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Atrial Flutter Medication

  • Author: Lawrence Rosenthal, MD, PhD, FACC, FHRS; Chief Editor: Jeffrey N Rottman, MD  more...
 
Updated: Dec 30, 2015
 

Medication Summary

Medications are usually administered in the acute setting or to patients who are not candidates for radiofrequency ablation (RFA). Agents can be used to control the ventricular rate, terminate acute episodes, prevent or decrease the frequency or duration of recurrent episodes, and prevent complications.

Drug initiation in an outpatient setting is generally accepted in patients without underlying structural heart disease who are in sinus rhythm. In addition, many specialists initiate outpatient drug therapy in patients with therapeutically anticoagulated atrial flutter who are awaiting outpatient electrical cardioversion in the near future.

Certain medications, such as sotalol and dofetilide, should be initiated in an inpatient setting because they can prolong the QT interval and be proarrhythmic. Regardless, close patient follow-up is mandated, with frequent electrocardiographic (ECG) or transtelephonic monitoring for potential signs of proarrhythmia.

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Antidysrhythmics, Class IC

Class Summary

Class IC antidysrhythmics are indicated for use in patients with atrial flutter and supraventricular tachycardia (SVT) without structural heart disease. Because conversion to atrial flutter with 1:1 conduction (producing fast ventricular rates) may occur with these agents, they are used in conjunction with atrioventricular (AV) nodal blocking agents in these cases.

Propafenone (Rythmol)

 

Propafenone treats life-threatening arrhythmias. It possibly works by reducing spontaneous automaticity and prolonging the effective refractory period. It is indicated for patients with atrial flutter and SVT without structural heart disease. Propafenone is used in conjunction with AV nodal blocking agents when administered to patients in atrial fibrillation because conversion to atrial flutter with 1:1 conduction (producing fast ventricular rates) is noted.

Flecainide (Tambocor)

 

Flecainide treats life-threatening ventricular arrhythmias. It causes prolongation of refractory periods and decreases action potential without affecting duration. This agent 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.

Effects on AV nodal conduction time and intra-atrial conduction times, though present, are less pronounced than those on ventricular conduction velocity. Flecainide is used in conjunction with AV nodal blocking agents when administered to patients in atrial fibrillation because conversion to atrial flutter with 1:1 conduction (producing fast ventricular rates) is noted.

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Antidysrhythmics, Class III

Class Summary

Class III antidysrhythmics are used to slow ventricular response by inhibiting AV nodal conduction during atrial fibrillation or flutter. They are also indicated for use in conjunction with class IA and IC antiarrhythmics, which slow atrial fibrillation or flutter rate and may cause more rapid ventricular response.

Beta blockers currently play more of a secondary role in rate control in atrial flutter or fibrillation. Patients receiving these agents require careful monitoring of blood pressure.

Amiodarone (Cordarone, Parcerone, Nexterone)

 

Amiodarone may inhibit AV conduction and sinus node function. It prolongs the action potential and refractory period in myocardium and inhibits adrenergic stimulation. It blocks sodium channels with high affinity for inactive channels, blocks potassium channels, and weakly blocks calcium channels. In addition, amiodarone noncompetitively blocks alpha- and beta-adrenergic receptors. Before administration, control ventricular rate and heart failure (if present) with digoxin or calcium channel blockers.

Dronedarone (Multaq)

 

Dronedarone blocks sodium channels, blocks beta1-adrenergic receptors, and alters adenyl cyclase generation (ie, it has negative inotropic effects). It blocks potassium channels (eg, hERG) and therefore prolongs cardiac repolarization.

Dronedarone is indicated for reducing the risk of cardiovascular hospitalization in patients with paroxysmal atrial fibrillation or atrial flutter who have had a recent episode of either arrhythmia, are in sinus rhythm or will be cardioverted, and have associated cardiovascular risk factors.

Sotalol (Betapace, Betapace AF, Sorine)

 

This class III antiarrhythmic agent blocks potassium channels, prolongs action potential duration, and lengthens the QT interval. It is a non–cardiac-selective beta-adrenergic blocker. Sotalol is be effective in the maintenance of sinus rhythm, even in patients with underlying structural heart disease. Class III effects are seen only at oral dosages of 160 mg/day or higher.

Ibutilide (Corvert)

 

Ibutilide is a newer class III antiarrhythmic agent that may work by increasing action potential duration and thereby changing atrial cycle length variability. It is indicated for acute termination of atrial fibrillation or flutter of recent onset. Potentially fatal arrhythmias can occur with ibutilide, usually in association with QT prolongation, during or within a number of hours after its administration.

Dofetilide (Tikosyn)

 

Dofetilide is the prototype of a "pure" class III agent. It has been approved by the US Food and Drug Administration (FDA) for maintenance of sinus rhythm after conversion from atrial fibrillation or atrial flutter lasting longer than 1 week. It is also indicated for conversion of atrial fibrillation and atrial flutter to normal sinus rhythm. If patients do not convert within 24 hours of initiation of therapy, electrical cardioversion should be considered.

Torsades de pointes is the only complicating arrhythmia showing a dose-response relation. The prevalence with supraventricular arrhythmia is 0.8%. The majority of torsades de pointes episodes occur within the first 3 days of therapy.

Dofetilide has no effect on cardiac output, cardiac index, stroke volume index, or systemic vascular resistance in patients with ventricular tachycardia, mild to moderate heart failure, angina, and either normal or reduced left ventricular ejection fraction (LVEF). It does not affect blood pressure.

Dofetilide blocks delayed rectifier current (IKr) and prolongs action potential duration; indeed, even at higher dosages, it has no effect on other depolarizing potassium currents (IKs and Ik1). It terminates induced reentrant tachyarrhythmias (atrial fibrillation or flutter and ventricular tachycardia) and prevents their reinduction. At clinically prescribed concentrations, it has no effect on sodium channels, which are associated with class I effects. Furthermore, no effect is noted on alpha- or beta-adrenergic receptors.

Dofetilide must be initiated with continuous ECG monitoring, and monitoring must be continued for at least 12 hours after conversion. The dosage must be individualized according to creatinine clearance (CrCl) and QTc (use the QT interval if the heart rate is below 60 beats/min). There is no information on use of this drug for heart rates lower than 50 beats/min.

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Antidysrhythmics, Class IV

Class Summary

Class IV antiarrhythmic drugs are used as rate control agents. They affect calcium channels by inhibiting calcium ions from entering areas of the vascular smooth muscle and myocardium during depolarization. These agents also slow automaticity and conduction of the AV node.

Diltiazem (Cardizem, Cardizem CD, Cardizem LA, Cartia XT)

 

Diltiazem is a nondihydropyridine calcium channel blocker that produces relaxation of coronary vascular smooth muscle and coronary vasodilation by inhibiting calcium ions from entering the "slow channels" and myocardium during depolarization. Intravenous (IV) diltiazem is indicated for control of rapid ventricular rate in patients with atrial fibrillation or atrial flutter.

Verapamil (Calan, Isoptin, Verelan)

 

During depolarization, verapamil inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium. It can diminish premature ventricular contractions (PVCs) associated with perfusion therapy and decrease the risk of ventricular fibrillation and ventricular tachycardia. By interrupting reentry at the AV node, it can restore normal sinus rhythm in patients with paroxysmal SVT.

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Antidysrhythmics, Class V

Class Summary

Cardiac glycosides decrease AV nodal conduction primarily by increasing vagal tone. They are used mainly in the context of atrial fibrillation and atrial flutter with congestive heart failure.

Digoxin (Lanoxin)

 

Digitalis slows sinus node and AV node conduction via a vagomimetic effect and is not very effective if sympathetic tone is increased. It has direct inotropic effects in addition to indirect effects on the cardiovascular system.

The effects on myocardium involve both direct action on cardiac muscle that increases myocardial systolic contractions and indirect actions that result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure. This agent is generally not recommended unless depressed left ventricular function is present.

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Anticoagulants, Cardiovascular

Class Summary

Anticoagulants are used to prevent thromboembolic complications.

Heparin

 

Heparin augments the activity of antithrombin III and prevents conversion of fibrinogen to fibrin. It does not actively lyse clots but can inhibit further thrombogenesis and prevent reaccumulation of clot after spontaneous fibrinolysis. Most data are related to use of unfractionated heparin (UFH). Low-molecular-weight heparin (LMWH) is probably as effective, but results from clinical studies are not yet available.

Warfarin (Coumadin, Jantoven)

 

Warfarin interferes with hepatic synthesis of vitamin K–dependent coagulation factors. It is used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. Tailor the dose to maintain an international normalized ratio (INR) of 2-3.

Dabigatran (Pradaxa)

 

Dabigatran is a direct thrombin inhibitor that has been approved by the FDA for the prevention of stroke and systemic embolism in patients with nonvalvular atrial fibrillation. The oral adult dose is 150 mg twice daily.

The American Heart Association (AHA) recommends dabigatran as a reasonable alternative to warfarin in patients who have 1 or more additional risk factors for stroke and a creatinine clearance greater than 30 mL/min. The American College of Chest Physicians (ACCP) recommends dabigatran over warfarin for primary and secondary prevention of cardioembolic stroke or transient ischemic attack.

Dabigatran is a prodrug that is converted to the active drug in vivo. It inhibits both free and fibrin-bound thrombin; it also inhibits coagulation by preventing thrombin-mediated effects. Dabigatran is not recommended for patients with a prosthetic heart valve or hemodynamically significant valve disease, severe renal failure (CrCl < 15 mL/min), or advanced liver disease.

Rivaroxaban (Xarelto)

 

Rivaroxaban is a direct factor Xa inhibitor approved by the FDA for the prevention of stroke and systemic embolism in patients with nonvalvular atrial fibrillation. Multiple strengths are available: 10 mg, 15 mg, and 20 mg. Dosing and administration depend on the indication and the presence and degree of renal impairment. The 15-mg and 20-mg tablets can be crushed and administered via a nasogastric or gastrostomy tube (the 10-mg tablet cannot be crushed).

Rivaroxaban should be discontinued 24 hours before a scheduled surgical procedure, to reduce the risk of bleeding. Contraindications include active bleeding and hypersensitivity to rivaroxaban. It is a pregnancy category C drug.

Apixaban (Eliquis)

 

Apixaban is a direct factor Xa inhibitor approved by the FDA in 2012 for the prevention of stroke and systemic embolism in patients with nonvalvular atrial fibrillation. The standard dose is 5 mg twice daily. Use 2.5 mg twice daily if any 2 of the following conditions are met:

*Age >80 years

*Serum creatinine level >1.5 mg/dL

*Weight < 60 kg

Apixaban is not recommended for use in patients with any of the following:

*CrCl < 15 mL/min or dialysis

*Prosthetic heart valve

*Severe hepatic impairment

Apixaban is contraindicated in patients with active bleeding or hypersensitivity to apixaban. It should be discontinued at least 48 hours before elective surgical procedures or invasive procedures with a moderate or high risk of unacceptable or clinically significant bleeding and at least 24 hours before elective surgical procedures or invasive procedures with a low risk of bleeding or in which the bleeding would be noncritical in location and easily controlled.

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Beta-Blockers, Beta-1 Selective

Class Summary

These agents are used to slow ventricular response by slowing AV nodal conduction during atrial fibrillation or flutter. They are also indicated for use in conjunction with class IA and IC antiarrhythmics, which slow atrial fibrillation or flutter rate and may cause more rapid ventricular response.

Beta blockers currently play more of a secondary role in rate control in atrial flutter and fibrillation. Patients receiving these agents require careful monitoring of blood pressure.

Metoprolol (Lopressor, Toprol XL)

 

Metoprolol is a selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor blood pressure, heart rate, and ECG.

Atenolol (Tenormin)

 

Atenolol selectively blocks beta1 receptors, with little or no effect on beta2 receptors.

Esmolol (Brevibloc)

 

Esmolol (Brevibloc)

Esmolol is excellent 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. Its short half-life of 8 min allows titration to desired effect and quick discontinuation if necessary.

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Contributor Information and Disclosures
Author

Lawrence Rosenthal, MD, PhD, FACC, FHRS Associate Professor of Medicine, Director, Section of Cardiac Pacing and Electrophysiology, Director of EP Fellowship Program, Division of Cardiovascular Disease, University of Massachusetts Memorial Medical Center

Lawrence Rosenthal, MD, PhD, FACC, FHRS is a member of the following medical societies: American College of Cardiology, Massachusetts Medical Society, American Heart Association

Disclosure: Nothing to disclose.

Coauthor(s)

Cynthia Anne Ennis, DO Assistant Professor, University of Massachusetts Medical Center

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

Acknowledgements

Brian Olshansky, MD Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, and Heart Rhythm Society

Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting

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

Disclosure: Medscape Salary Employment

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Anatomy of classic counterclockwise atrial flutter. This demonstrates oblique view of right atrium and shows some crucial structures. Isthmus of tissue responsible for atrial flutter is seen anterior to coronary sinus orifice. Eustachian ridge is part of crista terminalis that separates roughened part of right atrium from smooth septal part of right atrium.
Type I counterclockwise atrial flutter. This 3-dimensional electroanatomic map of tricuspid valve and right atrium shows activation pattern displayed in color format. Red is early and blue is late, relative to fixed point in time. Activation travels in counterclockwise direction.
12-Lead ECG of type I atrial flutter. Note negative sawtooth pattern of flutter waves in leads II, III, and aVF.
Atypical left atrial flutter.
3-Dimensional electroanatomic map of type I atrial flutter. Colors progress from blue to red to white and represent relative conduction time in right atrium (early to late). Ablation line (red dots) has been created on tricuspid ridge extending to inferior vena cava. This interrupts flutter circuit. RAA = right atrial appendage; CSO = coronary sinus os; IVC = inferior vena cava; TV = tricuspid valve annulus.
Type I atrial flutter unmasked by adenosine (Adenocard).
 
 
 
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