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Pediatric Atrial Flutter Medication

  • Author: M Silvana Horenstein, MD; Chief Editor: Steven R Neish, MD, SM  more...
 
Updated: Feb 11, 2014
 

Medication Summary

Drug therapy of atrial flutter in children can be classified under the 3 broad headings of ventricular rate control, acute conversion, and chronic suppression.

Digoxin is relatively safe for preventing rapid conduction of atrial flutter via the atrioventricular (AV) node to the ventricles, and some evidence indicates that this reduces symptomatology during flutter. Nevertheless, digoxin is unlikely to be particularly effective in the acute conversion or prevention of atrial flutter recurrence. It is devoid of negative inotropic effects (as is amiodarone) and is useful to control ventricular rate when using propafenone, flecainide, or procainamide.

Intravenous procainamide has been used with variable success to effect acute conversion of atrial flutter to sinus rhythm. Procainamide infusion should be preceded by digitalization to prevent procainamide-induced acceleration of AV node conduction to the ventricles.

The Vaughan Williams class III agents ibutilide and dofetilide may be used for acute conversion of atrial flutter and fibrillation. Both are more effective than other medications in converting atrial flutter, but their use is associated with QT prolongation with a nontrivial risk of induction of torsade de pointes polymorphic ventricular tachycardia. Clinical experience in adults is limited, and efficacy, dosing, and safety in children have not been established.

A more recent drug, dronedarone, a less-lipophilic amiodarone analog, has been shown to prevent recurrence of atrial flutter and atrial fibrillation in adult patients, according to several multicenter trials. However, it increases mortality in patients with decompensated heart failure and therefore should be avoided in such cases.[16] Safety and efficacy of this drug have not been confirmed in patients younger than 18 years.

Fetal atrial flutter is the second most common intrauterine tachyarrhythmia. Treatment is aimed at controlling ventricular rate and, thus, avoiding hydrops fetalis. First-line treatment is digoxin administered to the mother, which provides a conversion rate to sinus rhythm of 45-52%. In addition, its positive inotropic effect may be beneficial.

Sotalol has also been used in numerous cases with success. Maternal drug levels were not reliable predictors of successful therapy.[17, 18] Flecainide alone or in combination with digoxin is used as second-line treatment. Fetal atrial flutter in a structurally normal heart seldom recurs after conversion before or after birth, and postnatal suppressive antiarrhythmic therapy may not be necessary.

Flutter in patients with repaired or palliated structural congenital lesions is more likely to recur, and long-term antiarrhythmic therapy aimed at flutter suppression is often instituted after the first or the second flutter episode.

Vaughan Williams class IC (eg, flecainide, propafenone) or class III (eg, sotalol, amiodarone) agents have been prescribed with variable success. Some authors have cautioned against use of flecainide in this setting, but the data are equivocal. Combinations of agents occasionally succeed after failure of single-agent therapy.

Use of antiarrhythmic agents other than digoxin for the long-term suppression of atrial flutter in sinus node disease (a frequent coexisting finding) is particularly controversial. In patients with atrial flutter who have had the Mustard procedure, treatment with quinidine was associated with case reports of sudden death. This resulted in the recommendation of antibradycardia pacing initiation before antiarrhythmic drug therapy in these patients. This recommendation has gradually broadened to encompass other antiarrhythmic agents in patients with other types of repaired congenital heart disease.

Diltiazem can provide rapid, consistent, and safe temporary ventricular rate control in children.

Antibradycardia pacing may be directly advantageous in flutter suppression by reducing the frequency of flutter-inducing pauses and premature beats. It also provides a safety factor for more aggressive antiflutter drug therapy.

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Antiarrhythmic agents

Class Summary

These agents alter the electrophysiologic mechanisms responsible for arrhythmia.

Digoxin (Lanoxin)

 

Digoxin is a cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system. It 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.

Procainamide

 

Procainamide is a class IA antiarrhythmic used for premature ventricular contractions (PVCs). It increases the refractory period of the atria and ventricles. Myocardiac excitability is reduced by increase in threshold for excitation and inhibition of ectopic pacemaker activity.

Propafenone (Rythmol, Rythmol SR)

 

Propafenone treats life-threatening arrhythmias. It may work by reducing spontaneous automaticity and prolonging the refractory period.

Amiodarone (Cordarone, Pacerone)

 

Amiodarone may inhibit AV conduction and sinus node function. It prolongs the action potential and refractory period in myocardium and inhibits adrenergic stimulation. Before administration, control ventricular rate and congestive heart failure (if present) with digoxin.

Diltiazem (Cardizem, Tiazac, Dilacor XR)

 

Diltiazem is an AV nodal blocking agent. It is administered IV temporarily (ie, < 24 h) until definitive treatment can be initiated.

Flecainide (Tambocor)

 

This agent treats life-threatening ventricular arrhythmias. It causes a prolongation of refractory periods and decreases action potential without affecting duration. Flecainide blocks sodium channels, producing a dose-related decrease in intracardiac conduction in all parts of the heart with greatest effect on the His-Purkinje system (H-V conduction). Effects on AV nodal conduction time and intra-atrial conduction times, although present, are less pronounced than on ventricular conduction velocity.

Sotalol (Betapace, Betapace AF, Sorine)

 

Sotalol is a class III antiarrhythmic agent that blocks potassium channels, prolongs action potential duration, and lengthens the QT interval. It is a non–cardiac selective beta-adrenergic blocker.

Ibutilide (Corvert)

 

This newer class III antiarrhythmic agent may work by increasing action potential duration, thereby changing atrial cycle length variability. Mean time to conversion is 30 minutes. Two-thirds of patients who convert are in sinus rhythm at 24 hours. Ventricular arrhythmias may occur, mostly PVCs; torsade de pointes is a rare complication.

Dofetilide (Tikosyn)

 

Recently approved by FDA for maintenance of sinus rhythm, dofetilide increases monophasic action potential duration, primarily because of delayed repolarization. It terminates induced reentrant tachyarrhythmias (eg, atrial fibrillation/flutter, ventricular tachycardia) and prevents their reinduction. It does not affect cardiac output, cardiac index, stroke volume index, or systemic vascular resistance in patients with ventricular tachycardia, mild-to-moderate CHF, angina, and either normal or reduced LVEF. There is no evidence of a negative inotropic effect.

Dronedarone (Multaq)

 

Dronedarone is a benzofuran derivative indicated to reduce the risk of cardiovascular hospitalization in patients with paroxysmal or persistent atrial fibrillation (AF) or atrial flutter (AFL), with a recent episode of AF/AFL. It is not effective in patients with permanent atrial fibrillation. It may cause bradycardia and QT prolongation. Dronedarone is contraindicated in patients with NYHA class IV heart failure or NYHA class II and class III heart failure who had a recent decompensation. Safety and efficacy of this drug have not been confirmed in patients younger than 18 years.

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Contributor Information and Disclosures
Author

M Silvana Horenstein, MD Assistant Professor, Department of Pediatrics, University of Texas Medical School at Houston; Medical Doctor Consultant, Legacy Department, Best Doctors, Inc

M Silvana Horenstein, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Robert Murray Hamilton, MD, MSc, FRCPC Electrophysiologist, Senior Associate Scientist, Physiology and Experimental Medicine, Labatt Family Heart Centre; Professor, Department of Pediatrics, University of Toronto Faculty of Medicine

Robert Murray Hamilton, MD, MSc, FRCPC is a member of the following medical societies: American Heart Association, Canadian Medical Association, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada, Canadian Medical Protective Association, Heart Rhythm Society, Canadian Cardiovascular Society, Cardiac Electrophysiology Society, Pediatric and Congenital Electrophysiology Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Steven R Neish, MD, SM Director of Pediatric Cardiology Fellowship Program, Associate Professor, Department of Pediatrics, Baylor College of Medicine

Steven R Neish, MD, SM is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association

Disclosure: Nothing to disclose.

Acknowledgements

Alvin J Chin, MD Professor of Pediatrics, University of Pennsylvania School of Medicine; Attending Physician, Cardiology Division, Children's Hospital of Philadelphia

Alvin J Chin, MD, is a member of the following medical societies: American Association for the Advancement of Science, American Heart Association, and Society for Developmental Biology

Disclosure: Nothing to disclose.

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.

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Rhythm strip depicting lead II of a patient with atrial flutter with an atrial rate of 300 beats per minute (bpm). Atrioventricular conduction rate is variable at 2:1 and 3:1. Therefore, the ventricular rate ranges from 100-150 bpm.
 
 
 
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