APPROACH TO THE VARIOUS MULTIVALVULAR HEART DISEASES IN CLINICAL GROUNDS

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 impulse is visible in left 5th
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 5th
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……