sits betwen the ear pieces!
. Be isolated from surrounding and keep ear pieces tight to your ears.
.4 areas need to be auscultated 2 times change from diaphragm to bell.
. 2 positions need to be done by the patient other than supine.
. 2 radiation of the murmurs need to be checked.
. Start from mitral area “apex beat”. OR aortic area!
. start from MA - TA – PA – AA
.
These areas, although known as the mitral, tricuspid, pulmonary and
aortic areas, in fact have no anatomical meaning. They are the key areas
where the heart sounds and murmurs radiating from these valves are
traditionally considered to be best heard. Be prepared to hunt around
slightly to find the optimum position for your stethoscope but don’t move
too quickly or you could miss a sound.
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Technique of auscultation
A. Start from mitral area by putting the diaphragm of stethoscope
and Listen systematically to the cardiac cycle i.e. 1st and 2nd
heart sounds (S1 and 2) and listen in the systolic and diastolic
intervals for added sounds and murmurs. Time events with
simultaneous palpation of the carotid.
B. Roll your patient slightly onto his left side and listen in the 5th
ICS with the bell for the low frequency mid diastolic murmur of
mitral stenosis. (Listen in full expiration).
C. Auscultate in the axilla with the diaphragm for radiation and
comparative loudness of a systolic murmur. (e.g. the pan systolic murmur of mitral regurgitation radiates to the axilla.)
D. Go to TA then PA then AA ask patient to sit , lean forward
and exhale the air to check AA and listen at left lower sternal
edge for high frequency diastolic murmur of aortic regurgetation
E. auscultate with the diaphragm over both
carotids for bruits and radiation of
murmurs, (the ejection systolic murmur of
aortic stenosis radiates to the neck.)
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F. Use both the bell and diaphragm appropriately in the 4 areas –
That the bell should only be placed lightly on the skin.
The bell at the apex for low frequency sounds (i.e. murmurs)
The diaphragm at the base for high frequency sounds.
HEART SOUNDS
Heart sounds are discrete bursts of auditory vibrations of varying intensity
(loudness), frequency (pitch), quality, and duration.
Start by listening to the heart sounds. To help you differentiate between the
heart sounds they should be timed against the carotid pulse.
SUMMARY
S1 =1st heart sound best heard in MA
Muffled with MR as it is masked by pansystolic murmur
Very loud in MS with rumbling diastolc murmur
Timed with carotid pulsation
S2 =2nd heart sound heard in AA
Loud in PA in pulmonary HTN, loud in AA in systemic HTN
Timed with carotid pulsation “delay”
Soft A2 in AS , AR
S3 = Left ventricular failure-gallop rhythm
S4 = noncompliant ventricle LVH
S3 AND S4 DIASTOLIC SOUNDS , LOW PITCHED.
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S1 & S2 ARE NORMAL SOUNDS . S3&S4 ARE PATHOLOGICAL.
• The first heart sound is
. The sound of the mitral and tricuspid valves closing
.Systolic events tend to occur at the same time as the carotid pulse
. Loudest at the apex.
The S1 is muffled when there is an increased amount of tissue between the
heart and the stethoscope, as occurs with pleural effusion, pericardial
effusion, emphysema, pneumothorax, and obesity.
Conditions associated with a loud S1 include the following:



Increased transvalvular gradient (MS, TS, atrial myxoma)
Increased force of ventricular contraction (tachycardia, hyperdynamic
states [ie, anemia, fever, thyrotoxicosis, exercise, inotropic agents])
Shortened PR interval - Tachycardia, preexcitation syndromes (ie,
Wolff-Parkinson-White [WPW] syndrome)
Conditions associated with diminished intensity of S1 include the following:

Inappropriate apposition of the AV valves
(ie, mitral regurgitation [MR], tricuspid regurgitation [TR], dilated
cardiomyopathy)


Prolonged PR interval (ie, bradycardia, heart block, digitalis toxicity)
Decreased force of ventricular contraction
(ie, cardiomyopathy, myocarditis, myxedema, myocardial infarction [MI])

Increased calcification of the AV valve
(ie, calcific MS, postirradiation)

Increased distance from the heart
(ie, obesity, emphysema, pleural effusion, pericardial effusion)
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SO , S1 CAN BE HELPFUL FOR EVALUTING THE SEVERITY OF VALVULAR LESION.
.
• The second heart sound
.Closure of the aortic and pulmonary valves at end of systole.
.Follows the apical impulse and carotid pulsation.
. Best heard at the upper left sternal edge using the
diaphragm of the stethoscope.
A2 is best heard at the aortic area (second right intercostal space); P2 is best
heard at the pulmonary area. S2 is a high-pitched sound heard best with the
diaphragm of the stethoscope. The intensity depends on valvular factors, the
transvalvular gradient, mechanical factors, and size of the great vessels.
The intensity of A2 is increased in Systemic hypertension,
Coarctation of the aorta,
Aortic aneurysm,
Thin individuals,
and when the aorta is closer to the anterior chest wall as may occur with
tetralogy of Fallot and transposition of the great arteries (TGA).
The intensity of A2 is decreased with decreased aortic diastolic pressure ( AR),
with improper valvular apposition ( AR or aortic dissection), calcific immobile
valves ( calcific aortic stenosis [AS]), and decreased systemic arterial pressure.
The intensity of P2 is increased with pulmonary arterial hypertension
Split S2
Normally, the aortic valve closes slightly before the pulmonary valve. This
difference is more pronounced with inspiration due to increased RV stroke
volume.
The fixed-split S2-
ASD, right heart failure
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Third Heart Sound
The third heart sound (S3) is a low-pitched, early diastolic sound audible during
the rapid entry of blood from the atrium to the ventricle. When arising from the
LV, it is best audible at the apex with the patient in left lateral decubitus position
with breath held at end expiration. When it is of RV origin, S3 is best audible at
the left lower sternal border or the xiphoid with the patient in supine position.
These are best heard with the bell of the stethoscope. Conditions associated with
pathological S3 include the following:
A. Systolic and/or diastolic ventricular dysfunction
1. Ischemic heart disease
2. MR or TR
3. Sysetmic and pulmonary hypertension
4. Acute aortic regurgitation
5. Chronic AR with systolic dysfunction
B.Hyperkinetic states - Anemia, fever, pregnancy, thyrotoxicosis, AV fistula
C.Volume overload - Renal failure
Fourth Heart Sound
The fourth heart sound (S4) is a late diastolic sound that corresponds to late
ventricular filling through active atrial contraction. It is a low-intensity sound
heard best with the bell of the stethoscope. When of LV origin, S4 is best heard at
the apex with the patient in the left lateral decubitus position at end expiration.
When of RV origin, it is heard best at the left lower sternal border. Maneuvers
that increase the preload increase the intensity of S4 by increasing the separation
of S4 from S1.
Active atrial contraction is necessary for the generation of S4. Thus, S4 is not
audible with atrial fibrillation or flutter.
Some of the conditions associated with S4 include the following:




Ventricular hypertrophy - LV hypertrophy (systemic hypertension,
hypertrophic cardiomyopathy, AS); RV hypertrophy (pulmonary
hypertension, pulmonary stenosis [PS])
Ischemic heart disease - Acute MI,angina
Ventricular aneurysm
Hyperkinetic states that cause forceful atrial contraction
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Both S3 and S4 need to be differentiated from splitting of the normal heart
sounds. With splitting, the heart sounds are high pitched and best audible
with the diaphragm, whereas the S3 or S4 are low-pitched sounds best audible
with the bell of the stethoscope
Is there any audible sound other than heart sounds?
MURMURS
1.‘‘Inching’’ the stethoscope (i.e., slowly dragging it from site to site)
can be the best way to avoid missing important findings.
2. From MA TO TA THEN PA OT AA or THE REVERSE AA.
3. Murmurs are common in MA AND AA THAT IS LEFT SIDE.
Definition:
The production of murmurs results from turbulent flow across valves. Three main
factors have been attributed to cause a murmur:
(1) high flow rate through normal or abnormal orifices
(2) forward flow through a constricted or irregular orifice or into a dilated vessel or
chamber, (3) backward or regurgitant flow through an incompetent valve.
When evaluating a heart murmur, it is important to know the timing of the
murmur in the cardiac cycle, the location, the duration, character, configuration,
radiation, aggravating maneuvers, and diminishing maneuvers.
Types of murmurs:
1.Systolic (holosystolic, early/middle/late systolic)
2.Diastolic (early/middle/late) or
3.Continuous (ie, present in both systole and diastole).
All diastolic murmurs and any systolic murmur above grade 2
in severity requires further evaluation with echocardiography.
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TIME
The timing of the murmur is determined by palpating the
carotid pulse while listening to the murmur. The carotid upstroke
corresponds to the onset of systole.
LOCATION
This is the area of the heart where the murmur is heard the loudest.
While auscultating, one should concentrate on the apex, pulmonary
area, tricuspid, and aortic areas, in addition to the axilla, base of the
heart, and left fourth ICS for evidence of radiation of murmur.
INTENSITY:
The intensity of the murmur depends on the volume of blood flow
across the valve and the pressure gradient across which the blood
flow occurs.
What is the Levine system for grading the intensity of murmurs?
The intensity or loudness of a murmur is traditionally graded by the
Levine system from 1/6 to 6/6. Increased intensity usually reflects
increased flow turbulence. Thus, a louder murmur is more likely to be
pathologic and severe.






Grade I - Heard in a quiet room by an expert examiner
Grade II - Heard by most examiners
Grade III - Loud murmur without thrill
Grade IV - Loud murmur with a thrill
Grade V - Thrill with a very loud murmur audible with stethoscope
placed lightly over the chest
Grade VI - Thrill with a very loud murmur audible even with the
stethoscope slightly away from the chest
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Quality/character:
Different murmurs have different qualities, such as
harsh, blowing, rumbling, musical.
Pitch:
This can be high or low pitched depending on the frequency of the
murmur. The high-pitched sounds are best audible with a diaphragm
and the low-pitched sounds with the bell.
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Radiation:
Murmurs tend to radiate to certain specific areas that are often characteristic of a
particular murmur. The murmur of MR radiates to the axilla or base of the heart,
depending on which leaflet is involved. In the case of AS, the murmur radiates in
the direction of the jet of turbulent blood (ie, radiates to the carotids). Similarly,
the aortic regurgitant murmur tends to radiate along the left sternal border.
Configuration:
This corresponds to the shape of murmur intensity over time. It can be a plateau,
decrescendo, crescendo-decrescendo, or crescendo murmur.
Maneuver affect on murmur:
1.Affect of respiration
The murmurs generated from the right side of the heart increase in intensity
with inspiration by increasing the venous return to right side. ,
Murmurs arising from the left side of the heart become more prominent with
expiration as blood is forced from lung to the heart.
2.Standing up:
This causes a peripheral pooling of blood and a net decrease in venous return.
Most murmurs are thus decreased in intensity upon standing, except that of
hypertrophic obstructive cardiomyopathy (HOCM) and MVP, which become
more prominent.
3.Squatting:
Squatting causes an increase in the afterload and venous return (ie, preload).
The net effect is an increase in intensity of all the murmurs, except those
associated with MVP and HOCM, which become less prominent with
squatting.
4.Hand grip:
Hand grip is a form of isometric exercise and increases the afterload, arterial
pressure, LV volume, and LV pressure. The net effect of these changes is
complex and variable. Murmurs of MR, AR, and VSD worsen with hand grip,
while those of HOCM and MVP are less prominent.
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Cardiac cycle
As a rule , the stenosis will be evident once blood flow through the valve and the valve is
opened that with associated turbulent flow.
The 2nd rule is the regurgitation will be evident once there is no blood flow through the
valve and valve closed
In systole, left and right ventricles contract
Aortic valve and pulmonary valves opened
Mitral and tricuspid valves closed
Aortic and pulmonary valves opened. If there is stenosis “AS/PS” , ejection systolic
murmur will be heard in aortic area/ pulmonary area which is harsh high pithched loud of
crescendo- decrescendo in configuration as blood is pumped with high amount during
systole which became more audible by sitting leaning and in full expiration in AS.
Mitral valve and tricuspid valves closed. If there is regurgitation “MR/TR”, pansystolic
murmur will be heard in mitral area and tricuspid area which is blowing and high pitched
plateau in configuration which became more audible by telt to left side in apex beat in
the expiration and radiate to left axilla in MR.
In diastole, left and rig ventricles relaxed.
Mitral and tricuspid valves opened.
Aortic and pulmonary valves closed .
Mitral and tricuspid valves opened . If there is stenosis “MS/TS”, mid diastolic murmur
will be heard in mitral area and tricuspid area which is low-pitched rumbling , best heard
with the bell of the stethoscope placed over the cardiac apex with the patient in the left
lateral position in mitral stenosis in expiration with loud S1.
Aortic and pulmonary valves closed. If there is regurgitation, “AR/PR” early diastolic
murmur will be heard in aortic area and pulmonary area which is high-pitched sound, is
decrescendo in configuration , and is most audible at the left sternal border or the right
second ICS just to the right of sternum, with the patient leaning forward at end expiration
in AR.
AS/PS = EJCETION SYSTOLIC MURMU
MR/TR = PANSYSTOLIC MURMUR
AR/PR = EARLY DIASTOLIC MURMUR
MS/TS =MID DIASTOLIC MURMUR
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Systolic murmurs;
1. Pansystolic murmurMitral regurgitation
Tricuspid regurgitation
Ventricular septal defect
These murmurs last throughout ventricular systole. They usually start at S1 and
proceed through S2; the intensity of the murmur may overshadow both valve
closure sounds.
These murmurs are typically produced by emptying of the high-pressure
ventricle during systole into chambers that have lower pressure at that time (the
atria with MR or TR or the right ventricle in the case of VSD).
The murmur of MR is blowing and high pitched and is best heard at the apex
with radiation to the axilla or the base of the heart. It is usually plateau in
configuration. The MR murmur is increased during expiration, passive leg
raising, squatting, and handgrip and decreased in intensity with inspiration,
Valsalva, and standing. The radiation of the murmur depends on which leaflet
is involved. A murmur generated by the deformity of anterior leaflet radiates
more toward the axilla, thoracic spine, and scapula, while a murmur arising
from posterior leaflet involvement radiates to the base of the heart
Severe MR
. The presence of S3
. Signs of pulmonary hypertension and right heart failure
The murmur of TR is best heard at the left lower sternal border. It is a
blowing high-pitched murmur heard that increases in intensity with
inspiration (Carvallo sign). It can result primarily from involvement of the
tricuspid valve or secondarily from pulmonary hypertension. When due to
pulmonary hypertension, it is associated with a loud P2.
In VSD with normal pulmonary arterial pressures, a holosystolic murmur can
be heard over the left lower sternal border at the level of the third and fourth
ICSs. This murmur depends on the orifice size of the septal defect. The
smaller the defect, the greater the intensity of the murmur.
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2.Ejection systolic murmur “mid to late systole”
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Aortic
o Obstructive
 Supravalvular - Supravalvular AS, aortic coarctation
 Valvular - AS, aortic sclerosis
 Subvalvular - HOCM
o Increased flow, hyperkinetic states, aortic regurgitation,
complete heart block
o Dilatation of the ascending aorta, aortitis, atheroma
Pulmonary
o Obstructive
 Supravalvular - Pulmonary artery stenosis
 Valvular - Pulmonary valve stenosis
 Subvalvular - Infundibular stenosis
o Increased flow, hyperkinetic states, left-to-right shunt
o
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These murmurs are usually associated with ventricular outflow tract
obstruction (which can be valvular, supravalvular, or subvalvular) or an
abnormal amount of blood flow across normal valves as can happen in
hyperdynamic states (hyperthyroidism, fever, pregnancy, anemia, renal
failure).
AS/PS
The murmur associated with valvular stenosis (AS or PS) is usually a harsh murmur
which is crescendo- decrescendo in configuration and high pitched.
AS-associated murmurs are most audible at the right upper sternal border/right
third ICS with the patient in the upright position and breath held at end
expiration. In some cases, it is audible at the apex, in which case it can be confused
with the murmur of MR. Some of the findings that help delineate the murmur of
MR from that of AS include an audible S1, forceful apex, radiation to carotids,
changes with atrial fibrillation, and post-PVC accentuation. The AS murmur usually
radiates to the carotid arteries.
MAGDI AWAD SASI 2013
Early diastolic murmurs
Are produced by either AR or pulmonary regurgitation.
ar
The AR murmur is a soft high-pitched sound, is decrescendo in configuration, and is most
audible at the left sternal border or the right second ICS just to the right of sternum, with
the patient leaning forward at end expiration. The murmur radiates to the left lower
sternal border if it is due to primary valve disease. In patients with aortic root disease, the
murmur may radiate to the right sternal border. The murmur increases in intensity during
expiration and decreases in intensity with hand grip. The S2 is usually muffled with AR.
PR
The murmur of pulmonary regurgitation is best audible at the pulmonary area. The
character, quality, and pitch of the murmur vary depending on the presence or absence of
pulmonary hypertension. In the presence of pulmonary hypertension, it is a high-pitched,
decrescendo murmur also known as a Graham Steell murmur. S2 is usually loud in
association with pulmonary regurgitation. In the absence of pulmonary hypertension, it is a
low-pitched crescendo-decrescendo murmur.
Mid- to late diastolic murmurs
These murmurs are produced by the blood flow across stenotic AV valves.
MS produces a low-pitched, mid-diastolic, rumbling murmur with presystolic accentuation,
best heard with the bell of the stethoscope placed over the cardiac apex with the patient in
the left lateral position. S1 is loud. The murmur usually follows an OS, and the interval
between the A2 and OS is inversely proportional to the severity of obstruction.
The murmur of MS is increased in intensity with expiration and maneuvers that increase
cardiac output, such as exercise. The presystolic accentuation results from atrial
contraction in late diastole and is absent in patients with atrial fibrillation. The duration of
murmur corresponds to the period in which the LA-LV diastolic pressure gradient is
maintained. This duration correlates with the severity of obstruction; the longer the
murmur duration, the more severe the MS (provided the diastolic filling time is not
shortened, as may happen in tachycardia) except in high cardiac output and pulmonary
htpertension.
D/D OF MID DIASTOLIC MURMUR:
1.
2.
3.
4.
Tricuspid stenosis=tricuspid area
Atrial myxoma- change by position
Austin Flint murmur- due to AR
Carey Coombs murmur-rhematic heart disease
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Continuous Murmurs
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PDA
Coronary arteriovenous fistula
Ruptured sinus of Valsalva aneurysm
Aortopulmonary window
Anomalous left coronary artery from the pulmonary artery
Bronchial collateral circulation
Opening Snap
The opening snap (OS) is a high-pitched diastolic sound produced by rapid
opening of the mitral valve in MS or TS. When mitral in origin, it is best heard
at the apex following the aortic sound A2, with the patient in left lateral
decubitus position.
The time difference between the A2 and OS has a diagnostic implication. The
closer the OS is to A2, the more severe the stenosis. The OS signifies when the
left atrial pressure exceeds the LV diastolic pressure and marks the beginning of
blood entry into the LV from the LA. The more severe the stenosis, the greater
the LA pressure and the lesser the LA-LV early diastolic pressure gradient,
leading to an early opening of the mitral valve. In general, the relation between
A2 and the OS depends on LV pressure at A2 closure, LA pressure at A2 closure,
and the rate of LV pressure decline.
Pericardial rub
It indicates pericardial inflammation.
• Inflammation of the pericardial membrane or pleural sac at the 3rd and 4th
interspace at the left sternal border. Louder during inspiration
• Scratchy, like sandpaper being used, a match being struck, or leather
squeaking .
• Sound present when the epicardial & pericardial surfaces, roughened by
inflammation, slide over one another during atrial & ventricular systole &
during the passive motion of rapid ventricular filling.
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• 3 components
– Atrial Systolic (A)
– Ventricular Systolic (V)
– Ventricular Diastolic (D)
Percardial Knock
• Sharp, high-pitched sound present in 90% or more of patients
with constrictive pericarditis
• Heard in diastole
• Occurs .09 to .12 sec after S3
• Occurs after Heart Surgery, radiation therapy, viral infection, TB
pericarditis
• Diaphragm of the stethoscope listen at the lower left sternal
border
Tumor Plops
• Clues to a Myxoma
– Cardiac silhouette on X-Ray consistent with atrial
enlargement
– An ECG showing signs of LA enlargement
– Light-headedness
– A very short presystolic murmur
– Extra sound in diastole
• Left Atrial Tumors
– Loud, low-frequency thud heard in early diastole & caused
by abrupt movements of the tumor inside the LA
– It strikes the wall of the chamber or comes to a sudden halt
as the pedicle reaches the limit its stretch
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SUMMARY SHEET OF CVS EXAMINATION
1. INSPECTION
Chest deformity
Skin ,scars , pulsation, vessels
Respiratory movements
Accessory muscles of respiration
2. PALPATION
Trachea
Apex beat- line , space , character
Thrill- MA , TA ,PA & AA.
Heave - left parasternal
3. AUSCULTATION
Start in mitral area by diaphragm and listen for S1 ,S2 ,M
For murmur , site ,time ,radiation, character, grade ,pitch.
Tilt pt to left lateral and use the bell to here diastole in MA
Change the bell to diaphragm to auscultate axilla for PSM
Inch to TA and check S2 and ask pt to hold in inspiration
Inch to PA to hear P2 and murmurs if present
Concentrate on AA and ask pt to sit , lean ,and full expiration
Lastly check carotids by diaphragm for systolic radiation
MAGDI AWAD SASI 2013
MAGDI AWAD SASI 2013