Medication Summary
Medical therapy is used to avoid or decrease pulmonary congestion as well as to treat atrial tachyarrhythmias. These require medical therapy to prevent thromboembolic complications.
Loop diuretics
Class Summary
By promoting renal excretion of water and electrolytes, loop diuretics decrease pulmonary congestion. Pulmonary congestion results from back-flow to the lungs caused by obstruction across a narrowed mitral valve orifice.
Furosemide (Lasix)
Furosemide acts by inhibiting absorption of the electrolytes sodium and chloride in the proximal and distal tubules and in the loop of Henle, thereby promoting excretion of salt (sodium chloride) and water. It acts as a diuretic and as an antihypertensive.
Potassium-sparing diuretics
Class Summary
Potassium-sparing diuretics are used to prevent potassium depletion induced by the more potent loop-diuretics (such as furosemide).
Spironolactone (Aldactone)
Spironolactone retains potassium by competing with aldosterone for the receptor sites in the distal convoluted renal tubules. This increases sodium and water excretion while retaining potassium and hydrogen ions.
Anticoagulants
Class Summary
Anticoagulants are used in general for the prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. In the case of MS, they are used to prevent clot formation secondary to blood stasis in an enlarged, many times fibrillating, left atrium and in case of a prosthetic (mechanical) mitral valve.
Warfarin (Coumadin)
Warfarin inhibits vitamin K–dependent clotting factors II, VII, IX, and X and the anticoagulant proteins C and S. Its anticoagulation effect occurs 24 h after administration, but the peak effect may occur 72-96 h later. Antidotes are vitamin K and FFP.
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Congenital Mitral Stenosis. Hemodynamic changes in severe congenital mitral valve stenosis (MS). MS causes an obstruction (in diastole) to blood flow from the left atrium (LA) to the left ventricle (LV). Increased LA pressures are transmitted retrograde to pulmonary veins and pulmonary capillaries, resulting in capillary leak with subsequent development of pulmonary edema. To overcome pulmonary edema, the arterioles constrict, increasing pulmonary pressures. With time, capillaries develop intimal thickening, causing fixed (permanent) pulmonary hypertension. The right ventricle (RV) hypertrophies to generate enough pressure to overcome the increased afterload. Eventually, the RV fails, which manifests as hepatomegaly and/or ascites, edema of the extremities, and cardiomegaly on radiography.
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Congenital Mitral Stenosis. Two-dimensional echocardiograph, parasternal long axis view of a 5-month-old boy with congenital mitral valve stenosis. A small mitral valve annulus (star) is appreciated when compared with the normal-sized tricuspid valve annulus. Mitral valve stenosis has caused left atrial (LA) enlargement. AoV = Aorta; LA = Left atrium; LV = Left ventricle; RA = Right atrium; RV = Right ventricle.
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Congenital Mitral Stenosis. Two-dimensional echocardiograph, parasternal long axis view of a patient who required mitral valve replacement with a St. Jude's prosthetic mitral valve (star). He developed a stroke one month after mitral valve replacement despite anticoagulation with warfarin and required re-replacement of the prosthetic mitral valve. He will eventually outgrow this new prosthetic mitral valve and require subsequent mitral valve replacements with a larger mitral valve prosthesis. AoV = Aorta; LA = Left atrium; LV = Left ventricle; RA = Right atrium; RV = Right ventricle.
