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APPROACH TO THE VARIOUS MULTIVALVULAR HEART DISEASES IN CLINICAL GROUNDS
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MULTI VALVULAR HEART DISEASE
PROF.M.K.SUDHAKAR
SRMC
OBJECTIVES A CLINICAL SHORT CASE DISCUSSION
APPROACH TO THE VARIOUS MULTIVALVULAR HEART DISEASES IN CLINICAL GROUNDS.
CASE PRESENTATION.
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
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.
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
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
CARDIOVASCULAR SYSTEM
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.
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.
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.
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.
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
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.
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.
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.
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
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
1.What are the common causes of Multivalvular heart diseases ?
Multivalvular lesions are almost always due to Rheumatic fever
Collagen vascular diseases or myxomatous degeneration are rare causes
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.
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
2.What are the factors which modify the clinical presentation of MVD ?
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
Non valvular Factors Myocarditis Volume overload states Pressure overload states CAD Infective endocarditis Arrhythmias
WHEN DO U SUSPECT A MVD ?
MVD Atrial fibrillation Pulmonic hypertension Pulmonic congestion Systemic emboilsm
What is graham steel murmur? What are the recent views on it?
Features of Combined AS/AR:
AS + AR Apico carotid delay
S2 paradoxical split A2 – soft or absent S3 S4
Prolonged Aortic ESM Prolonged Aortic EDM Austin Flint Murmur
Dominant AS vs Dominant AR
DOMINANT ASAnacrotic pulse
Apex heave
Systolic decapitation
Systolic Ejection Click
S2 reverse split S3 – later S4 Systolic murmur – late, loud, longer
DOMINANT AR
Wide pulse pressure Pulsus bisferiens Diffuse apical impulse Early diastolic murmur S3 – earlier
What is silent AS, severe AS?
SILENT AS
Old age – non fused, calcified cusps
Cardiac failure
Severe AS
AS + MS
SEVERE ASJVP a wave (Bernheim effect)
Apico carotid delay
S2 single or paradoxical split
AEC absent
S4
Systolic murmur - late, loud, longer
Mitral pansystolic functional murmur
What is silent AR, severe AR?
SEVERE AR Hills sign > 60 mm hg S2 soft S3 EDM – louder & longer Cole Cecil murmur Austin Flint murmur
Cole Cecil murmur – AR EDM heard in the apex or axilla
Austin Flint murmur – MDM heard in severe and acute AR
SILENT AR
Acute AR CCF AR + AS AR + MS
COMBINED MITRAL LESION:
MS + MR Mitral valve orifice < 1.5 sq.cm MS is
predominant Mitral valve orifice > 1.5 sq.cm MR is
predominant
MS + MR Parasternal heave - prominence Apical impulse - prominence Apical MDM Apical PSM
DOMINANT MS ?
DOMINANT MS Parasternal lift – early systolic & brisker Tapping apical impulse S1 - loud OS MDM/LDM
DOMINANT MR?
DOMINANT MR Parasternal impulse – slower & late systolic
Hyperdynamic apical impulse Pansystolic murmur S1 - soft S3
WHAT IS….. SILENT MS? SEVERE MS?
SILENT MS Severe MS with pulmonary hypertension
RV enlarges and LV rotates clockwise - tight or silent MS
TS + MS AS + MS
SEVERE MS A2 OS interval - closer MDM – longer Severe PHT
What is Silent MR? Severe MR?
SILENT MR Obesity Emphysema Chest wall deformity LV infarction / dilatation Para prosthetic leakage
SEVERE MR S1 – soft S2 – wide and variable S3 PSM – intensity MDM – short low pitch flow murmur.
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
MS + AS Carotid pulse & Apex prominent Parasternal heave Loud S1 OS Ejection systolic murmur Grade < 3/6 Mid diastolic murmur
MS < AS Angina Syncope
Carotid thrill Apical impulse heave Ejection systolic murmur
MS > AS Dyspnea Pulmonic hypertension Atrial fibrillation Systemic thromboembolism
MDM
MS + AR Wide pulse pressure Apical prominence Parasternal impulse
Loud S1 OS S3 S4
Early diastolic murmur Mid diastolic murmur
MR + AS Geriatric – calcific Rheumatic
MR + AS AS augments the severity of MR
Systemic hypotension Pulmonic hypertension
MR + AS Hyperdynamic AI
S3 / S4
Mitral – PSM Aortic – ESM
MR < AS Angina Syncope Fatigue
Carotid thrill S4 Systolic murmur decreased on squatting or
hand gripping
MR = AS Angina Dyspnea Syncope Fatigue
Pulmonic congestion Systemic embolism
Atrial fibrillation Carotid thrill Diffuse & sustained apical impulse S2 soft S3 S4
WHAT IS GALLIVARDIAN PHENOMENON?
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
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
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
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
MR + AR MR is worsened by AR
Wide pulse pressure Peripheral signs Diffuse apical impulse
P2 S3 S4 Mitral PSM Aortic EDM
MR < AR Wide pulse pressure Longer EDM Longer PSM S4
MR = AR Wide pulse pressure Parasternal heave Longer EDM Longer PSM
MR > AR Atrial fibrillation Parasternal heave Longer PSM
AS / AR / MS /MR Rheumatic
Murmurs of all four hemodynamic lesions
Pulmonary congestion
TVD
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
MS precedes TS TS masks MS
TS is to be suspected when RHF persists after adequate mitral valvotomy
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
TS > TR Tricuspid OS
The Tricuspid diastolic murmur increases and whereas Tricuspid systolic murmur decreases with inspiration
TR > TS Tricuspid S3
The Tricuspid diastolic murmur decreases and whereas Tricuspid systolic murmur increases with inspiration
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
How will you investigate MVD ?
History or Physical examination provides insignificant clues to recognize pulmonary valve disease in multivalvular disease
INVESTIGATIONS: ECG CXR 2D ECHO Cardiac catheterization
How do you manage multivalvular diseases ?
In Ideal conditions all lesions should be corrected simultaneously
In practice distal lesions are corrected first followed by proximal lesions.
PROCEDURES. Valvotomy
Valvuloplasty
Valve replacement
THANK YOU……