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……