The first heart sound (S1) is loud when the mitral or
tricuspid valve cusps remain wide open at the end of
diastole and shut forcefully with the onset of ventricular
systole. This occurs in mitral stenosis because the
narrowed valve orifice limits ventricular filling so that
there is no diminution in flow towards the end of
diastole. The normal mitral valve cusps drift back
towards the closed position at the end of diastole as
ventricular filling slows down. Other causes of a loud
S1 are related to reduced diastolic filling time (e.g.
tachycardia or any cause of a short atrioventricular
conduction time).
Soft first heart sounds can be due to a prolonged
diastolic filling time (as with first-degree heart block)
or a delayed onset of left ventricular systole (as with
left bundle branch block), or to failure of the leaflets
to coapt normally (as in mitral regurgitation).
The second heart sound (S2) may have a loud aortic
component (A2) in patients with systemic hypertension.
This results in forceful aortic valve closure secondary
to high aortic pressures. Congenital aortic stenosis
is another cause, because the valve is mobile but
narrowed and closes suddenly at the end of systole.
The pulmonary component of the second heart sound
(P2) is traditionally said to be loud in pulmonary
hypertension, where the valve closure is forceful because
of the high pulmonary pressure. In fact, a palpable P2
correlates better with raised pulmonary pressures than a
loud P2.16
A soft A2 will be found when the aortic valve is
calcified and leaflet movement is reduced, and in aortic
regurgitation when the leaflets cannot coapt.
Splitting
Splitting of the heart sound is usually most obvious
during auscultation in the pulmonary area. Splitting
of the first heart sound is usually not detectable
clinically; however, when it occurs it is most often due
to the cardiac conduction abnormality known as
complete right bundle branch block (see the OCSE
ECG library no. 22 at ).
Increased normal splitting (wider on inspiration)
of the second heart sound occurs when there is any
delay in right ventricular emptying, as in right bundle
branch block (delayed right ventricular depolarisation),
pulmonary stenosis (delayed right ventricular ejection),
ventricular septal defect (increased right ventricular
volume load) and mitral regurgitation (because of earlier
aortic valve closure, due to more rapid left ventricular
emptying).
In the case of fixed splitting of the second heart
sound, there is no respiratory variation (as is normal)
and splitting tends to be wide. This is caused by an
atrial septal defect where equalisation of volume loads
between the two atria occurs through the defect. This
results in the atria acting as a common chamber.
Reversed splitting is present when P2 occurs first
and splitting occurs in expiration. This can be due
to delayed left ventricular depolarisation (left bundle
branch block [see the OCSE ECG library no.
Extra heart sounds:
The third heart sound (S3) is a low-pitched (20–70 Hz)
mid-diastolic sound that is best appreciated by listening
for a triple rhythm.17 Its low pitch makes it more easily
heard with the bell of the stethoscope. It has been
likened (rather accurately) to the galloping of a horseand is often called a gallop rhythm. Its cadence is similar
to that of the word ‘Kentucky’. It is more likely to be
appreciated if the clinician listens not to the individual
heart sounds but to the rhythm of the heart. It is
probably caused by tautening of the mitral or tricuspid
papillary muscles at the end of rapid diastolic filling,
when blood flow temporarily stops.
A pathological S3 is due to reduced ventricular
compliance, so that a filling sound is produced even
when diastolic filling is not especially rapid. It is strongly
associated with increased atrial and ventricular
end-diastolic pressure.
A left ventricular S3 is louder at the apex than at
the left sternal edge, and is louder on expiration. It can
be physiological when it is due to very rapid diastolic
filling, associated with an increased cardiac output, as
occurs in pregnancy and thyrotoxicosis and in some
children. Otherwise, it is an important sign of left
ventricular failure and dilation, but may also occur in
aortic regurgitation, mitral regurgitation, ventricular
septal defect and patent ductus arteriosus.18
A new third heart sound after a myocardial
infarction is an indicator of increased mortality risk
(LR+, 8.0).19
A right ventricular S3 is louder at the left sternal
edge and with inspiration. It occurs in right ventricular
failure or constrictive pericarditis.
The fourth heart sound (S4) is a late diastolic sound
pitched slightly higher than the S3.20 The cadence of
an S4 is similar to that of the word ‘Tennessee’. Again,
this is responsible for the impression of a triple (gallop)
rhythm. It is due to a high-pressure atrial wave reflected
back from a poorly compliant ventricle. It does not
occur if the patient is in atrial fibrillation, because the
sound depends on effective atrial contraction, which is
lost when the atria fibrillate. Its low pitch means that,
unlike a split first heart sound, it disappears if the bell
of the stethoscope is pressed firmly onto the chest.
A left ventricular S4 may be audible when
left ventricular compliance is reduced owing to
aortic stenosis, acute mitral regurgitation, systemic
hypertension, ischaemic heart disease or advanced age.
It is sometimes present during an episode of angina
or with a myocardial infarction, and may be the only
physical sign of that condition.
A right ventricular S4 occurs when right ventricular
compliance is reduced as a result of pulmonary
hypertension or pulmonary stenosis.
If the heart rate is greater than 120 beats per
minute, S3 and S4 may be superimposed, resulting in
a summation gallop. In this case, two inaudible sounds
may combine to produce an audible one. This does not
necessarily imply ventricular stress, unless one or both
of the extra heart sounds persists when the heart rate
slows or is slowed by carotid sinus massage. When both
S3 and S4 are present, the rhythm is described as a
quadruple rhythm. It usually implies severe ventricular
dysfunction.
Additional sounds
An opening snap is a high-pitched sound that occurs
in mitral stenosis at a variable distance after S2. It is
due to the sudden opening of the mitral valve and is
followed by the diastolic murmur of mitral stenosis.
It can be difficult to distinguish from a widely split
S2, but normally occurs rather later in diastole than
the pulmonary component of the second heart sound.
It is pitched higher than a third heart sound and so
is not usually confused with this. It is best heard at
the lower left sternal edge with the diaphragm of the
stethoscope. Use of the term opening snap implies
the diagnosis of mitral stenosis or, rarely, tricuspid
stenosis.
A systolic ejection click is an early systolic
high-pitched sound that is heard over the aortic or
pulmonary and left sternal edge areas, and that may
occur in cases of congenital aortic or pulmonary stenosis
where the valve remains mobile; it is followed by the
systolic ejection murmur of aortic or pulmonary
stenosis. It is due to the abrupt doming of the abnormal
valve early in systole.
A non-ejection systolic click is a high-pitched
sound heard during systole that is best appreciated
at the mitral area. It is a common finding. It may be
followed by a systolic murmur. The click may be due
to prolapse of one or more redundant mitral valve
leaflets during systole. Non-ejection clicks may also be
heard in patients with atrial septal defects or Ebstein’s
anomaly (p 141).
An atrial myxomaz is a very rare tumour that may
occur in either atrium. During atrial systole a loosely
pedunculated tumour may be propelled into the mitral
or tricuspid valve orifice, causing an early diastolic
CHAPTER 5 THE CARdiAC ExAminATion 101
(Adapted from Etchells EE, Bell C, Robb K. Does this patient
have an abnormal systolic murmur? JAMA 1997;
277(7):564–571.)
GOOD SIGNS GUIDE 5.1
LRs of signs suggesting that a systolic
murmur is significant (abnormal)
SignLR+LR−
Systolic thrill120.73
Pansystolic murmur8.70.19
Loud murmur6.50.08
Plateau-shaped murmur4.10.48
Loudest at apex2.50.84
Radiation to carotid0.911.0
aa The same study showed that if a cardiologist thought a murmur was
plopping sound: a tumour plop. This sound is only
rarely heard, even in patients with a myxoma (about
10%).
A diastolic pericardial knock may occur when there
is sudden cessation of ventricular filling because of
constrictive pericardial disease.21
Prosthetic heart valves produce characteristic
sounds (p 138).22 Rarely, a right ventricular pacemaker
produces a late diastolic high-pitched click due to
contraction of the chest wall muscles (the pacemaker
sound).
Murmurs of the heart
Murmurs are continuous sounds caused by turbulent
blood flow. Some turbulence is inevitable as the blood
is accelerated through the aortic and pulmonary valves
during ventricular systole. Increased turbulence across
normal valves occurs in association with anaemia and
thyrotoxicosis. The normal velocity of flow through
these valves is about 1 metre per second. This may
be enough to produce a soft swishing sound audible
with the stethoscope, an innocent murmur. Greater
turbulence—flow velocities of 4 metres per second or
more across narrowed aortic valves and even higher
velocities when the mitral valve leaks—lead to more
prominent murmurs. Certain features have been shown
to indicate a likelihood that a murmur is significant
(see Good signs guide 5.1aa).
In deciding the origin of a cardiac murmur, a
number of different features must be considered. These
are: associated features (peripheral signs), timing,
the area of greatest intensity and radiation (see Fig.
5.35), the loudness and pitch and the effect of dynamic
manoeuvres, including respiration and the Valsalva
manoeuvre. The presence of a characteristic murmur
is very reliable for the diagnosis of certain valvular
abnormalities, but for others less so.
Associated features
As already mentioned, the cause of a cardiac murmur
can sometimes be elicited by careful analysis of the
peripheral signs.
Timing
Systolic murmurs (which occur during ventricular
systole) may be pansystolic, midsystolic (ejection
systolic) or late systolic (see Table 5.4).
The pansystolic murmur extends throughout systole,
beginning with the first heart sound and going right
up to the second heart sound. Its loudness and pitch
do not vary during systole. Pansystolic murmurs occur
when a ventricle leaks to a lower-pressure chamber
or vessel. As there is a pressure difference from the
moment the ventricle begins to contract (S1), blood
flow and the murmur both begin at the first heart sound
and continue until the pressures equalise (S2). Causes
of pansystolic murmurs include mitral regurgitation,bb
tricuspid regurgitation, ventricular septal defect and
aortopulmonary shunts.
The midsystolic ejection murmur does not begin
right at the first heart sound; its intensity is greatest
in midsystole or later, and wanes again late in systole.
This is described as a crescendo–decrescendo murmur.
These murmurs are usually produced by turbulent flow
through the aortic or pulmonary valve orifices or by
greatly increased flow through a normal-sized orifice
or outflow tract. Causes include aortic or pulmonary
stenosis, hypertrophic cardiomyopathy and atrial septal
defect.
When it is possible to distinguish an appreciable gap
between the first heart sound and the murmur, which
then continues right up to the second heart sound,
bb The older term incompetence