Pathology to any of the above said components can lead to MR
PATHOPHYSIOLOGY
Can be divided into three stages
ACUTE PHASE CHRONIC COMPENSATED CHRON IC DECOMPENSATED
There is usually a sudden rupture of Chordae tendineae or
papillary muscles, which leads to volume overload in Lt atrium and
Lt ventricle
The Volume overload in left ventricle is because of the
increased total stroke volume as now the left ventricle has to pump
blood both into the aorta and also the regurgitating blood. ie :
Total Stroke Volume of LV = Forward stroke volume + Regurgitation
Volume
The regurgitated blood causes a volume overload into the left
atrium and this in turn increases the pressure in left atrium. The
increased pressure hampers the blood flow into the atrium from the
pulmonary veins. Thus it can lead to pulmonary congestion and
pulmonary hypertension
This occurs if the MR is slow in onset or if the initial acute
phase is managed for long periods with medical therapy.
Here there is LV hypertrophy and LA dilatation. This in turn
causes a normal (compensated) forward stroke volume and increased
emptying of pulmonary veins respectively(therefore no pulmonary
hypertension)
Thus the patient usually has normal exercise tolerance
In decompensated phase the left ventricular muscles are no
longer able to pump the increased stroke volume.
This leads to increased end diastolic volume and increased
filling pressure leading to CCF.
Further the increased blood volume in the LV causes LV
dilatation, this causes dilatation of the annulus of mitral valve
which further increase the MR.
CLINICAL FEATURES
Clinical features depends on the phase of the disease
1. Acute phase and decompensated phase presents with shortness
of breath, orthopnoea,
PND, decreased exercise tolerance and sometimes cardiovascular
collapse.
2. Patients are mostly asymptomatic in compensated phase (with a
normal exercise tolerance)
3. SIGNS:
a. Soft S1
b. Laterally displaced apex with a HEAVING character
c. High pitched pansystolic murmur radiating towards the axilla
or back (loudness of
the murmur is inversely proportional to the severity of MR)
d. In case of pulmonary HTN
i. Palpable P2(loud P2 on auscultation)
4. Atrial fibrillation can occur
INVESTIGATIONS
1. ECG
a. Shows evidence of LV hypertrophy and LA enlargement in long
standing MR
b. Shows evidence of AF
2. X RAY CHEST
a. Enlargement of LV and LA
3. ECHOCARDIOGRAM
a. To confirm diagnosis. Colour Doppler on transthoracic
echocardiogram(TTE) shows a
jet of blood flow from the LV to LA during systole
TREATMENT
Acute Mitral Valve regurgitation require immediate valve
replacement. If the patient is hypotensive
then an intra-aortic balloon pump is placed to increase
perfusion. If the patient is hypertensive then
vasodilators like nitroprusside can be given to reduce e the
after load.
In Chronic case vasodilators like ACE inhibiters and hydralazine
can be given.
SURGICAL TREATMENT:
Mitral Valve Repair or
Mitral Valve Replacement
