MITRAL REGURGITATION
Causes
MI
MVP(most common cause)
DILATATION OF LEFT
VENTRICLE e.g. CAD,
CARDIOMYOPATHY
RHD
CONNECTIVE TISSUE
DISORDERS LIKE MARFANS
SYNDROME
INFECTIVE
ENDOCARDITIS(usually Staph
aureus)
MITRAL VALVE ANATOMY (Refer diagram )
1. CUSPS : Anterior and Posterior (Posterior has three lobes)
2. Annulus
3. Chordae Tendineae
4. Papillary muscles
Pathology to any of the above said components can lead to MR
 |
| MITRAL VALVE ANATOMY |
PATHOPHYSIOLOGY
Can be divided into three stages\
ACUTE PHASE
1. There is usually a sudden rupture of Chordae tendineae or papillary muscles, which leads to volume overload in Lt atrium and Lt ventricle
2. 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
3. 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
CHRONIC COMPENSATED
1. This occurs if the MR is slow in onset or if the initial acute phase is managed for long periods with medical therapy.
2. 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) 3. Thus the patient usually has normal exercise tolerance
CHRONIC DECOMPENSATED
1. In decompensated phase the left ventricular muscles are no longer able to pump the increased stroke volume.
2. This leads to increased end diastolic volume and increased filling pressure leading to CCF.
3. 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
e. 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
