eMedicine Specialties > Emergency Medicine > Cardiovascular

Mitral Regurgitation: Treatment & Medication

Author: Daniel DiSandro, MD, Clinical Assistant Professor, Department of Emergency Medicine, Drexel University
Contributor Information and Disclosures

Updated: Jun 8, 2009

Treatment

Emergency Department Care

  • Acute mitral regurgitation is a specific case in which immediate intervention in the ED can make a difference.
    • If the etiology is myocardial infarction, infusion of thrombolytics may reestablish the blood flow to the papillary muscle, possibly restoring function.
    • The mainstay of medical treatment in most other cases of mitral regurgitation is afterload reduction.
    • Afterload reduction decreases the impedance to left ventricular ejection and, as a result, decreases the regurgitant volume.
    • The treatment of pulmonary edema should include oxygen, diuretics, nitrates, and early intubation if respiratory failure results.
    • These individuals can benefit from afterload reduction with nitroprusside, even in the setting of a normal blood pressure.
    • Do not attempt to alleviate tachycardia with beta-blockers. Mild-to-moderate tachycardia is beneficial in these patients because it allows less time for the heart to have backfill, which lowers regurgitant volume.
    • Rapid atrial fibrillation secondary to chronic mitral regurgitation should be controlled with digoxin or diltiazem.
    • The physician should consider cardioversion in refractory or unstable patients. If cardioversion is effective, however, the restored sinus rhythm usually is transient due to the left atrium being severely dilated.

For more information, see the American College of Cardiology/American Heart Association guidelines for the management of patients with valvular heart disease.1

Consultations

  • In the setting of acute regurgitation secondary to an acute myocardial infarction, a cardiologist should be involved early. Echocardiography is necessary in order to look for papillary muscle rupture. Interventional cardiology for emergency angioplasty, as an alternative to thrombolysis, should be obtained as per protocol in institutions with such capability.
  • For highly suspicious cases, a cardiothoracic surgeon should be notified as soon as possible, even before echocardiography is performed. This will allow the surgical team to mobilize.

Medication

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

Diuretics

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.

Adult

1 mg/kg PO/IV; range of 20-120 mg

Pediatric

2 mg/kg PO/IV

Metformin decreases furosemide concentrations; furosemide interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides and furosemide; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently; increased plasma lithium levels and toxicity are possible when taken concurrently

Documented hypersensitivity; hepatic coma; anuria; severe electrolyte depletion

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus

Precautions

Perform frequent serum electrolyte, CO2, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter

Nitrates

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


Nitroglycerin (Nitro-Bid)

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

Adult

0.4 mg SL
Spray: 1-2 sprays per dose
Paste: 1-2 inches of paste q8h
50 mg in 250 mL D5W IV; start at 5 mcg/min and titrate until desired effect; not to exceed 200 mcg/min; watch for hypotension

Pediatric

Not established

Aspirin may increase nitrate serum concentrations; marked symptomatic orthostatic hypotension may occur with coadministration of calcium channel blockers (dose adjustment of either agent may be necessary)

Documented hypersensitivity; severe anemia; shock; postural hypotension; head trauma; closed-angle glaucoma; cerebral hemorrhage

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in coronary artery disease and low systolic 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.

Adult

50 mg in 250 mL D5W IV; start at 3 mcg/kg/min up to 10 mcg/kg/min

Pediatric

Not established

Documented hypersensitivity; idiopathic hypertrophic subaortic stenosis; atrial fibrillation or flutter

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in increased intracranial pressure, hepatic failure, severe renal impairment, and hypothyroidism; in renal or hepatic insufficiency, nitroprusside levels may increase and can cause cyanide toxicity; sodium nitroprusside has the ability to lower blood pressure and should be used only in patients with mean arterial pressures >70 mm Hg

Anti-arrhythmics

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.

Adult

0.25 IV q6h up to 1 mg loading dose followed by a maintenance dose of 0.125-0.25 mg PO/IV qd

Pediatric

Digitalization must be individualized

Medications that may increase digoxin levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, oral amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil
Medications that may decrease serum digoxin levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid

Documented hypersensitivity; beriberi; heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; carotid sinus syndrome

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus

Precautions

Hypokalemia may reduce positive inotropic effect of digitalis; IV calcium may produce arrhythmias in digitalized patients; hypercalcemia predisposes patient to digitalis toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are normal; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients diagnosed with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis


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.

Adult

Bolus 0.25 mg/kg up to 20 mg IV over 2 min
Rebolus with 25 mg or 0.35 mg/kg prn, then start infusion of 5-15 mg/h

Pediatric

Not established

May increase carbamazepine, digoxin, cyclosporine, and theophylline levels; when administered with amiodarone, may cause bradycardia and a decrease in cardiac output; when given with beta-blockers, may increase cardiac depression; cimetidine may increase diltiazem levels

Documented hypersensitivity; severe CHF; sick sinus syndrome; second- or third-degree AV block; hypotension (<90 mm Hg systolic)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in impaired renal or hepatic function; may increase LFT levels, and hepatic injury may occur

More on Mitral Regurgitation

Overview: Mitral Regurgitation
Differential Diagnoses & Workup: Mitral Regurgitation
Treatment & Medication: Mitral Regurgitation
Follow-up: Mitral Regurgitation
Multimedia: Mitral Regurgitation
References
[ CLOSE WINDOW ]

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].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

mitral regurgitation, mitral valve prolapse, MVP, MVP syndrome, acute mitral regurgitation, chronic compensated mitral regurgitation, chronic decompensated mitral regurgitation, myocardial infarction, rheumatic heart disease, acute pulmonary edema, dyspnea, left ventricular hypertrophy, increased left atrial pressure, pulmonary congestion, acquired mitral valve disease, coronary artery disease, CAD, orthostatic hypotension, left ventricular failure

[ CLOSE WINDOW ]

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.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

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.

CME Editor

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, Assistant Professor, Department of Medicine, Division of Emergency Medicine, Harvard Medical School; Associate-Chief, Attending Physician, 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: Schering  Honoraria Speaking and teaching

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.