Mitral Regurgitation in Emergency Medicine 

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

Background

Mitral regurgitation, in the acute and chronic decompensated states, is commonly encountered in the emergency department. An understanding of the underlying etiologies and pathophysiology of the condition is critical to direct appropriate treatment.

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Pathophysiology

Mitral regurgitation can be divided into the following 3 stages: acute, chronic compensated, and chronic decompensated.

In the acute stage, which usually occurs with a spontaneous chordae tendineae or papillary muscle rupture secondary to myocardial infarction, a sudden volume overload occurs on an unprepared left ventricle and left atrium. The volume overload on the left ventricle increases left ventricular stroke work. Increased left ventricular filling pressures, combined with the transfer of blood from the left ventricle to the left atrium during systole, results in elevated left atrial pressures. This increased pressure is transmitted to the lungs resulting in acute pulmonary edema and dyspnea.

If the patient tolerates the acute phase, the chronic compensated phase begins. The chronic compensated phase results in eccentric left ventricular hypertrophy. The combination of increased preload and hypertrophy produces increased end-diastolic volumes, which, over time, result in left ventricular muscle dysfunction. This muscle dysfunction impairs the emptying of the ventricle during systole. Therefore, regurgitant volume and left atrial pressures increase, leading to pulmonary congestion.

Severe mitral regurgitation as depicted with colorSevere mitral regurgitation as depicted with color Doppler echocardiography.
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Epidemiology

Frequency

United States

Previously, chronic rheumatic heart disease was the most common cause of acquired mitral valve disease in the Western world. More recently, however, mitral valve prolapse (MVP) has become the most common cause, being responsible for 45% of cases of mitral regurgitation. MVP has been estimated to be present in 4% of the population; however, significant regurgitation in this population only occurs in those with abnormalities of the valve.

International

In areas other than the Western world, rheumatic heart disease remains the leading cause of mitral regurgitation.

Mortality/Morbidity

The prognosis of patients with mitral regurgitation depends on the underlying etiologies and the state of the left ventricular function.

  • Acute pulmonary edema and cardiogenic shock often complicate the course of acute regurgitation. The operative mortality in these cases approaches 80%. A patient with ruptured chordae tendineae and minimal symptoms has a much better prognosis.
  • With chronic regurgitation, volume overload is tolerated very well for years before symptoms of failure develop. Left atrial enlargement predisposes patients to the onset of atrial fibrillation with the subsequent complication of embolization. In addition, these patients are susceptible to endocarditis. A study of the survival of patients with chronic regurgitation was performed using randomly selected patients. The study revealed that 80% of the patients were alive 5 years later, and 60% were alive after 10 years.
  • Most patients with mitral valve prolapse are asymptomatic. Prolapse in those older than 60 years is frequently associated with chest pain, arrhythmias, and heart failure. The prognosis of these patients is good; however, sudden death, endocarditis, and progressive regurgitation occur rarely.
  • When ischemic heart disease is the mechanism for regurgitation, the extent of anatomic disease and left ventricular performance are prognostic determinants. Complicating events include sudden death and myocardial infarction.

Sex

  • In those younger than 20 years, males are affected more often than females.
  • In those older than 20 years, no sexual predilection exists.
  • Males older than 50 years are affected more severely.

Age

Of those cases caused by prior rheumatic disease, the mean age is 36, plus or minus 6 years.

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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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