Examining the precordium

The precordium refers to that

part of the chest overlying the

heart.
Inspection
Palpation
Percussion
Auscultation

Inspection
For most of the cardiac
examination, the patient should be
supine with the upper body raised
by elevating the head of the bed or
table to about 30.
Two other positions are also
needed: (1) turning to the left side,
and (2) leaning forward.
The examiner should stand at the
patients right side. Look for:

Inspection
Scars
Cutaneous venous colllaterals
Chest shape and movements,

precordial projection
Apical impulse
Visible pulsations

Scars : A midline sternotomy scar usually

indicates previous coronary bypass surgery

or valve replacement.
A left lateral thoracotomy may be evidence of
previous closed mitral valvotomy, resection
of coarctation, or ligation of a patent ductus
arteriosus.
Cutaneous venous colllaterals: over the
anterior chest suggest obstruction of the
superior vena cava or subclavian vein
Abnormal chest shape or movements:
Unilateral asymmetry of the left side of the

chest because of right ventricular

hypertrophy before puberty.

Pectus excavatum (posterior

displacement of the lower sternum) seen

in Marfans syndrome and in mitral valve
prolapse, and pectus carinatum ('pigeon
chest') associated with Marfans
syndrome , may displace the heart and
affect palpation and auscultation.
Barrel shaped chest can be related to
COPD and cor pulmonale
Pacemaker or implantable defibrillator,
usually implanted over the left pectoral
region.

Precordial projection
congenital heart disease: tetralogy of Fallot
Valvular heart disease--

MS,PS
pericardial effusion (large , childhood)
The second right intercostal space(2nd ICS-RS)
aneurysm of aortic arch
dilatation of ascending aorta
Abnormal chest wall movements: in-drawing of
the intercostal spaces during systole because
the left ventricle is tethered to the chest wall
by the diseased pericardium in chronic
constrictive pericarditis.

Apical impulse: Careful inspection of the

anterior chest may reveal the location
of the apical impulse or point of
maximal impulse.
Abnormal apical impulse-Inward
impulse:
apex excavation in the systole is seen
in :
adhesive pericarditis
prominent RV hypertrophy

Visible pulsations
In the right second and third intercostal

space, parasternal- a dilated or aneurysmal

aorta.
In the left second and third intercostal
space-dilatation of the pulmonary artery or
increased flow in the pulmonary artery.
Left parasternal area in the 3rd, 4th, and 5th
interspaces: right ventricular hipertrophy .
Pulsation in the epigastric or subxiphoid
area- right ventricular hipertrophy-Harzer
sign
Pulsation in the supraombilical areaabdominal aorta (in asthenic patients or in
aneurysm of the abdominal aorta).

Cardiac palpation
Palpation of the apical impulse (the apex

beat)
Palpation of visible pulsations
Palpable heart sounds
Palpable murmurs: thrills
Pericardial friction rub
The apex beat or apical impulse:
The lowest and most lateral position on
the chest wall where a cardiac impulse can
be felt representing the brief early
pulsation of the left ventricle as it moves
anteriorly during contraction and touches
the chest wall.

Palpation of the apex beat:

Locate the apex beat by laying your fingers on the chest

parallel to the rib spaces .

Position of the patient for palpation of the apex beat:
supine . If you cannot identify the apical impulse with
the patient supine, ask the patient to roll partly onto the
left sidethis is the left lateral decubitus position.
Palpate again using the palmar surfaces of several
fingers. If you find in this position the apex beat, count
back 2 cm medially, as the apex beat moves laterally 2
cm-s .
If you cannot find the apical impulse, ask the patient to
exhale fully and stop breathing for a few seconds.
Assess:
Location
Diameter
Amplitude
Duration

Location:
The apex beat is normally found in the 5th

left intercostal in the mid-clavicular line or 11,5 cm medial to the MCL

Diameter
In the supine patient, it usually measures
less than 2.5 cm and occupies only one
interspace. 3 cm or less in left sided position.
Amplitude
It is usually small and feels brisk and
tapping.
Some young persons have an increased
amplitude, or hyperkinetic impulse,
especially when excited or after exercise; its
duration, however, is normal.

Duration
Duration is the most useful characteristic

of the apical impulse for identifying

hypertrophy of the left ventricle.
To assess duration, listen to the heart
sounds as you feel the apical impulse, or
watch the movement of your stethoscope
as you listen at the apex.
Estimate the proportion of systole
occupied by the apical impulse.
Normally it lasts through the first two
thirds of systole, and often less, but does
not continue to the second heart sound.

Abnormalities of the apical impulse:

Amplitude
Reduced or impalpable apex beat: chest

deformity, obesity, emphysema, a very muscular

chest wall, pericardial effusion, a markedly dilated
failing heart , ,death.
Beware of dextrocardia. If no beat is felt, check
the right side.
Impalpable: apex beat is behind a rib.
Increased amplitude:
A hyperkinetic impulse results from increased
stroke volume and does not necessarily signify
heart disease, thus can be caused by
hyperthyroidism, severe anemia, fever.
An impulse may feel hyperkinetic when the chest
wall is unusually thin, in young patients especially
after exercise or excitement.

A forceful or thrusting apex

either in the normal position or

slightly displaced to the left is
usually due to concentric left
ventricular hypertrophy caused
by pressure overload (e.g aortic
stenosis, hypertension).
Increased amplitude may also
reflect volume overload of the
left ventricle (e.g., mitral or
aortic regurgitation).
A heave is a palpable impulse

Displacement of the apex beat:

Upward and to the left by pregnancy or a

high left diaphragm.

The apex may be displaced laterally in
subjects with:
chest deformity, or because of
mediastinal shift (in these situations the
trachea may also be deviated) secondary
to
a large pleural effusion,
tension pneumothorax (away from the
affected side)
pneumonectomy
lung collapse (towards the affected

Diffusely displaced inferiorly and

laterally (to the left) in: volume overload

(e.g. mitral or aortic regurgitation) or
severe left ventricular dysfunction with
left ventricular enlargement.
Diameter:
Increased in pressure or volume
overload.
When a ventricle works under conditions
of chronic pressure overload or increased
afterload, its walls gradually thicken or
hypertrophy.
Volume overload (increased preload), in
contrast, produces dilatation of the
ventricle as well as thickening of its

Duration:
Sustained: impulse longer than expected

(left ventricular hypertrophy, aortic stenosis,

hypertrophic cardiomyopathy or hyperkinesia).
Double impulse: (palpable atrial systole)
characteristic of hyptertrophic cardiomyopathy.
Palpation of visible pulsations:
Left and right second and third interspace
Left parasternal (right ventricular) heave
A significantly hipertrophied and/or dilated
right ventricle will produce an abnormal
impulse at the lower end of the
sternum,usually to the left side

Apical beat modifications

Normal

Hyperkinet
ic

Pressure
Overload

Volume
Overload

Location

5th ICS MCL

Normal

Normal

Displaced
left and
downward

Diameter

Little more
Normal
than 2 cm in
adults

Increased

Increased

Amplitude

Small,
gentle

Increased

Increased

Increased

Duration

Usually less
than 2/3 of
systole

Normal

Prolonged,
Often
may be
slightly
sustained up prolonged
to s2

Anxiety,
severe
anaemia,
hyperthyroid
osis

Aortic
stenosis,
systemic
hypertensio
n

Examples of
causes

Aortic or
mitral
regurgitatio
n

Pressure overload: means that

the ventricle works under

conditions of increased afterload,
its walls gradually thickens
(hypertrophy)
Volume overload: means that the
ventricle works under increased
preload, this produces dilatation
of the ventricle and also
thickening of its walls.

Palpable heart sounds:

The 'tapping' apex beat: this is the description

given to a palpable 1st heart sound in severe

mitral stenosis.
A palpable S2 a sharp snapping felt in the left
2nd interspacepulmonic area -suggests
increased pressure in the pulmonary artery
(pulmonary hypertension).
A palpable S2 a sharp snapping felt in the right
2nd interspace-aortic area-suggests systemic
hypertension.
A brief mid-diastolic impulse indicates an S3gallop, in cases of advanced heart failure.
An impulse just before the systolic apical beat
itself indicates an S4 gallop in cases of poor left
ventricular distensibility during diastole.
The opening snap of mitral stenosis felt at the
apex.

Palpable murmurs are called thrills and are felt

as a shudder beneath your hand or rather like

placing your hand on a purring cat.
Thrills are the superficial vibratory sensations
felt on the skin overlying an area of turbulence.
One of characteristic signs of organic heart
disease.
The presence of a thrill indicates a loud murmur,
4/6 or louder.
They are usually best felt using the heads of
your metacarpal bones rather than the fingertips
and applying very gentle pressure on the skin in
the areas where the murmur is best heard
Caused by severe valvular disease (If systolic:
aortic stenosis, ventricular septal defect or
mitral regurgitation; diastolic: mitral stenosis.)

Pericardial friction rub

1) Precordium-4th ICS-LS
2) both phases of the cardiac cycle
3) systolic period, sitting erect and
leaning forward, the end of expiration
4) mechanism: rub of the visceral and
parietal layers of pleura
5) felt in acute pericarditis

Cardiac percussion
Percussion may provide an estimate of a

patients heart size the cardiac dullness.

It is seldom used nowadays.
With percussion we can determine the
absolute cardiac dullness, where the heart
is in direct contact with the chest, and the
relative cardiac dullness, where we
determine the dullness of the heart
including those portions where the heart is
partially covered by the lung.
Superior margin: percussion in the midclavicular line downward, normally in the
third intercostal space we find the cardiac
dullness.

Right margin: percussion in the right

midclavicular line downward until we find

the hepatic dullness, after that we change
the position of the hand on the chest in
vertical position and continue the
percussion in a the latero-medial direction
toward the sternum until we find dullness.
Normally this will be at the right border of
the sternum-sternal line.
Inferior margin: is determined by the apical
impulse and the superior margin of the
liver.
Left margin: it is a curve line between the
apex and the superior margin of the third
rib in the sternal line. The percussion is
performed in a radial way in the superoinferior and latero-median direction .

Abnormalities of cardiac dullness

Relative cardiac dullness is

increased :
In all directions:
Cardiomegaly
Pericardial effusion
Transversally-to the left and right:
right ventricular dilatation ,
hipertrophy
Downward: left ventricular
hipertrophy , dilatation
Relative cardiac dullness is decreased
or disappeared: emphysema, left

Modification of cardiac dullness

due to extracardiac diseases:

Abdominal: tumors, ascites,
meteorism, gravidity, diaphragm
paralysis CD is moved upwards
Pulmonary: right pleural effusion,
pneumothorax, lung tumor moves
cardiac dullness to the left
Left pulmonary
atelectasis,pulmonary fibrosis
toward the left

Cardiac auscultation
It is an important aspect of the clinical

cardiovascular examination, but

auscultatory skills are decreasing with
the almost universal availability of
echocardiography.
Auscultation requires a stethoscope
equipped with a bell and a diaphragm.
The bell emphasizes low-pitched sounds
such as the murmur of mitral stenosis.
The diaphragm filters out these sounds
and helps to identify high-pitched
sounds such as normal heart sounds and
most systolic murmurs.

You must know :

the surface anatomy of the heart
to understand how and where the
sounds and murmurs radiate and
basic cardiac physiology to

appreciate their timings.

Surface Projections of the

Heart and Great Vessels
The right ventricle
occupies most of the
anterior cardiac
surface.
and to the left of the
sternum.
The left ventricle,
behind the right
ventricle and to the
left, forms the left
lateral margin of the
heart. Its tapered
inferior tip is often
termed the cardiac
apex.

The cardiac cycle

Technique of cardiac auscultation

1. Where to listen- areas of

auscultation
2. What and how to identify and
describe by listening:
the first and second heart sounds
extra heart sounds (third and fourth
heard in diastole)
additional sounds, e.g. clicks and
snaps
pericardial rubs
murmurs in systole and/or diastole.

Where to listen-areas of auscultation

1. Mitral: at and around the cardiac apex. Sounds

and murmurs arising from the mitral valve are

usually heard best here.
2. Tricuspid: 5th intercostal space at the left sternal
edge. Sounds and murmurs originating in the
tricuspid valve are heard best here.
3. Pulmonary: 2nd intercostal space at the left
sternal edge.
4. Aortic: 2nd intercostal space at the right sternal
edge.
5. Erb-Botkin: 3rd intercostal space at the left
sternal edge, for listening the murmur in aortic
insufficiency.
These areas do not relate exactly to the anatomical
position of the valves but are the areas at which
the sound of each valve can be best heard.

Practice is needed here and many hearts should be

listened to in order to be familiar with the normal

sounds.
Make sure the room is quiet when auscultating.
Position of the patient:
The patient lying at approximately 45 .
Left lateral decubitus (bringing the left ventricle
close to the chest wall) for listening murmur of
mitral stenosis, leftsided S3 and S4
Sitting, leaning forward , exhaling completely and
withholding breath for listening aortic
regurgitation.
Standing up for listening mitral valve prolapse
Ask the patient to briefly stop breathing while you
are listening.
Normal heart valves make a sound when they close
(lub-dub) but not when they open.

Use a regular routine for auscultation.

Sequence of auscultation is not important, one can

start either at the apex or at the base, just do not

leave out any of the areas of auscultation.
You can then go back and concentrate on any
abnormalities.
First step should be identifying the two heart
sounds.
Simultaneously feel the carotid pulse with your
thumb to time the sounds and murmurs. The carotid
pulsation occurs with S1.
Another way to recognize sounds is the duration of
the pause: between sounds: the sound which
appears after a longer pause (diastole) is S1
Listen with the diaphragm at each area and then
repeat using the bell.
Listen over the carotid arteries and in the left axilla.

At each site :
Identify the first and second heart sounds
Assess their character and intensity
Note any splitting (relation of splitting to

respiratory phases, wideness of splitting)

Concentrate in turn on systole (the interval
between S1 and S2) and diastole (the interval
between the S2 and S1).
Listen for added sounds and then for murmurs
(note location, timing, intensity, pitch, effect of
resppiration)
Use special positions as mentioned above.
Use inspiratory or expiratory apneea
Note the character and intensity of any murmur
heard.
Sometimes listen after exercise.

Effects of respiration on auscultation

If a murmur or sound is made

louder by inspiration it is nearly

always right sided since right
heart blood flow is increased
during inspiration.
If a murmur is made louder by
expiration it may be left sided,
but this is not definite since
expelling air from the lungs
decreases the amount of air
between the heart and chest wall

Normal heart sounds

Normal findings
S1 and S2 are usually the only heart

sounds heard on auscultation of a normal

heart, although in young and athletic
subjects a soft third sound S3 may be
present.
The first heart sound (S1)
Is caused by the closure of the mitral and
tricuspid valves at onset of ventricular
systole and
It is best heard at the apex (mitral area)
It has low intensity, it is low pitched and
longer duration than S2.

The second heart sound (S2)

Is caused by closure of the

pulmonary and aortic valves at the

end of ventricular systole , and
Is best heard at the basis of the
heart.
The second sound is louder and
higher pitched than the first
sound, has a shorter duration and
normally the aortic component is
louder than the pulmonary one.

Physiological splitting of the second

heart sound occurs because contraction

of the left ventricle slightly precedes
that of the right ventricle so that the
pulmonary valve closes after the aortic
valve.
This splitting increases at endinspiration because the increased
venous filling of the right ventricle
further delays pulmonary valve closure.
This separation disappears on
expiration .
Splitting of the second sound is best
heard at the left sternal edge using the

Heart sounds other than S1 and S2 are

usually abnormal, but S3 and an ejection

sound and very rarely S4 can occur in
normal subjects.
A third heart sound (S3)
Is a low-pitched early diastolic sound
best heard with the bell at the apex.
It coincides with rapid ventricular filling
immediately after opening of the
atrioventricular valves.
A third heart sound is therefore heard
after the second as 'lub-dub-dum'.
A third heart sound is a normal finding in
children, young adults and during
pregnancy.

Ejection sound: an ejection sound occurs

as the aortic or pulmonary valve opens

and is close to S1 .
Ejections sounds are sometimes heard in
normal subjects but the most common
cause in an asymptomatic patient is a
bicuspid aortic valve.
S4 also called atrial sound is
exceptionnaly rare in normal subjects

Abnormalities of the heart sounds

Intensity of heart sounds can be

influenced by :
Thickness and elasticity of the
chest wall
Elasticity and density of the lungs
Phases of respiration
Ventricle contractility and output
Distance from which valves are
closing
Speed at which valves are closing

Pathological third heart sound

This is a low frequency (can just be heard with the

bell) sound occurring just after S2 at the end of

rapid ventricular filling, early in diastole and is
caused by tautening of the papillary muscles or
ventricular distension.
It can be heard as Da-da-dum or ken-tuck-y.
Is usually pathological after the age of 40 years
Combined with the normal heart sounds produces
a triple rhythm or gallop rhythm as it
resembles galloping horses-protodiastolic or
ventricular gallop
Left sided S3 is best heart at the apex in the left
lateral position during expiration
Right sided S3 is best heard along the lower left
sternal border or below the xifoid, in supine
position, durin inspiration

Clinical implication of a pathological S3:

LV impairment (decreased conpliance) or

increased filling.
The commonest causes are:
left ventricular failure (IHD, hypertensive
heart disease, MI, severe myocarditis)
dilated cardiomyopathy,
mitral regurgitation
tricuspid regurgitation
aortic regurgitation.
In cardiac failure S3 is usually
accompanied by a tachycardia and S1
and S2 are quiet.

4th heart sound (atrial sound or atrial

gallop or pre-systolic gallop) occurs

just before S1 in the late diastole.
Clinical implication: left ventricular
impairment or hypertrophy.
It is soft and low pitched, best heard
with the bell of the stethoscope at
the apex.
It is caused by decreased compliance
or increased stiffness of the
ventricular myocardium.
Can be heard Da-lub dubor Tenne-ssee.

Coincides with abnormally forceful

atrial contraction and raised end

diastolic pressure in the left
ventricle.
It is almost always pathological.
Causes of left sided S4 (heard at
the apex in left lateral position)
hypertrophic cardiomyopathy
aortic stenosis and
systemic hypertension
ischaemic heart disease

Causes of right sided S4 (best heard

along the lower left sternal border or

below the xifoid):
Pulmonary hypertension
Pulmonic stenosis
Occasionally, a patient has both an
S3 and an S4, producing a quadruple
rhythm of four heart sounds.
At rapid heart rates the S3 and S4
may merge into one loud extra heart
sound, called a summation gallop.

Additional or extra heart sounds

Extra heart sounds in systole:
Ejection clicks
Mid-systolic clicks
Extra heart sounds in diastole:
opening snap
pericardial knock
Mechanical prosthetic valves

Extra heart sounds in systole:

Ejection click occur early in systole just after the

first heart sound, caused by the opening of

stiffened but not too calcified semilunar (aortic,
plmonary)valves or by systemic or pulmonary
hypertension
This is a high-pitched sound , sharp, clicking
quality, which can be heard with the diaphragm
of the stethoscope at the aortic or pulmonary
areas and down the left sternal edge.
Clinical significance: indicate cardiovascular
disease.
Causes:
Over the aortic area: aortic stenosis, bicuspid
aortic valve, systemic hypertension
Over the pulmonary area: pulmonic stenosis,
pulmonary hypertension

Midsystolic clicks
Occur in mitral valve prolapse (abnormal

systolic ballooning of part of the mitral

valve into the left atrium)
The prolapsing mitral valve tenses in
mid/late systole and this produces single
or multiple clicks.
May be associated with a late systolic
murmur .
They are high pitched , clicking in quality
and best heard at or medial to the apex
with the diaphragm.
Squatting delays the murmur, standing
moves it closer to S1.

Extra heart sounds in diastole:

Opening snap
An opening snap is commonly heard in mitral

(rarely tricuspid) stenosis (if the valves are

not calcified and almost immobile)
The mitral valve normally opens immediately
after S2.
In mitral stenosis, sudden opening of the
stiffened valve , due to high atrial pressure
can cause an audible high-pitched snap,
early in diastole, just after the second heart
sound .May be followed by the murmur of
mitral stenosis.
The opening snap of mitral stenosis is best
heard at the apex and over the left sternal
edge in 4-5 th ICS, with the diaphragm.

Pericardial knock:
May be heard in early diastole .
Appears in constrictive

pericarditis
Is due to the high pressure
atrium rapidly decompressing into
a restricted LV producing an
audible reverberation.

Extra heart sounds in systole and diastole:

pericardial friction rub

It is a superficial scratching , high pitched
sound, comparable with creaking leather, best
heard with the diaphragm of the stethoscope
Often has systolic and diastolic components.
It may be audible over any part of the
precordium ,usually heard best in the 3rd
interspace to the left of the sternum (Erb
Botkin)and is often very localized, does not
radiate.
Intensity varies over time, increases when the
patient leans forward and during expiration.
It is most often heard in acute viral pericarditis
and sometimes 24-72 hours after myocardial
infarction.

MURMURS
Murmurs are audible vibrations produced

by turbulent flow through the heart, across

an abnormal valve, septal defect or outflow
obstruction, or by increased volume or
velocity of blood flow through a normal
valve.
Murmurs are differentiated from heart
sounds by their longer duration.
Whatever constricts an orifice, whatever
dilates a cavity, whatever establishes an
orifice or cavity where none shall be, will
disturb the even flow of blood and produce
vibrations and a murmur.
Samuel Jones Gee (18391911

Clinically murmurs can be:

Innocent murmurs
Functional or relative murmurs
Organic murmurs
Innocent murmurs : no anatomic or

physiologic abnormality exists

Occur in a healthy heart in situations
where the circulation is hyperdinamic,,
e.g. normal children, during pregnancy,
fever, anaemia and hyperthyroidism.
They are always systolic, usually soft or
moderate in intensity and with musical
quality.
It may require an echocardiogram to be
sure that murmurs are innocent.

Functional or relative murmurs:

Without anatomical lesions of the

valves
They reflect cardiac diseases
Can be caused by:
Dilatation of great vessels
Dilatation of valvular orificies
(secondary to left or right ventricle
dilatation)
Papillary muscle dysfunction
Congenital heart disease (ASD, VSD)
Organic murmurs: are produced by
anatomical lesions of the valves,
leading to stenosis or incompetence

For each murmur heard, you should

determine:
1. Timing: relation to cardiac cycle
(systolic, diastolic, systolodiastolic)
2. Pattern (shape)
3. Intensity (loudness)
4. Location of Maximal Intensity
5. Radiation
6. Character and pitch
7. Variation of the murmur: with
position, with respiration, with

1. Timing: relation to cardiac cycle (systolic,

diastolic, systolo-diastolic)
Decide if you are hearing a systolic murmur,
falling between S1 and S2, or a diastolic
murmur.
Murmurs that coincide with the carotid
upstroke are systolic.
Within systole or diastole they can be
heard :
At the beginning-early or proto-systolic ,
early or proto-diastolic
In the middle: mid-systolic, mid-diastolic,
At the end : late systolic or telesystolic,
late-diastolic or tele-diastolic or pre-systolic.
Throughout the systole: pansystolic or
holosystolic.

2. Pattern (shape)
The shape of a murmur is determined by

its intensity over time.

A crescendo murmur grows louder : MS
presystolic(only in sinus rhythm)
A decrescendo murmur grows softer :AI
A crescendodescrescendo murmur first
rises in intensity, then falls :AS
A plateau murmur has the same intensity
throughout :MI
Continuous :PDA

3. Intensity (loudness)
Based on Levine 6 grade classification

expressed as a fraction (1/6).

Grade 1 Very faint murmur, heard by an expert
in optimum conditions.
Grade 2 Soft, heard by a non-expert in optimum
conditions.
Grade 3 Easily heard, moderately loud, without
an associated thrill (palpable murmur)
Grade 4 Loud murmur with barely palpable thrill
Grade 5 Loud murmur with easily palpable thrill.
May be heard when the stethoscope is partly off
the chest.
Grade 6 Loud murmur with thrill and audible
with stethoscope removed from chest wall.

4. Location of Maximal Intensity

Where the murmur is best heard
This is determined by the site where the

murmur originates.
For example, a murmur best heard in the
2nd right interspace usually originates at or
near the aortic valve.
5. Radiation-precordial and other (e.g.
carotids) radiation of the murmur.
Murmurs radiate in the direction of the
blood flow causing the murmur to specific
sites outwith the precordium.
The radiation of cardiac murmurs is complex
and any cardiac murmur from any structure
can be heard anywhere in the chest.

There are, however some typical

radiations.
The pansystolic murmur of mitral
regurgitation radiates towards the
left axilla.
The systolic murmur of
ventriculoseptal defect towards
the right sternal edge.
The ejection systolic murmur of
aortic stenosis to the aortic area
and the carotid arteries.

6. Character and pitch

The quality of murmurs is hard to define.
Terms such as harsh, blowing, musical, rumbling, high

or low pitched are used.

Some examples:
blowingMI

musical MI of ischaemic cause (papillary muscle

dysfunction -Mweschrei), calcified mitral or aortic

valves (degenerative mitral regurgitation or aortic
stenosis)
rumblingMS
sighing- AI
Harsh AS
machinery--PDA
High-pitched murmurs often correspond with high-

pressure gradients, so the diastolic murmur of aortic

incompetence is higher pitched than that of mitral
stenosis.

7. Variation of the murmur:

With position
With respiration
With exercise
Variation with position:
Some murmurs will become louder if you

position the patient so as to let gravity aid

the flow of blood creating the sound.
Aortic regurgitation is heard louder if you
ask the patient to sit up, leaning forwards,
and listen at the left sternal edge.
Mitral stenosis is louder if you ask the
patient to lie on their left-hand side (listen
with the bell at the apex).

Variation with respiration

Ask the patient to breathe deeply whilst

you listen.
Right-sided murmurs (e.g. pulmonary
stenosis) tend to be louder during
inspiration and quieter during expiration
(because of increasedvenous return.
Left-sided murmurs are louder during
expiration.
Variation with exercise:
murmurs are louder after exercise
Description of a murmur: a medium
pitched, grade 3/6, blowing holosystolic
murmur, best heard at the apex, radiating
to the left axilla (mitral regurgitation)

SYSTOLIC MURMURS

1. Ejection systolic murmur

2. Pansystolic murmurs
3. Late systolic murmurs

1. Causes of ejection systolic or myd-

systolic murmurs (S1 and S2 can be

heard clearly)
Increased flow through normal valves
'Innocent systolic murmur':
fever
athletes (bradycardia , large stroke

volume)
pregnancy (cardiac output maximum at
15 weeks)
Atrial septal defect (causing high

pulmonary flow)
Severe anaemia

Normal or reduced flow through stenotic valve

Aortic stenosis
Pulmonary stenosis
Other causes of flow murmurs
Hypertrophic obstructive cardiomyopathy

(obstruction at subvalvular level)

Aortic regurgitation (aortic flow murmur,
relative stenosis)
Aortic sclerosis
Physiopathology of ejection murmurs
The flow of blood through a pathological
structure generates the murmur and this flow is
determined by the pressure difference on
opposite sides of the responsible pathology
(abnormal valve, septal defect, coarctation
etc. )

The sound generated (murmur) is louder

when the pressure difference is greater.

The murmur does not start until ejection
begins and peaks when blood flow is
greatest.
The murmur stops before S2 since
ejection is finished.
Thus the murmur has a
crescendo/decrescendo character.
The murmur is flow dependent, meaning,
that it gets softer and may disappear if
transvalvular flow starts to fall when a
lesion is very severe and causes heart
failure.

2. Causes of pansystolic or holosystolic murmurs

This is a murmur that lasts for the whole of

systole, S1 and S2 cannot be heard in all areas.

All caused by a systolic leak from a high to a
lower pressure chamber (regurgitant murmurs)
Mitral regurgitation
Tricuspid regurgitation
Ventricular septal defect
Leaking mitral or tricuspid prosthesis
Regurgitant systolic murmurs through the AV
valves, e.g. mitral regurgitation, may start
immediately isovolumic contraction begins,
before ejection, since the leak occurs as soon as
the pressure rises in the ventricle and continues
up until S2 or slightly beyond.

This is because there is a continuing pressure

difference between the LV and the LA during this

period of time.
Often the S2 is swamped by the end of the murmur.
3. Late systolic murmurs
There is an audible gap between S 1 and the start of
the murmur which then continues until S 2.
Typically due to tricuspid or mitral regurgitation
through a prolapsing valve.
In these cases the valve does not become
incompetent until is has prolapsed and the
murmur begins in mid-or even late systole and then
continues up to and slightly beyond the second
heart sound.
Late systolic murmur may have a crescendo rather
similar to an ejection systolic murmur but are much
later in the cycle .

DIASTOLIC MURMURS
1. Early diastolic murmur
2. Mid-diastolic murmur
Diastolic murmurs can be

extremely difficult to hear.

They are often very low pitched
and rumbling.
Almost always they are produced
by a heart disease.

1. Early diastolic murmur

Early diastolic murmurs occur from

regurgitation through incompetent aortic

or pulmonary valves.
They are descrescendo and follow the S2.
This is because the biggest pressure
difference between the outflow vessel and
the ventricle is at the beginning of the
diastole.
They are heard at the left sternal edge
(occasionally louder at the right sternal
edge) and are most obvious in expiration
with the patient leaning forward. (brings
the heart closer to the chest wall)

Since the regurgitant blood volume

must be ejected during the

subsequent systole, significant aortic
regurgitation leads to increased
stroke volume and is almost always
associated with a systolic flow
murmur (relative stenosis)
Pulmonary regurgitation is
uncommon. It may be caused by
pulmonary artery dilatation in
pulmonary hypertension (Graham
Steel murmur) or to a congenital
defect of the pulmonary valve.

2. Mid-diastolic murmur
A mid-diastolic murmur is usually caused

by mitral stenosis.
This is a low-pitched, rumbling sound
which may follow an opening snap .
It is best heard with the bell of the
stethoscope at the apex with the patient
rolled to the left side.
The murmur can be accentuated by
listening after exercise.
The whole cadence sounds like 'lup-ta-taroo' where 'lup' is the loud first heart
sound, 'ta-ta' the second sound and
opening snap and 'roo' the mid-diastolic
murmur.

If the patient is in sinus rhythm, left atrial contraction

increases the blood flow across the stenosed valve

leading to presystolic accentuation of the murmur. The
murmur of tricuspid stenosis is similar but rare.
An Austin Flint murmur is a mid-diastolic murmur
caused by the vibration of the mitral valve during
diastole as it is hit by flow of blood due to severe
aortic regurgitation.
Carey Coombs murmur: occurs in patients with

mitral valvulitis and secondary valve incompetence

due to acute rheumatic fever.
It is a short, mid-diastolic rumble best heard at the
apex, which disappears as the valvulitis improves.
Can be distinguished from the diastolic murmur of
mitral stenosis by the absence of an opening snap
before the murmur.
The murmur is caused by a increased blood flow
across a thickened mitral valve. (relative stenosis)

CONTINUOUS MURMURS

Continuous murmurs are rare in adults.

These are murmurs heard throughout

both systole and diastole murmur begins

in the systole and continues through the
second sound into all or part of diastole.
The systolic component is usually louder
than the diastolic component .
Causes:
1. Patent arterial duct
2. Shunt-acute communication between
the right and the left side
3. Pericardial friction rub
4. Venous hum

1. Patent arterial duct, which connects the upper

descending aorta and pulmonary artery in the

fetus and normally closes just after birth.
The murmur is best heard at the upper left
sternal border and radiates over the left scapula.
It is continuous and harsh described as
'machinery-like as it sounds like heavy machinery
working in the background.
2. Most commonly in adults continuous murmurs
are due to some acute communication developing
between the right and the left side of the heart
through which flow occurs both in systole and
diastole. The commonest situation is a ruptured
sinus of Valsalva, but infective endocarditis can
lead to arteriovenosus and right/left heart
communication.

3. Pericardial friction rub

It is a superficial scratching , high

pitched sound, comparable with

creaking leather, best heard with
the diaphragm of the stethoscope
Often has systolic and diastolic
components.
It may be audible over any part of
the precordium ,usually heard best
in the 3rd interspace to the left of
the sternum (Erb Botkin)and is often
very localized, does not radiate.

Remember

Auscultation remains an

important clinical skill despite the

ready availability of
echocardiography.
You must be able to detect
abnormal signs to prompt
appropriate investigation.
Furthermore, certain auscultatory
signs, such as the third or fourth
heart sounds and pericardial
friction, have no direct equivalent