Heart sounds DR. MUHAMMAD SHAHID SAEED

First heart sound - M1T1Produced by sudden closure of mitral (M) and Tricupsid (T) valve .

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 M1High frequency T1Small frequency vibrations coincides with

acceleration of blood into the great vessel

Factors affecting s1

1. 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 timeLV 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 contractionIncreased 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 s1Reasons – 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

TSASD - increased tricuspid flow

Anomalous pulmonary venous connection - increased tricuspid flow

Soft S1MR- decreased mobility, poor coaptation, loss

of isovolumic contractionSome 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 valvea/c myocardial infarction- - decreased ventricular contractility, - associated MR, -LBBB

Variable S1AF - varying cycle length - varying force of

ventricular contractionS1 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

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 – 150HzEvents associated with closure of aortic & pulmonary valvesSudden deceleration of reterograde bloodflow in the aorta & PA, which

sets the entire cardiohemic system into vibrationsA2 louder (higher pressure in aorta) P2 later to (longer RV ET and

more HI)Normal split- <30 ms exp, 40-50 ms inspInspiratory 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)

S3Mechanism of productionImpact 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

s3Follows 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 S3Normal-

Children and young adultsHyperkinetic states( diastolic overload with

high atrial pressure)Diastolic overload states-

MR(earlier, higher frequency), VSD, PDALVF

Normal S3 disappears in upright positionAbnormal S3 better heard after isotonic

exercise, passive leg raising ( augments the venous return & mid diastolic atrio ventricular flow)

S4The s4 occurs just after atrial contraction and

immediately before S120 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 apexbecome more apparent with exercise, with

the patient in left lateral position in expiration

RVS4 most evident LLSBlouder with exercise, inspiration

Method of study Heart SoundsAscultation 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.