Rheumatic heart disease Mitral stenosis Valvular heart disease

Rheumatic heart disease Mitral stenosis

Valvular heart disease • Rheumatic • Age related • congenital

Mitral valve • Stenosis • Regurgitation • Prolapse

Mitral stenosis • • 2/3 females Usually rheumatic Rarely congenital 40% of all RHD

Structural defects • Diffusely thickened –fibrous tissue /calcified deposits • Mitral commisures fuse • Corde tendinae fuse /shorten • Narrowing of the apex of funnel shaped valves

• Calcification of slender valves immobilises the leaflet and narrows the orifice –thrombus formation –arterial thrombus from calcified Valves

Pathophysiology • Normal mv –dia -4 -6 cm 2 • <2 cm 2 -atrial to ventricular flow is maintained by increased av pressure gradient –the hallmark of ms • <1 cm 2 –LAP should be atleast 25 mm hg is required to maintain normal output.

• Increased Lap ----increased pulm pressure -----increased capillary pressure -----decreased pulm compliance -------exertional dyspnoea. • Increased heart rate –decreased transvalvular gradient ----increased LAP • Lv diastolic pressure in normal in ms • Co is normal at rest ---at exercise –decreased co.

$ Clinical /hemodynamic Features –influenced by Passive backward transmission of LAP Pulmonary arteriolar constriction Intertitial edema Organic obliterative changes in the pul vascular bed • Phtn----Tr------rt sided failures---bornheimeffect • • •

symptoms • Carditis---ms-----2 decades, • Dyspnoea on exertion ----4 th decade— progressive worsening to death---2 -5 yrs • Doe , orthopnoea , pnd, arrthmia-premature atraial complex, paroxysysmal tachycardia, flutter, fibrilation • Haemoptysis –increased pulm venous pressure

Recurrant pulm embolism Pulm infection Endocarditis Chest pain -10% Thrombus formation in the left atrium-af— appendages of LA • Pedunculated thrombus –ball valve thrombi • -syncope-angina –changing ascultatory signs • • •

On examination • Malar flush-pinched blue facies • JVP-a wave prominence –af –a wave absent • Palpation-tapping apical impulse , s 1 loud, palpable , s 2 p 2 loud • Diastolic thrill • Auscultation-s 1 accentuated /snapping – delayed –mv doesn’t close till LVP>LAP • Qs prolongation , p 2 loud

• • • A 2 -p 2 -os -0. 05 -0. 12 P 2 -os –severity of ms Intensity of s 1/os –pliability of le. AFLET MDM after os Duration correlates with ms severity S 1 -closure of mitral /tricuspid valve

• • • Intensity of s 1 Pos of mv at onset of vent systole Rate of increase in LAP Degree of structural damage of the valve Amt of tissue bet heart and sthetoscope

• S 1 loud –diastole is shortened by tachycardia • S 1 split -10 -30 msec • S 1 –m 1 t 1 -----prolonged in rbbb • t 1 m 1 –severe ms , left atrial myoma lbbb

Mitrl regurgitation

etiology • Chronic rhd –severe mr- 1/3 • Seen in males mostly • Rheumatic processrigidity, deformity, retraction of the valve cusps -commisural fusion • Congenital-endocardial cushion defects • Fibrosis of papillary muscles in MI • Ischeamia –paplillary dysfn

• • Lv dilated in DCM HOCM-ant displace ment of the ant leaflet Mitral prolapse –MR Acute MR-inf endocarditis

pathophysiology • Clinical pic depends on p-v relation ship of LA AND PUL -VENOUS BED • Increased LAP-Increased pulm edema • Effective forward pressure of lv decreases • Inc-LA volume –due to atrial compliance • Low cardiac out put • Atrial fibrillation

SYMPTOMS • • FATIGUE Doe Orthopnea Pnd Haemoptysis Sys embolism Rh f-jvp inc, tr, phtn, hep congestion

Physical examination • • • Sys thrill-left apex Hyperdynmic apical impulse Laterally displaced Palpable p 2 Parasternal heave

auscultation • S 1 -absent/softor buried in systolic murmur • Decreased co-aorta closes early-a 2 early-wide spliting of s 2 • Os –indicates ms • Gallop rhythm • Pansystolic murmur

lab • Ecg –sinus rhythm , prominent p waves , af lvh • Echo • Cxr-kerley b lines

management • • Medical Dec exertion Dec NA intake Diuretics Digitalis/vasodilators-inc co Ace inhibitors /hydralazine Surgical-valve replacement