Dynamic auscultation

1. DYNAMIC AUSCULTATION

2. This is a technique of altering circulatory dynamics by means of a variety of physiological and pharmacological maneuvers and determining their effects on heart sounds and murmurs

3. Interventions most commonly employed are Respiration Postural changes Valsalva maneuver Isometric exercise Premature ventricular contractions Vasoactive agents- amyl nitrite , methoxamine ,phenylephrine

4. RESPIRATION History Pontain in1866 was the first to note the normal respiratory variation in splitting of the second heart sound . In 1954 leatham brought pontain’s observations to clinical attention through emphasis on their significance

5. Hemodynamics On inspiration the intra thoracic pressure decreases and results in augmentation of right heart blood flow and decrease in left heart flow Murmurs generated in the right heart there fore generally become louder on inspiration and those in left heart chambers decrease as a result of reduced left heart flow as well as increased insulation by the air filled lungs

6. Second heart sound Respiration alters the splitting and loudness of second heart sound In normal young adults in supine position inspiration S2 split increase expiration split narrows and s2 becomes single Failure of S2 to fuse in EXP may occur in normal children and 15 to 20 % of young adults In up to 50% of normal adults > 50 yr single audible S2 is seen in supine position both in INSP and EXP

7. During inspiration A2 becomes softer because 1. aortic pressure decreases 2. increased lung space between heart and chest wall During ispiration P2 becomes soft in 2 nd LICS and Louder in lower LSB ( increased flow in the pulmonary artery has greater effect lesser deree of lung space interposed in this area )

8. Heart sounds Accentuated during Inspiration RVS3 and RVS4 Tricuspid OS Expiration LVS3 and LVS4 mitral OS

9. Pulmonary ejection click Inspiration diminish intensity of valvular PEC PA diastolic pressure is very low Inspiration causes elevation of RV DP RV late diastolic Pr almost equlises PA diastolic Pressure Causes partial presystolic opening of PV Less upward motion of valve during systole

10. MURMURS Respiration exerts more pronounced and consistent alterations on murmurs of right side than left side Especially tricuspid murmurs 100 % sensitivity, 88% specificity Inspiration increases venous return to right side of heart Expiration increases venous return to left side of heart

11. Murmurs accentuated during Inspiration TS TR ( Carvallo’s sign) PR Mild or moderate PS Severe PS no further increase in gradient Expiration MS MR AS AR VSD Pericardial rub (AP diameter)

12. MVP MSC and systolic murmur occur earlier during systole in inspiration Inspiratory reduction in LV size Increased redundancy of MV Increase valvular prolapse

13. IHSS murmur may decrease in loudness and intensity with inspiration This is because of inspiratory increase in Lv transmural pressure, with resultant decrease in LVOT obstruction

14. In general it is best to assess respiratory variation during normal respiration. Effects of inspiration on auscultatory findings may be accentuated by Muller maneuver Converse of Valsalva Maneuver Forced inspiration against closed glottis Forcibly inspires while the nose is held closed and mouth is firmly sealed for about 10 sec.

15. Patients who have pulmonary hypertension and severe RVF may not demonstrate inspiratory augmentation of Rt heart murmurs and gallops This is due to high Rt heart filling pressures that does not allow venous return to increase in inspiration By requesting these patients to stand and by repeating cardiac ausculation we can appreciate the expected respiratory changes

16. Widens split S2 and augments murmur and filling sound originating in right side of the heart.

17. POSTURAL CHANGE RAPID STANDING Decrease in venous return, thus stroke volume and the ensuing reflex increses the cardiac rate and systemic vascular resistance immediately

18. Width of the splitting become reduced No change in patients with true fixed split Decrease in intensity RVS3 and RVS4 LVS3 and LVS4

19. Decrease in intensity Semilunar valve stenosis AV valve regurgitation murmurs VSD Most functional systolic murmurs

20. Since LV EDV is decreased Increase in murmurs HOCM(95 % sensitivity, 84% specificity) Early MSC and murmur of MVP

21. Physiological changes that cause increase in obstruction in LVOT include a smaller ventricular size and reflex inotropic stimulus from increased catecholamines

22. SQUATTING Sudden change from standing to squatting position Increase venous return and augmentation of peripheral resistance due to kinking of femoral arteries simultaneously Squatting abruptly increases ventricular preload and afterload Arterial pressure rise may cause transient reflex bradycardia

23. Increase in stroke volume causes augmentation of S3 and S4(of both ventricles ) Right sided systolic murmurs AS Diastolic murmur of MS augmented due to increase in CO with increased flow across mitral valve

24. Elevation of arterial pressure Increase in aortic reflux AR Increase in MR volume Increase in LT to RT shunt in VSD Increase in blood flow through RVOT in TOF

25. Combination of elevated arterial pressure and venous return Increase LV size and reduce LVOT obstruction Decrease murmur in HOCM (95% sensitivity, 85% specificity) Click and murmur of MVP delayed

26. LEFT LATERAL RECUMBENT POSITION Accentuate intensity of S1 LVS3 and LVS4 OS of MS Murmurs of MS and MR Click and murmur of MVP Austin Flint murmur

27. SITTING AND LEANING FORWARD Accentuate AR and PR murmur ( mechanical )

28. Lying flat or passive leg raising in supine position Results in increase in venous return with sequential increase in right and then left ventricular end diastolic volumes, stroke volume, and ejection velocities

29. Augmented Valvular AS/PS murmurs TR murmur S3 and S4 Diminished EDM of AR Murmur of HOCM MVP murmur and click are delayed

30. ISOMETRIC EXERCISE This can be carried out by using a calibrated handgrip device or a handball Better to carryout bilaterally Performed in supine posture Should be sustained for 30 to 40 secs Valsalva maneuver during the handgrip must be avoided Contraindicated in patients with myocardial ischemia and ventricular arrhythmias, severe HTN, cerebral ischemia

31. Hemodynamic effects Increases cardiac contractility cardiac output arterial pressure without significant change in ventricular chamber size

32. Isometric exercise results in significant increase in Systemic vascular resistance Arterial pressure Heart rate COP LV filling pressure Heart size

33. Systolic murmur of AS diminished –reduction of pressure gradient across AV Diastolic murmur of AR and systolic murmurs of rheumatic MR and VSD increases LVS3 and LVS4 accentuated Diastolic murmur MS becomes louder –increase in flow across valve

34. Increase LV volume Systolic murmur of HOCM decreased Click and murmur of MVP delayed

35. VALSALVA MANEUVER Forced expiration against a closed glottis Standard test consists of asking the patient to blow against an aneroid manometer and maintain a pressure of 40mmhg for 30seconds

36. Relatively deep inspiration followed by forced exhalation against a closed glottis for 10 to 20 seconds Physician has to keep flat of the hand on the abdomen to provide the patient a force to breathe against Normal response has four phases

37. PHASE I Intrathoracic pressure rises Transient increase in LV output and SBP

38. PHASE II STRAINING PHASE Systemic venous return decrease Filling of right and then left side reduced Stroke volume reduced Mean arterial and pulse pressures falls Reflex tachycardia

39. Since LV volume is reduced Murmur of HOCM increased (65% sensitivity, 95% specificity ) Systolic click and murmur of MVP commence earlier

40. PHASEIII VALSALVA RELEASE Brief sudden Decrease SBP Due to sudden decrease in intra thoracic pressure

41. Phase IV Over shoot of SBP due to increased venous return and reduced systemic vascular resistance Followed by reflex bradycardia

42. PHASE IV OVERSHOOT PHASE Murmurs and heart sounds transiently augmented

43. Square wave response Seen in Severe LV dysfunction +_ Heart failure MS with significant PAH ASD with significant L to R shunt Apparently normal persons aged above 55 yr

44. Phase I: Intra thoracic pressure rises with increase in sys and pul arterial pressures with no increase in CO Phase II: ventricular filling is not decreased and venous return is maintained during continued straining. Arterial pressure remains mildly elevated with insignificant changes in PP , HR , LV SV , CO

45. Phase III/IV: post release phase pressures return to normal pre strain level No transient increase invenous return,SV or over shoot BP rise or reflex brady cardia

46. The maneuver should be performed with patient in supine position or upper part of body elevated no more than 30 degrees Strain phase to be limitied to 10 to 12 sec Should not be performed in patients with active myocardial ischemia or cerebral ischemia and unstable cardiac rhythm

47. Valsalva Maneuver I/T Pr = VR = BP sympathetic tone HR sudden return of peripherally pooled blood to the vaso-constricted arterial system (2 to the increased sympathetic tone) PHASE II PHASE IV MAXIMAL SYMPATHETIC ACTIVATION FLAT PART OF STARLING’S CURVE HEART FAILURE ASD MS

48. Valsalva maneuver is helpful in differentiating rt sided systolic murmurs from those of the left side and of considerable importance in identifying systolic murmur of HOCM

49. During strain phase Attenuation of S3 and S4 AS & PS MR & TR AR & PR TS & MS Most of the heart sounds and murmurs decrease in the strain phase of valsalva

50. Up on release of valsalva murmurs on the right side of the heart return to baseline intensity in 2 to 3 cardiac cycles where as left sided murmurs donot return to baseline intensity till 5 to 10 cardiac cycles

51. Second heart sound Normal splitting of S2 narrows during the strain phase of valsalva and widens markedly immedaitely during the release phase Paradoxical plitting of S2 w idens during the strain phase and then becomes more narrow during the release phase

52. POSTPREMATURE VENTRICULAR CONTRACTIONS Followed by a significant pause Increase in ventricular filling Augmentation of cardiac contractility- post extra systolic potentiation Onset of LV ejection at a lower diastolic pressure

53. During postpremature beat – augmented are ESM of AS and PS volume contractility HOCM contractility-increase dynamic LVOT obstruction increase volume decrease LVOT obstruction net increase gradient

54. PSM of MR and of VSD - not altered(relatively little further increase in mitral valve flow or change in the LV-LA gradient) (ventricle has has 2 openings aorta and LA in MR not in AS) Systolic murmur of papillary muscle dysfunction diminish Increase in LV size delays systolic click and murmur of MVP (depend mainly on volume)

55. Similar auscultatory changes follow prolonged diastolic pauses in AF After a long R-R interval augmented unchanged AS/PS TOF IHSS VSD TR MR AR

56. PR interval variations When PR interval becomes abnormal atrial contribution to ventricles decrease and the stroke volume falls Varying atrial contribution will cause significant alteration in ESMs S1 soft with long PR and loud with short PR

57. PHARMACOLOGICAL AGENTS AMYL NITRITE INHALATION Crush ampule in towel take 3-4 deep breaths over 10 – 15 secs First 30 secs – Systemic art pressure decrease 30 to 60 secs – Reflex Tachycardia > 60 secs - positive inotropic effect, SV, EF, CO,HR and Ejection Velocity Significant increase in venous return

58. S1 augmented A2 diminished OS mitral and tricuspid valve become louder A2 OS interval shortens RVS3 and LVS3 augmented –rapidity of ventricular filling LVS3 associated with MR diminished(MR reduced)

59. Systolic murmurs accentuated are HOCM AS PS TR Functional systolic murmurs Increased ventricular contractility and SV

60. Due fall in systemic arterial pressure murmurs diminished are PSM of MR PSM of VSD EDM of AR Austin flint murmur Continuous murmur of PDA Continuous murmur of AVF

61. Systolic ejection murmur of TOF diminished Decrease in arterial pressure Increase right to left shunt Decrease blood flow in RVOT

62. Reduction cardiac size leads to Early appearance of click and murmur of MVP Murmur intensity show variable response

63. Amyl nitrate response useful in distinguishing Systolic murmur of AS(^)and MR(v) Systolic murmur of TR(^) and MR(v) Systolic murmur of PS(^) and TOF(v) Systolic murmur of PS(^) and VSD(v) Diastolic murmur of MS(^) and Austin flint(v) EDM of PR(^) and AR(v)

64. In HOCM there an additional and earlier( 5 to 10 after inhaltion ) augmentation of murmur due to decrease in LV Vol and sys art pressure with resultant increase in LVOT obstruction This earlier response helps in differentiating HOCM from valvular AS where murmur augmentation starts 15 to 20sec after inhalation

65. METHOXAMINE AND PHENYL EPHRINE Increase systemic arterial pressure Reflex bradycardia and decreased contractility and COP Contraindicated in CHF and HTN

66. Methoxamine 3-5 mg IV increase arterial pressure by 20-40 mm Hg with in 2-3 min lasting for 30 to 40 min Phenylephrine 0.5mg IV elevates systolic pressure around 30mm Hg for 3-5min Phenylephrine preferred due to shorter duration action

67. S1 reduced A2 becomes louder A2 OS prolonged S3 and S4 response variable Click of MVP occurs later and accentuated

68. Increase in arterial pressures cause following murmurs louder EDM of AR and Austin Fli nt murmur PSM of MR VSD TOF Continuous murmurs of PDA and AVF

69. Systolic murmur of HOCM softens(^ LV size) Click and murmur of MVP delayed(^ LV size) Decrease in COP diminish ESM of AS Functional systolic murmurs MDM of MS

70. TRANSIENT ARTERIAL OCCLUSION Transient external compression of both brachial arteries By bilateral cuff inflation to 20 mm Hg greater than peak systolic pressure Augments the murmurs of MR, VSD, and AR

71. MS Inspiration, Sudden standing Dec pulmonary venous return, Reduces LAP MDM reduced OS softens A2-OS gap widen Three sequential sounds (A2, P2, and OS) may be audible Exercise ,Squatting ,Amyl Nitrate, isometric hand grip MDM accentuated

72. Valsalva maneuver may show square wave response A2 OS interval directly related to R-R interval

73. MR Varies little with respiration Decrease murmur Sudden standing Valsalva Amyl Nitrate Augments the murmur Squatting Isometric Exercise

74. AS Murmur increases on Post PVC beat squatting Lying flat from standing Reduces AS murmur Valsalva Standing Handgrip Abnormal PR

75. AR EDM increases on Expiration sitting up and leaning forward Squatting Isometric exercise Vasopressors Decreases with Amyl Nitrate Valsalva

76. MVP Murmur and click earlier(intensity decreases) LV Volume decrease Standing Valsalva Murmur and click later LV Volume increase Squatting Post ectopic Isometric Exercise (intensity increases)

77. HOCM Increase murmur in Expiration Valsalva strain Standing Post ectopic Amyl nitrate Decrease murmur in Inspiration Sustained Handgrip squatting Methoxamine

78. Valsalva strain following amyl nitrate in HCM In 20 to 30% of patients systolic murmur of HCM remains unchanged after valsalva strain When valsalva strain is repeated after amyl nitrate inhalation most of these pts will now show augmentation This maneuver increases the sensitivity of valsalva for diagnosing HOCM

79. Dynamic auscultation helpful in AS X HOCM squatting (^/ v) valsalva /standing ( v/^) AS x MR handgrip (v/^) phenyl ephrine ( v /^) post pvc (^/ v) amyl nitrate (^/ v)

80. MS X TS respiration MR X TR respiration MS X AUSTIN FLINT amyl nitrate(^/v) PS X AS respiration PS X Small VSD amyl nitrate (^/v) phynylephrine (v/^) respiration PR X AR squatting (_/^) sus handgrip (-/^)

81. Thank you