DR. MUHAMMAD SHAHID SAEED Heart sounds DR. MUHAMMAD SHAHID SAEED

First heart sound - M1T1 Produced 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 M1 High frequency T1 Small frequency vibrations coincides with acceleration of blood into the great vessel

Factors affecting s1 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 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 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

Hypertension ( higher pressure in the aorta ) 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- Diastolic overload states- LVF 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.