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 cm2 <2 cm 2-atrial to ventricular flow is maintained by increased av pressure gradient –the hallmark of ms <1 cm2 –LAP should be atleast 25mm 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 decades, Dyspnoea on exertion th decade— progressive worsening to death 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,s1 loud,palpable,s2 p2 loud Diastolic thrill Auscultation-s1 accentuated /snapping – delayed –mv doesn’t close till LVP>LAP Qs prolongation,p2 loud

A2-p2-os P2-os –severity of ms Intensity of s1/os –pliability of leAFLET MDM after os Duration correlates with ms severity S1-closure of mitral /tricuspid valve

Intensity of s1 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

S1 loud –diastole is shortened by tachycardia S1 split msec S1 –m1t1-----prolonged in rbbb t1m1 –severe ms,left atrial myoma lbbb

Mitrl regurgitation

etiology Chronic rhd –severe mr- 1/3 Seen in males mostly Rheumatic process- rigidity,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 p2 Parasternal heave

auscultation S1-absent/softor buried in systolic murmur Decreased co-aorta closes early-a2 early-wide spliting of s2 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