Heart sounds,murmurs & Dynamic auscultation.pptx

Heart sounds , murmurs & Dynamic auscultation.pptx

1. HEART SOUNDS, MURMURS AND DYNAMIC ASCULTATION Dr Awadhesh Kumar Sharma Consultant Cardiologist LPS Institute of Cardiology,Kanpur

2. Heart sounds are relatively brief discrete auditory vibrations which are produced by sudden deceleration of blood within the cardiovascular system that are usually characterized by intensity ( loudness ) and frequency ( pitch ) Normal heart sounds. Abnormal heart sounds.

3. Normal human acoustic acuity 20-20000 hz normal human capability 1000-5000 hz Normal human ear sensitivity 1000-2000 hz Optimal human auditary acuity 30-1000 hz Most cardiovascular sounds and murmurs 20-30 msec interval between two sounds Human ear capable of detecting two sounds

4. Characterstics of cardiac sounds Low frequency ( 25-125 hz ) S3, S4, pericardial knock, MDM of mitral and tricuspid stenosis Medium frequency (125-300 hz ) Innocent systolic murmurs High frequency (>300 hz ) S1, S2, opening snap, ejection sounds, MR murmur, AR murmur Mixed frequency SM of AS and PS

5. Depending upon the cardiac cycle Diastolic sounds Early diastolic Opening snap, tumour plop, pericardial knock, opening sounds of prosthetic valves Mid diastolic Physiological S3 Lat e diastolic S4 Systolic sounds Early systolic Aortic and pulmonary ejection sounds, closing sounds of prosthetic valves Mid to late systolic Non ejection sounds or clicks

6. First heart sound ( S1) Signals the onset of ventricular contraction. Consists of two audible ( M1 and T1) and two inaudible components. First inaudible component is muscular in origin and coincide with the beginning of the LV contraction. Followed by high frequency audible M1 and T1 components, which are produced due to closure of the mitral and tricuspid valves, The last inaudible low frequency vibrations coincide with the opening of semilunar valves with ejection of blood into aorta and pulmonary trunk. ( clinical recognition– S1 immediately precedes the palpable carotid arterial upstroke and beginning outward thrust of apex beat whereas S2 occur immediately after the peak of carotid pulse and apex beat)

7. The apex phonocardiography is recorded with the mitral valve echocardiogram (left panel) and tricuspid valve echocardiogram (right panel) in a normal subject. The mitral (M1) and tricuspid T1 components of the first heart sound are coincident with the closure points C. of the mitral and tricuspid valves respectively. A small low frequency vibration (m) is seen prior M1, and a few low frequency vibrations follow T1 in early systole

8. CHARACTERISTICS OF S1 Characters Value Frequency Medium to high pitched Duration 0.14 sec M1-T1 interval 20-30ms C point of mitral valve echocardiogram Coincide with M1 Down stroke of c wave of LA pressure (delayed from LV-LA pressure crossover by 30ms Coincide with M1 Down stroke of c wave of RA pressure Coincide with T1

9. Determinants of intensity of S1 Determinants Mechanism Structural integrity of AV valve Thickness and mobility of the leaflets Velocity of MV closure Position of AV valve at the time of ventricular systole Status of ventricular contraction Myocardial contractility, heart rate Transmission characteristics Thoracic cavity and chest wall

10. Structural integrity of mitral valve Thickened but mobile valve (MS) – loud S1. Inadequate coaptation of the valve (severe MR) – soft S1. Loss of leaflet tissue (infective endocarditis) – soft S1. Calcification (long standing MS) – soft S1. Velocity of valve closure Normal PR interval (120-200ms) – normal S1. Short PR interval (30-100ms) – mitral leaflets are maximally separated by the LA contraction at end diastole– MV close at high speed with a large excursion– loud S1 Long PR interval (200-500ms)– premature MV closure due to LV diastolic pressure exceed LA pressure – less excursion of MV with LV contraction– soft S1. Very long PR interval (>500ms ) – mitral valve reopens and closes with rapid velocity – loud S1

11. Status of ventricular contraction. Increased myocardial contractility (increase the rate of rise of LV pressure– increase the velocity of the closing mitral leaflets – loud S1 Exercise, thyrotoxicosis, anaemia, pregnancy, fever, AV fistula, catecholamine Decreased myocardial contractility (decreased rate of rise of LV pressure– soft S1 Acute MI, cardiomyopathy, myocarditis, ventricular aneurysm, beta blockers, myxoedma Loss of isovolumic contraction (decrease velocity of MV closure – soft S1 Severe MR, AR, large VSD,ventricular aneurysm HEART RATE (tachycardia – loud S1)

12. Variable intensity of S1 Atrial fibrillation Complete heart block with AV dissociation Atrial flutter with varying block Atrial tachycardia with varying block Wide splitting of S1 (M1-T1 gap >30ms) Reverse splitting (delayed mitral component) (best found at lower left sternal border) Complete RBBB Complete LBBB, RV pacing LV ectopics , LV pacing. RV ectopics Ebstein’s anamoly Mitral stenosis TS and right atrial myxoma left atrial myxoma

13. Second heart sound S2 Signals onset of ventricular diastole. Sudden deceleration of retrograde flow of blood column in the aorta and pulmonary artery which initiates the vibrations of haemocardiac structures coinciding with the closure of aortic and pulmonary leaflets. Two components – A2 and P2. Higher in pitch than S1 due to low elasticity of semilunar valves and arterial trunks than that of AV valves. Less blood volume in arteries than ventricles and so low inertia of the vibrating structures producing higher frequency of vibrations.

14. The aortic (A2) and pulmonic (P2) closure sounds are coincident with the incisura of their respective arterial traces. Although the left and right ventricular mechanical systole are nearly equal in duration, the right ventricular(RV) systolic ejection terminates after left ventricular(LV) ejection because of an increased right sided "hangout" interval.

15. Characteristic of S2 Frequency High pitched Duration 0.11 sec A2 -P2 interval During expiration During inspiration <30ms 40-50ms Incisura of aortic pressure coincides Incisura of pulmonary pressure coincides With A2 With P2 A2 is louder than P2 High pressure in aorta than pulmonary artery A2 occur earlier than P2 RV ejection begins earlier, lasts longer than LV ejection and ends after LV ejection. Aortic hang out interval (30ms) < pulmonary hang out interval(80ms) A2 well heard at the aortic area P2 well heard at the pulmonary area

16. Normal splitting of S2 (inspiration) Delayed P2 – 73% Early A2 – 27%. Inspiratory increase in systemic venous return inspiratory decrease in pulmonary venous (due to fall in intrathoracic pressure) return ( pooling of blood in pulmonary vascul - ature ) Increase RV stroke volume Decrease LV stroke volume Prolonging the RV ejection Decreasing the LV ejection Decreasing the pulmonary vascular impedence Increasing the pulmonary hang out interval Decreasing the aortic hang out interval Delayed P2 Early A2

17. Abnormal splitting of S2-- Presence of audible expiratory split (>30ms) in both supine and standing position Persistant physiological wide splitting Delayed pulmonary closure Delayed electrical activation of right ventricle – complete RBBB, LV ectopics , LV pacing prolonged RV mechanical systole – moderate to severe PS, acute pulmonary embolism. Increased hang out interval – mild PS, idiopathic dilatation of pulmonary artery, ASD Early aortic closure – severe MR, VSD, cardiac tamponade , CP, atrial myxoma Benign causes – pectus excavatum , straight back syndrome Narrow physiological splitting – splitting in both inspiration and expiration (but A2 and P2 are separated by <30ms interval because of increased intensity and high frequency of P2) – found in pulmonary hypertension.

18. Reversed or paradoxical splitting Audible split during expiration and inaudible split during inspiration Type I paradoxical splitting- Inspiration- Single S2 Expiration- Split S2 (P2-A2) Type II paradoxical splitting- Inspiration – Split S2 (A2-P2) Expiration- Split S2 (P2-A2) Type III paradoxical splitting - Inspiration- Single S2 Expiration- Single S2 (P2-A2, but separation is 20 msec or less) Thus in type II, we get split in both phases. In type III, we do not get any split. In type I, split in expiration, no split in inspiration. Valsalva maneuver in reversed split – wide split – narrow split – wide split. only type I is clinically detectable type II and III by phonocardiograpy

19. Causes of reverse split of S2 Due to delayed aortic closure Delayed electrical activation of LV – complete LBBB, RV pacing, RV ectopics . Prolonged LV mechanical systole -- AS, hypertension, chronic ischemic heart disease. Increase hang out interval – post stenotic dilatation of aorta secondary to AS or AR, PDA. 2 . Due to early pulmonary closure – WPW syndrome (type B) (type II reverse splitting).

20. Reversed splitting of S2 with paradoxical movement in a patient with complete LBBB. A2 is confirmed by the simultaneous indirect carotid pulse and with inspiration there is slight narrowing of the splitting interval. At cardiac catheterization, a marked increase in the Q to left ventricular rise interval of 80ms was documented and was primarily responsible for the delayed A2. A slight increase in the isovolumic contraction time was also present

21. Single S2- Absent P2- Severe PS Pulmonary atresia Severe TOF Most cases of tricuspid atresia, TGA, Absent A2- Severe AS Absent A2 and P2- Truncus arteriosus Fusion of A2 with P2- Eisenmenger VSD Single ventricle Apparently absent P2- COPD Obesity Pericardial effusion  

22. Wide fixed splitting of S2 Interval between A2 and P2 is wide and persistent and remain unchanged during the respiratory cycle. ( A2 and P2 are widely separated during expiration and exhibit little or no change with inspiration or with valsalva maneuver . Causes – OS-ASD, RV failure, acute and chronic pulmonary embolism. Wide split in ASD – caused by delay in P2 which is due to increase venous return and increased RV filling during inspiration – prolong RV systole, prolong hang out interval. Fixed splitting in ASD – increase venous return during inspiration – no L-R shunt Decrease venous return during expiration – L-R shunt. ( impedence of pulmonary vascular bed is decreased and no additional decrease in pulmonary vascular impedence during inspiration)

23. Simultaneous base and apex phonocardiogram recorded together with the carotid pulse during with quiet respiration in a young woman with a large atrial septal defect. Wide, fixed splitting of S2 is present, and P2 is easily recorded at the apex. A prominent systolic ejection murmur (SEM) is recorded at the base and is due to the large stroke volume across the right ventricular outflow tract.

24. Third heart sound S3 Low frequency mid diastolic sound produced due to rapid ventricular filling phase of cardiac cycle. Non stenotic AV valve is prerequisite for its generation. Sudden deceleration of the onrushing column of blood in the ventricular inflow during rapid ventricular filling phase produce S3. (VENTRICULAR THEORY). Coincides with rapid filling phase of apex cardiogram. Coincides with y descent of atrial pressure. Physiological S3– 120-200ms after A2. Pathological S3 – 140-160ms after A2. When heard in diseased state called protodiastolic gallop or ventricular diastolic gallop. Best heard with bell of stethoscope at the apex in left lateral position.

25. Causes of S3 Physiological Children and young adults (men <40years), (women <50years), 3 rd trimester of pregnancy, exercise, anxiety Pathological S3 Excessive rapid ventricular filling. 1. Hyperkinetic states Anaemia, thyrotoxicosis, AV fistula 2 AV valve incompetence MR, TR 3. Left to right shunt VSD, ASD, PDA 4. Cyanotic heart disease with increase blood flow TAPVC, DORV without PS, TA, TGA with VSD Increase end systolic and end diastolic volume with high filling pressure Ischemic heart disease, DCMP, systemic hypertension,

26. Clinical recognition of S3 LV S3 is best heard at the apex in left lateral position during expiration and increase in intensity with isometric hand grip exercise. RV S3 is best heard at the lower left sternal edge in supine position and is exaggerated during inspiration but no change with isometric hand grip exercise. Maneuvers which Increase S3 audiability (increase venous return) Maneuvers which decrease S3 (decrease venous return) Passive elevation of legs Upright posture Coughing Strain phase of valsalva maneuver Isotonic exercise Tourniquets about the extremities Abdominal exercise Release phase of valsalva maneuver

27. PERICARDIAL KNOCK Early diastolic rapid filling sound characteristic of constrictive pericarditis. Produced due to sudden cessation of rapid ventricular filling due to pericardial constriction. Occurs 0.10-0.12 seconds after A2. Best heard with bell in supine position along the left sternal border. Earlier and higher frequency than typical S3. May be confused with opening snap of MS. ( rapid y descent, kussmaul’s sign, helps in detection).

28. Fourth heart sound S4 Low frequency late diastolic or pre systolic sound heard during atrial contraction (last rapid ventricular filling phase) Also called presystolic or atrial diastolic gallop ( though ventricular in origin). Indicate a hard working ventricle ( S3 usually means ventricular failure). A healthy contracting atrium, non obstructive AV valve, and non complaint ventricle is prerequisite for genesis of S4 Follows the onset of P wave in ECG by approx. 70ms and precedes S1. Presence of S3 or S4 indicate triple rhythm ( gallop), while presence of both S3 and S4 indicate quadruple rhythm. During tachycardia or long PR interval, S3 may summate with S4, producing a loud single summation gallop (hyperkinetic states).

29. CAUSES OF S4 Physiological Pathological Recordable in elderly subjects (>60 years) Hyperkinetic circulatory states (anaemia , thyrotoxicosis, AV fistula) Acute MR, AR, TR LV outflow tract obstruction (AS) RV outflow tract obstruction (PS) Mod to severe systemic and pulmonary hypertension Ischemic heart disease, HOCM First and second degree heart blocks

30. Clinical recognition LV S4 is best heard at apex with bell in left lateral position. RV S4 is best heard at the left lower sternal border during inspiration. S4 S1 complex – S4 attenuates with firm pressure on stethoscope and in upright position. S4 accentuates with handgrip or coughing.

31. A. The S4 occurs in presystole and is frequently called an atrial or presystolic gallop. B. The S3 occurs during the rapid phase of ventricular filling. It is a nornal finding and is commonly heard in children and young adults, disappearing with increasing age. When it is heard in the patient with cardiac disease, it is called a pathologic S3 or ventricular gallop and usually indicates ventricular dysfunction or AV valvular incompetence. C. In constrictive pericarditis, a sound in early diastole, the pericardial knock (K) is heard earlier and is louder and higher pitched than the usual pathologic S3. D. A quadruple rhythm results if both S4 and S3 are present. E. At faster heart rates, the S3 and S4 occur in rapid succession and may give the illusion of a middiastolic rumble. F. When the heart rate is sufficiently fast, the two rapid phases of ventricular filling reinforce each other, and a loud summation gallop (SG) may appear; this sound may be louder than either the S3 or S4 alone.

32. OPENING SNAP Coined by Thayer WS in 1908. Early diastolic, crispy, sharp, high pitched sound correlates with the mobility of AV valve (anterior mitral leaflet in MS and septal leaflet in TS). Thickened but mobile AV leaflets, high atrial pressure, high velocity flow across AV valve is prerequisite for genesis. Sudden stopping of the opening movements of the valve ( Margolies and Wolferth theory). Phonocardiographically correlates with the maximum opening motion of anterior mitral leaflet in MS. ( and near O point apex cardiogram). Occurs at the maximal MV opening shortly (20-40ms) after LV-LA pressure crossover. Intensity correlates with intensity of M1 of S1. (mobile valve – loud OS, calcified valve – decreased or absent OS).

33. Base and apex phonocardiograms are recorded simultaneously with the mitral valve echocardiogram in three patients with chronic rheumatic mitral valvular disease. In the left panel, a soft opening snap is coincident with the maximal opening of a thickened, relatively immobile, stenotic mitral valve. In the center panel, calcified fixation of the severely stenotic mitral valve is present, and an opening snap is absent. Note that the onset of the diastolic rumble begins after the maximal anterior excursion of the heavily calcified valve. In the right panel, an opening snap occurs at the maximal opening of the nonstenotic rheumatic valve A holosystolic murmur of mitral regurgitation is present and no gradient was found across of the mitral valve at cardiac catheterization. A loud S1 gallop follows the opening snap and occurs during the early E-F slope of the rheumatic mitral valve

34. Causes of OS Stenotic OS – MS, TS Non stenotic OS – due to high velocity and Increased flow across the AV valves causing rapid excursion of the leaflets. Mitral OS Tricuspid OS Thyrotoxicosis TR MR, VSD, PDA ASD, EBSTEIN ANOMALY, TOF Tricuspid atresia with a large ASD HOCM

35. A2-OS INTERVAL OS follows A2 by an interval of 0.03-0.15s. Predicts the level of left atrial pressure and severity of MS. Higher the LAP pressure (severe MS) earlier the OS (shorter A2-OS interval ) and vice versa . Mild MS – A2-OS interval >120ms with LAP 15mmhg (mean LAP < 5mmhg). Mod MS – A2-OS interval 60-80ms with LAP 20mmhg (mean LAP 5-10mmhg) Severe MS – A2-OS interval 40-60ms with LAP 25mmhg (mean LAP > 10mmhg). FEATURE A2-OS A2-P2 site Mid precordial area (between apex and sternal area) Base of the heart (pulmonary area) interval Long interval (30-150ms) Short interval (<30ms) Postural variation Wider on standing Narrows on standing Variation with respiration Narrows on inspiration Wider on inspiration

36. FEATURES A2-OS A2-S3 Interval 30-150ms >150ms site Mid precordial Apex pitch high Low Association Loud S1, MDM of MS,TS Normal or soft S1, pansystolic murmur of MR, TR Variation on standing increase No change

37. Factors affecting A2-OS interval Heart rate Tachycardia – decrease A2-OS interval due to shortening of diastole Bradycardia – increase A2-OS interval due to prolonged diastole. Atrial fibrillation – varies with cycle length. HYPERTENSION – increase A2-OS interval ( LV systolic pressure takes longer time to descend below the LAP and there is early occurrence of A2) INCREASED LVEDP – increase A2-OS interval due to obliteration of the trans-mitral gradient ( LV failure, LV dysfunction, CAD) AS– decrease A2-OS interval due to delayed occurrence of A2. Amyl nitrite inhalation– decrease A2-OS interval .

38. Clinical recognition of OS Mitral OS– high frequency, best heard with diaphragm, in the mid precordium just inside the apex, increase with inspiration. Often well heard at the base of the heart. Tricuspid OS –frequently not detected, maximum intensity closer to the left sternal border during inspiration. Absent OS– severly calcified mitral valve, significant MR, severe AR, LV dysfunction.

39. Systolic ejection sounds Valvular ejection sounds – high frequency early systolic sounds caused by the abrupt cephalad doming and halting movements of the SL valves at the onset of ejection coinciding with fully opened position of the valve. (indicate thickened but mobile valve with maximum) excursion of the domed valve when its elastic limits are met) Found in Valvular AS and PS, congenital bicuspid aortic valve, truncus arteriosus with quadricuspid valve, TOF with Valvular PS. 2 . Vascular or root ejection sound – due to reverberation of proximal arterial wall of the dilated great artery or opening movement of the leaflets that resonate in the arterial trunk.

40. Etiology - 1. due to increased pressure beyond the valve – systemic and pulmonary hypertension 2. Due to an increased flow across the valve – anaemia, thyrotoxicosis, ASD. 3. Due to dilatation of the vessel beyond the valve – dilatation or aneurysm of ascending aorta idiopathic dilatation of pulmonary artery.

41. Aortic Valvular ES High frequency, sharp, discrete sound that follow S1 by >0.05sec. Coincident with sharp anacrotic notch on the upstroke of the aortic pressure tracing. Delayed 20 to 40ms after the onset of pressure rise in the central aorta and is coincident with the sharp anacrotic notch on the upstroke of the aortic pressure curve Defines LVOTO at the Valvular level. Most often indicates bicuspid aortic valve. Intensity correlates with the mobility of the valve not with the severity of the obstruction. Best heard at the base in the sitting and leaning forward position. (also better heard at the apex). Does not vary with respiration (constant ejection sound) (LVEDP in AS does not vary with respiration and is never higher than the aortic diastolic pressure)

42. A prominent aortic valvular ejection sound(AVES) of a congenital nonstenotic and stenotic bicuspid aortic valve is shown on the left and center panels, respectively. On the right panel there is no evidence of valvular ejection in a patient with severe fixed orifice aortic stenosis. The valvular ejection sound of the nonstenotic bicuspid aortic valve is widely separated from S1 and unassociated with a subsequent murmur. The ejection sound of the stenotic bicuspid valve introduces the typical crescendo-decrescendo murmur of valvular aortic stenosis in both conditions,A2 is well preserved

43. Pulmonary Valvular ES High frequency sound occur at maximum excursion of the stenosed pulmonary valve. Best heard at the 2 nd and 3 rd intercostal space. Best heard during expiration Elevated RVEDP in mod to severe PS Increase venous return to RV during inspiration leads to the further elevation of RVEDP beyond the pulmonary diastolic pressure Premature opening of the pulmonary valve in the diastole Decrease intensity of ES during inspiration S2 is usually widely split with P2 soft or inaudible and delayed.

44. Simultaneous right ventricular and pulmonary artery pressures are recorded with the phonocardiogram showing the mechanism of the attenuation of the pulmonary ejection sound (PES) during respiration in a patient with mild valvular pulmonary stenosis. In the second complex the valvular ejections sound has disappeared and there is complete equalization of the diastolic pressures in the right ventricle and pulmonary artery. With equalization of the pressure there is preopening of the deformed stenotic valve and with the onset of right ventricular systole no further excursion of the domed valve is possible, and the ejection sound is absent.During expiration, the pulmonary diastole pressure is significantly higher than the right ventricular end-diastolic pressure, and the prominent ejection sound is a gain recorded. Considerable the variation of the ejection sound occurs during various phases of respiration and is caused by varying degrees of preopening of the valve. Note the tendency of the ejection sound to occur later during the expiratory phase

45. Non ejection click Cuffer B in 1887 first described these sounds. Carl potain in 1894 describe these sounds as small short clicky sounds. Mid to late systolic systolic sounds, sharp, high frequency and clicking quality single or multiple often occurs with late systolic murmur in AV valve prolapse. Occurs due tensing of the redundant leaflets and elongated chordea tendinea of the AV valve during systole. Coincides with maximum systolic excursion of the prolapsed leaflet into the atrium. Causes – MVP,TVP LV aneurysm Incompetent heterograft valves. Atrial myxomas Adhesive pericarditis.

46. Base and apex phonocardiography phonocardiograms in two patients with nonejection clicks. The apex phonocardiogram shows an isolated systolic click the ( left). In the right panel are two close clicks 40 millisecond apart. On examination multiple clicks may sound like a scratchy murmur rather than individual clicks.

47. Clinical recognition Click of MVP Better heard at the apex with diaphragm. Click of TVP better heard over the lower left sternal border. Often associated with loud S1 (increased amplitude of leaflet excursion with prolapse beyond the line of closure) and systolic murmur. Maneuvers which decrease the LVEDP and LV size cause earlier and greater degree of prolapse cause louder and earlier click (standing, valsalva II, nitroglycerine and amyl nitrite inhalation) and vice versa (squatting, supine position, valsalva IV, sustained hand grip).

48. A midsystolic nonejection sound C occurs in mitral valve prolapse and is followed by the late systolic murmur that crescendos to S2. With the assumption of the upright posture venous return decreases, the heart size become smaller, the C point moves closer to S1 and the mitral regurgitant murmur has an earlier onset. With prompt squatting both venous return and afterload increase, the heart becomes larger, the C moves toward S2,and the duration of the murmur shortens

49. Pericardial rub High pitched, leathery and scratchy sound produced to movement of parietal and visceral pericardium against each other. Triple phased – systolic (ventricular systole), mid diastolic (rapid filling), late diastolic (atrial systole ). All three phases in only <50% patients. Systolic phase is most consistent followed by pre systolic phase . Best heard over 2 nd and 3 rd left intercostal spaces, with diaphragm in leaning forward position and holding the breath after forced expiration. Can be present even with large pericardial effusion. Found in acute pericarditis, post cardiotomy pericarditis, uremic pericarditis, after acute phase of transmural MI.

50. HEART MURMURS Defined as series of audible signals/vibrations of varying intensity, frequency, configuration and duration produced by the turbulence of blood flow. high flow velocity small orifice diameter low kinetic viscosity turbulence jet impact cavitation vortex shedding eddies formation flitter periodic wake murmur

51. Turbulence (Reynolds number) = flow/2(diameter)(viscosity). Reynolds number >2000 – turbulence. Vortex shedding = blood flow through a narrow orfice – vortices produced at the tip of orfice – shed laterally to hit the vessel wall producing vibrations – murmur. Jet impact = turbulent blood flow – hit the wall of the heart or blood vessel– vibrations – murmur. Cavitations = turbulent blood flow– cavitations (micro bubbles) generate heart sounds of different frequencies. Eddies = high velocity jet of blood – eddy current in the adjacent slow moving blood – vibrations – murmur. Periodic wake phenomenon = blood passes to either side of structure placed in its path – producing high velocity pure musical tones – murmur. Flitter = high speed jet of blood may pull the wall of blood vessel inward by Bernoulli effect –variations in the speed of jet produce vibrations in the wall of vessel – murmur.

52. Characteristics of murmurs 1. TIMING OF MURMUR systolic murmur diastolic murmur continuous murmur ( begin with or after S1 and ends (begins with or after S2 and ends (begins in systole and continues At or before S2) before the subsequent S1) without interruption through S2 into all or a part of diastole) early mid late holo

53. LOCATION OF MURMUR APEX LOWER STERNAL AREA LEFT 3 RD ICS PULMONARY AREA AORTIC AREA MDM of MS MDM OF TS PSM OF VSD ESM OF PS ESM OF AS SM OF MR SM OF TR EDM OF AR EDM OF PR EDM OF AR (AORTIC EsM OF CALCIFIED AS ESM OF INFUND- CM OF PDA ROOT) IBULAR PS FLOW MURMUR OF PULMONARY ORIGIN OF ASD EDM OF AR PSM OF MR AND VSD VALVULAR PS ESM OF AS ESM OF AS AND PS TR MURMUR MDM OF TS PSM OF TR PSM OF VSD

54. INTENSITY OR LOUDNESS OF MURMUR GRADED by FREEMAN AND LEVINE in 1933 into 1 to 6 DURATION OF LENGTH OF MURMUR May be short, long, or holo ( pansystolic / pandiastolic ) Correlates with the severity of the murmur (except in acute AR, complicated wit LVF, associated with systemic hypertension) GRADE SYSTOLIC MURMUR DIASTOLIC MURMUR I Very soft (quiet room, special effort) Very soft II Soft (readily detected) Soft III Moderately loud murmur without thrill Loud without thrill IV Loud murmur with thrill Loud with thrill V Extremely loud murmur (edge of the stethoscope in contact) VI Exceptionally loud murmur (stethoscope away from chest wall)

55. FREQUENCY OR PITCH OF MURMUR High pitched (>300 CPS) = AR, MR. Mixed (combination of high and medium 125-300 CPS) = AS, PS, VSD. Low pitched (25-125 CPS) = MS,TS. CONFIGURATION OR SHAPE OF MURMUR Crescendo = ESM of AS Decrescendo = EDM of AR Crescendo-Decrescendo (diamond shaped) = SM of AS and PS. Plateau = PSM of MR. TRANSMISSION OF MURMUR

56. INNOCENT MURMURS Occurs without the evidence of physiologic or structural heart disease, usually <3/6, no radiations to carotids or axilla. INNOCENT MURMURS SYSTOLIC CONTINUOUS Still’s murmur Venous hum Pulmonary artery systolic murmur Continuous mammary souffle Branch pulmonary artery systolic murmur Cephalic continuous murmur Supraclavicular systolic murmur Systolic mammary soufflé Aortic sclerotic systolic murmur Cardiorespiratory systolic murmur

57. STILLS’S MURMUR Seldom heard in infants, prevalent after 3 years of age and diminishing frequency in adolescence. Ranges from grade 1-3/6. Loudest between apex and lower left sternal edge in the supine position. Increase during exercise, excitement or fever. Uniform, medium pitch frequency. Begins shortly after S1 and confined to first half of systole. Mechanism = 1. periodic vibrations of the base of the cusp of pulmonary valve due to low right ventricular ejection pressure and velocity. 2.Due to presence of ventricular bands or false tendons that are vibrating periodically during ventricular systole. Pulmonary artery systolic murmur Most prevalent in children, adolescents and young adults. Midsystolic , maximum intensity in 2 nd left ICS, grade 1-3/6, medium pitched, best heard in supine position. Increase with exercise, fever excitement.

58. Represent normal ejection vibrations from within the main pulmonary artery during right ventricular systole. Commonly heard in pregnancy, anaemia or hyperthyroidism, loss of thoracic kyphosis. Branch pulmonary artery systolic murmur Found especially in premature neonates, occasionally in healthy neonates, seldam persist beyond 3-6 months of age. Grade 1-2/6 in intensity, medium pitched distributed to left and right anterior chest, axilla and back. Cause= pulmonary trunk in fetus is relatively dilated domed shaped ( receive the output of high pressure right ventricle proximal right and left pulmonary artery arise as small lateral branch and receive paucity of blood flow After birth, difference in the size persist especially in premature infants. (in addition branches arises at right angle from the inferior and posterior wall of pulmonary trunk This difference produce systolic murmur

59. Supraclavicular systolic murmur Heard in children and young adults. Always maximally heard above the clavicles, louder on the right, generally bilateral, prominent over the suprasternal notch. Originate from the aortic origins of major brachiocephalic arteries, especially the subclavians . 3-4/6 in intensity, may be associated with thrills, crescendo-decrescendo, abrupt, brief and confined to first 2/3 rd of systole. Partial compression of subclavian artery intensifies the murmur. Best heard in sitting upright and straight head. Aortic systolic murmur in adults Most common form of normal mid systolic murmur found in older adults. Caused by fibrous or fibrocalcific thickening of the bases of the inherently normal aortic cusps. Does not causes obstruction across the valve and called aortic sclerotic murmur of old age. Grade 2-3/6, midsystolic , high pitched, best heard in sitting position.

60. Venous hum First recognised by potain in 1867. Laminar flow in the internal jugular vein is disturbed by the deformation of the vein at the level of the transverse process of the atlas during head rotation. Continuous murmur typically louder in diastole. Best heard in sitting posture with head rotated to the opposite side and chin upwards with bell on the right side mainly. Abolished by digital compression over vein, supine position, head returned to neutral position, valsalva maneuver . Found in healthy children and young adults, later stage of pregnancy, hyperkinetic state. Mammary soufflé Found in 10-15% of pregnant women during 2 nd and 3 rd trimester and early postpartum. Medium to high pitched, best heard over the breast on either side between the 2 nd and 6 th ICS, with no significant change with respiration. Usually began S1 with a distinct gap and systolic component is the loudest. Light pressure auguments the murmur whereas firm pressure abolish the murmur. Valsalva meneuver has no significant effect on the murmur.

61. SYSTOLIC MURMUR Early systolic mid systolic late systolic holosystolic (begin with S1 and confined) (begin after S1 and end be-) (begin with S1, occupy all of) ( begin with mid to late To 1/3 rd to ½ of systole) fore S2) systole and end with S2 ) systole and end with S2 High pitched high to medium pitched high pitched high pitched, blowing, Decrescendo crescendo-decrescendo sometimes musical Regurgitant murmurs Due to regurgitant flow “diamond shaped” plateau configuration From high to low pressure Region eg - acute severe MR eg - AS, HOCM, PS eg - MVP due to prolapse of eg - chronic MR,TR Acute TR with normal functional-dilatation of posterior mitral leaflets Restrictive VSD RV systolic pressure aortic root and pulmonary PDA WITH PH Nonrestrictive VSD with PAH trunk AP window Small VSD increased flow into Ao or PA innocent mid systolic murmur

62. DIASTOLIC MURMUR EARLY DIASTOLIC MID DIASTOLIC LATE DIASTOLIC HOLODIASTOLIC (begin with S2 and confined (begin with clear interval (occurs in presystole (begins after S2 occupy To early 1/3 rd to ½ of diastole) after S2 and end before S1) immediately before S1) whole diastole and ends before S1) Soft, high pitched, blowing Low pitched, rumbling, Regurgitant murmur rough murmur. Ex- AR Ex- MS, TS Ex- severe chronic AR. Functional PR (GRAHAM Austin flint murmur severe PR STEELL MURMUR)

63. Diagram contrasting the auscultatory findings in chronic and acute aortic regurgitation (AR). In chronic AR, a prominent systolic ejection murmur (SEM), resulting from the large forward stroke volume, is heard at the base and apex and ends well before the second heart sound (S 2 ). The aortic diastolic regurgitant murmur begins with S 2 and continues in a decrescendo fashion, terminating before the first heart sound (S 1 ). At the apex, the early diastolic component of the Austin Flint (AF) murmur is introduced by a prominent third heart sound (S 3 ). A presystolic component of the AF is also heard. In acute AR, there is a significant decrease in the intensity of the SEM compared with chronic AR because of the decreased forward stroke volume. S 1 is markedly decreased in intensity because of preclosure of the mitral valve; at the apex, the presystolic component of the AF murmur is absent. The early diastolic murmur at the base ends well before S 1 because of the equilibration of the left ventricular (LV) and aortic end-diastolic pressure. Significant tachycardia is usually present.

64. MID DIASTOLIC MURMUR LV and RV inflow mitral and tricuspid flow MV opening interface other causes Obstruction murmurs Ex – MS Ex- severe MR Ex- Austin flint murmur organic PR left atrial myxoma VSD,, PDA carey coomb’s murmur CHB ( rytand’s cor triatriatum AP window murmur) constriction around AV RSOV into right ventricle groove severe TR TS ASD, PAPVC, TAPVC right atrial myxoma RSOV to right atrium carcinoid syndrome single atrium ebstein’s anomaly hyperkinetic states

65. CONTINUOUS MURMUR (begin in systole, continues without interruption through S2 into all or a part of diastole without change in character) DUE TO HIGH TO LOW PRESSURE SHUNT DUE TO RAPID BLOOD FLOW DUE TO LOCALIZED ARTERIAL OBSTRUCTION Ex- PDA Ex- cervical venous hum coarctation of aorta ALCAPA mammary soufflé branch pulmonary artery stenosis Blalock, watersons and pott’s shunt haemangioma carotid occlusion (50-80%) TAPVC hyperthyroidism AV fistula Pulmonary atresia ( TO AND FRO MURMUR) RSOV into RA,RV VSD WITH AR Truncus arteriosus with PS MS WITH MR AP window AS WITH AR Porto systemic shunt

66. DYNAMIC AUSCULTATION Technique of altering circulatory dynamics by a variety of physical and pharmacological manuvers and determining the effects of these manuvers on heart sounds and murmurs. Types of bed side manuvers . Physical = respiration, postural changes, isometric hand grip, valsalva and Muller manuvers . Non deliberate = change in cardiac cycle length by PVC, atrial fibrillation in heart blocks. Pharmacological = amyl nitrate, methoxamine , phenylephrine.

67. NORMAL RESPIRATION Inspiration Increase in systemic venous return due to fall decrease in pulmonary venous return due to in intra thoracic pressure. Pooling of blood in pulmonary vasculature. Increase RV SV and duration of RV ejection. Decrease LV SV and LV ejection Decrease pulmonary vascular impedence and decreases hang out interval on the aortic side Increasing the pulmonary hang out interval (<30ms). (>80ms)

68. EFFECTS ON HEART SOUNDS INSPIRATION EXPIRATION S2 normal split in A2 and P2 single sound S3,S4 OS right sided increase in intensity left sided increase in intensity Aortic ejection sound no change with respiration Pulmonary ejection sound (Valvular) decrease increase Pulmonary vascular section sound increase EFFECTS ON HEART MURMURS Right sided murmurs increase (no change in RVF as little or no increase in venous return) Left sided murmurs increase MR murmur no change with respiration MVP increase

69. VALSALVA MANEUVER Deep inspiration followed by forced expiration against a closed glottis for 10-20sec. Blowing into a BP manometer to maintain level of 40mhg for 30ms. PHASE I STRAINING COMMENCES Rise in intra thoracic pressure Transient rise of LV output and systemic arterial pressure. Fall in heart rate PHASE II STRAINING PHASE Perceptible decrease in systemic venous return and SV (initially right sided than left sided Decrease of systolic, diastolic and pulse pressure. Reflex tachycardia. PHASE III CESSATION OF STRAINING PHASE Sudden increase in systemic venous return 1. Abrupt transient decrease in arterial pressure equivalent to the fall in intra thoracic pressure PHASE IV OVERSHOOT PHASE Transient overshoot of systemic arterial pressure, wide pulse pressure. Reflex bradycardia (return of pooled blood in venous return)

70. Effects on heart sounds Phase II – S2 split narrows, S3, S4 attenuated. Phase III – right sided S3, S4 augments and S2 split widens. Phase IV – left sided S3, S4 may transiently accentuated. Effects on heart murmurs Phase II – SV and systemic arterial pressure falls ( attenuation of systolic murmurs of AS,PS, MR, TR and diastolic murmurs of AR, PR, MS, TS.) increase in LVOTO with increased pressure gradient increase SM of HOCM. increase in degree of prolapse – loud and early occurrence of systolic murmur(MVP) Phase III – augmentation of all right sided murmurs (increase in systemic venous return) Phase IV – left sided murmurs return to controlled levels and may transiently accentuated.

71. Arterial pressure tracing in MS, ASD, HEART FAILURE Phase I and phase III responses are normal but as baroreceptors reflexes are not activated. Absence of normal decrease in arterial pressure during phase II. No overshoot of arterial pressure in phase IV. This gives arterial pressure tracing a “square wave response” (instead of distinct 4 phases) Valsalva ratio of 1.0 (normal 1.6). MULLERS MANEUVER – converse of valsalva maneuver Forced inspiration against closed glottis (with closed nose and firmly sealed mouth) for 10sec This maneuver exaggerates the inspiratory effort. S2 split widened, RV S3 and S4 are accentuated. All right murmurs are augmented.

72. POSTURAL CHANGES Sudden lying down from standing or sitting position or passive elevation of both legs Increase in systemic venous return initially increase the RV SV followed by increase LV SV and LV size after several cardiac cycles. Effects on heart sounds Widening of S2 split. Initially RV S3, S4 accentuated followed by LV S3, S4 after several cardiac cycles. Effects on heart murmurs Increase in SM of PS, AS, MR, TR, VSD, functional murmurs (increase in systemic venous return) Increase in LVEDP and LV size – SM of HOCM decrease ( pressure gradient decreases) mid systolic click and late SM of MVP delayed (little or no prolapse).

73. Sudden standing from supine position Response— sudden decrease in venous return SV decreases, RVEDP and LVEDP decreases. Reflex increase in cardiac output and SVR Effects on heart sounds and murmurs S2 split narrows, RV and LV S3 and S4 decreases. all right and left sided heart murmurs decreases. murmur of HOCM and MVP increase.

74. SQUATTING FROM STANDING POSTURE increase in systemic venous return and SV. Increase in SVR due to kinking of iliac arteries and reduction of distending pressure of gravity on the lower limbs vessels. Increase in systemic arterial pressure with transient reflex bradycardia Effects on heart sounds – S3 and S4 of both ventricle accentuated Effects on heart murmurs 1. Due to increase venous return and stroke volume – SM of AS, PS and DM of TS, MS increase 2. Increase LV size– decrease LVOTO in HOCM – decreased SM little or no prolapse with MVP – late SM and click delayed.

75. 3. Due to increase in aortic reflex – inaudible DM of AR becomes audible and augmented. 4. Due to elevated SVR– right to left shunt decreased – increased pulmonary blood flow– immediate improvement of arterial oxygen saturation. 5. Elevated SVR and systemic pressure – increased regurgitant volume – augmentation of SM of MR. left to right shunt increase through VSD – loud SM.

76. ISOMETRIC EXECRISE Done by sustained hand grip Ideally by using calibrated hand grip device simultaneously by both hands. By pressing a hand ball simultaneously with both hands. By simply making a hand grip with both hand simultaneously for 20-30sec. -- Inadvertently doing valsalva maneuver during handgrip must be avoided -- Avoided in patients with ventricular arrhythmias and myocardial ischemia . Physiological effects – increase in -- systemic vascular resistance. -- arterial pressure -- heart rate. -- cardiac output -- LV filling pressure and size.

77. Effects on heart sounds S2 split widens, and LV S3, S4 increased. Effects on heart murmurs DM of MS becomes louder due to increase cardiac output. DM of AR and SM of MR and VSD increased due to increased systemic vascular resistance SM of AS diminished ( reduction in pressure gradient – due to increase arterial pressure and SVR Increased LV size – SM of HOCM decrease (due to decreased pressure gradient) mid systolic click and late SM of MVP delayed (decrease in prolapse).

78. CHANGE IN CARDIAC CYCLE LENGTH (PVE AND AF) During compensatory pause following a PVC or AF— -- increase in the ventricular filling and size. -- Secondary augmentation of ventricular contractility of the next beat and transient elevation of arterial pressure. Effects Varying intensity of S1 (with AF) SM of AS accentuates (increase ventricular filling prolonging the preceding diastole and contractility. DM of AR becomes louder (transient elevation of arterial pressure). SM of HOCM augmented due to increase LVOTO as a result of increased ventricular contractility (with decreased volume of pulse ( brokenbrough braunwald sign). Mid systolic click and late SM of MVP delayed (increased LV filling and size). No change – MR and VSD.

79. AMYL NITRITE INHALATION 3 to 4 deep breath of amyl nitrite (taken over a piece of gauze) over 10-15 sec. Changes – Marked vasodilatation (due to decreased SVR) with reduction in systemic arterial pressure in first 30sec. After 30-60sec, followed by reflex tachycardia, increase in cardiac output and velocity of blood flow. Effects on heart sounds S1 is augmented and A2 is diminished. Mitral and tricuspid OS becomes louder and A2-OS interval shortens (arterial pressure falls) S3 of either ventricle augments (rapid ventricular filling) S3 of MR origin diminished.

80. Effects on heart murmurs Due to increased cardiac output – increase in SM of AS, PS and TR. All functional SM DM of MS, TS, and PR. 2. Due to decreased SVR – decrease in SM of MR and VSD. DM of AR. Austin flint murmur of AR Diastolic phase of continuous murmur of PDA SM of TOF ( decreased arterial pressure increase right to left shunt and decrease the pulmonary blood flow).

81. 3. Due to decreased LV volume and size – LVOTO increase and SM of HOCM accentuated. Degree of prolapse increased and early onset of mid systolic click and murmur of MVP. AMYL NITRITE INHALATION EFFECT INCREASED DECREASED AS Vs MR SM OF AR SM OF MR TR Vs MR SM OF TR SM OF MR PS Vs TOF SM OF PS SM OF TOF DM OF MS Vs AR DM OF MS AFM OF AR EDM OF AR Vs PR EDM OF PR EDM OF AR

82. METHOXAMINE AND PHENYLEPHRINE 3-5 mg of methoxamine IV is given which increase arterial pressure by 20-40mmhg for 10-20min. 0.3-0.5 mg of phenylephrine IV is preferred as it elevates the arterial pressure by 30mmhg for only 3-5min. Effects – Increase arterial pressure Causes reflex bradycardia and decreased contractility and cardiac output. Not used in CHF and HTN. Effects on heart sounds and murmur – low intensity DM of AR increased and AFM of AR augmented. No change in SM of AS, PS and DM of PR , TS.

83. MURMURS MANEUVERS MANEUVERS 1. SM of AS Vs HOCM valsalva Squatting SM of AS ↓ ↑ SM of HOCM ↑ ↓ 2. SM of AS Vs MR Amyl nitrate Post PVC SM of AS ↑ ↑ SM of MR ↓ No change 3. SM of MR Vs TR Respiration SM of MR No change SM of TR ↑inspiration 4. SM of PS Vs TOF Amyl nitrate SM of PS ↑ SM of TOF ↓ 5. SM of PS Vs VSD Amyl nitrate SM of PS ↑ SM of VSD ↓ 6. Ejection sound of PS Vs AS Respiration ES of PS Expiration ↑ Inspiration ↓ ES of AS No change

84. THANKS