Ebook Bedside cardiology: Part 2

15

Second Heart
Sound (S2)

Mechanism
During the closure of the semilunar valves, clapping of the leaflets does not
produce the sound. Sudden deceleration of the retrograde flow of the blood
column in the aorta or pulmonary artery by the closed tensed valves set the
vibration of the cardiohemic system. The high frequency components of this
vibration produce the S2.

Splitting
Physiological Splitting (Fig. 15-1)
Left ventricular ejection begins and completes earlier than right ventricle.
Thus, aortic component (A2) occurs 10 to 15 ms earlier than the pulmonary
component (P2). One cannot appreciate two components unless the split is
more than 30–50 ms. This causes the S2 single during expiration, where the
split is less than 15–20 ms.
In inspiration, the split is appreciable because P2 is delayed and A2
occurs earlier. Delayed P2 contributes 70% and early A2 30% for the
inspiratory split. P2 is delayed because of the effect of inspiration on the
aortic and pulmonary hang out time.
Hang-out time is defined as the interval between the end of the ventricular
ejection and closure of the semilunar valve. This time is longer in pulmonary
artery than the aorta. Pulmonary hang out time may be up to 60 to 70 ms,
whereas aortic hang-out time may be below 20 to 30 ms. Semilunar valve
is closed only when the pulmonary artery or aortic diastolic pressure crosses
that of the respective ventricle. Pulmonary vasculature is more compliant
than the systemic vasculature, pulmonary vascular resistance is one tenth
of that of aorta and pulmonary artery has less elastic recoil power than

that of the aorta. Thus, it takes a longer time for the diastolic pressure
building up in the pulmonary artery than in the aorta for this cross
over (Fig. 15-2).


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Bedside Cardiology

Fig. 15-1: Physiological splitting of S2. (A) During inspiration, P2 is delayed and A2 occurs
earlier. Inspiratory shifting of P2 is more than shifting of A2; (B) In lying down posture,
due to increased preload, S2 may appear as persistently splitted, due to audibly wide
expiratory splitting; (C) In sitting posture, expiratory splitting narrows down and becomes
audibly single. Thus proper assessment of S2 splitting should be done with patient in
sitting posture.

Incisura: Point of cross over of aorta or pulmonary artery over its respective
ventricle in the pressure curve is called incisura, which coincides with S2.
Hang-out time can also be defined as the distance between the ventricular
pressure curve and the aortic or pulmonary incisura. Actual cusp apposition
occurs before the incisura. Due to inertia, the forward flow continues. Duration
of this forward flow determines the hang-out time and depends on the
vascular capacitance, vascular resistance and the recoil property of the aorta
vs pulmonary artery.
During inspiration, there is increased pulmonary vascular capacitance
resulting in longer pulmonary artery hang-out time and increased venous
return resulting in longer right ventricular ejection time. P2 is delayed by
both of these factors, more important being the hang-out time. Inspiration
causes decreased intrathoracic pressure, which is transmitted in the pulmonary
veins with a pulling effect, without any change in the aortic capacitance. Left

Second Heart Sound (S2)

Fig. 15-2: Hang-out interval, which is defined as the interval between the end of the ventricular
ejection and closure of the semilunar valve. It is up to 70 ms for P2 and 30 ms for A2

ventricular stroke volume is decreased with shortening of ejection time,
resulting in early A2.

Pathological Splitting (Table 15-1)
Pathological splitting of S2 may be related to either the wideness of the split
or the effect of respiration on it.

TABLE 15-1

Pathological
splitting of S2

A. Persistent splitting
1. Fixed
2. Nonfixed
B. Reverse splitting
C. Persistently single.

Persistent splitting means aortic and pulmonary components are audible in
both phases of respirations.
Persistent nonfixed splitting means normal inspiratory widening on the
backdrop of persistent splitting.

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Bedside Cardiology

Wide Splitting (Persistent Nonfixed Splitting) (Table 15-2)
S2 is said to be widely splitted:
 When both its components can be appreciated in expiration,
particularly in standing position; there may be further widening
during inspiration.
 Inspiratory widening more than 60 msec; may be single on expiration.
Commonest causes are the electrical abnormalities including RBBB,
WPW syndrome with left ventricular pre-excitation. There is late activation
of the right ventricle resulting in delayed P2. Mechanical causes include
pulmonary valvular stenosis, infundibular stenosis and peripheral
pulmonary artery stenosis, all of which prolong right ventricular activation
time resulting in delayed P2. In pulmonary valvular stenosis, severity is
directly proportional to expiratory splitting. When the splitting is 70–80
ms, right ventricular systolic pressure approximates 70–80 mm Hg. Severe
MR and large VSD cause wide expiratory splitting due to early A2 by
shortening left ventricular mechanical systole. Wide inspiratoy splitting
due to early A2 occurs in constrictive pericarditis. Inspiration causes
decreased intrathoracic pressure as well as decreased pulmonary venous
pressure, which is an extracardiac structure. But this thoracic pressure
swinging is not reflected on cardiac chambers due to constricted
pericardium. Thus, left atrial pressure remains normal during inspiration.
This diminished pulmonary vein—left atrial pressure gradient during
inspiration causes reduced left ventricular venous return and ejection

time. Wide split is found in Idiopathic dilatation of pulmonary artery due
to prolonged hang-out time.

TABLE 15-2

Wide splitting of S2

Electrical causes
1. RBBB
2. WPW syndrome.
Mechanical causes
1. Delayed P2 (RVOT stenosis)
2. Early A2 (Severe MR, large VSD,
constrictive pericarditis).
Prolonged hang-out time:
1. Idiopathic dilatation of pulmonary artery
2. ASD (fixed)
3. RV systolic dysfunction (fixed).


Second Heart Sound (S2)

Wide Fixed Splitting (Fig. 15-3)
The split is defined fixed when the respiratory variation is less than 20 msec.
This is one of the most consistent auscultatory finding and hallmark of all
forms of ASD. Increased pulmonary flow causes increased pulmonary

Fig. 15-3: ASD: In normal situation, pulmonary hang-out interval widens more in inspiration,
which is responsible for insptratory split. In ASD, hang-out interval is fixed in both phases
of respiration, causing the fixed splitting of S2

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Bedside Cardiology
capacitance and prolonged hang-out time which results in persistent expiratory
(wide) splitting of S2. As capacitance is already increased, inspiration does
not cause any additional increase. This fixed hang-out time in both phases
of respiration causes the fixed splitting. Another causative factor is ejection
time of two ventricles. Inspiration causes increased right ventricular venous
return with prolonged ejection time, thus delaying P2. At the same time,
increased right ventricular volume causes decreased left to right shunt, causing
longer left ventricular ejection time and delayed A2. As a consequences,
there is no inspiratory widening of S2.
Another cause of wide fixed splitting is severe right ventricular systolic
dysfunction. Wide expiratory splitting is due to prolonged right ventricular
ejection time. During inspiration the failing right ventricle cannot increase
its stroke volume or ejection time and S2 remains fixed. Wide split is
appreciable when RBBB is associated with right ventricular failure.
Pseudofixed splitting: Sometimes S2 is mistakenly diagnosed as having
fixed splitting. In children with rapid respiratory rate, there is little variation
of right ventricular volume and S2 appears fixed. A late systolic click before
S2 and an opening snap after S2 may be mistaken as wide fixed S2.
Narrow split in ASD: In ASD, the split may be less than 60 msec. Grade
of shunt, probably is not related with degree of splitting.

Splitting in Pulmonary Hypertension
Expiratory splitting usually persists. Inspiratory splitting in pulmonary

hypertension depends on two opposing factors. Pulmonary hypertension causes
prolonged right ventricular ejection with delayed P2. At the same time it
causes decreased pulmonary capacitance and hang-out time resulting in narrow
S2. Inspiratory splitting is usually preserved; loud P2, however, may mask A2
in pulmonary area; then, split can better be assessed at the apex.
In MS with pulmonary hypertension, split is physiological. In MR with
pulmonary hypertension, split is wide. In VSD with hyperkinetic pulmonary
hypertension, split is physiological, whereas in Eisenmenger syndrome, S2
is single. In ASD, both with hyperkinetic or obstructive pulmonary
hypertension, split is wide and fixed. In PDA with hyperkinetic pulmonary
hypertension, split may be physiological or reverse, whereas in Eisenmenger
syndrome, splitting is physiological. In idiopathic PAH, expiratory splitting
can be appreciated and inspiratory splitting is narrower.

Reverse Splitting (Fig. 15-4)
Reverse splitting is appreciable when S2 is splitted during expiration and
becomes narrow or single during inspiration. During expiration, A2 shifts


Second Heart Sound (S2)

Fig. 15-4: Reverse split: S2 in AS. Here, A2 is delayed. In inspiration, P2 is delayed. Thus,
A2 merges to P2 in severe AS in inspiration. In expiration, P2 occurs earlier as usual, and
A2 is delayed, resulting in wider split

beyond P2. Inspiration have its usual effect on S2, i.e. P2 is delayed. That
results in either closely splitted or single S2 during inspiration. Common
cause of reverse splitting is delayed electrical activation of the left ventricle,
like, LBBB, right ventricular pacing and pre-excitation of the right ventricle.
Prolonged left ventricular ejection time is another cause of reverse splitting.

Increased left ventricular stroke volume, like Severe AR, large PDA and left
ventricular outflow obstruction, like AS, HCM cause prolonged left ventricular
ejection time (Table 15-3).

TABLE 15-3

Reverse splitting

Electrical causes:
1. LBBB
2. Right ventricular pacing
3. WPW syndrome.
Mechanical causes:
1. Increased LV stroke volume (Severe AR,
Large PDA)
2. LVOT obstruction
3. Ischemic episodes
4. LV systolic dysfunction

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Reversed splitting can be classified as:
• Type 1: S2 is usually single during inspiration, and reversely splitted in
expiration.
• Type 2: S2 shows normal inspiratory splitting and reverse splitting in
expiration.

• Type 3: S2 in single in inspiration, as well as in expiration, though A2P2 sequence is reverse in expiration. This is because, during reverse
splitting, P2-A2 separation is less than 20 ms.
Reverse splitting can be occasionally found in ischemic heart disease, during
acute ischemic event. Severe left ventricular systolic dysfunction is another
cause of reverse splitting, particularly when it is associated with LBBB.

Persistently Single (Table 15-4)
Single S2 in both phases of respiration can occur when either of the two
components is absent or two components remain synchronous. P2 is absent
in pulmonary atresia, severe PS, dysplastic pulmonary valve, Truncus
arteriosus and absent pulmonary valve.
Pulmonary component is present but inaudible in conditions where pulmonary
artery is abnormally positioned, like DTGA or other malposed great arteries.
Aortic component is absent in calcific aortic stenosis or aortic atresia. Both
the components occur simultaneously in VSD with bidirectional shunt, having

TABLE 15-4

Single S2

Absent P2
1. Pulmonary atresia
2. Severe PS and dysplastic pulmonary valve
3. Truncus arteriosus.
4. Absent pulmonary valve.
5. Occasionally in old age.
Inaudible P2
1. D-TGA
2. MPGA
Absent A2

1. Calcific AS
2. Aortic atresia
Inaudible A2
1. Loud P2 in pulmonary area
2. Loud pansystolic murmur (VSD, MR)
3. Prolonged ejection systolic murmur (PS)
Synchronous A2 and P2
1. VSD with bidirectional flow
2. Single ventricle


Second Heart Sound (S2)
equal pulmonary and systemic vascular resistance. Sometimes, P2 is inaudible
in old age with increased anteroposterior diameter of chest.

Intensity
Loudness or intensity of S2 depends on the closing force, which is the
diastolic gradient across the aortic and pulmonary valve. This gradient between
aorta and left ventricle is much higher than between pulmonary artery and
right ventricle. For this reason, A2 is louder than P2. This loudness makes
A2 audible both at the base as well as apex, whereas P2 is audible at the
left second or third intercostals space. That left ventricle forming the apex
can be another contributing factor for the transmission of A2 at the apex.
A2 is louder than P2 in 95% cases, even at left 2nd intercostal space.
Normally, P2 is not audible down to the 2nd intercostal space and only in
5% cases, it is audible at apex.
Commonest cause of loud A2 is Hypertension, hyperkinetic circulation
and aneurysm of the ascending aorta. Hyperkinetic flow causes stretching of
the aorta by increased volume during systole with vigorous recoiling during
diastole contributing to loud A2. Diminished intensity of A2 is calcific AS

and severe AR.
Cause of louder P2 is pulmonary hypertension. Left to right shunt by
increasing flow along with dilatation of pulmonary artery and hyperkinetic
circulation by increasing flow also cause loud P2. P2 is equal to A2 in mild
PAH; louder than A2 in moderate PAH; it becomes audible all through the
precordium in severe PAH. Apical transmission of loud P2 in PAH caused
by mitral stenosis and VSD, is somehow rare. A very loud P2 can mask A2
in pulmonary area. P2, without PAH is usually not audible at apex. When
apex is formed by the right ventricle as in ASD or primary tricuspid
regurgitation, P2 is audible at the apex with normal pulmonary artery pressure.
Depressed sternum may cause louder S2, due to the closer proximity of the
chest wall with the heart.

Further Reading
1. Curtis EL, Mathews RG, and Shaver JA. Mechanism of normal splitting of the
second heart sound. Circulation 1975;51:157.
2. Gray I: Paradoxical splitting of the second heart sound. Br Heart J. 1956;18:21.
3. Harris A and Sutton G. Second heart sound in normal subjects. Br Heart J. 1968
30:739-42.
4. Sutton G, Harris A and Leatham A. Second heart sound in pulmonary hypertension.
Br Heart J. 1968;30:743-56.

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16

Third Heart
Sound (S3)

Physiology (Fig. 16-1)
S3 is a low frequency, low-pitched ventricular filling sound. It follows A2
by 120 to 200 ms in the ventricular early rapid filling phase and coincides
with y descent of the atrial pressure pulse. Sudden halting of the opening
AV valves in early diastole or the impact of the ventricular wall on the chest
wall are some of the mechanism suggested, regarding the genesis of S3.
Sudden deceleration of the blood flow after opening of the AV valve, setting
the cardiohemic system in vibration and producing the S3, is the most
acceptable mechanism.

Fig. 16-1: Physiology of S3: During rapid ventricular filling phase, higher atrial-ventricular
gradient, due to higher v wave causing higher atrial pressure and rapidly expanding
ventricle with lower filling pressure causes S3

How to Detect it
S3 is relatively a faint sound and often can be missed. It can be best picked
up by the bell of the stethoscope lightly pressing on the skin at the apex,
the patient lying in left lateral decubitus in a quiet room. Coughing a few


Third Heart Sound (S3)
times or a few sit-ups can make a S3 better audible. This sound waxes and
wanes with respiration and postures and may be present on every second
third or fourth beat. This is an event around the S2.

Left Sided vs Right Sided S3
Right ventricular S3 is best heard at left parasternal area in supine position
and is increased in intensity with respiration and passive leg rising.

Physiologic S3 vs Gallop Sound

When S3 is present in a normal heart, it is called physiologic S3.When it
is associated with pathologic or hemodynamic abnormalities, it is called
gallop sound.

Gallop Sound
Presence of S3 or S4 causes tripling or quadrupling of sound and creates an
auscultatory impression of the canter of a horse. This effect is more impressive
in presence of tachycardia. When both S3 and S4 are present, they produce
a diastolic rumble. When very closed to each other, they produce a single
filling sound, called summation gallop.

Physiologic S3
It may be normally found in children, and 25% young adults. Thin body
habitus and enhanced early diastolic flow are the probabable explanations.

How to Differentiate Physiologic S3 vs Pathologic S3
Clinical situation is the most important factor. Physiologic S3 is softer and
disappears completely on sitting or standing. A palpable S3 is usually
pathological which is louder and sharper (higher pitch) than physiological
S3.

S3 due to High Flow
High flow across the atrioventricular valves may produce S3. Mitral
regurgitation and tricuspid regurgitation with a large v waves cause left and
right sided S3 respectively. Posttricuspid and pretricuspid shunt may cause
left and right sided S3 respectively. Any high output state, like pregnancy,
thyrotoxicosis may produce S3. In these conditions, S3 is not any indicator
of ventricular dysfunction.

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S3 in Ventricular Dysfunction
Ventricular dysfunction, either systolic or diastolic, leading to increased
ventricular end diastolic pressure, may cause S3. One explanation is the noncompliant ventricle in which rapid early diastolic flow causes S3. Another
explanation is that the distended ventricle with increased preload causes a
suction effect and a rapid inflow in early diastole Its presence, in these
conditions indicates ventricular end diastolic pressure more than 15 mm Hg,
EE less than 20% and high serum BNP. Presence of S3 in chronic aortic
regurgitation is an important hallmark of left ventricular dysfunction. In
chronic mitral regurgitation, S3 might be an indicator of either increased
flow or left ventricular dysfunction. S3 may be the earlier marker of left
ventricular dysfunction. A persistent, loud S3 along with sinus tachycardia
even after optimal antifailure medications is a poor prognostic sign.

Further Reading
1. Abrams J. The third and fourth heart sound. Primary Cardiol. 1982;8:47.
2. Marcus GM, Michaels AD, DeMarco T, et al. Usefulness of the third heart sound
in predicting an elevated level of B- type natriuretic peptide. Am J Cardiol.
2004;93:1312.
3. Nixon PGF. The genesis of the third heart sound. Am Heart J. 1963;65:712.


17

Fourth Heart

Sound (S4)

Physiology (Fig. 17-1)
S4, like S3 is a low frequency low pitched ventricular filling sound during
atrial contraction. Presystolic expansion of left ventricle, during atrial
contraction, produces this sound. Physiology of origin of this sound is similar
to that of S3. Pressure over loaded ventricle, or ventricle with raised end
diastolic pressure, requires a vigorous atrial support to maintain an optimal
preload. A functionally competent atrium and nonstenotic AV valve are
prerequisite for the S4. It occurs at the same time of a wave in atrial pressure
pulse and after the p wave of ECG.

Fig. 17-1: Physiology of S4: During presystolic phase, higher atrial-ventricular pressure
gradient, due to higher a wave causes S4. Mean atrial pressure is not very high

How to Detect it
It can be best picked up, like S3, by the bell of the stethoscope lightly
pressing on the skin at the apex, the patient lying in left lateral decubitus
in a quiet room. S4 is coupled with S1 in its timing. Sometimes, it is better
palpable than audible (vide palpation). Palpable S4 is always pathological.


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Bedside Cardiology

Pressure Over Load
Commonest causes of left sided S4 are systemic hypertension, aortic stenosis
and hypertrophic cardiomyopathy. Presence of S4 in aortic stenosis indicates
a gradient around 70 mm Hg and left ventricular end diastolic pressure

around 15 mm Hg, in a young adult.

Raised End Diastolic Pressure (Fig. 17-2)
Acute coronary syndrome, during the ischemic episode, is consistently
associated with S4. Dilated cardiomyopathy, restrictive cardiomyopathy and
acute mitral or aortic regurgitation can cause S4, due to raised left ventricular
end diastolic pressure. These conditions are also associated with S3.

Fig. 17-2: Acute MR and S3, S4: Both a wave (causing S4) and v wave (causing S3)
are high and mean left atrial pressure is high

TABLE 17-1
1.
2.
3.
4.
5.
6.
7.
8.
9.

Causes of S4

Systemic hypertension
Aortic stenosis
Hypertrophic cardiomyopathy
Acute ischemic episode
Dilated cardiomyopathy
Restricted cardiomyopathy

Acute regurgitant lesions
PAH (right sided S4)
Pulmonary stenosis (right sided S4).


Fourth Heart Sound (S4)

Right-sided S4
It is best heard at the left parasternal area and may be accentuated with
inspiration. Pulmonary hypertension and pulmonary stenosis are the
commonest causes.

AV Block
S4 is better audible in presence of first degree AV block due to its separation
from S1 (S4 sound occurs after the completion of atrial contraction, around
0.16 sec after the beginning of the p wave in the ECG). In complete heart
block, S4 is intermittently heard and at a faster rate than S1 or S2.

Others
Increased stroke volume and cardiac output like thyrotoxicosis, anemia and
large AV fistula can cause S4 along with S3.

Further Reading
1. Goldblatt A, Aygen MM, Braunwald E: Hemodynamic phonocardiographic
correlation of the fourth heart sound in aortic stenosis. Circulation, 1962;26:92.

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18

Ejection Sound

Ejection sounds are high-pitched sound occurring in ventricular systole at
the onset of ejection phase. They are pulmonary or aortic in nature and either
valvular or vascular in origin. Valvular clicks are due to sudden halting of
the diseased semilunar valve at the end of its maximal excursion. It occurs
at the end of the isovolumic contraction phase, around 40–60 ms after S1.
Vascular click occurs during ejection of blood commonly in a dilated
pulmonary or aortic root.

Pulmonary Valvular Click (Fig. 18-1)
Pulmonary click occurs 0.09 second after Q wave on ECG. Mild to moderate
pulmonary stenosis is the commonest cause of pulmonary valvular click. It
is a high-pitched sound, localized in the pulmonary area. Its most important
characteristic is that it’s the only right-sided event, which is decreased in

Fig. 18-1: Pulmonary valvular click (EC): During inspiration, increased preload causes
higher right ventricular end-diastolic pressure (RVEDP) resulting in lower pulmonary
artery end-diastolic to RVEDP gradient. This leads to absent EC during inspiration. During
expiration, RVEDP comes down, with higher pulmonary artery to RVEDP and EC can be
heard


Ejection Sound
intensity in inspiration. During inspiration, the increased inflow of blood
in right ventricle increases the right ventricular end diastolic pressure, thus
reducing the pulmonary end diastolic (which is already low in the setting of
pulmonary stenosis) to right ventricular end diastolic pressure gradient,
which causes forward movement of the pulmonary valve and its partial

reopening. At the onset of systole, there is less excursion of the partially
opened valve, thus decreasing the intensity of the ejection click. In early
mild pulmonary stenosis, the click may not be appreciably diminished in
inspiration. More severe is the stenosis, more the click is shifted to S1. In
severe stenosis, the click is absent, either due to its merging with S1 or the
valve’s immobility. Click indicates obstruction at valvular level and is absent
in infundibular stenosis.

Pulmonary Stenosis vs ASD
Mild pulmonary stenosis has the features of ejection systolic murmur, normal
intensity of P2 and a persistent split of S2. Sometimes it is difficult to
differentiate it from small ASD. Valvular click is the clue in favor of
pulmonary stenosis.

Pulmonary Vascular Click
Pulmonary hypertension, idiopathic dilatation of pulmonary artery and other
conditions with dilated pulmonary artery produce an ejection click, which
is vascular in origin. It is also a localized high pitch sound but does not show
the effect of inspiration (constant click).

Aortic Valvular Click (Fig. 18-2)
Aortic click occurs 0.12 second after Q wave on ECG, i.e. it occurs later
than pulmonary click. It occurs in aortic stenosis and bicuspid aortic valve.
It corresponds in timing with the anacrotic notch in the upstroke of the
aortic pressure curve. The click is often better heard at the apex, rather
than the base and does not show any variation with respiration (constant
click). In case of aortic stenosis, severe the stenosis, earlier will be the
click in relation to S1. Click will be absent in calcific aortic stenosis with
nonpliable leaflets.

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Fig. 18-2: Aortic valvular click: It occurs at the end of isovolumeric contraction, once LV
pressure pulse crosses over the aortic pressure pulse, only when it can open the aortic
valve against aortic pressure

Bicuspid Aortic Valve
In an uncomplicated bicuspid aortic valve, the click is best heard at the apex.
It is louder than S1, followed by a short systolic murmur, relatively louder
A2 and a short early diastolic murmur. Increased area of large cusp,
responsible for the ejection sound during its opening, is responsible for the
louder A2.

Aortic Vascular Click
It occurs in situations with dilated aortic root, like systemic hypertension,
ascending aortic aneurysm, coarctation of aorta and Fallot’s physiology. Its
timing is after the anacrotic notch of the aortic pressure pulse. Vascular click
is localized in nature.

Clinical Importance of Click
A valvular click indicates the obstruction across the RVOT or LVOT is at
the valvular level and not at the supra or subvalvular level. Secondly, it
indicates that the valve is still pliable. Vascular click has its clinical relevance
only in case of Fallot’s physiology, where its presence indicates a severe

Ejection Sound
RVOT stenosis or atresia, resulting in most of the flow across the aorta with
a dilated aortic root. Sometimes, in ‘pink’ Fallot’s tetralogy, where RVOT
stenosis is mild and at valvular level, a valvular click may be present.

Further Reading
1. Hultgren H N, Reeve R, Cohn K, et. al. The ejection click of valvular pulmonic
stenosis. circulation 1969;40;631-40.
2. Leech G, Mills P and Leatham A. The diagnosis of a non-stenotic bicuspid aortic
valve. Br Heart J. 1978;40:941-50.

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19

Nonejection Sound

Midsystolic Click (Fig. 19-1)
Physiology: Mitral valve prolapse is the commonest cause of nonejection
click. It occurs due to sudden tensing of the prolapsing atrioventricular valve
during systole. A long, redundant leaflet, too large for the contracting ventricle
is prolapsed in mid to late part of systole when the click dimension (ventricular
volume at which leaflet cannot be accommodated) is reached.
Location: This high frequency, sharp clicking sound, best heard at the apex,
is audible over a wider area on the precordium. There might be multiple
clicks, which, depending on the degree of malcoaptation, may or may not
be associated with murmur.
Dynamic auscultation: It bears a very important application on this click.

Any maneuver, which reduces the ventricular volume like standing, valsalva
phase 2, causes an early prolapse of the mitral valve followed by a long
murmur. Supine posture and valsalva phase 4 by increasing ventricular
volume cause late prolapse and late systolic murmur. Click may even merge
with S1, making it louder in very early prolapse. By this hemodynamic

Fig. 19-1: Nonejection click (NEC) of MVP: Depending upon the severity and dynamic
maneuvers, click may be classically midsystolic, late systolic or early systolic


Nonejection Sound
maneuver, S1-nonejection click can be differentiated from S4-S1, S1-ejection
click and M1-T1.
Clinical significance: Isolated click does not have much clinical relevance.
Associated mitral regurgitation determines the overall prognosis.

Other Causes of Nonejection Click (Table 19-1)
Left sided pneumothorax, adhesive pericarditis, complete absence of
pericardium, left ventricular aneurysm, atrial and ventricular septal aneurysm
and left atrial myxoma may cause systolic nonejection click, which does not
change appreciably on hemodynamic maneuvers.

TABLE 19-1

Causes of nonejection click

1. Mitral valve prolapse
2. Left sided pneumothorax
3. Ahesive pericarditis/complete absence of pericardium
4. Left ventricular aneurysm

5. Atrial and ventricular septal aneurysm
6. Atrial myxoma

Pseudoejection Sound
This sound occurs in hypertrophic cardiomyopathy. Either the anterior mitral
leaflet abutting on the septum or sudden deceleration of blood in the LVOT
causes this apparent ejection sound. Dynamic auscultation does not
appreciably change the timing of this sound in relation to S1.

Mitral Opening Snap (OS)
Physiology: Opening of a normal AV valve is acoustically silent. Sudden
tensing of the stenosed mitral valve at its full opening produces the mitral
opening snap. It is mostly contributed by AML.
Location: It is a high-pitched sound; best heard medial to the apex. As it
is a loud sound, can be heard over a wide area of the precordium.
Timing: It occurs 40 to 120 ms after S2, corresponding with isovolumic
relaxation time (Fig. 19-2).

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Bedside Cardiology
Clinical significance: Opening snap is absent when stenosed mitral valve
is calcified and nonpliable. Thus an audible OS indicates the valve, is suitable
for valvuloplasty. This sound is often absent in congenital MS as because
the leaflets are not pliable. OS may persist even after vlavuloplasty.

Fig. 19-2: Events around S2

Severity assessment: Severe the stenosis, higher will be the left atrial
pressure. Left atrial pressure cross over the left ventricular pressure pulse,
which indicates opening of mitral valve, will be earlier. Thus, OS will be
closed to A2. Shorter the A2-OS interval, severe will be the MS. This does
not hold true in presence of tachycardia (shortened diastole), bradycardia
(longer diastole), AS (delayed A2), low cardiac output (low atrial pressure)
and high LVEDP (lower gradient across mitral valve) (Fig. 19-3).

Fig. 19-3: Severity assessment of MS: Severe the MS, higher will be the LA-LV
diastolic pressure gradient and shorter will be the S2-OS distance


Nonejection Sound
MS vs ASD: OS can often be heard at the left upper parasternal area and
can be confused as pulmonary component of widely splitted S2. In ASD,
there can have a diastolic flow murmur; S1 can also be loud due to T1
component. Assuming A2-OS as widely splitted S2, MS can wrongly be
diagnosed as ASD. But during inspiration, MS should have three high
frequency components at pulmonary area—A2, P2 and OS. Other points in
favour of second component being OS are: It is equally loud at the apex as
well base; its intensity is decreasing with inspiration; split is getting narrowed
on inspiration and wider on standing (Table 19-2 and Fig. 19-4).

TABLE 19-2

MS vs ASD

Similarities
S2-OS/A2-P2

Diastolic murmur
Differences
Inspiration

Standing

MS

ASD

S2-OS
MS

A2-P2
Flow murmur

A2-P2-OS
S2-OS narrows
OS intensity downs
S2-OS widens

A2-P2
A2-P2 widens
P2 intensity ups
A2-P2 narrows

Fig. 19-4: MS vs ASD: In ASD, in both phases of respiration, there will be two components
around S2 (A2 and P2). In MS, whereas during inspiration, there will be three components,
A2, P2 and OS and during expiration, only one component, S2

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Bedside Cardiology

Tricuspid Opening Snap
Tricuspid OS is associated with a rare entity like tricuspid stenosis, large
ASD and Ebstein’s anomaly. Like any right-sided event, its intensity is
increased with inspiration.

Pericardial Sound
Pericardial Knock
Physiology: In constrictive pericarditis, there is high filling pressure
with large atrial v wave. It occurs in ventricular rapid filling phase.
During this phase, there is sudden halting of the expanding ventricle, due
to the constricted, restrained pericardium, causing the pericardial knock
or S3.
Timing: It occurs 100 to 120 ms after S2, later than mitral OS, but earlier
to left ventricular S3. It corresponds with the rapid y descent.
Clinical significance: Features of constrictive pericarditis may simulate
those of CHF. Pericardial knock may be confused as S3. That the knock
occurs earlier and higher in frequency than S3 may be a differentiating
point.

Pericardial Rub
Physiology: It is a leathery, high frequency sound and is scratchy in
quality.
Timing: It occurs in three phases of cardiac cycle, in atrial systole, in

ventricular systole and in ventricular rapid filling phase.
Clinical significance: It may be found in acute pericarditis of any
etiology. However, all the three components are found in idiopathic
pericarditis, post-traumatic pericarditis and pericarditis associated with CRF.
Some systolic murmurs, as in hyperthyroidism (Means-Lerman sign) and in
Ebstein anomaly, due to its scratchy superficial nature, may be simulated as
pericardial rub.
Pericardial rub is best heard with patient in sitting forward with held
expiration.


Nonejection Sound

Mediastinal Crunch (Hamman Sign)
Physiology: It consists of multiple scratchy sounds in various phase of
cardiac cycle, due to presence of air in pericardial and mediastinal spaces.
Clinical significance: It may be found after cardiac surgery with open
pericardium. Associated mediastinal emphysema, with crepitations in the
neck, is the clue.

Prosthetic Sound (Fig. 19-5)
Mechanical Prosthesis
Mechanical prosthetic valve produces sound louder and higher in frequency
than the native valves. Nature of opening and closing sounds depend on the
nature of the prosthetic valve.

Ball-and-cage Valve
In aortic position, ball-and cage valve produces a loud opening click (OC)
after S1 and relatively softer closing sound (CS). Opening click may be
followed by early to mid peaking ejection systolic murmur associated with

multiple clicks as the ball is bouncing on the cage.
In mitral area, caged-ball prosthesis produces a loud OC after S2 along
with a midsystolic murmur at the left parasternal area, due to turbulent flow
in left ventricular outflow tract.

Tilting-disk Valve
In aortic area, single-tilting-disk valve produces CS louder than OC. OC is
followed by a midsystolic murmur, which may radiate to carotids. There may
be a soft diastolic murmur. In mitral area, single-tilting-disk valve produces
louder CS than OC. There is associated low-frequency diastolic rumbling
murmur.
Bileaflet-tilting-disk valve produces same pattern of sound, excepting
that in aortic area, it does not produce any diastolic murmur.
Clinical significance: Malfunction of the mechanical valve prosthesis
includes ball degeneration, strut fracture, thrombus and pannus formation,
infection or dehiscence. Multiple clicks may indicate a malfunctioning
valve. Both early and late opening of the valve, in relation to S2, indicate

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