DR. MUHAMMAD SHAHID SAEED
First heart sound - M1T1
 Produced by sudden closure of mitral (M) and Tricupsid (T) valve
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32-80 vib/sec is the frequency.
Mitral valve closes after Tricupsid (T) valve and this is called as
Physiological splitting of first heart sound.
Sudden tensing of MV leaflet after closure of mitral valve, which
sets the surrounding cardiac structures including the blood into
vibrations
Complete coaptation of valve leaflets& final tensing are not
simultaneous
Final tensing responsible for M1
S1 – 4 sequential components
(phono)
 Small frequency vibrations, coincides with the
beginning of LV contraction- felt to be muscular origin
 High frequency M1
 High frequency T1
 Small frequency vibrations coincides with acceleration
of blood into the great vessel
Factors affecting s1
1.
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structural integrity of valve :
inadequate coaptation of mitral valve - soft S1 (severe
MR )
Loss of leaflet tissue – soft S1 (IE)
thickness & mobility of the valve
In mild- mod MS, the increased LA pressure causes the
mobile portions of the mitral valve leaflets to be more
widely separated  accentuated M1
The stiff noncompliant leaflets & chordae tendinae
appear to resonate with increased amplitude
Calcified mitral valve( long standing MS) immobilizes
the valve- soft S1
2. velocity of the 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
3. 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)
 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
- loss of isovolumic contraction
decreased dp/dt
4. Heart rate
 Tachycardia- loud s1
 Reasons – short PR interval
- wide opened valves due to short diastole
- increased myocardial contractility
5. Transmission characteristics of thoracic cavity &
chestwall
-Obesity, emphysema,pericardial effusion decrease
the intensity of all auscultatory events
-Thin chest wall increases the intensity
conditions
causing
Loud
S1
(M1)
 MS-thickened mobile leaflets, high LA pressure
 Interval from LV-LA pressure crossover to mitral valve closure is same
as in normal state, rate of ventricular pressure development (dp/dt)
during this period is higher
 summation of normal M1& nonejection click
 Exercise – tachycardia induced short PR
-Increased LV contractility
- increased flow across the valve
Loud T1
 TS
 ASD - increased tricuspid flow
 Anomalous pulmonary venous connection
- increased tricuspid flow
Soft S1
 MR- decreased mobility, poor coaptation, loss of
isovolumic contraction
 Some of the energy of ventricular contraction may be
spent developing kinetic energy responsible for the
regurgitant flow, diminishing the rate of rise of
intraventricular pressure
 Calcific MS- immobility of mitral valve
 LBBB- delay in onset of LV contraction-
delayed M1
- decreased LV contractility
- concomitant 1st degree AV block
- presence of noncompliant LV leading to
preclosure of mitral valve
 a/c myocardial infarction- decreased ventricular contractility,
- associated MR,
-LBBB
Variable S1
 AF - varying cycle length - varying force of ventricular
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contraction
S1 intensity & mitral valve closure velocity closely related in
AF (Mills& Craige)
With short ventricular cycle lengths AV valve closure may
begin during the rapid filling phase of the immediately
preceding diastole,during which MV leaflets are relatively
divergent, leading to loud S1
If S1 occur after rapid filling phase, intensity is likely to be
related to rate of ventricular pressure development
S1 amplitude & rate of pressure development tend to
increase with increase in cycle length until a critical length
is reached, little changes thereafter
So difficult to relate the observed intensity to the cycle
length
SECOND HEART SOUND
Produced by Sudden closure of aortic (A) and Pulmonary (P) valve
 High pitch shorter duration 0.02 sec.
 Pulmonary valve closes after the aortic valve during inspiration due to
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increase in venous return to the right atrium and during expiration
aortic valve closes later and pulmonary earlier this is called
physiological splitting of second heart sound.
High frequency, 120 – 150Hz
Events associated with closure of aortic & pulmonary valves
Sudden deceleration of reterograde bloodflow in the aorta & PA, which
sets the entire cardiohemic system into vibrations
A2 louder (higher pressure in aorta) P2 later to (longer RV ET and
more HI)
Normal split- <30 ms exp, 40-50 ms insp
Inspiratory split- P2 delay accounts for 73% & early A2 accounts for27%
 Factors affecting intensity of A2 / P2
• Great artery pressure
• Elastic recoil of great artery root- determined primarily by
the rate at which stroke volume is ejected
• status of Semilunar valve
• Size of vessel
• Position of vessel
Loud A2• Hyperkinetic states( increased flow across normal valve)
 Hypertension ( higher pressure in the aorta )
 Aortic root dilation(increased flow, dilated vessel)
 TGA ( Aorta arises more anteriorly )
Loud P2 Pulmonary hypertension( dilated pulmonary
trunk,increased PA pressure)
 ASD ( dilated pulmonary trunk, increased flow across
the valve)
 straight back syndrome( decreased AP diameter)
Diminished A2• Valvular AS ( distorted valve ,diminished mobility)
• AR (restricted valve mobility, poor coaptation)
Diminished P2
• Valvular PS (thickened leaflet, diminished mobility)
• Dysplastic valve (distorted valve anatomy& diminished
mobility)
S3
 Mechanism of production
 Impact theory - ventricular filling occurs early in the
diastole, if ventricles resist this rapid flow, vibratory
activity results which are transmitted to the chest wall
 Ventricular theory - sudden cessation of ventricular filling
resulting in distension & vibration of ventricular wall,
papillary muscles & chordae
 Valvar theory- sudden limitation of longitudinal expansion
of LV wall during early diastole
 Abnormal s3 - altered physical properties of the recipient
ventricle &/or increase in the atrioventricular flow during
rapid filling phase of ventricle
s3
 Follows A2 by 140 to 160 msec (physiological 120-200
msec)
 Gallop rhythm - auscultatory phenomenon of tripling
or quadrupling of heart sounds resembles the canter of
a horse
Causes of S3
 Normal Children and young adults
 Hyperkinetic states( diastolic overload with high atrial
pressure)
 Diastolic overload states MR(earlier, higher frequency), VSD, PDA
 LVF
 Normal S3 disappears in upright position
 Abnormal S3 better heard after isotonic exercise,
passive leg raising ( augments the venous return & mid
diastolic atrio ventricular flow)
S4
 The s4 occurs just after atrial contraction and
immediately before S1
 20 to 30 Hz
 caused by stiffening of the walls of the ventricles
(usually the left), which produces abnormally
turbulent flow as the atria contract to force blood into
the ventricle
 audible in the elderly due to a more rigid ventricle
 LVS4 heard best at the cardiac apex
 become more apparent with exercise, with the patient
in left lateral position in expiration
 RVS4 most evident LLSB
 louder with exercise, inspiration
Method of study Heart Sounds
 Ascultation by stethoscope. First and second heart
sound is heard by this method.
 By using microphones which ampliphie heart sounds .
 First second and third heart sound can be heard by
this.
 Phonocardiogram.. A electronic transducer is placed
 over chest and connected to recording device and
heart sound are recorded.