Mitral Regurgitation in Emergency Medicine Medication

  • Author: Daniel DiSandro, MD; Chief Editor: David FM Brown, MD   more...
 
Updated: Nov 1, 2010
 

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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Contributor Information and Disclosures
Author

Daniel DiSandro, MD  Clinical Assistant Professor, Department of Emergency Medicine, Drexel University

Daniel DiSandro, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Robert M McNamara, MD, FAAEM  Chair and Professor, Department of Emergency Medicine, Temple University School of Medicine

Robert M McNamara, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, Pennsylvania Medical Society, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Paul Blackburn, DO, FACOEP, FACEP  Program Director, Department of Emergency Medicine, Maricopa Medical Center; Assistant Professor, Department of Surgery, University of Arizona

Paul Blackburn, DO, FACOEP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Medical Association, and Arizona Medical Association

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

David FM Brown, MD  Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

References
  1. [Guideline] Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD, et al. 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1998 guidelines for the management of patients with valvular heart disease). Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. Sep 23 2008;52(13):e1-142. [Medline]. [Full Text].

  2. Borer JS, Bonow RO. Contemporary approach to aortic and mitral regurgitation. Circulation. Nov 18 2003;108(20):2432-8. [Medline].

  3. Carabello BA. Management of valvular regurgitation. Curr Opin Cardiol. Mar 1995;10(2):124-7. [Medline].

  4. Carabello BA. Mitral valve disease. Curr Probl Cardiol. Jul 1993;18(7):423-78. [Medline].

  5. Fenster MS, Feldman MD. Mitral regurgitation: an overview. Curr Probl Cardiol. Apr 1995;20(4):193-280. [Medline].

  6. Filsoufi F, Salzberg SP, Adams DH. Current management of ischemic mitral regurgitation. Mt Sinai J Med. Mar 2005;72(2):105-15. [Medline].

  7. Gaasch WH, Eisenhauer AC. The management of mitral valve disease. Curr Opin Cardiol. Mar 1996;11(2):114-9. [Medline].

  8. Schon HR. Medical treatment of chronic valvular regurgitation. J Heart Valve Dis. Oct 1995;4 Suppl 2:S170-4. [Medline].

  9. Wisenbaugh T. Mitral valve disease. Curr Opin Cardiol. Mar 1994;9(2):146-51. [Medline].

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Transesophageal echocardiogram demonstrating prolapse of both mitral valve leaflets during systole.
Transthoracic echocardiogram demonstrating bioprosthetic mitral valve dehiscence with paravalvular regurgitation.
Severe mitral regurgitation as depicted with color Doppler echocardiography.
Four-chamber apical view of a 2-dimensional transthoracic echocardiogram demonstrates mitral valve prolapse (MVP), a common cause of mitral regurgitation.
 
 
 
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