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Mitral Stenosis in Emergency Medicine Medication

  • Author: Ethan S Brandler, MD, MPH; Chief Editor: Barry E Brenner, MD, PhD, FACEP  more...
 
Updated: Dec 28, 2015
 

Medication Summary

The goal of medical therapy is to control the rapid ventricular rate and to prevent thrombus formation and embolization. Conversion of atrial fibrillation to sinus rhythm may also decrease symptoms.

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Antiarrhythmics

Class Summary

These agents alter the electrophysiologic mechanisms that are responsible for arrhythmia.

Amiodarone (Cordarone)

 

Class III antiarrhythmic. Has antiarrhythmic effects that overlap all 4 Vaughn-Williams antiarrhythmic classes. May inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation. Only agent proven to reduce incidence and risk of cardiac sudden death, with or without obstruction to LV outflow. Very efficacious in converting atrial fibrillation and flutter to sinus rhythm and in suppressing recurrence of these arrhythmias.

Has low risk of proarrhythmia effects, and any proarrhythmic reactions generally are delayed. Used in patients with structural heart disease. Most clinicians are comfortable with inpatient or outpatient loading with 400 mg PO tid for 1 wk because of low proarrhythmic effect, followed by weekly reductions with goal of lowest dose with desired therapeutic benefit (usual maintenance dose for AF 200 mg/d). During loading, patients must be monitored for bradyarrhythmias. Prior to administration, control the ventricular rate and CHF (if present) with digoxin or calcium channel blockers.

Oral efficacy may take weeks. With exception of disorders of prolonged repolarization (eg, LQTS), may be DOC for life-threatening ventricular arrhythmias refractory to beta-blockade and initial therapy with other agents.

Esmolol (Brevibloc)

 

Ultra–short-acting that selectively blocks beta1-receptors with little or no effect on beta2-receptor types. Particularly useful in patients with elevated arterial pressure, especially if surgery is planned. Shown to reduce episodes of chest pain and clinical cardiac events compared with placebo. Can be discontinued abruptly if necessary.

May be used with class I antiarrhythmics if digoxin therapy does not abort atrial arrhythmia. Administer in patients needing prompt slowing of ventricular rate in response to atrial flutter or fibrillation and who are most likely to become hemodynamically unstable if left without treatment or in those waiting for the start of the therapeutic effects of digoxin (average, 10 h). Useful in patients at risk for experiencing complications from beta-blockade; particularly those with reactive airway disease, mild-moderate LV dysfunction, and/or peripheral vascular disease. Short half-life of 8 min allows for titration to desired effect and quick discontinuation if needed.

Digoxin (Lanoxin)

 

Cardiac glycoside that has direct inotropic effects in addition to indirect effects on the cardiovascular system. Effects on myocardium involve a direct action on the cardiac muscle that increases myocardial systolic contractions as well as indirect actions that result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.

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Beta-adrenergic Blockers

Class Summary

These drugs inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation.

Metoprolol (Lopressor)

 

Selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions. During IV administration, carefully monitor blood pressure, heart rate, and ECG.

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Calcium Channel Blockers

Class Summary

In specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. The calcium channel blockers inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity.

Diltiazem (Cardizem CD, Cardizem SR, Tiazac, Dilacor)

 

During the depolarization, 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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Anticoagulants

Class Summary

These agents inhibit thrombogenesis.

Heparin

 

Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis. Most data are related to use of unfractionated heparin. Low molecular weight heparin probably is as effective but awaits the results from clinical studies.

Warfarin (Coumadin)

 

Inhibits vitamin K–dependent clotting factors II, VII, IX, and X and anticoagulant proteins C and S. Anticoagulation effect occurs 24 h after drug administration, but peak effect may happen 72-96 h later. Antidotes are vitamin K and FFP.

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Contributor Information and Disclosures
Author

Ethan S Brandler, MD, MPH Clinical Assistant Professor, Attending Physician, Departments of Emergency Medicine and Internal Medicine, University Hospital of Brooklyn, Kings County Hospital

Ethan S Brandler, MD, MPH is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Eric M Suess, MD Clinical Assistant Instructor, Resident Physician, Department of Emergency Medicine, Kings County Hospital Center, State University of New York Downstate Medical Center

Eric M Suess, MD is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Paul Blackburn, DO, FACOEP, FACEP Attending Physician, Department of Emergency Medicine, Maricopa Medical Center

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

Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, Society for Academic Emergency Medicine, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians

Disclosure: Nothing to disclose.

Additional Contributors

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, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Drugs & Diseases gratefully acknowledge the contributions of previous authors, Yiju Teresa Liu, MD, and Richard H Sinert, DO, to the development and writing of this article.

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Mitral stenosis.
Echocardiography of mitral stenosis. Courtesy of Michael B. Stone, MD, RDMS.
 
 
 
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