Ms mr

mulyivalvular heart disease

1. MULTI VALVULAR HEART DISEASE PROF.M.K.SUDHAKAR SRMC

2. OBJECTIVES A CLINICAL SHORT CASE DISCUSSION APPROACH TO THE VARIOUS MULTIVALVULAR HEART DISEASES IN CLINICAL GROUNDS.

3. CASE PRESENTATION.

4. GENERAL EXAMINATION 46 yr / male Conscious , Oriented to time, place and person Weight – 60 kg Height – 162.5 cm Arm span – 145 cm BMI – 22.8 kg/m2

5. Vitals Temperature - 98.2 F Pulse 80/min, Regular , large volume , Collapsing in nature (water hammer pulse) Bis feriens in character, Carotid thrill +. Normal vessel wall No radio-radial or radio-femoral delay All peripheral pulses are well felt No apex- pulse deficit noted.

6. 110/50 mm of Hg over right brachial artery in supine position 110/50mm of Hg over Lt. brachial artery Systolic BP measured in lower limb is 160 mm of Hg Hill’s sign - positive ( systolic BP difference between upper & lower limbs is 50 ) Blood Pressure

7. JVP – elevated 5 cms above the sternal angle, but the waveforms masked by carotid pulsations in neck. Respiration - Rate- 17/min, Regular, Abdomino-thoracic type No other peripheral signs of AR. No P I C C L E. No external markers of Rheumatic fever / Infective Endocarditis Fundus Examination – Normal

8. CARDIOVASCULAR SYSTEM

9. INSPECTION Chest symmetrical, no spinal or chest deformity noted Trachea appears to be in midline Carotid pulsations are visible in the neck. Apical i mpulse is visible in left 5 th intercostal space in Midclavicular line confined to single intercostal space. Visible pulsations noted in left parasternal area. Parasternal heave is visible. No sinus , dilated veins over chest wall. A healed surgical scar of 15 cms in the left thoracic wall extending from mid clavicular line(6 ICS) to the post axillary line.

10. PALPATION Trachea centrally placed. Apex beat localized in the Left 5 th Intercostal space Midclavicular line confined to single Intercostal space, tapping in nature, systolic thrill palpable. Parasternal heave felt and not obliterable ( grade 3 ) Systolic thrill noted in aortic area and all over precordium. Palpable P2 noted in pulmonary area. Supra sternal and epigastric pulsations are felt.

11. Aortic Area S1 heard A2 soft . A harsh ejection systolic murmur occupying almost of entire systole ; crescendo-decrescendo in nature with delayed peaking, of grade 4 intensity conducted to both carotids which is best audible with diaphragm of stethoscope in sitting and leaning forward position with breath held in expiration No ejection click noted. Dynamic auscultation: murmur is augmented on squatting Reduces on standing and isometric hand grip.

12. Pulmonary Area : S1heard P2 loud and s2 single. Systolic Crescendo decrescendo murmur same as heard in aortic area best heard in expiration with pt leaning forward. No ejection click noted. Dynamic auscultation: murmur is augmented on expiration; squatting and reduced on isometric hand grip.

13. 2nd Aortic Area ( Erb’s Area ) S1 heard A2 soft A harsh ejection systolic murmur occupying almost of entire systole ; crescendo-decrescendo in nature with delayed peaking, of grade 4 intensity conducted to both carotids which is best audible with diaphragm of stethoscope in sitting and leaning forward position with breath held in expiration

14. A grade 3 high pitched , blowing , early diastolic decrescendo murmur which is best audible with diaphragm of stethoscope in sitting and leaning forward position with breath held in expiration . No ejection click noted. Dynamic auscultation: The early diastolic murmur is augmented on isometric hand grip and expiration.

15. Tricuspid Area : S1 , S2 heard A High pitched Pan systolic murmur grade 4 intensity ;best heard with the diaphragm which increases on inspiration is heard. No s3,s4 heard.

16. Mitral Area: S1 S2 heard. S1 loud. Low pitched rough rumbling mid diastolic murmur of grade 3 intensity noted at the apex with the bell of the stethoscope with best heard in left lateral position and pt in expiration. A high pitched holo systolic murmur is noted of grade 4 intensity radiating from the tricuspid area confirmed by inch auscultation. Which increases on inspiration . No opening snap heard. No s3 ,s4 heard.

17. OTHER SYSTEMS Respiratory System : Bilateral normal vesicular breath sounds heard No added sounds Abdominal System : Soft , Non tender , No organomegaly No ascites Nervous System : No focal neurological deficit

18. CLINICAL DIAGNOSIS Anatomical : Mitral and Aortic valves with tricuspid valve. Etiology :Acquired Rheumatic Valvular Heart Disease Pathological : Severe mitral re stenosis Severe aortic stenosis Moderate aortic regurgitation Functional tricuspid regurgitation . Complication : Pulmonary hypertension Patient is in sinus rhythm No evidence of Cardiac failure No evidence of Infective endocarditis No evidence of Thromboembolic event

19. 1.What are the common causes of Multivalvular heart diseases ?

20. Multivalvular lesions are almost always due to Rheumatic fever Collagen vascular diseases or myxomatous degeneration are rare causes

21. Significant stenosis at multiple valves are usually Rheumatic Significant regurgitation at multiple valves are usually Non Rheumatic Significant stenosis and regurgitation together are usually rheumatic.

22. MVD Quadrivalvular disease is most likely due to combination of causes – congenital , rheumatic, infective, degenerative disease A unitary cause for quadrivalvular disease is either rheumatic or myxomatous degeneration

23. 2.What are the factors which modify the clinical presentation of MVD ?

24. The natural history and clinical presentation of combined lesions is determined by the relative severity of each individual lesion and by chronology and chronicity of development Proximal lesions mask the features of distal lesions

25. Non valvular Factors Myocarditis Volume overload states Pressure overload states CAD Infective endocarditis Arrhythmias

26. WHEN DO U SUSPECT A MVD ?

27. MVD Atrial fibrillation Pulmonic hypertension Pulmonic congestion Systemic emboilsm

28. What is graham steel murmur? What are the recent views on it?

29. Features of Combined AS/AR:

30. AS + AR Apico carotid delay S2 paradoxical split A2 – soft or absent S3 S4

31. Prolonged Aortic ESM Prolonged Aortic EDM Austin Flint Murmur

32. Dominant AS vs Dominant AR

33. DOMINANT AS Anacrotic pulse Apex heave Systolic decapitation Systolic Ejection Click

34. S2 reverse split S3 – later S4 Systolic murmur – late, loud, longer

35. DOMINANT AR Wide pulse pressure Pulsus bisferiens Diffuse apical impulse Early diastolic murmur S3 – earlier

36. What is silent AS, severe AS?

37. SILENT AS Old age – non fused, calcified cusps Cardiac failure Severe AS AS + MS

38. SEVERE AS JVP a wave ( Bernheim effect ) Apico carotid delay S2 single or paradoxical split AEC absent S4 Systolic murmur - late, loud, longer Mitral pansystolic functional murmur

39. What is silent AR, severe AR?

40. SEVERE AR Hills sign > 60 mm hg S2 soft S3 EDM – louder & longer Cole Cecil murmur Austin Flint murmur

41. Cole Cecil murmur – AR EDM heard in the apex or axilla Austin Flint murmur – MDM heard in severe and acute AR

42. SILENT AR Acute AR CCF AR + AS AR + MS

43. COMBINED MITRAL LESION:

44. MS + MR Mitral valve orifice < 1.5 sq.cm MS is predominant Mitral valve orifice > 1.5 sq.cm MR is predominant

45. MS + MR Parasternal heave - prominence Apical impulse - prominence Apical MDM Apical PSM

46. DOMINANT MS ?

47. DOMINANT MS Parasternal lift – early systolic & brisker Tapping apical impulse S1 - loud OS MDM/LDM

48. DOMINANT MR?

49. DOMINANT MR Parasternal impulse – slower & late systolic Hyperdynamic apical impulse Pansystolic murmur S1 - soft S3

50. WHAT IS….. SILENT MS ? SEVERE MS?

51. SILENT MS Severe MS with pulmonary hypertension RV enlarges and LV rotates clockwise - tight or silent MS TS + MS AS + MS

52. SEVERE MS A2 OS interval - closer MDM – longer Severe PHT

53. What is Silent MR? Severe MR?

54. SILENT MR Obesity Emphysema Chest wall deformity LV infarction / dilatation Para prosthetic leakage

55. SEVERE MR S1 – soft S2 – wide and variable S3 PSM – intensity MDM – short low pitch flow murmur.

56. MS + AS The combination of Mitral stenosis and Aortic stenosis is almost always due to rheumatic The combinations is usually associated with significant regurgitation at either valve Mitral stenosis masks Aortic stenosis

57. MS + AS Carotid pulse & Apex prominent Parasternal heave Loud S1 OS Ejection systolic murmur Grade < 3/6 Mid diastolic murmur

58. MS < AS Angina Syncope Carotid thrill Apical impulse heave Ejection systolic murmur

59. MS > AS Dyspnea Pulmonic hypertension Atrial fibrillation Systemic thromboembolism MDM

60. MS + AR Wide pulse pressure Apical prominence Parasternal impulse Loud S1 OS S3 S4

61. Early diastolic murmur Mid diastolic murmur

62. MR + AS Geriatric – calcific Rheumatic

63. MR + AS AS augments the severity of MR Systemic hypotension Pulmonic hypertension

64. MR + AS Hyperdynamic AI S3 / S4 Mitral – PSM Aortic – ESM

65. MR < AS Angina Syncope Fatigue

66. Carotid thrill S4 Systolic murmur decreased on squatting or hand gripping

67. MR = AS Angina Dyspnea Syncope Fatigue Pulmonic congestion Systemic embolism

68. Atrial fibrillation Carotid thrill Diffuse & sustained apical impulse S2 soft S3 S4

69. WHAT IS GALLIVARDIAN PHENOMENON?

70. GALLIVARDIAN PHENOMENON An acoustic phenomenon whereby the aortic ejection systolic murmur radiates to the mitral area with reduced intensity but prolonged duration so as to be heard as a pansystolic murmur AS often confused with MR

71. Inch auscultation along the sash line appreciates the transformation Sash line is an imaginary line through right carotid, aortic area, second aortic area ,mitral area

72. MR + AR Most common cause is rheumatic with or without AS / MS Pure MR and AR is due to connective tissue disorders with myxomatous degeneration of valve tissue when TR coexists Infective endocarditis or chordal rupture produce regurgiation in congenital or rheumatic valve diseases

73. When MR > AR , it attenuates AR When AR > MR , it worsens MR Pulmonary symptoms are earlier and severe with MR + AR combination than in isolation

74. MR + AR MR is worsened by AR Wide pulse pressure Peripheral signs Diffuse apical impulse

75. P2 S3 S4 Mitral PSM Aortic EDM

76. MR < AR Wide pulse pressure Longer EDM Longer PSM S4

77. MR = AR Wide pulse pressure Parasternal heave Longer EDM Longer PSM

78. MR > AR Atrial fibrillation Parasternal heave Longer PSM

79. AS / AR / MS /MR Rheumatic Murmurs of all four hemodynamic lesions Pulmonary congestion

80. TVD

81. TS TS is very unusual as an isolated lesion TS is almost always due to rheumatic valvulitis and is associated with coexisting disease of mitral and aortic valves TS almost always coexists with MS and only rarely with predominant MR

82. MS precedes TS TS masks MS TS is to be suspected when RHF persists after adequate mitral valvotomy

83. TR Functional TR is more frequent than organic TR and is due to severe Pulmonary hypertension Severe organic TR is almost always due to rheumatic origin and accompanies TS Severe organic TR coexists with Mitral or Aortic valve disease

84. TS > TR Tricuspid OS The Tricuspid diastolic murmur increases and whereas Tricuspid systolic murmur decreases with inspiration

85. TR > TS Tricuspid S3 The Tricuspid diastolic murmur decreases and whereas Tricuspid systolic murmur increases with inspiration

86. PVD Pulmonic valve disease is unusual in rheumatic heart disease , when it occurs it is usually in quadrivalvular disease Carcinoid tumor should be suspected when pulmonary and tricuspid valve lesions coexist

87. How will you investigate MVD ? History or Physical examination provides insignificant clues to recognize pulmonary valve disease in multivalvular disease

88. INVESTIGATIONS: ECG CXR 2D ECHO Cardiac catheterization

89. How do you manage multivalvular diseases ?

90. In Ideal conditions all lesions should be corrected simultaneously In practice distal lesions are corrected first followed by proximal lesions.

91. PROCEDURES. Valvotomy Valvuloplasty Valve replacement

92. THANK YOU……