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Heart sounds – origin,normal & abnormal

Heart sounds – origin,normal & abnormal. Dolly mathew. Brief discrete auditory vibrations charecterized by intensity(loudness),frequency(pitch),& quality high frequency sounds – related to opening :OS, ES Closure sounds-S1,S2

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Heart sounds – origin,normal & abnormal

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  1. Heart sounds –origin,normal& abnormal Dolly mathew

  2. Brief discrete auditory vibrations charecterized by intensity(loudness),frequency(pitch),& quality • high frequency sounds – related to opening :OS, ES Closure sounds-S1,S2 • Low frequency sounds - early & late diastolic filling events of the ventricle

  3. 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

  4. First heart sound - M1T1 • 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

  5. 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 & chordaetendinae appear to resonate with increased amplitude • Calcified mitral valve( long standing MS) immobilizes the valve- soft S1

  6. 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

  7. Longer PR(180-500ms)- ventricular contraction accelerate blood towards the AV valve only during the time required to stretch the closed valve to its elastic limit • the rate of ventricular pressure development is negligible & insignificant VA pressure gradient

  8. when PR markedly prolonged (>550ms) re opening occurs due to continuing blood inflow from pulmonary arterial to venous bed • The valve is open at the onset of ventricular systole,s1 loud

  9. Short PR – valve cusps are in their most divergent position when ventricular contraction begin, ventriculoatrial pressure gradient greater, louder s1 • Very short PR- atrial systole coincides with ventricular systole, diminishing the VA gradient at the time of AV valve closure- s1 soft/ inaudible

  10. 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

  11. 4. Heart rate • Tachycardia- loud s1 • Reasons – short PR interval - wide opened valves due to short diastole - increased myocardial contractility

  12. 5. Transmission characteristics of thoracic cavity & chestwall -Obesity, emphysema,pericardial effusion decrease the intensity of all auscultatory events -Thin chest wall increases the intensity

  13. 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 • 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, • summation of normal M1& nonejection click • Exercise – tachycardia induced short PR -Increased LV contractility - increased flow across the valve

  14. Loud T1 • TS • ASD - increased tricuspid flow • Anomalous pulmonary venous connection - increased tricuspid flow

  15. 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

  16. Severe AR- - pre closure of mitral valve as a result of rapid increase in the LV filling pressure In a/c AR, aortic pressure markedly reduced, LV pressure markedly elevated, leading to equilibration of pressure at the onset of LV systole Since the energy of ventricular contraction is immediately converted into kinetic energy in the form of aortic transvalvular flow, the energy producing the mitral valve displacement is reduced

  17. 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

  18. 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

  19. CHB- varying PR interval- Intermittent loud S1- cannon sound • VT with AV dissociation - varying position of AV valves at ventricular systole • Atrial flutter with varying conduction • Pulsusalternance – regular alternation in the intraventricular pressure development • Electrical alternance- heart is swinging in a pendular arc , whose period is twice the heart rate , ventricular systole occur at each end of the pendular arc • Alternating distance & fluid volume between the source of sound production & chestwall

  20. wide splitting S1 • Electrical delay(delayed RV contraction)-RBBB ( with normal sequence) - LV pacing - Ectopics from LV • Mechanical delay -Ebstein’s anomaly (sail sound due to delayed activation, increased RA pressure) - TS& RA myxoma ( due to increased RA pressure) • Reverse splittingT1M1- RV pacing( delayed LV contr) -RV ectopics(delayed LV contr) -LBBB(delayed LV contr) - MS, LA myxoma (Hemodynamically significant mitral valve obstruction can cause reverse splitting, mitral valve closure delayed due to increased LA pressure that must be overcome by rising the LV pressure before closure can occur)

  21. Second heart sound • High frequency, 120 – 150Hz • Events associated with closure of aortic & pulmonary valves • Sudden deceleration of reterogradebloodflow 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%

  22. P2 delay 2/3rd due to increased hangout interval during inspiration, and 1/3rd due to increased RV ejection time • Expiratory split of S2 must be confirmed in sitting position- P2 occurs earlier and the split disappears Hangout interval • Semilunar valves expected to close at the point of cross over of pressures, however these valves closes slightly later • Hangout interval (30 ms Ao &80ms PA)

  23. 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

  24. 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)

  25. 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)

  26. Inspiration may attenuate P2 due to increased lung interposition • Massive pulmonary embolism- A2 soft due to decreased cardiac output P2 loud due to increased PA pressure (may be soft in very large embolus A2 early, P2 late

  27. Wide physiological split Late P2- • Electrical causes like RBBB (ET) • PS (ET, HI) • ASD (HI, ET, RBBB) • PH + RVF (ET) • IDPA (HI) Early A2- • Severe MR (decreased LV ET- due to loss of isovolumic contraction) • VSD (decreased LV ET due to loss of isovolumic contraction) ) • Pericardial tamponade (ET) Both- • PE • VSD

  28. Wide fixed split • When the RV or LV stroke volume doesnot change with inspiration • RVF • PE • Simultaneous increase in RV & LV filling- ASD • Delayed P2 due to increased venous return to RV • Delayed A2 due to decreased left to right shunt • No further increase in hi is possible

  29. Reversed split S2 • Types I, II & III (latter two by phono) • inspiration : single S2(P2A2) / Expiration : P2-A2 • Typeii - inspiration :A2-P2 / Expiration : P2-A2 • Late A2- • Electrical delay- LBBB(delayed activation LV,prolongedisovolumic contraction time) ,RV pacing, RBBB VPCs, • AS, HOCM(due to large systolic gradient, ?prolonged LV relaxation) • Early P2- • TR

  30. Single S2 • Aging (early P2, delayed A2) • Murmur obscuration (MR, VSD, AS, PS, PDA) • Absent P2 (PS, TOF, PA, TA) • fusionA2-P2 Eisenmenger VSD (same inspiratory delay), single ventricle • Apparently single S2(inaudible P2)- Emphysema, obesity, pericardial effusion

  31. 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

  32. 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

  33. 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 • CCP (earlier, louder, higher pitched, due to rapid rise of LV pressure)

  34. 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) • RV S3- TR , ASD, CCP

  35. S4- atrial gallop- presystolic gallop • 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

  36. 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

  37. Absent in chronic MR (poor LA contractility • Present in acute MR (hyperdynamic atrial systole)

  38. Causes- CAD, HT, AS, HCM ( decreased ventricular compliance) acute MR( hyperdynamic atrial systole) a/c AR (Decreased LV compliance) AV blocks (prolonged PR 220-260ms atrial gallop heard in addition to s1) • CHB - (S4/ summation sound occur randomly in diastole- P&QRS relationship is random) • RV S4- PH( increased resistance to ventricular filling) PS, PE ( RV pressure overload) • S3 & S4- non obstructive AV valve • S4- healthy atrium S3 has more inspiratory decrease than S4. • Upright posture- physiological S3 & S4 vanishes

  39. Systolic ejection sounds • Valvular- arising from deformed valve • vascular or root events - Rapid forceful ejection into great vessels • Coincident with maximal excursion of domed valve when its elastic limits are met • Mechanism - Deceleration of oncoming blood column sets the entire cardiohemic system into vibration • high frequency sound • Intensity of ES correlates directly with mobility of the valve • No correlation with severity of obstruction

  40. Ejection sounds Semilunar valve stenosis- • Absent in extremely severe stenosis and in calcification. • Aortic stenosis- common in BAV, less common in acquired valvular AS • Pulmonic stenosis- • Common in valvular PS • Softens or disappears with inspiration • Absent in very mild PS

  41. Pulmonary valvular ejection soundsOccurs at maximal excursion of stenotic pulmonary valve

  42. Nonejection sounds • MVP/TVP • a/w systolic regurgitantmr • Caused by tensing of AV valves during systole • Produced by vibrations of the entire cardiohemic system when the elastic limits of prolapsed valve are suddenly reached • Standing – click moves earlier, greater degree of prolapse • Squatting- later prolapse, moves towards s2

  43. diastolic sounds - Opening snap • Sharp, high pitched brief early diastolic • 60-100ms after A2 • Represents the isovolumic relaxation period of the ventricle, inversely proportional to LA pressure • Sudden stoppage of the opening movements of the valve(Margolies & Wolferth theory) • Sudden tensing of the valve leaflets by the chordaetendinae

  44. AF- shorter A2-OS with short R-R cycles -With Longer preceding R-R, the LA pressure falls, A2-OS widens • Stenotic OS-MS,TS • Nonstenotic mitral- MR, ( increased flow,swift opening of nonstenotic valve); VSD( functional OS) • Nonstenotic tricuspid –TR, ASD(functional opening snap), ebstein anomaly( increased flow , rapid excursion)

  45. Mild MS A2-OS>120ms mean LAP <5mmHgModerate MS60-80 ; 5-10MmmHgSevere MS 40-60ms ;>15mmHg

  46. Factors affecting OS • 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& early occurance of A2) • Increased LVEDP- increased A2-OS (obliteration of transmitral gradient)

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