Heart Sounds - 1

Theme of the presentation
 PART I: Cardiac Cycle
S1 S2 : GENESIS,PATHOLOGY AND
CONTROVERSIES
 PART II: S3 S4
Added Sounds
Ejection Sounds

 Mechanical events from the beginning of one heart beat to the
beginning of next one constitutes one cardiac cycle
 Constitutes of Ventricular Systole and V. Diastole
 Systole: 1. Isovolumetric Contraction (0.05sec)
(0.27) 2. Ejection Phase(Rapid + Slow( 0.09 + 0.13sec) (70%
+30%)
Diastole: 1. Isovolumetric Relaxation(including Protodiastole)
(0.12sec)
(0.53) 2. Rapid Ventricular Filling(0.11sec)
3. Reduced/Slow Ventricular Filling(Diastases)
(0.19sec)
4. Atrial Kick/Booster (0.11sec)

POLYGRAM
 Graphical representation of the pressure
volume relationship of Aorta, Ventricle and
Atria along with ECG and Phonocardiogram
tracings is called polygram.

Heart Sounds - Basics
 Human Ear Capacity 20- 20,000Hz
 Best Acuity heard at 1000-5000Hz
 Most Sounds and Murmurs 30- 1000Hz

Stethoscope
 Invented by Dr Rene Laennec in France in
1816
 Monaural and wooden tube structure

 First Binaural Stethoscope was invented by
Dr George Cammann in 1841 in New York

 Conventional Stethoscope developed by 1960
Bell: Low frequency Sounds(30- 150HZ
Diaphragm: High Frequency >300HZ
Tube : Ideally Double Tubing 10-12in
Best Inner Diameter 1/8 – 3/16in

RUSHMER THEORY
 Cardiac Sounds represent the vibrations
produced by the reverberations of the cardiac
structures like ventricular mass, Valvular
Apparatus and fibrous skeleton of the heart
due to sudden accleration or
deceleration of the blood mass during
each cardiac cycle

 No normal valvular apparatus is thick and rigid
enough to produce the cardiac sound just by
leaflet apposition thus the sound is actually
due to sudden tensing of the surrounding
structures(*)
 More rapid the tensing due to blood mass and
pressure crossover between two chambers
,higher is the frequency of the sound.

 The low frequency sounds like S3 and S4 is
not due to the sudden tensing rather than due
to large amount of blood mass moving at low
velocities.

FIRST HEART SOUND- S1
(M1 T1)
 Medium to High frequency Sound signalling
the onset of LV contraction.
 50- 60 msec after the electrical initiation of
ventricular depolarisation the first high
frequency component of S1 is heard.
 In actuality there are 3-6 components of S1
but out of these, high frequency and audible
are only 2 components.

 Calling the components of S1 as M1 and T1 is
more of a convenient acronym rather than the
fact, as various controversies surround the
production of the same.

FIRST COMPONENT OF S1
 LUISADA THEORY
States that MV cusps have nil or minimal role to
play in the origin of this component and this
component is due to the sudden tensing of LV
walls , Septum and the MV apparatus at the
onset of IVC.
He assumed that MV closure precedes the first
high frequency component of S1.
He was against the terminology M1

 LEATHEM,CRAIGE AND OTHERS
They proposed that the first component is due to
the maximal closing excursion of mitral cusps
and M1 reflects the sudden tensing of the
closed MV leaflets causing the vibration in the
surrounding structures.
MV leaflets play a role in the production of M1
and Closure conincides with the M1
More confirmed theory

Second Component of S1
 LUISADA AND SHAVER THEORY
Due to the vibrations caused by the ejection
component occuring with the opening of Aortic
Valve
Controversial but most authors concur that the
second component is due to the onset of
ejection into the aorta and this is accentuated
and delayed in the diseased states resulting to
be heard diffirently

 CRAIGE AND LEATHAM THEORY
Due to closure of the tricuspid valve.

CHARACTERISTICS OF S1
 Normally heard as fused single heart sound
 Medium to High Frequency
 Low Pitched
 Best heard with diaphragm
 M1 louder than T1
 M1 best heard at apex
 T1 best heard at Left LSB
 Splitting can be heard in Expiration and @ L-
LSB

 Normal M1 is followed by T1 by 30msec
 If the gap between is <20msec its sounds as a
single sound

FACTORS AFFECTING S1
STRUCTURAL INTEGRITY OF
VALVE
1.Inadequate coaptation of mitral valve
2. Loss of leaflet tissue – soft S1 (IE)
3. Thickness & mobility of the valve

VELOCITY OF VALVE CLOSURE
determined by the position of mitral valve at the
onset of ventricular systole
Position of mitral valve is altered by relative
timing of atrial & ventricular systole( PR interval )
Long PR: longer diastolic filling time-LV
pressure gradually increases - mitral valve leaflets
slowly drift together- lesser distance between
leaflets
Short PR - mitral leaflets are farther apart at the
onset of ventricular systole- closes with a high
velocity large excursion

 Very short PR- atrial systole coincides with
ventricular systole, diminishing the VA gradient
at the time of AV valve closure- s1 soft/
inaudible
 Max Intensity is heard between 80-140msec
 Soft S1 heard with PR >200msec

STATUS OF VENTRICULAR CONTRACTION
 Increased myocardial contractility increases the rate
of LV pressure(dP/dt) – loud S1
( Exercise, high output state)
 Decreased dP/dt – soft S1
(A/c MI, myocarditis, LBBB)
 Loss of isovolumic contraction- decreases dp/dt-
decreased velocity of mitral valve closure - soft S1
MR ,large VSD - S1 may be masked by the
murmur

EXTRACARDIAC CAUSES
-Obesity, emphysema, pericardial effusion
decrease the intensity of all auscultatory events
-Thin chest wall increases the intensity
Straight Back Syndrome: Loss of thorasic
Kyphosis causes a very narrow thorasic cavity:
Loud delayed T1

LOUD S1
 Labelled when its louder than A2 at the apex
or Louder than or equal to A2 at base.

LOUD M1
1.Mitral Stenosis
3 major reasons
1. Persistently elevated LA pressure in late
diastole leads to higher rate of ventricular
pressure development (dp/dt) during
isovolumetric systolic phase
2. Wide closing excursion of MV leaflets
3. Stiff non compliant leaflet and the
subvalvular structures (in RHD)

2. MVP ( non rheumatic MR): Holosystolic
prolapse– S1
loud- due to delay in checking action of mitral
valve caused by increased valve displacement,
increased amplitude of leaflet excursion and
summation of normal M1& nonejection click
3. Exercise – Tachycardia induced short PR
- Increased LV contractility
- Increased flow across the valve

4. LA Myxoma : Physiologically similar to MS.
(Booming S1-coined by Shaver et al in 1985)

LOUD T1
 TS
 ASD - increased tricuspid flow
 Anomalous pulmonary venous connection
- increased tricuspid flow
 Ebstein anomaly( noted by Barlow in 1969
postulated due to increase in RV pressure rising
rate- Sail Sound(coined by Fontana nd Wooly
1972))
 Straight Back Syndrome(Distance b/w Mid of
Ant Br of T8 and line between T4 and T12 on
lateral CXR <1.2cm)

Soft S1
 MITRAL REGURGITATION - decreased
mobility, poor coaptation, loss of isovolumic
contraction(in cases of LV dysfunction)
 CALCIFIC MS- immobility of mitral valve
 SEVERE AR
Steep rise in LV diastolic pressure causes
LVP>LAP in late diastole only leading to
premature closure of MV

 LBBB- delay in onset of LV contraction-
delayed and soft M1
decreased LV contractility
concomitant 1st
degree AV block
 Acute Myocardial infarction-
decreased ventricular contractility,
associated MR,
LBBB

VARIABLE S1
 AF (variable diastolic cycle length and thus
variable position of the cusps as the onset of
systole.Short cycle Loud S1 and Long cycle :
Soft S1)
 CHB
 VT with AV dissociation
 Atrial flutter with varying conduction
 Frequent Ectopics

ABNORMAL SPLITTING OF S1
 WIDE SPLITTING
2 MAJOR CAUSES
1. Electrical: Delayed ventricular activation time
2. Mechanical : Increased IVC time

CAUSES
1. RBBB
2. VPC`s with RBBB morphology
3. LV Pacing
4. LBBB,RV pacing( Can cause reverse splitting
T1-M1)
5. RA Myxoma,TS ( Extremely Delayed T1)
6. Ebstein Anomaly(Delayed closure of Septal
leaflet of Tricuspid Valve)
7. Older Adults
8. Acute M.I.
Longer LV pre-ejection time

 Normally Splitting is heard in expiration and at
the apex but if heard at the base it should be
suspected as a ejection click

Difference between Split S1 and
S4
Split S1
1.Best heard at apex
and Left LSB
2. No Variation with
Respiration
3. No Presystolic
accentuation
palpable
4. Best heard with
Diaphragm
S4
1.Best heard at apex
alone
2. Varies with
Respiration
3. Presystolic
accentuation
palpable
4. Best heard with
Bell

 S1 and AF
 S1 and relation to murmur in MVP

Second Heart Sound
 Produced by the sudden deceleration of the
blood mass at closure of Semilunar Valves
leading to vibration of the cardiohemic system
 2 components Aortic and Pulmonary
 Respiratory variations were described by
Potaine in 1866.

GENESIS OF S2(A2 P2)
LV End Systole
Flow into great vessels complete
Sudden deceleration of the blood mass towards the Semilunar
Valves (Ao-LV and PA-RV pressure crossover)
Cessation of Forward flow into great vessels
Coaptation of the Semilunar Valves
Abrupt tensing of the closed leaflets and vibration of LVOT
And RVOT and Great Vessels
A2 and P2

 As compared to S1 there are limited
controversies over the exact genesis of S2
and the most accepted theory is by Shaver et
al who states that the highest frequency
sound is heard due to the vibrations of the
great vessels due to sudden tensing of the
supporting structures of the semilunar valves
at the time of pressure crossover between the
ventricles and the great arteries due to the
deceleration of the blood mass.

CHARACTERISTICS OF S2
 High Frequency
 Best Heard with Diaphragm
 A2 louder than P2
 Normally A2-P2 gap : 10-60msec
 Average A2-P2 gap :40 msec best heard in
Mid to late inspiration.
 Narrow Splitting is gap < 30msec
 Splitting can be heard if gap >20msec
 With age the the A2-P2 gap reduces and its
normal to find single S2 in both phases in

 A2: Can be heard at R/L 2nd
ICS and apex
Best heard at apex
If palpable /Tambour A2(*) : Always
pathological
P2: Best heard at Left 2-4th
ICS
If heard at apex or if palpable:
Pathological

RESPIRATION AND S2
INSPIRATION
Increased Intrathorasic Volume
Decreased Intrathorasic Pressure
Increased Blood to RV and relatively less blood from PV to LA
Prolonged RV systole and LV systole either unchanged or decrease
RV ejection and Q-P2 increases and Q-A2 unchanged or decreased
Several beats later and during expiration this increased BV enters
LV and Q-A2
Increases and Q-P2 again decreases

HANGOUT INTERVAL
 Distance between the Ventricular Systolic
Pressure and its great vessels at the level of
Incisura is called HANGOUT INTERVAL.
 Termed by Shaver and associates.
 Insicura: Peak deceleration of the blood
mass in the great arteries and is followed by
rebound pressure.

 After the pressure cross over the valves
should close but due to the inertia of the
moving blood mass the valves remain open for
a brief period and this period is hangout
interval and it depends upon the vascular
impedance of the great vessels.
 Higher the resistance lower the H.I.

Importance of Hangout Interval
Aorta
High Resistance and Low Compliance
Lesser distensibility
Recoil from the ejection of blood from
Aorta is brisk
Vibrations are relatively sooner
A2 and incisura come immediately after
LV ejection
Smaller Hangout Interval
Pulmonary Artery
Low Resistance & High
Compliance
Recoil is delayed
As there is higher
distensiblity
P2 and incisura come
delayed after
RV ejection
Longer Hangout Interval

 Aortic HI is <15msec
 Pulmonary Hangout Interval is 2-5 times
higher than the Aortic Hangout Interval and
can be 43-86msec.
 PHI has more variation with respiration and is
Inversely related to PVR
 PHI is the most responsible for the widening of
A2-P2 in inspiration.

CONTRIBUTION OF VARIOUS
COMPONENTS IN DELAY OF P2
 INCREASED Q-P2 : 73%
Increased PA hangout interval: 45%
Increased RV ejection time : 28%
 DECREASED Q-A2 : 27%

FACTORS AFFECTING S2
 AFFECTING SPLITTING:
1. Increase or decrease in the RV or
LV ejection time.
2. Increase or decrease in great
vessel impedance and/or distensibility
Ex: Electrical activation pattern, Abnormal
contraction of ventricle, Outflow tract
obstruction , changes in PVR/SVR

 AFFECTING INTENSITY:
Its directly propotional to the rate of change of the
diastolic pressure gradient across the valve i.e.
driving force that’s acclerating the blood mass
retrograde into the base of the great vessels
This pressure gradient is dependent on:
1. Level of diastolic pressure in great vessels
2. Rate of pressure decline in the ventricles

1. Increase in the pressure of Ao or PA leading
to sudden deceleration of blood mass
2. Valve Morphology

Assessment of relative
loudness –perloff 172

INCREASED A2
1.Increased Pressure in Central Aorta: ex
Hypertension
2. Aortic Root Dilatation: Syphilis, Marfans, RA
Takayasu
3. Congenital Positional variation in CHD: ex
dTGA in which Aorta is pushed anteriorly., TOF
with absent P2 and dilated dextroposed Aorta

LOUD P2(relative to A2)
 Pulmonary Hypertension: Due to dilated PA,
Increased PAP.
 ASD: With large L-R shunt. Apex is occupied
by RV.

DECREASED A2
 Valvular AS due to distorted fibrosed and
calcified valve.Also seen in Supravalvular AS
but A2 is normal in Subvalvular AS.
 Aortic Regurgitation(destruction of the valve
tissue and impairment of elastic tensing
mechanism of the leaflets)

Decreased P2
 Valvular PS causes diminished and delayed
P2.Right sided maneuvers like Leg raising can
increase the intensity of P2.
 Deep Inspiration causes insulation of the PA
with air filled lung tissue and can lead to
diminished P2.
 Absent Pulmonary Valve
 CHD like TOF P2 can be inaudible

SPLITTING OF S2
 PHYSIOLOGICAL SPLITTING
Determined by
1. Electromechanical Coupling(Q-
P2,Q-A2)
2. Mechanical Systole
3. Hangout intervals and thus the
PVR and
SVR
4. RV and LV inflows

 Normally, A2 will be heard at the apex and P2
will not be heard at apex even in inspiration.
 Thus while assessing the split, base should be
auscultated first and traced to the apex.

WIDE SPLIT S2
 Delayed P2
1. RBBB,LV Pacing(Prolonged Q-P2)
2. Pulmonary Embolism(Increased Systole)
3. Valvular PS: Delay corelates with the
severity of
lesion.
A2-P2 interval >100msec indicates RV-PA gradient
>100mmhg.
This corelation is not seen in infundibular PS as the delay
is also caused by infundibular hypertrophy and not
valvular obsruction alone.
4. Idiopathic dilatation of PA: Delayed P2 due
to increased Hangout interval

5. RV failure(Increased Systole)
6. Late Pregnancy or Adv. Renal
Failure
(Hypervolumia)

 Early A2:
1: VSD with normal PAP
2 : Severe MR with Normal LVEF
3: LA Myxoma
4: Constrictive Pericarditis(reduced
diastolic inflow)
5:Pericardial Tamponade
3rd
and 4th
due to Decreased LV inflow and reduced
LV systole

EXPIRATORY SPLIT
 Presence of A2 and P2 at end Expiration
 In supine position Pts may have expiratory
split due to A2-P2 gap>30msec but it becomes
single in upright position and hence basal
areas should be auscultated in upright
postions only.
 Persistent expiratory split is pathological
 All the causes of Wide Split will cause
expiratory split also

FIXED SPLIT
 When the RV or LV SV does not change with
inspiration or changes equally with respiration
the splitting heard is FIXED.
 Diagnosis should be made only in both
recumbent and upright position as it
occasionally can be seen in supine position
also.

Major Physiological Reasons
 SIMULTANEOUS EQUAL CHANGE IN
LV/RV SV WITH INSPIRATION
 FAILURE TO INCREASE RV-SV WITH
INSPIRATION

Equal change in LV/RV SV
1. Atrial Septal Defect
In cases of ASD with L-R shunt there is RV
overload and RA and LA act hemodynamically
as a single reservoir.
In inspiration, increased flow to RV which
causes decreased flow from LA to RA and thus
momentarily increased flow from LA to LV
increasing LV inflow.

This leads to Increased Q-A2 and hence both
RV and LV SV increase in inspiration.
In cases of ASD without PAH, this fixed splitting
is occasionally variable and respiratory variation
can be heard in sitting position.

 ASD with PAH: Always fixed splitting with loud
P2

ASD and Valsalva Maneuver
In Normal population, in strain phase of
Valsalva, there is decrease in both LV and RV
inflow and thus reduced SV leading to fused S2.
During the release phase, there is sudden
increase in RV inflow and thus RV-SV increases
leading to prominent S2 splitting for 6-8beats
Finally when the augmented blood again
reaches LV, Q-A2 again increases leading to
narrowing of the A2-P2 gap.

 In patients with ASD, S2 splitting widens
during strain phase due to increased L to R
shunting and in the release phase the
expected S2 splitting doesn’t occur.

ASD and Atrial Fibrillation
 Long cycle lengths in patients with ASD
results in Increased A2-P2 splitting

Longer RR cycles cause wide split
S2 in AF(James O Toole et al Circulation 1977)
 Two factors responsible
1) QP2 progressively increased with increasing
cycle length due to a selective increase in the
duration of RV electromechanical systole
2) at relatively long cycle lengths, the duration of
LV electromechanical systole was relatively
fixed.

 This is related to the differences in compliance
between the right and left ventricles.
 The longer cycle lengths allow greater time for
diastolic filling and because the left ventricle is
thicker and less compliant than the right, there
is selectively more filling of the right ventricle.
 This greater filling of the right ventricle then
leads to selective prolongation of the right
ventricular electromechanical interval with
increase in the width of splitting of S2.

2. Ventricular Septal Defects:
S2 is normally split in patients with VSD and
normal PAP.

VSD WITH SEVERE PAH
Increased PVR, Decreased PA compliance and
decreased PA hangout Interval.
Both chambers eject into high resistance
vessels resulting in equal inspiratory delay on
both sides accompanied by nil respiratory
variation as both ventricles act as a common
chamber
This leads to single S2 in both the phases of
respiration

Note:
S2 in supracristal VSD: (Farru et al , BMJ
1971)
1.Pathological Splitting of S2 in expiration
2. Attenuated and delayed P2
3. Crescendo-Decrescendo murmur

 The main cause was a delay in pulmonary valve
closure due to a lengthening of the ejection
period of the right ventricle.
 The mechanism is analogous to that of valvular
PS due to overloading of the infundibulum during
systole by left-to-right shunt at this level which
acts as an obstruction to RVOT and interferes
with its emptying; consequently, the systolic
ejection period of the right ventricle is
lengthened.

FAILURE TO INCREASE
RV-SV WITH
INSPIRATION
 In cases of major pressure overload of RV
1. RV Failure
2. Acute/ Chronic PE
3. Severe PAH(uncommon)
4. RBBB with Congestive Cardiac Failure: RV
systole is substantially prolonged and A2- P2
coupling will be both wide and fixed. In such
cases maneuvers that decrease the venous
return as torniquets and upright position bring
about the respiratory variation.

REVERSED/PARADOXICAL
SPLIT
 Here S2 is maximally split at expiration and
narrows or fuses at inspiration
 As the directional changes also occur its also
called as paradoxical splitting.

Paradoxical Split
Paradoxical
Splitting
Paradoxical
Splitting
Type 1
(classical)
Type 1
(classical)
Type 2Type 2 Type 3Type 3
Incrased Q-A2 interval due
to LV mechanical delay
During Expiration
Prolonged LV systole
makes A2 follow P2 and is
heard in expiration
During Inspiration
Q-P2 increases normally but
Q-A2 remains unchanged
and ear appreciates only
single S2
Mild delay in Q-A2
and
Marked Q-P2
interval
During Inspiration
Normal split may
be heard
During Expiration
S2 reverse split
heard
Both Expiratory
And Inpiratory
separation
Is <20msec and S2
is
Fused in both the
phases

Increased Q-A2 interval
1. LBBB: Most common cause of the Reversed
Split.
Increased LV systole due to
1.Increased interval from the beginning of
electrical activation ie onset of QRS to IVC
2.Increased LV IVC time secondary to imapired
LV contractility.

2. WPW syndrome with Rt Ventricular
Pre excitation from Rt Bypass tract
Q-P2 may shorten with inspiration.
May cause type 2 paradoxical splitting.
3.RV pacing and RV-PVC

4. Increased LV ejection time:
Uncommon but Large SV in LV overload
conditions may lead to prolonged Q-A2 and
paradoxical Splitting.
Ex: PDA
Severe AR
Severe LV dysfunction

5. LVOT Obstruction:
Valvular AS and HCM
In valvular AS ,not only its because of the
prolonged ejection time but also due to the post
stenotic dilatation of the Aorta and thus
increased Hangout interval.

Decreased Q-P2(uncommon)
 Shortened RV systole : seen in TS and RA
myxoma

Key to Auscultate Reverse
Splitting
 As per Constant et al
 2 approaches:
1. Assess the amplitude of both components of
S2 as the stethoscope moves from base to
apex.
Component that softens at apex is P2
2. Valsalva Maneuver: Widening of S2 in strain
phase, narrowing on release and
subsequent widening again

PSEUDOPARADOXICAL
SPLITTING
1.COPD:
2. Large chests:
Deep Inspiration in these patients will
cause artificial muffling Of P2 due to
insulation of the PA by the expanded
lungs and hence S2 appears single with
inspiration and split in expiration

SINGLE S2 / NARROW SPLIT
S2
 Heard when the A2-P2 gap is <30msec
1. Aging: Incidence of Auditary splitting with
inspiration decrases with age.
50% subjects with age >60yrs have single S2.
Due to either age related increased LV ejection
time
Or due to age related increase in PVR and
subsequent decrease in PA hangout interval.

2. Artifactual Muffling of P2: Lung insulation of
the P2 during inspiration in COPD and large A-P
diameter chest individuals.
3. Pulmonary Hyertension: Pts with Severe PAH
and Normal RV function narrow A2-P2 is a must
and loud P2 can backwards mask A2 causing it
to appear as single S2.

4. Pathological Absence of P2:
Severe Pulmonic deformity with low or absent
PBF and great vessel malposition causes single
A2/S2
ex: TOF
Pulmonary Atresia and stenosis
Tricuspid Atresia
Truncus Arteriosus
TGA

5. Semilunar Valve Stenosis:
In severe AS,A2 can be obscured by a murmur
of AS or it itself can be soft or absent.
6. Eisenmenger VSD, Single Ventricle
Common ventricular chamber ejects into 2
vessels with equal compliance,resistance and
hangout interval, the systole lengths will be
equal and S2 will be fused in all phases.

DIFFERENTIATING SHUNTS
ON S2
 ASD:
Normal PAP:
Delayed normal intensity P2 with wide
inspiratory split
May or may not have Fixed split
With PAH: Loud P2 with Fixed Split as a rule
In post operative cases of ASD,P2 may remain loud but
the split becomes physiological or wide in 70% cases.

 VSD:
Hyperkinetic but Normal PAP:
Wide physiological split S2 with
early A2 and normal P2
Fixed+/-
With PAH :
Delayed and loud P2
With Eisenmengrisation:
Single Fused S2

PDA:
Large PDA: (Increased H.I sec to
decreased
SVR)
Delayed A2 +/- Loud P2
Paradoxical Split
Eisenmenger PDA:
Loud P2
Narrow Split(Fused also can

Third Heart Sounds
 Low frequency , Low amplitude diastolic
Sounds
 Heard after A2(120-140msec after A2)
 Heard at the cardiac apex(LVS3) and L-
LSB(RVS3)
 Best heard with Bell of stethoscope
 Can be heard normally in children and young
adults
 Normal S3 can persist after 40yr but only in

 Presystolic Sound
 Also termed as Ventricular Diastolic Gallop,
Protodiastolic gallop and S3 gallop.
 With respect to presence or absence of S4, its
called as Triple or Quadruple Gallop or
Summation Gallop(in cases of tachycardia)

Physiology of Origin of S3
 S3 occurs when there is rapid active
ventricular filling phase which is associated
with ventricular relaxation.
 Follows MV opening and near the end of RVF
 Initial Vibrations conincide with the maximal
excursion or `checking` of the LV septum and
posterior free wall by MV leaflets

 Final component is due to rapid deceleration
of blood during inflow to LV is translated into
vibratory energy of the cardiohemic system
which produces S3
 It occurs when the active ventricular relaxation
ends and passive distension begins

OTHER SCHOOL OF THOUGHTS
1.Potain: He suggested the origin of S3 to be a
ventricular sound due to sudden cessation of
ventricular distension in early diastole.
2.Shaver reddy et al: Nature of coupling of the LV
with inner chest wall

Factors affecting genesis of S3
1. Transmitral blood flow velocity or volume
2. LV relaxation properties
3. LV End Diastolic Volume
4. Blood Viscosity
5. Coupling of LV with chest wall
6. Character of the Chest

 Intensity of S3 increases with Isotonic
exercises,Coughing(Increased HR) and leg
raising(increased venous return)

Why is it heard normally in
Children and Young Subjects
1. Young have rapid diastolic filling secondary to
higher Cardiac Output as compared to elderly
2. Altered LV compliance physiology with age
3. Altered sound transmission in adults
4.Decrease in LV-chest wall coupling in adults

 Physiological S3 heard in children in mainly
contributed by LV and involvement of RV is
questionable in normal S3

Clinical Significance of S3
Mainly present in
1. Normal Hearts
2. Diastolic Overload states
3. LV dysfunction with or without overt CCF
4. Constrictive Pericarditis

S3 in Normal Hearts
 Uncommon to be heard in subjects aged >40
yrs under normal circumstances
 Increased Cardiac Output states
Acoustically similar to the pathological gallop
Usually attenuate or disappear in upright
position
Can be associated with flow murmurs
Pregnant females can have S3 in 80% cases
and out of that 60% <20wks

 Thin Chest Wall
Associated with Flow murmurs
Can be palpable also

S3 in Mitral Regurgitation
Seen in hemodynamically significant MR
Loudest S3 amongst all the conditions.
Frequency may reach >150 Hz and may
simulate OS
May be associated with a mid diastolic flow
rumble.
Hemodynamically its due to significantly
elevated LV filling pressure with high diastolic
filling rates.

 If LVEF is normal in MR, it does not hold an
ominous prognosis and indicates volume
overload state.
 In such cases the velocity and amplitude of
early diastolic filling is increased and LV apical
impulse is hyperactive.

 Development of significant PAH after severe
MR will soften the S3 but if it causes RV
failure S3 may appear again.
 Usually RV S3 is uncommon in cases of high
flow situations like TR and ASD on the right
side unless there is high RV volume overload
or RV failure.
 This is seen because RV compliance is much
more than the LV compliance.

S3 in LV dysfunction
Characteristic of global LV impairment
If S3 is related to a new clinical event like AMI or
acclerated hypertension, its transient and
disappears once the LV function improves.
In cases of S3 associated with functional MR in
severe LV dysfunction, its mailnly due to poor
LV function rather than LA volume overload as
seen in valvular MR

 A pathological S3 in LV dysfunction will persist
in upright position but may soften with this
maneuver

Hemodynamics in LV
dysfunction
Depressed LVEF
LA,PA and PCWP are elevated
LV early diastolic pressure is elevated
End diastolic pressure may or may not
increase with atrial contraction
Increased vibration in the early diastolic phase

 Along with other attributes, LV dilation leads to
increased coupling of LV and chest wall.
(shaver reddy theory)

S3 in Constrictive Pericarditis
 Different from usual S3
 Early, Loud, High pitched diastolic sound
 Earlier than normal S3 i.e 80-100 msec after
A2
 Caused by elevated LA pressure and a rapid
rise of early ventricular diastolic pressure due
to stiff pericardial casing.
 S3 is usually loudest of all sounds in these
patients
 Pericardial Knock

Other causes of S3
 LV aneursym in CAD
 Decompsated hypertensive and AV disease
 Dilated cardiomyopthy

EVIDENCE
 S3 is the best predictor of mortality at 2.5 yr in
cases with CAD

Fourth Heart Sound(S4)
 Low frequency sound after atrial systole
 Bell of stethoscope
 Ventricular origin
 20-40Hz
 Follows P wave by 140-200msec
 Precedes S1
 Actual contraction of atria doesn’t produce any
sound and the sound is due to the sudden
tensing of cardiohemic system

 As S3 increases with isotonic exercise, S4
increases with isometric exercise which
causes an increased afterload on LV reducing
the LV compliance.

Hemodynamic correlates
LV hypertrophy with normal LV dimensions and
LVEDP
Low compliance ventricle
Impaired velocity of LV diastolic filling in
presence of preserved cardiac output

Physiology of a stiff LV
 Normal in LV diastole, 80% is rapid ventricular
filling and 15% is atrial booster(end diastole)
 In cases of stiff LV, atrial booster becomes
responsible for the greater proportion of LV
filling and may provide upto 30-40 % of
LVEDV

 At this stage, S4 appears as a prominent
sound but as the LV dysfunction appears in
course of disease, early and mid diastolic LV
pressure increases and LA contraction
produces relatively lesser further increase in
LVEDV
 Now, S4 becomes soft or even inaudible.

Importance of LA function
Because S4 appears after atrial systole, LA
contractility plays a huge role in genesis of S4 at
the end of LV diastole.
Fibrosis, Ischemia or dilatation causes diminution of
S4
Ex:
S4 in AF: Absent
S4 in chronic severe MR: Absent(LA enlarged and
reduced LA
contractility)
S4 in CHB: Loud when LA contracts against closed
MV(not from LV walls but due to tensing of MV

CLINICAL CORREALTES
 Common denominator of all the causes in all
the conditions causing S4 is LVH with
restricted early diastolic filing due to stiff
ventricle
Sensitivity
 Ventricular compliance: S4>>S3
 Cardiac decompensation: S3>>S4

Causes of LVS4
1. Coronary Artery disease
2. Hypertension
3. Aortic Stenosis
4. Hypertrophic Cardiomyopathy
5. Acute MR
6. Other causes: CHB

Coronary Artery Disease
 S4 is hallmark of CAD
 Reduced LV compliance due to prior MI
produces S4
 Acute MI causes S4 in 80-90% cases which
manifests 24-48hrs after onset of infarction.
 S4 persisting after MI has been shown to
portend poor prognosis for subsequent cardiac
events
 S4 may appear during angina and disappears
with NTG

 Many believe that isolated S4 in a normal
individual may predict a future coronary event.
 In patients with LV aneursym, S4 is common
and is even palpable.

Evidence-Marcus et al`2005-
JAMA
Patients underwent Left heart catheterization and coronary assesment and it was
found that
Patients with isolated S4 in absence of S3 had much more incidence of isolated CAD
irrespective of the LV systolic function

Acute MR
 Acute MR will cause large regurgitant volume
to be pushed forcibly into a normal sized LV
resulting in S4 .
 Chronic MR leads to decreased LA contraction
due to enlarged LA leading to loss of S4

RVS4
 In PAH and PS leading to severe RV pressure
overload can lead to S4
 Inspiratory augmentation and maximal
intensity at the Left LSB is indicative of RV
origin.

Differentiating LV and RV gallop
 Leg raising, Inspiration and pressure over liver
can augment right sided sounds but not the LV
type

S4 audibility and PR interval
 In cases of acute/chronic LV decompensation,
S4 closely follows the P wave of ECG and is
more widely separated from S1 at any given
PR interval and thus is readily heard.
 As the LV pressure decreases with therapy,
S4 and S1 move closer decreasing the
audibility of S4.
 Thus with long PR interval S4 is more readily
heard and separated from S1.

SUMMATION GALLOP
 When HR is high, atrial contraction will move
into rapid filling phase of diastole and thus S3
and S4 will occur together leading to a very
loud summation gallop.
 CSM and rate control can separate the two
components.
 When S3 and S4 both are heard, the term
quadruple gallop is used.

Systolic Ejection Sounds
 Early systolic ejection sounds from either Left
or Right side of the heart
 High frequency
 Immediately after S1
 Always pathological
 Also called as Ejection clicks
 Can be Vascular or Valvular

Location:Aortic ES
Aortic ES : valvular ES: best at the apex
vascular origin best at the base

Location: Pulmonary ES
 Best heard at the 2nd
and 3rd
ICS in upright
position
 Whenever a loud sound best heard in the
above mentioned area is seen to have
variation with respiration, Pulmonary click
should be strongly considered.

Pathophysiology of Ejection
sounds
2 different mechanisms:
1.Snapping open or doming of a stenotic
thickened or malformed pulmonary or aortic
valve(Valvular)
2.Sudden tensing of proximal Aorta or pulmonary
artery at the time of early ejection coincident
with the upstroke of pressure rise in the
responsible great vessel(Vascular)

 Valvular ES are classically found in congenital
aortic and pulmonary valvular stenosis.

SEMILUNAR VALVE
STENOSIS

Commissural fusion of semilunar valve and
leaflet thickening and rapidly rising ventricular
pressure in early systole drives the abnormal
leaflets upwards and the taut valve leaflets
bulge or dome into their respective great
vessel producing a high frequency sound.

 Flow across the valve occurs after the
maximal valve opening followed by the
ejection systolic murmur and followed by S2
 In cases of severe calcification or reduced
mobility ES and S2 is diminished or even
absent.

Aortic Valvular Ejection Sounds
 Ejection click is almost always present in
Congenital Nonstenotic Bicuspid Aortic Valvea
and across the entire spectrum of mild to
severe AS
 In acquired AS and of rheumatic origin,
Ejection click is much less common and is not
heard due to severe anatomic
deformity,calcification and rigid leaflets
producing reduced excurtion.

 High frequency sound followed by the ejection
murmur
 Best heard at apex
 Aortic valvular ES is delayed 20-40msec after
the onset of pressure rise in central aorta and
is coincident with sharp anacrotic notch on
upstroke of Aortic pressure curve

 Sound is conincident with the maximal
excursion of domed valve when its elastic
limits are met which causes the sudden
deceleration of the blood mass leading to
vibrations of cardiohemic system causing the
sound
 Thus for this sound to be produced, the valve
leaflet mobility is imperative.
 Calcified deformed valves doesn’t produce the
sound

 Aortic ES have no corelation with the intensity
of the stenosis.
 In cases of mobile,non stenotic valve, the ES
is widely placed from S1 due to prolonged
excursion of the mobile valve leaflets

Pulmonic Stenosis
 Seen in only valvular PS
 Variability with respiration :
In contrast to all other Right sided sounds,
Pulmonary click softens or diminishes with
inspiration.
In very mild PS respiratory variation may be
absent

Cause of this respiratory
variation
PA diastolic pressure is low and RV compliance
is low due to RVH due to PS
With inspiration, augmented venous return
causes more forceful RA contraction causing
increased RV EDP
RV late diastolic pressure exceeds diastolic
pressure of PA

 PV cusps get literally pushed towards an open
position during late diastole and thus the
actual opening excursion of valve cusps is
minimal or even absent thus leading to soft
opening click.

 In cases of very severe PS, there is vigorous
atrial contraction leading to increase in
RVEDP to be more than PA diastolic pressure
at the time to RA booster phase.
 As the severity of PS increases, both the
excursion of deformed valve and RV
isovolumetric contraction time decrease thus
causing the Pulmonary ES to appear early
towards S1.

NonValvular ES
 An ES with a normal semilunar valve is
typically associated with dilated aorta or PA
which occurs in conditions with either
increased SV and/or increased force of
ejection.

Aortic Vascular ES
 Usually found in cases of systemic HTN in
setting of sclerotic tortuous aortic root and a
tight non compliant arterial tree with forceful
LV ejection.
 Coincident with the upstroke of the central
aortic pressure.
 In contrast to the valvular type,they are poorly
transmitted from base and are poorly heard at
the apex.

Pulmonary Vascular ES
 Common denominator to these sounds is
dilation of PA whether it is idiopathic or due to
PAH.
 Conditions causing PAH in which there is
ejection of blood into a tense non compliant
vessel is a cause of ES and it thus coincides
with the maximal opening of PV.
 Higher the pulmonary pressure, later is the
ejection sound which is due to increased RV
systolic time and delayed opening of PV

 Usually ASD is not associated with ejection
sounds unless it is associated with PAH and if
even after closure of ASD there is persistence
of ES, it indicates chronic changes in PA
compliance.

Non Ejection Sounds
 Mid systolic click due to prolapse of the mitral
or tricuspid valve is the most frequent cause of
systolic non ejection sounds and are often
associated with a systolic regurgitant murmur.
Proposed mechanism is due to tensing of the
Atrioventricular valves during systole when the
elastic limits of the prolapsed valve is
suddenly reached.

Characteristics
 Sharp high frequency clicking quality
 Often confined to apex but can be transmitted
widely to the precordium.
 Can present as either an isolated click in
middle to late systole or as multiple clicks
throughout the systole due to different areas of
large redundant scalloped mitral leaflets
prolapsing at different times in the systole

 Click usually occurs at the time of maximal
prolapse of the leaflets.

Variability of non ejection clicks
 A classical feature of these sounds is
variability of the findings from one examination
to the other and even beat to beat.
 Timing of the click and click with the late
systolic murmur changes considerably
 Variation with posture:
In upright posture,the heart becomes
smaller due to decreased venous return and
the click moves early in systole.

Squatting increases the venous return as well as
afterload increases the LV volume,causes late
prolapse and movement of the click towards S2.
Conclusively, it has been documented that the
timing of the click depends upon the size of LV
leading to valvuloventricular disproportion.

 In general,maneuver that reduces LV volume
like sitting,standing, strain at valsalva and
amyl nitrite inhalation causes the click to come
early in systole closer to S1.
 Maneuvers increasing the LV size like
squatting,vasopressor infusion and supine
position will move the click towards S2.

Opening Snaps
 Coined by Thayer in 1908
 High frequency diastolic sounds in mitral
stenosis.
 Margolies and Wolferth proposed the
mechanism of OS ie sudden stopping of the
opening motion of the valve after the elastic
limits are met.
 Sound is contributed more by the AML rather
than PML.

Characteristics
 Crisp sharp high frequency sound
 Best heard in area from L-LSB to just inside of
the cardiac apex.
 Followed by the diastolic rumble of the MS
 No variation with respiration

 Intensity of the OS corelates with the opening
of the valve.
 Loud OS is present in mobile stenotic valves
with good excursions while calcified MS has
absent or diminished OS.
 Intensity of OS corelates directly with loudness
of M1

 Although its generally said that calcified MV
will not have OS but 50-60% calcified valves
may have OS which supports the fact that it is
due to lack of mobility in calcified valves that
causes absence of OS and not the calcium
itself.

Hemodynamics
 OS occurs at the maximal MV opening shortly
after LV-LA pressure crossover.
Factors affecting A2-OS gap
1. Rate of LV pressure decline
2. Level of LV pressure at the time of A2
3. Level of LA pressure

 Heart rate- tachycardia decreases A2-OS
(shortening of diastole)
 Brady increases A2-OS (prolonged
diastole)
 Hypertension – A2-OS increased
( LVpressure takes longer time to descend
below LAP)
 Increased LVEDP- increased A2-OS
(obliteration of transmitral gradient and
increased LV ejection time)

 More severe MS will have high LA pressure
thus a short A2-OS gap.
 Isolated TS is rare and when TS present its
usually accompanies MS who`s OS
overshadows that of TS

 As compared to OS of MV, OS of TV is found
closer to L-LSB and its intensity increases with
inspiration and it usually appears after OS of
MV.

OS with Normal Valves
 Although rare but OS can be heard in high
flow situations across the atrioventricular
valves
1. Large ASD
2. Severe MR(rheumatic with diastolic doming of
the the deformed mitral valve leaflets)
3. Large VSD
4. Thyrotoxicosis
5. Tricuspid atresia with large ASD

Prosthetic Valve Sounds
 Sound depends upon the type of valve and
position.
Starr Edwards Ball cage valve
 Loudest sound is produced by any valve
 In aortic position, opening click occurs 60-70
msec after S1 and is due to maximal ball
excurtion.
 Absence or decrease occurs with Valve
obstruction and LV dysfunction.

 In mitral position prominent opening click
occurs 50-150msec after A2 and narrowing of
this interval indicates raised LA pressure.
 Closing click is also prominent at mitral area
and behaves exactly as S1.

 Tilting disc valve(Medtronic Hall,Bjork
Shirley and St Judes)
These valves produce more prominent closing
sound rather than the opening click
LV dysfunction,1st
degree AV block will cause the
disc to move to partial closed position prior to
LV contraction leading to a softer sound.

Tumour plop;
 high frequency heard in atrial myxomas
 Abrupt diastolic seating of mobile myxoma
within Rt or Lt AV orifice
 Later than OS

Pericardial knock
 Diastolic sound caused by loss of pericardial
elasticity that limits ventricular filling
 High pitched sound
 Louder with inspiration, squatting (increased
venous return)
 Mechanism-structural restriction of diastolic
filling by the restricting pericardial shell
 Disappear following pericardiectomy

Pacemaker sounds
Occuring nearly synchronously with
pacemaker spike
Caused by stimulation of intercostal nerves
adjacent to endocardial electrodes which
results in contraction of intercostal muscles
Should always rule out myocardial
perforation

Pericardial friction rubs
 High pitched, leathery, scratchy sound
heard in end expiration.
 Has three components according to the
cardiac cycle when heart has the maximal
excursion against the pericardium
1.Atrial systole
2. Ventricular systole
3.Rapid early disatolic filling

Usually only 2 components are heard except in
uremic pericarditis where all 3 components are
heard.
It’s a misconception that fluid between 2 layers
decreases the rub but it doesn’t because some
portion of 2 layers continue to stay in touch.

Mediastinal crunch(Hamman Sign)
 Scratchy sounds, due to air in the mediastinum
 Most frequently during ventricular systole due to
heart beating against the air filled tissue & in a
random fashion

Heart Sounds - 1

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