• Mitral Stenosis

    by  • 07/10/2013 • Cardiology

    Definition

    characterized by the narrowing of the orifice of the mitral valve of the heart

    Presenting complaint

    1. p/c: dyspnoea, palpitations, ftigue, haemoptysis, large LA, (+AF), loud S1 and S2.
    2. first heart sound is unusually loud (loud M1: mitral valve closure) and may be palpable (tapping apex beat)
    3. If PAH = secondary to mitral stenosis, P2 (pulmonic) component of the second heart sound (S2) will become louder

     

    Murmur: An opening snap, followed by a mid-diastolic rumbling murmur, accentuated in pt rolled to left side.

    Peripheral signs include:

    1. Malar flush – due to PAH
    2. Peripheral oedema – when there is right heart failure
    3. Atrial fibrillation – irregular pulse and loss of ‘a’ wave in jugular venous pressure due to atrial stretch
    1. Left parasternal heave – presence of RVH due to PAH
    2. Tapping apex beat which is not displaced

     

    Diagnostic tools/investigations

    1. Echo
    2. Doppler echocardiography for severity
    3. Simultaneous left heart catheterization and right heart catheterization = Swan-Ganz catheterization = mean pulmonary capillary wedge pressure, which is a reflection of the left atrial pressure.

     

    Aetiology

    1. Rheumatic heart disease
    2. Congenital heart disease

     

    Pathophysiology

    1. When the mitral valve area goes below 2 cm2, the valve causes an impediment to the flow of blood into the left ventricle, creating a pressure gradient across the mitral valve.
    2. As the gradient across the mitral valve increases, the amount of time necessary to fill the left ventricle with blood increases.
    3. As the heart rate increases, the amount of time that the ventricle is in diastole and can fill up with blood (called the diastolic filling period) decreases. When the heart rate goes above a certain point, the diastolic filling period is insufficient to fill the ventricle with blood and pressure builds up in the left atrium, leading to pulmonary congestion.
    4. This left atrial pressure is transmitted to the pulmonary vasculature and causes pulmonary hypertension. Pulmonary capillary pressures in this level cause an imbalance between the hydrostatic pressure and the oncotic pressure, leading to extravasation of fluid from the vascular tree and pooling of fluid in the lungs (congestive heart failure causing pulmonary edema).

     

    Treatment and management (conservative/medical/surgical)

    1. B-blockers/CCB/digoxin for AF
    2. Prevent emboli with anti-clotting
    3. Prophylaxius for RF = penicillin)
    4. Surgical replacement of the valve = best option!!
    5. Percutaneous balloon valvuloplasty
    6. Once an individual develops NYHA class III or IV symptoms, the progression of the disease accelerates and the patient’s condition deteriorates – this warrants a valve replacement 
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