Atrial Tachycardia Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent recurrences and complications. Consider using antiarrhythmics when the arrhythmia is causing symptoms and does not respond to correction or treatment of underlying diseases. A calcium channel blocker or beta-blocker also may be required as well, in combination therapy.

Class Summary

Beta-blockers are effective for reducing frequency and severity of episodes via control of ventricular response during tachycardia and by reduction of frequency in a subgroup of patients for whom tachycardia is sensitive to catecholamine.

Acebutolol (Sectral)

Acebutolol is a selective, hydrophilic beta-blocking drug, as well as a class II antiarrhythmic agent with mild intrinsic sympathomimetic activity.

Atenolol (Tenormin)

Atenolol selectively blocks beta-1 receptors, with little or no effect on beta-2 receptors.

Esmolol (Brevibloc)

Esmolol is an excellent drug for use in patients at risk for experiencing complications from beta-blockade. It selectively blocks beta-1 receptors with little or no effect on beta-2 receptors. Esmolol is also classified as a class II antiarrhythmic agent.

Metoprolol (Lopressor)

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

Class Summary

Amiodarone and sotalol have been shown to be effective in maintaining sinus rhythm after converting from atrial tachycardia.

Amiodarone (Cordarone)

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

Sotalol (Betapace)

This is a non–cardiac-selective beta-adrenergic blocker that blocks potassium channels, prolongs the action potential duration, and lengthens the QT interval.

Dofetilide (Tikosyn)

Dofetilide can terminate some atrial tachycardias but it is effective for maintaining sinus rhythm after conversion to a normal sinus rhythm.

Ibutilide (Corvert)

Ibutilide can terminate some atria tachycardias. Ibutilide works by increasing the action potential duration and, thereby, changing atrial cycle-length variability.

Class Summary

These drugs have been tried in patients with refractory recurrent atrial tachycardia and disabling symptoms in whom beta-blockers or calcium channel blockers were unsuccessful. These drugs prolong the atrial refractoriness and slow the conduction velocity, thereby disrupting the reentrant circuit. They also suppress the atrial premature depolarizations that commonly initiate the tachycardia. These agents are proarrhythmic; use caution. The adverse effects of class IA drugs are significant. Therefore, the use of class IA drugs is limited. These drugs are effective only approximately 50% of the time.

Procainamide (Procanbid, Pronestyl)

Procainamide increases the refractory period of atria and ventricles. Myocardial excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity.

Quinidine

Quinidine depresses myocardial excitability and conduction velocity.

Class Summary

These agents have been used in patients with atrial tachycardia and disabling symptoms in whom beta-blockers or calcium channel blockers were unsuccessful. Recommended use is with a beta-blocker or calcium channel blocker.

Flecainide (Tambocor)

Flecainide blocks sodium channels, producing a dose-related decrease in intracardiac conduction in all parts of the heart. It increases electrical stimulation of the threshold of the ventricle and His-Purkinje system. It shortens phase 2 and 3 repolarization, resulting in decreased action potential duration and effective refractory period.

Flecainide is indicated for the treatment of paroxysmal atrial fibrillation/flutter associated with disabling symptoms and paroxysmal SVTs, including AV nodal reentrant tachycardia, AV reentrant tachycardia, and other SVTs of unspecified mechanism associated with disabling symptoms in patients without structural heart disease. It is also indicated for prevention of documented life-threatening ventricular arrhythmias (eg, sustained ventricular tachycardia). It is not recommended in less severe ventricular arrhythmias, even if patients are symptomatic.

Propafenone (Rythmol)

Propafenone shortens upstroke velocity (phase 0) of the monophasic action potential. It reduces fast inward current carried by sodium ions in Purkinje fibers and, to a lesser extent, myocardial fibers. It may increase the diastolic excitability threshold and prolong the effective refractory period. It reduces spontaneous automaticity and depresses triggered activity.

It is indicated for treatment of documented life-threatening ventricular arrhythmias (eg, sustained ventricular tachycardia). Propafenone appears to be effective in the treatment of SVTs, including atrial fibrillation and flutter. It is not recommended in patients with less severe ventricular arrhythmias, even if symptomatic.

Class Summary

Via specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. Calcium channel blockers inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity. They are especially effective in atrial tachycardia, with triggered activity as the underlying mechanism.

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

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

Verapamil (Calan, Calan SR, Covera HS, Verelan)

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

Class Summary

Digoxin and adenosine alter the electrophysiologic mechanisms responsible for arrhythmia.

Digitalis in toxic doses can cause atrial tachycardia. In therapeutic doses, digitalis may be useful in some focal atrial tachycardias. It should be considered if beta-blockers are contraindicated or if beta-blockers and calcium channel blockers are unsuccessful in controlling the arrhythmia medically.

Adenosine is an ultra–short-acting drug that is useful in SVTs of unknown origin both in making the diagnosis and in terminating those that are dependent on the AV junction and some focal atrial tachycardia. If adenosine successfully terminates an atrial tachycardia, those patients may respond to beta-blockers or calcium channel blockers.

Digoxin (Lanoxicaps, 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. It is used to control the ventricular rate when administering propafenone, flecainide, or procainamide.

Adenosine (Adenocard)

Adenosine is a short-acting agent that alters potassium conductance into cells and results in hyperpolarization of nodal cells. This increases the threshold to trigger an action potential and results in sinus slowing and blockage of AV conduction. As a result of its short half-life, adenosine is best administered in an antecubital vein as an IV bolus followed by rapid saline infusion.

Class Summary

Electrolyte replacement therapy involving magnesium is important because magnesium deficiency may lead to hypokalemia.

Magnesium sulfate

Magnesium is used for replacement therapy in magnesium deficiency, especially in acute hypomagnesemia accompanied by signs of tetany similar to those observed in hypocalcemia. When magnesium sulfate is administered to correct hypokalemia, most patients convert to normal sinus rhythm (NSR). In a small number of patients, high-dose magnesium levels cause a significant decrease in the patient's heart rate and conversion to normal sinus rhythm.