Acute Mitral Regurgitation Medication

Updated: Dec 28, 2015
  • Author: Daniel DiSandro, MD; Chief Editor: Barry E Brenner, MD, PhD, FACEP  more...
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Medication

Medication Summary

The mainstay of treatment is preload and afterload reduction, particularly in the setting of mitral regurgitation with pulmonary edema.

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Diuretics

Class Summary

These agents are used to reduce preload and the left ventricular volume.

Furosemide (Lasix)

An excellent preload reducer. Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.

Dose must be individualized. Depending on response, administer at increments of 20-40 mg, no sooner than 6-8 h after the previous dose, until desired diuresis occurs. When treating infants, titrate with 1-mg/kg/dose increments until a satisfactory effect is achieved.

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Nitrates

Class Summary

These agents are useful in preload reduction and as antianginal agents.

Nitroglycerin topical (Nitro-Bid)

Causes relaxation of the vascular smooth muscle via stimulation of intracellular, cyclic guanosine monophosphate production, which causes a decrease in blood pressure.

Nitroprusside (Nipride, Nitropress)

DOC for afterload reduction. Has an effect on afterload reduction but also some effect on preload; produces vasodilation and increases inotropic activity of the heart. In addition, reduces peripheral resistance by directly acting on arteriolar and venous smooth muscle.

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Anti-arrhythmics

Class Summary

These agents are used for the control of atrial fibrillation in the setting of chronic mitral regurgitation.

Digoxin (Lanoxin)

DOC in rate control of atrial fibrillation. Cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system.

Diltiazem (Cardizem)

Useful as second line of therapy in rate control of atrial fibrillation and chronic mitral regurgitation. During the depolarization, it inhibits the calcium ion from entering the slow channels or the voltage-sensitive areas of the vascular smooth muscle and myocardium.

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