HEART SOUNDS

There are two major groups of heart sounds, they are classified according to their
mechanism, i.e. valvular or ventricular filling. Also the slight asynchrony between the
two sides of the heart doubles the number of sounds making a total of 12.
Note that, as with heart murmurs, what is heard in the heart is not an isolated
event - there may be clues elsewhere in the body which permit the astute clinician to
predict sounds even before the stethoscope is placed on the chest.
Low and medium frequency sounds (eg third and fourth heart sounds) are more
easily heard with the bell applied lightly to the skin. High frequency sounds (eg first and
second heart sounds, opening snap) are more easily heard with a diaphragm.

VALVE SOUNDS
These include:
 The first and second heart sounds
 Eejection sounds
 Opening snaps

First (1st) heart sound

The first heart sound is caused by the closing of the mitral valve and the closing
of the tricuspid valve - the latter contributing little.
It is heard loudest at the apex.

Heart sounds (first, soft)

Possible causes of a soft first heart sound include:
 Early atrioventricular closure (in this situation the leaflets are semi-closed at the
end of diastole)
o A low flow at the end of diastole
o A P-R interval that is greater than 0.2 s
 A rigid calcified valve will cause a soft first heart sound
 If the left ventricle is not contracting efficiently then there may be a soft first heart
sound produced
 A delayed onset of left ventricular systole
Hence, causes include:
 Mitral regurgitation
 Low blood pressure, for example with M.I.
 Rheumatic carditis
 Severe heart failure
 Left bundle branch block

Heart sounds (first, loud)

A loud first heart sound occurs when the leaflets are wide open at the end of
ventricular diastole and shut forcefully at the beginning of ventricular systole.
Possible causes of a loud first heart sound include:
  Late atrioventricular closure
o This occurs when there is rapid flow at the end of diastole e.g. mitral stenosis,
the short diastole of tachycardic states and left to right shunts
o Where the P-R interval is less than 0.12 s. This situation results in an opened
valve that is not closed at the time of ventricular contraction.
Hence:
 Atrial fibrillation
 Short diastole - tachycardia
 Atrial premature beat
 Mitral stenosis where high left atrial pressure delays mitral valve closure

Heart sounds (first, split)

The differential contraction of the left and right ventricle causes a splitting of the
first heart sound.
An abnormally large splitting of the first heart sound is heard when there are:
 Either conduction abnormalities:
o Right bundle branch block
o Pacing from an electrode on the LV
o Left ventricular ectopics
 or mechanical causes:
o Ebsteins anomaly
o Atrial septal defect
o Tricuspid stenosis

Heart sounds (first, variable)

If the blood flow from atria to ventricles varies from one beat to the next, then the
intensity of the first heart sound will change accordingly.
Causes include:
 varying duration of diastole
 complete atrioventricular block

Haemodynamics
 loudest sound in the cardiac cycle
 caused by the abrupt halt of the closing movement of the mitral valve (M1) which
is followed by the softer sound caused by the closing of the tricuspid (T1)
 the first heart sound is initiated by the contraction of the left ventricle (LV)
followed by the right ventricle (RV)
o the differential contraction of the LV and the RV causes a splitting of the first
heart sound
o an abnormally large splitting of the first heart sound is heard when closure of
the tricuspid is delayed as in right bundle branch block, pacing from an
electrode on the LV, or with LV ectopics
 intensity of the first heart sound is closely related to the timing of the final halt of
the closing atrioventricular valves (mitral mainly) in relation to the ventricular
pressure pulse:
 o soft first heart sound is produced if closure occurs during the initial slow rise
of LV pressure
o a loud first heart sound is produced if valve closure occurs on the steep part of
the LV pressure pulse

Heart sounds (ejection)

These are caused by the opening of the aortic and pulmonary valves.
These sounds are high pitched and often described as clicky. They occur in early systole
and are best heard with a rigid diaphragm chest piece.
Mitral valve prolapse causes mid- or late- systolic clicks.

Heart sounds (ejection, aortic)

This is heard in early systole after the first heart sound. The sound is often best
heard at the apex.
The sound is generated by the abrupt halt of the fused aortic cusps in systole when they
fail to fold onto the wall of the aorta.
Possible causes include:
 An aortic valve that does not open fully - a bicuspid aortic valve
 Aortic stenosis where there is a mobile valve. An aortic ejection sound signifies
that the stenosis is at valve level. Calcification causes the ejection sound to
disappear. The sound is also absent in supravalvular and subvalvular stenosis

Heart sounds (ejection, pulmonary)

This sound occurs in early systole. It coincides with the final halt in upward
movement of the pulmonary valve.
Possible causes include:
 pulmonary valve stenosis
 pulmonary hypertension

Heart sounds (second)

The second heart sounds are produced as a result of the closure of the aortic (A2)
and the pulmonary (P2) valves as ventricular pressures fall below those in the aorta and
the pulmonary artery.
A2 and P2 separate on inspiration (P2 following A2). This is because of the increased
right ventricular stroke volume that occurs as the result of increased venous return. In the
expiratory phase of continuous respiration (in normal subjects reclining at 30-40 degrees
to reduce venous return) A2 and P2 are almost fused because the systoles of the left
ventricle and the right ventricle occur almost simultaneously.

Wide split second (2nd) heart sound

The second heart sound is widely split if there is an early A2 or if the P2 is delayed.
 Early A2 can occur in mitral regurgitation or ventricular septal defect. There is a
shortening of left ventricular systole because of diminished resistance to left
ventricular ejection.
 Delayed P2 - possible causes include :-
 o right bundle branch block, where there is delay in the activation of the right
ventricle
o pulmonary stenosis - the P2 is soft and delayed;
o atrial septal defect with left to right shunt - there is an increase in right
ventricular stroke volume which causes a delayed P2
o prolonged right ventricular contraction as a result of right ventricular failure.

Second (2nd) heart sound (reversed split)

In this condition, P2 occurs before A2.
On expiration, A2 is delayed such that it occurs after P2. Inspiration causes P2 to be
delayed and the split is diminished.
Possible causes of a delayed A2 include:
 Electrical delay - left bundle branch block
 Systolic hypertension
 Severe aortic stenosis or HOCM
 Patent ductus arteriosus
 Left heart failure
In patients with aortic stenosis, A2 is often very soft or even absent, in such
circumstances there appears to be a single component to the second heart sound.
Note that an early P2 may occur in type B Wolff-Parkinson- White syndrome.

Single second (2nd) heart sound

This may be present in:
 A calcified aortic stenotic valve
 Pulmonary stenosis - here the P2 component may be soft
 Fallot's tetralogy
 Ebstein's anomaly
 Pericardial effusion
 Where pulmonary pressure approaches systemic blood pressure, for example in a
large ventricular septal defect
 Other causes eg obesity, pulmonary emphysema

Heart sounds (second, loud)

Loud second heart sounds can be loud A2 or a loud P2.
 Loud A2 occurs in systemic hypertension where there is a dilated proximal aorta
 A loud P2 is heard in pulmonary hypertension
 A loud P2 occurs in an atrial septal defect without pulmonary hypertension. This
is caused by a sharp rise and fall of pulmonary arterial pressure
 In thin-chested people with a forward projecting aorta

Heart sounds (second, soft)

A soft, or absent, A2 is heard in:
 Poorly mobile cusps - e.g. calcification as occurs in some forms of aortic stenosis
 Dilatation of the aortic root - e.g. syphilitic aortitis
 P2 is soft in pulmonary stenosis
Heart sounds (opening snaps)
In the healthy heart the mitral and tricuspid valves open silently during diastole, at
the end of isovolaemic relaxation. In certain pathological states the AV valves open more
rapidly than normal, this results in an audible opening snap.
A mitral opening snap is said by some experts to be pathognomonic of mitral stenosis.
The intensity of the snap is directly proportional to the area of the fused cusps. The
timing of the opening snap is influenced by the atrial pressure (higher the pressure earlier
the snap) and the duration of the isovolumic relaxation phase (the shorter the relaxation
phase the earlier the opening snap).
Differentiation of the opening snap from P2 is achieved by listening to the heart sounds
during inspiration: the examiner will hear A2, P2 and the opening snap in quick
succession. A mitral opening snap may be caused by:
 Mitral stenosis with a mobile valve
 Rapid mitral flow causes a soft snap e.g. left to right shunts such as a VSD or
PDA. Also may occur in severe mitral regurgitation
A tricuspid opening snap is rare and may be caused by:
 Tricuspid valve abnormalities e.g. rheumatic stenosis
 Increased tricuspid flow e.g. left to right shunt occuring in an atrial septal defect

VENTRICULAR FILLING SOUNDS

These sounds are of much lower frequency than the valve sounds and may be
difficult to hear.
They are best heard with the bell gently applied to the chest and are described as a dull
thud becoming palpable when loud.
Ventricular filling sounds include:
 rapid filling (third) - left ventricle and right ventricle
 atrial (fourth) - right ventricle and left ventricle
The third sound is normally audible in children, with the intensity diminishing with age.
The third heart sound becomes inaudible (but recordable) in normal subjects in middle
age with increasing ventricular stiffness.

Heart sounds (third)

This is heart sound is caused by rapid ventricular filling in early diastole. Third
heart sound may be divided into left ventricular (LV) third heart sounds and right
ventricular (RV) third heart sounds.
Note that an early third heart sound may occur in constrictive pericarditis.
Clinical features:
 Louder at the apex and the left sternal edge
 If right ventricular then louder on inspiration
 If left ventricular then louder on expiration
Evidence base:
 In patients referred for non-emergency left sided heart catherisation, third and
fourth heart sounds detected by phonocardiography (1)
 o Neither the phonocardiographic S3 nor the S4 is a sensitive marker of left
ventricular dysfunction
o The phonocardiographic S3 is specific for left ventricular dysfunction and
appears to be superior to the moderate specificity of the phonocardiographic
S4
 Thus the absence of a gallop rhythm should not be used to indicate the absence of
left ventricular dysfunction and certainly cannot replace other diagnostic testing
when screening for left ventricular dysfunction

Heart sounds (fourth)

The fourth heart sound is due to atrial contraction inducing ventricular filling towards the
end of diastole. They are never audible in normal subjects. A fourth heart sound is the
result of powerful atrial contraction filling an abnormally stiff ventricle.
Left atrial heart sound is maximal at the apex, with possible causes including:
 Left ventricular hypertrophy
 Fibrotic left ventricle
 Hypertrophic cardiomyopathy
Right atrial heart sound is maximal at the lower left sternal edge and on inspiration. This
may occur in right ventricular hypertrophy.
Evidence base:
 In patients referred for non-emergency left sided heart catherisation, third and
fourth heart sounds detected by phonocardiography (1)
 Neither the phonocardiographic S3 nor the S4 is a sensitive marker of left
ventricular dysfunction
 The phonocardiographic S3 is specific for left ventricular dysfunction and appears
to be superior to the moderate specificity of the phonocardiographic S4
 Thus the absence of a gallop rhythm should not be used to indicate the absence of
left ventricular dysfunction and certainly cannot replace other diagnostic testing
when screening for left ventricular dysfunction (2)

TIMING OF SOUNDS AND EVENTS IN THE CARDIAC CYCLE

 First sound: closure of AV valves, indicates the beginning of ventricular systole
 Ejection sound:
o Systolic ejection click: this is an early systolic high pitched sound heard over
the aortic area - may occur in cases of congenital sclerosis where the aortic
valve remains mobile
o Non-ejection systolic click: high pitched sound heard during systle and best
heard over the mitral area; may occur in mitral valve prolapse
 Second sound: closure of semilunar valves, marks the beginning of diastole,
which is generally longer than systole
 Opening snap: opening of abnormal AV valves; occurs at a variable distance after
the second sound
 Third sound: ventricular filling (beginning); mid - diastolic heart sound
 Fourth sound: ventricular filling with atrial contraction; late diastolic heart sound
 CARDIAC MURMURS (AUSCULTATION SITES)

The preferred sites of auscultation of valvular heart murmurs are different from the
surface markings of the valves on the anterior chest wall. This is because the transmission
of murmurs is dependent on factors such as the proximity of the respective chamber to
the thoracic cage and the direction of blood flow.
Hence, the following are locations at which there is the greatest probability of discerning
valvular murmurs:
 Aortic area:
o Right second intercostal space close to the sternum
o The site where the ascending aorta is nearest to the thoracic cage
 Pulmonary area:
o Left second intercostal space close to the sternum
o The site where the infundibulum is closest to the thoracic cage
 Mitral area:
o At position of apex beat
o Left ventricle is closest to thoracic cage at this point
 Tricuspic area:
o Inferior left sternal margin
o Point closest to valve in which ausculation is possible

CARDIAC VALVES (surface markings)

The surface markings on the anterior chest wall of the cardiac valves is typically
retrosternal:
pulmonary valve: junction of superior and middle thirds of body of sternum and slightly
to the left side; near to left third costal cartilage
aortic valve: just below and to the right of the pulmonary valve on left side of middle
third of sternum; level with the third intercostal space
tricuspid valve: median plane in the inferior third of the sternal body; opposite the fourth
costal cartilage
mitral valve: overlapping tricuspid area but more superior and to the left of sternal body
The surface markings of the valves are not the same locations as the preferred sites of
auscultation of murmurs which emanate from them. This is because the murmurs are
dependent on the proximity of the heart chambers to the thoracic cage and the direction
of blood flow.

Diagram of the site for auscultation

 CARDIAC MURMURS

Heart murmurs are caused by turbulent of blood flow through valves or

ventricular outflow tracts.
It must be appreciated that the phenomena which cause murmurs may have effects
throughout the body. Indeed a thorough examination may be sufficient for diagnosis and
auscultation is required only as supportive evidence. In practise there is a limited
combination of physical signs and murmurs.
Likewise, it will become apparent that the terms used to describe findings are a code
which implies a specific diagnosis e.g. a continuous machinery-like murmur in a neonate
indicates a patent ductus arteriosus.
Note low and medium frequency sounds (eg mid-diastolic murmurs) are more easily
heard with the bell applied lightly to the skin. High frequency sounds (eg some
regurgitant murmurs, ejection murmurs) are more easily heard with a diaphragm.
Note also that as far as a cardiologist is concerned, a heart murmur is not a sound - it is a
murmur.

TYPES OF HEART MURMURS

This section contains information concerning different types of murmur that may be
heard.
Note, with reference to valvular lesions that:
 systolic murmurs imply incompetence of atrioventricular valve or
stenosis/sclerosis of semilunar valve.
 diastolic murmurs imply stenosis of atrioventricular valve or incompetence of
semilunar valve
Systolic heart murmurs
Systolic heart murmurs are divided into ejection or midsystolic murmurs, and
pansystolic murmurs.
1. Heart murmur (midsystolic)
These occur during ejection of blood through the ventricular outflow tracts into the great
arteries. Ejection murmurs start with the ejection sound, if present, and end before the
relevant valve closure sound.
The most common causes of an ejection systolic murmur are aortic stenosis and aortic
sclerosis.
ETIOLOGY
aortic causes
Left ventricular ejection murmurs are maximal at the aortic area, lower left sternal
edge and apex. Possible causes include:
 aortic stenosis (valvar, subvalvar, supravalvar)
 hypertrophic obstructive cardiomyopathy
 increased stroke volume e.g. ASD
 aortic cusp sclerosis
 bicuspid aortic valve with no obstruction
 coarctation of the aorta - a coarctation murmur, when heard anteriorly, can be
confused with an ejection murmur
 post-valvar dilation eg aortic aneurysm, hypertension
An ejection systolic murmur may occur in aortic regurgitation due to increased blood
flow

pulmonary causes
 Functional, particularly in young people
 Increased flow rate
o Atrial septal defect
o Total anomalous pulmonary venous drainage
o Hyperdynamic circulation
 Post valvular dilatation eg pulmonary hypertension
 Pulmonary stenosis

DISTIGUISHING FEATURES OF DIFFERENT CAUSES

Ejection systolic murmur that is:
 Maximal over the aortic area:
o Aortic stenosis
o Aortic sclerosis
o Aoarctation of the aorta
o Hypertrophic cardiomyopathy
 Pulmonary area:
o Innocent
o Pulmonary stenosis
 o Pulmonary hypertension
o Atrial septal defect
 Apex:
o Innocent
o Aortic sclerosis
o Aortic stenosis
2. Heart murmur (pansystolic)
Pansystolic murmurs occur throughout systole, and may be caused by:
 Mitral regurgitation:
o The murmur is maximal at the apex and often in late systole
o It is transmitted to the axilla
 Ventricular septal defect with a left to right shunt:
o The murmur is maximal at the left lower sternal edge, and may be loudest
when the defect is small
 Tricuspid regurgitation:
o The murmur is maximal at the fourth left interspace with inspiratory
augmentation and a systolic wave in the jugular venous pulse

Innocent murmurs
Many babies and children have heart murmurs in the absence of any structural
abnormality.
The diagnosis of an innocent murmur is usually on the basis of clinical symptoms and
signs but if investigations are necessary they are always normal.
Types of innocent murmurs include:
 venous hum - a continuous blowing noise heard just below the clavicles. It varies
with respiration and disappears if the child lies down. It is due to turbulent flow in
the systemic great veins
 pulmonary flow murmur - is a soft ejection murmur heard in the second left
intercostal space. It is a flow murmur of a normal pulmonary valve. The increased
flow of anaemia, pyrexia and exercise makes this murmur louder
 vibratory murmur - this is a buzzing noise heard around the apex. It varies with
posture
If a murmur has any of the following characteristics then it probably is NOT innocent:
 Pansystolic
 Diastolic
 Loud or long
 Associated with a thrill or cardiac symptoms

Characteristics of innocent childhood murmurs

 No other abnormality - just a murmur
 No thrill
 The murmur usually has characteristics listed below:
o Heard over a local area
o Does not radiate outside the praecordium
 o Of a short, low frequency
o Occurs in early or midsystole
o Never diastolic
o shows variation in intensity with changes in posture; may disappear
completely with the Valsalva manoeuvre; sitting or deep inspiration makes the
murmur quieter
o Increased with tachycardia eg crying, anxiety
o ECG and chest X-ray normal
o Child is asymptomatic

Diastolic heart murmur

Diastolic heart murmur may be:
 early diastolic murmurs
 mid-diastolic murmurs

Mid-diastolic murmur
Mid diastolic murmurs:
 mitral stenosis - maximal at the apex with the patient inclined to the left. The
murmur begins after the opening snap. The murmur is long if severe and short if
mild.
 tricuspid stenosis - maximal at the lower left sternal edge. The murmur is
increased by inspiration.
 a murmur mimicking mitral stenosis may occur when there is greatly increased
flow across the mitral valve. This may occur in mitral regurgitation, VSD, patent
ductus, causes of a hyperdynamic circulation e.g. thyrotoxicosis.

Early diastolic murmur

Early diastolic murmurs:
 aortic regurgitation - maximal at the 4th interspace below the aortic valve. If the
aorta is dilated then heard higher and to the right of the sternum. Maximal if the
patient leans forwards. Radiates to the back.
 pulmonary regurgitation - maximal about the third left space.
 these murmurs are best heard if the patient momentarily holds his breath in
expiration.

Austin Flint murmur

An Austin Flint murmur is a mid-diastolic, low-pitched rumbling heard at the
apex.
Austin Flint murmurs occur in aortic regurgitation due to the vibration of the anterior
leaflet of the mitral valve as it is buffetted simultaneously by the blood jets from the left
atrium and the aorta.

Graham Steel murmur

 A Graham Steel murmur is a diastolic murmur audible along the left sternal
border due to functional incompetence of the pulmonary valve in patients with pulmonary
hypertension.
The Graham Steel murmur is a high-pitched, decrescendo murmur, loudest during
inspiration

Carey Coombs murmur

A Carey Coombs murmur is a soft, short filling murmur due to vegetations on the
mitral valve.
It is usually heard in rheumatic fever.

Heart murmur (continuous)

These occur when there is a communication in the circulation with a continuous
pressure gradient throughout the cardiac cycle. Continuous murmurs are often maximal in
late systole. This fact helps to discriminate a continuous murmur from an ejection
murmur accompanied by an early diastolic murmur. Possible causes of a continuous
murmur include:
 Aorta to pulmonary artery communication such as patent ductus arteriosus -
maximal below the left clavicle
 Systemic arteriovenous communication: - congenital e.g. aortic sinus of Valsalva
aneurysm rupturing into the right heart - acquired as the result of trauma e.g. knife
wound
 Pulmonary arteriovenous communications
 Bronchial artery anastomosis in pulmonary atresia
 Artificial ducts (Waterson or Blalock shunt)
 Prosthetic valve
 Venous hum

Pericardial friction rub

This is produced by pericarditis. The murmur sounds closer to the stethoscope and
coincides with heart movement in midsystole and during ventricular filling. All these
features are louder during inspiration when increased flow of blood into the heart
increases the apposition of pericardial layers.
The sound of the friction rub is like a 'snowball being rolled in the snow'.

Summary of signs
 Scratchy, superficial noise heard in systole and diastole.
 Brought out by stethoscope pressure.
 Sometimes variable with respiration.

HEART MURMURS (GRADING)

Murmurs are recorded in six gradations:
1/6 murmur is just audible by an expert in optimal conditions
2/6 is quiet
3/6 is moderately loud
4/6 is markedly loud } are accompanied by
5/6 is very loud } a thrill
6/6 is audible without a stethoscope
The intensity of a murmur does not indicate the severity of a valve defect. The sound
produced by a valve defect depends as much on flow as on valve aperture.

SUMMARY OF SIGNS OF DIFFERENT MURMURS

These summaries contain the clusters of signs seen with any particular murmur,
and thus also summarise the language used to communicate the diagnosis to the
cardiologist colleague.
Clinical features of mitral stenosis
There are two main presentations of mitral stenosis.
Patients with a normal pulmonary vascular resistance present principally with dyspnoea
and pulmonary oedema, a result of increased left atrial pressure. This presentation is more
common in younger patients and is exacerbated by situations of increased blood volume,
for example, during pregnancy.
Patients with an increased pulmonary vascular resistance present principally with fatigue,
mitral facies, a raised JVP, and right ventricular hypertrophy. This presentation is more
common in older patients with a low cardiac output and right heart failure. Dyspnoea is
less prominent in this group. When the mitral valve is immobile, these patients frequently
present with a diagnosis of cor pulmonale as the opening snap and murmur may not be
detected.
In general, features of mitral stenosis on examination include:
 Small pulse, which may be irregularly irregular
 Jugular venous pressure is only raised if there is heart failure
 Right ventricular hypertrophy, tapping apex beat
 Loud S1, loud P2 if pulmonary hypertension
 Opening snap
 Mid-diastolic murmur heard at the apex only
 Pre-systolic accentuation murmur if no atrial fibrillation
The more severe the stenosis, the larger the left atrium, the worse the dyspnoea, the closer
the opening snap is to the second heart sound, and the longer the murmur.

Clinical features of mitral incompetence

In cases of mild regurgitation the patient may be asymptomatic. Ventricular
ectopics may occur in patients with prolapsing mitral valves. There are often non-specific
chest pains in patients with prolapsing valves but these are usually skeletal in origin and
are exaggerated by anxiety.
When left ventricular failure occurs then the patient will complain of symptoms of
dyspnoea on exertion, orthopnoea and paroxysmal nocturnal dyspnoea. If there is
associated angina on exertion then this makes ischaemic heart disease a likely to be the
cause of the mitral regurgitation.
Signs of mitral incompetence:
 Pulse, which may be fibrillating
 JVP raised only if heart failure
  Right and left ventricular hypertrophy.
 Soft S1; loud P2 if there is pulmonary hypertension
 High frequency pan systolic murmur best heard in the apex and radiating to the
axilla.
The statement is: A soft blowing pansystolic murmur with a reduced or absent S1,
radiating to the axilla and back, heard best at the apex, especially in the left lateral
position with the breath held in expiration.

Clinical features of aortic stenosis

Symptoms include:
 often asymptomatic
 angina, syncope, exertional dyspnoea, dizziness, sudden death
Signs include:
 pulse: slow rising, small volume, narrow pulse pressure - plateau pulse
 blood pressure is normal.
 apex beat is heaving, undisplaced. There may be a systolic thrill, best felt with the
patient sitting forward at the end of expiration
 heart sounds
o second heart sound is normally split in mild aortic stenosis, P2 preceding A2.
As stenosis increases in severity then reversed splitting occurs ie A2
preceding P2. If there is calcification of the aortic valve then A2 will become
softer and may be inaudible all together.
o fourth heart sound (S4) may be present.
o ejection systolic murmur heart loudest in the aortic area which radiates to the
apex and the carotids.
o other sounds: ejection click if the valve is pliable. An ejection click excludes
supra- or subaortic stenosis.
Note that the murmur of aortic sclerosis is identical, but is distinguished from aortic
stenosis by the presence of a normal radial pulse wave and the absence of a thrill.

Clinical features of aortic incompetence

Aortic regurgitation is often asymptomatic because the left ventricle adapts to the
increased stroke volume. Dyspnoea is a late feature indicating left ventricle failure.
Acute left ventricular failure is more common when the onset of aortic regurgitation is
sudden, e.g. infective endocarditis, when the left ventricle has no time to adapt to the
increase in workload.
Angina pectoris may occur and is often atypical; in syphilitic regurgitation where there is
a narrowing of the coronary ostia.
Clinical features include:
 Waterhammer pulse - wide pulse pressure
 Pulse visible in the carotids - Corrigan's sign - plus a number of other eponymous
signs
 JVP only raised if there is heart failure
 apex beat is displaced and volume overloaded:
 o Typically there is dilatation of the left ventricule with relatively little
hypertrophy
 early diastolic murmur:
o Blowing high pitched
o Starting immediately after A2, loudest at 3rd and 4th intercostal spaces and
also heard in the aortic area and at the apex
 ejection murmur:
o Loudest in the aortic area and goes to the carotid arteries
o Due to increased blood flow
 Austin Flint murmur:
o Low-pitched rumbling presystolic murmur
o In severe cases may occur as a mid-diastolic murmur

Clinical features of atrial septal defect

These are considered by reference to the different types of defect and the general
features of any defect.

Clinical features of primum defect

The clinical features include:
 heart failure: this in infancy or childhood
 pulmonary hypertension: especially in Downs syndrome - pulmonary ejection
systolic murmur and mid-diastolic tricuspid murmur reflecting increased flow
 cardiac enlargement
 breathlessness at rest
 Harrison's sulci
 pink with normal pulses
 apical pansystolic murmur: if mitral valve is incompetent

Clinical features of secundum defect

Patients are usually asymptomatic throughout infancy and childhood, often
presenting in the third or fourth decades of life. Rarely the symptoms include:
 breathlessness on exertion
 recurrent chest infections
On examination:
 the child is pink with normal pulses
 there is a right ventricular heave
 there is a murmur in the 2nd intercostal space in the left parasternal region - this is
usually a flow murmur across a normal valve
 if the ASD is large there may be a similar murmur across the tricuspid valve
 the second sound is split because the over-filled right atrium takes longer to empty
 the splitting is fixed because the atria act as a single unit and therefore inspiration
affect them both equally
 mitral valve prolapse has been demonstrated in up to 30% of patients with ostium
secundum ASD
Clinical features common to primum and secundum defect
Small defects cause no abnormalities and are associated with normal
development. Larger defects may cause:
 exercise intolerance with easy fatiguability
 frequent chest infections
 atrial dysrhythmias, especially atrial fibrillation, may occur, the incidence
increasing with age
 in later life, there is the possible development of right heart failure
Other features may include:
 prominent V waves in the JVP
 narrow arterial pulse pressure
 normal blood pressure, unless complicated by atrial fibrillation
 hyperdynamic cardiac impulse with parasternal heave
 hepatomegaly if there is cardiac failure
 S1 loud, sometimes split
 S2 widely split, fixed, unchanged on respiration
 a loud S2 implies increased pulmonary resistance
 there are no murmurs of the defect because the defect is large with no pressure
gradient across it.
 ejection systolic murmur over the pulmonary area - due to blood flow over the
pulmonary valve, not the defect
 short mid-diastolic ejection murmur heard over the tricuspid area
 in ostium primum defects there may be associated mitral incompetence
 murmurs are louder on inspiration because of increased venous return

Clinical features of ventricular septal defect

The patient may be asymptomatic with a small shunt. Large shunts may cause:
 dyspnoea
 recurrent chest infections
 in infancy, failure to thrive, depending on the size of the defect.
On examination there may be:
 bulging sternum - enlarged right ventricle
 cyanosis - if pulmonary vascular resistance is intermittently reversing the
direction of the shunt.
 pulse and jugular venous pressure are normal.
 praecordial impulse - if there is a significant shunt then there may be a left
parasternal heave and a forceful apical impulse - biventricular hypertrophy.
 rarely there may be a groove in the ribs corresponding to the insertion of the
diaphragm, if the lungs have been chronically stiff because of pulmonary plethora.
Auscultation:
 Heart sounds - the loudness of P2 is an indicator of pulmonary vascular
resistance. If there is an increase in pulmonary resistance then the pulmonary
diastolic pressure increases and P2 becomes louder.
 Murmur of the defect:
 o a very small defect may close in late systole so that the murmur is only heard
during early systole.
o pansystolic murmur and thrill, maximal at the lower left sternal edge in a
moderate or large defect
o if a large defect is not surgically rectified then there is a gradual increase in
pulmonary vascular resistance and the murmur diminishes.
 flow murmurs mid-diastolic, through the mitral valve, but usually hidden by the
pansystolic murmur
 aortic incompetence may develop in a small percentage of sub-arterial VSDs.

Clinical features of patent ductus arteriosus

Children are often asymptomatic and may be only diagnosed on findings of
examination. Possible symptoms include:
 Fatigue
 Failure to thrive
 Breathlessness on exertion
 Recurrent chest infections
On examination:
 The patient often appears normal, unless the patent ductus is part of the rubella
syndrome.
 The pulse is of large amplitude with a sharp upstroke, and the aortic diastolic
pressure is low
 The jugular venous pressure is normal
 The dilated and hypertrophied left ventricle results in a prominent apex beat
On auscultation:
 Continuous machinery murmur maximal under the left clavicle. As the pulmonary
vascular resistance increases the velocity of the shunt decreases and the murmur
may become confined to systole. A very high pulmonary vascular resistance will
mean that there is no shunt and no murmur.
 Flow murmurs - an apical mid-diastolic flow murmur can be heard when the
pulmonary blood flow is about twice the systemic. This murmur is produced by
excessive return across the mitral valve.
 Second sound is dependent on the size of the ductus. The larger the ductus the
larger the volume of the left ventricular systolic volume, and hence the longer the
delay of the closing of the aortic valve (A2). These features mean that with a large
ductus the two heart sounds may become merged or even become paradoxically
split, i.e. P2 before A2.

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