Atrioventricular Node Reentry Supraventricular Tachycardia Medication

  • Author: Glenn T Wetzel, MD, PhD; Chief Editor: Stuart Berger, MD   more...
 
Updated: Apr 12, 2012
 

Medication Summary

Emergency treatment in the patient with hemodynamic instability is directed at immediate cardioversion. If the patient is stable, the goal is to convert the rhythm to sinus through a brief episode of AV block. Adenosine is the drug of choice for short-term termination of AVNRT. Esmolol, other beta-adrenergic blockers, verapamil, and digoxin also have been used with some success.

Drugs used for long-term therapy that have some effect in AV node reentrant tachycardia include digoxin, beta-blockers, and verapamil.[10] Avoid intravenous verapamil use in infants because of its negative inotropic effects and avoid its use in combination with beta-blockers.

Digoxin, in particular, has been used in cases of fetal supraventricular tachycardia (SVT) and atrial flutter (AF). However, it is sometimes ineffective especially in cases of fetal hydrops. One retrospective review of pregnancies with fetal tachycardia at one center found sotalol, alone or combined with digoxin, to be an effective alternative treatment for fetal SVT and AF.[11]

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Antiarrhythmic agents

Class Summary

These agents alter the electrophysiologic mechanisms responsible for arrhythmia.

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Adenosine (Adenocard)

 

Slows conduction time through AV node. Can interrupt reentry pathways through AV node and restore normal sinus rhythm in PSVT.

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Esmolol (Brevibloc)

 

Excellent drug for use in patients at risk for experiencing complications from beta-blockade; particularly those with reactive airway disease, mild-to-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.

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Digoxin (Lanoxin, Lanoxicaps)

 

Cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system. Acts directly on cardiac muscle, increasing myocardial systolic contractions. Its indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.

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Propranolol (Inderal)

 

Class II antiarrhythmic nonselective beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions.

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Atenolol (Tenormin)

 

Selectively blocks beta1-receptors with little or no effect on beta2 types. The advantage is the requirement of administration only twice per day in young infants. Causes less central nervous system effects than propranolol, because atenolol doesn't cross the blood brain barrier.

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Verapamil (Calan)

 

Acts on the slow calcium current in SA and AV nodal cells. Decreases the rate of phase 4 automaticity and phase 0 depolarization, prolonging refractoriness and conduction time. Interrupts AVNRT by slowing down the AV node.

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Contributor Information and Disclosures
Author

Glenn T Wetzel, MD, PhD  Professor of Pediatrics, University of Tennessee College of Medicine; Director, Pediatric Arrhythmia Service, Le Bonheur Children's Medical Center

Glenn T Wetzel, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Heart Association, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Coauthor(s)

Ryan Jones, MD  Fellow, Division of Pediatric Cardiology, Department of Pediatrics, University of Tennessee Health Science Center, Memphis

Ryan Jones, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Cardiology

Disclosure: Nothing to disclose.

Specialty Editor Board

Charles I Berul, MD  Professor of Pediatrics and Integrative Systems Biology, George Washington University School of Medicine; Chief, Division of Cardiology, Children's National Medical Center

Charles I Berul, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, Pediatric and Congenital Electrophysiology Society, and Society for Pediatric Research

Disclosure: Johnson & Johnson Consulting fee Consulting

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Hugh D Allen, MD  Professor, Department of Pediatrics, Division of Pediatric Cardiology and Department of Internal Medicine, Ohio State University College of Medicine

Hugh D Allen, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, American Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography, and Western Society for Pediatric Research

Disclosure: Nothing to disclose.

Gilbert Z Herzberg, MD  Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center

Gilbert Z Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD  Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin

Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Robert Hamilton, MD, and Rejane Dillenburg, MD, to the development and writing of this article.

References

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The patient's heart rate is approximately 146 beats per minute with a normal axis. Note the pseudo S waves in leads II, III, and aVF. Also note the pseudo R' waves in V1 and aVR. These deflections represent retrograde atrial activation.
 
 
 
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