Mitral Stenosis

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  MITRAL STENOSIS  Etiology and pathophysiology: –

1)almost always rheumatic in origin

2)sometimes due to calcification of the valves in the adults

3)can also be congenital but very rarely

4)the mitral orifice is slowly diminished by: –

a.progressive fibrosis

b.calcification of the valve leaflets

c.fusion of the cusps and subvalvular apparatus

5)the flow of blood from LA to the LV is restricted and hence the LA progressively dilates and the LAP rises leading to PVC and hence there is breathlessness

6)there is dilatation and hypertrophy of the LA, the left ventricular filling become more dependent on left atrial contraction

7)any increase in heart rate shortens diastole when the mitral valve is open and produces a further rise in left atrial pressure

8)exercise and pregnancy are poorly tolerated as they require an increase in CO and hence it causes an increase in LAP

9)mitral valve orifice is normally about 5cm^2 in diastole and is reduced to about 1cm^2 in mitral stenosis

10)asymptomatic until less than 2cm^2

11)breathless due to PVC and fatigue due to low CO

12)atrial fibrillation due to progressive dilation of the LA is very common

13)its onset often precipitates pulmonary edema due to tachycardia and loss of atrial contraction and hence there is marked hemodynamic changes that occur as there is a rapid rise in LAP

14)there is gradual rise in LAP and hence the pulmonary vascular resistance increases leading to pulmonary hypertension which can decrease the chances of pulmonary edema but cause right ventricular hypertrophy leading to right heart failure

15)20% patients develop sinus rhythm; many have small fibrotic LA and severe pulmonary hypertension

Clinical features: –

1)breathless due to PVC

2)fatigue due to low CO

3)oedema, ascites (right heart failure)

4)palpitation (atrial fibrillation)

5)hemoptysis (PVC, PE)

6)cough (PVC)

7)chest pain (PHTN)

8)thromboembolic complications (stroke, ischemic limb)

Signs: –

1)atrial fibrillation

2)mitral facies

3)auscultation: –

a.loud S1, opening snap due to increase LAP and it is palpable (tapping apex beat)

b.mid – diastolic murmur due to turbulent flow

4)crepitations, pulmonary edema, effusions (Raised pulmonary capillary pressure)

5)RV heave, loud P2 (PHTN)

6)There might be pansystolic murmur due to coexisting mitral regurgitation and it radiates towards the axilla

7)Also PTHN can lead to RVH and dilatation with secondary tricuspid regurgitation which causes a systolic murmur and giant “v” waves in the venous pulse.

Investigations: –

1)ECG: –

a.P mitral or atrial fibrillation

b.RVH: – tall R waves in V1 – V3

2)chest X – ray: –

a.enlarge LA and appendage

b.signs of PVC

3)echo: –

a.thickened immobile cusps

b.reduced valve area

c.reduced rate of diastolic filling of LV

d.enlarged LA

4)Doppler: –

a.Pressure gradient across mitral valve

b.Pulmonary artery pressure

c.Left ventricular function

5)cardiac catheterization: –

a.coronary artery disease

b.mitral stenosis and regurgitation

c.pulmonary artery pressure

Management: –

1)Balloon valvuloplasty

2)Mitral valvulotomy

3)Mitral valve replacement: – indications: –

a.significant symptoms

b.isolated mitral stenosis

c.no mitral regurgitation

d.LA free of thrombus

e.Mobile, non – calcified valve / subvalve apparatus on echo

4)medical management: –

a.to be done when minor symptoms are present

b.anticoagulant therapy to reduce risk of systemic embolism

c.ventricular rate control (digoxin, beta blockers or rate limiting calcium antagonists) should be given

d.antibiotics to be given for IE is no longer done

 
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