Atrial Flutter Medication

Medications are usually used in the acute setting or in patients who are not candidates for radiofrequency ablation. 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 as they can prolong the QT interval and be proarrhythmic. Regardless, close patient follow-up is mandated, with frequent ECG monitoring or transtelephonic monitoring for potential signs of proarrhythmia.

Class Summary

These agents are used to slow ventricular response by slowing atrioventricular (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/flutter rate and may cause more rapid ventricular response.

Beta-blockers currently have more of a secondary role in rate control in atrial flutter/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 beta-1 receptors with little or no effect on beta-2 receptors.

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.

Class Summary

These agents reduce the rate of AV nodal conduction and control ventricular response. Formulations administered IV are discussed only as they relate to the control of severe symptoms (eg, rapid ventricular rate in emergent situations). Only nondihydropyridine calcium channel blockers are effective for rate control.

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 risk of ventricular fibrillation and ventricular tachycardia. By interrupting re-entry at the AV node, it can restore normal sinus rhythm (NSR) in patients with paroxysmal supraventricular tachycardias.

Diltiazem (Cardizem, Dilacor XR, Diltzac, Matzim LA)

During depolarization, diltiazem inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.

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.

Digitalis, 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 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.

Class Summary

These agents are indicated for use in patients with atrial flutter and supraventricular tachycardia 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 AV nodal blocking agents in these cases.

Propafenone (Rythmol)

Propafenone treats life-threatening arrhythmias. It possibly works by reducing spontaneous automaticity and prolonging the refractory period. It is indicated for patients with atrial flutter and supraventricular tachycardia without structural heart disease. It 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 (HV conduction).

Effects on AV nodal conduction time and intra-atrial conduction times, although present, are less pronounced than on ventricular conduction velocity. It 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.

Class Summary

Class III drugs are used in maintenance of sinus rhythm in patients with atrial flutter. These agents establish a chemical conversion to sinus rhythm. In most patients, ablation is preferable to starting patients on long-term antiarrhythmics, owing to concerns about adverse effects.

Amiodarone (Cordarone, Parcerone)

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. Prior to administration, control ventricular rate and heart failure (if present) with digoxin or calcium channel blockers.

Sotalol (Betapace, Sorine)

This class III antiarrhythmic agent blocks K+ channels, prolongs action potential duration (APD), and lengthens the QT interval. It is a non–cardiac selective beta-adrenergic blocker. Sotalol is shown to be effective in the maintenance of sinus rhythm, even in patients with underlying structural heart disease.

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. Mean time to conversion is 30 min. Two thirds of patients who convert are in sinus rhythm at 24 h. Complications include ventricular arrhythmias, mostly PVCs, occurring in 9.6% of patients; and torsades de pointes, occurring in < 2%.

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 h of initiation of therapy, electrical cardioversion should be considered. This agent has not been effective for patients with paroxysmal atrial fibrillation.

Torsade de pointes is the only complicating arrhythmia showing dose-response relationship. The prevalence with supraventricular arrhythmia is 0.8%. Majority of torsade de pointes episodes occur within first 3 d 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 magnitudes, it has no effect upon other depolarizing potassium currents (IKs and IKl). It terminates induced re-entrant tachyarrhythmias (atrial fibrillation/flutter and ventricular tachycardia) and prevents their re-induction. 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 >12 h after conversion. Dose must be individualized according to creatinine clearance (CrCl) and QTc (use QT interval if heart rate < 60/min). There is no information on use of this drug for heart rates < 50/min.

Class Summary

Dronedarone is an antiarrhythmic agent with properties belonging to all 4 Vaughn-Williams antiarrhythmic classes.

Dronedarone (Multaq)

Dronedarone blocks sodium channels, blocks beta1-adrenergic receptors, and alters adenyl cyclase generation (ie, negative inotropic effects); it blocks potassium channels (eg, hERG) and therefore prolongs cardiac repolarization. It is indicated to reduce the risk for cardiovascular hospitalization in patients with paroxysmal atrial fibrillation or atrial flutter who have had a recent episode of either arrhythmia and have associated cardiovascular risk factors (ie, age >70 y, hypertension, diabetes, history of stroke, left atrial dimension (LAD) >50 mm or LVEF < 40%) who are in sinus rhythm or who will be cardioverted.

Class Summary

These agents are used to prevent thromboembolic complications.

Heparin

Heparin augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. It does not actively lyse clots but is able to inhibit further thrombogenesis. It prevents reaccumulation of clot after spontaneous fibrinolysis. Most data are related to use of unfractionated heparin. Low–molecular-weight heparin 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.

Class Summary

These agents are used for chemical conversion into sinus rhythm. They alter the electrophysiologic mechanisms responsible for arrhythmia.

Quinidine

Quinidine prolongs the effective refractory period and increases conduction time. It also has indirect anticholinergic effects, decreases vagal tone, and facilitates conduction in conversion of atrial fibrillation.

Procainamide

Procainamide is a class IA antiarrhythmic used for PVCs. It increases the refractory period of the atria and ventricles. Myocardial excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity.