Atrial Tachycardia Medication
- Author: Adam S Budzikowski, MD, PhD, FHRS; Chief Editor: Jeffrey N Rottman, MD more...
The goals of pharmacotherapy are to reduce morbidity and to prevent recurrences and complications. Consider using antiarrhythmic agents 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.
Calcium channel blockers are especially effective in atrial tachycardia with triggered activity as the underlying mechanism. Beta-blockers can reduce the frequency and severity of atrial tachycardia episodes by controlling ventricular response.
Beta Blockers, Intrinsic Sympathomimetic
Beta-blockers are effective for reducing the frequency and severity of episodes via control of the ventricular response during tachycardia and by reduction of frequency in a subgroup of patients for whom tachycardia is sensitive to catecholamine. Beta-blockers that have intrinsic sympathomimetic activity are capable of demonstrating low-level agonist activity at a beta receptor while also acting as an antagonist.
Acebutolol is a selective, hydrophilic beta-blocking drug, as well as a class II antiarrhythmic agent with mild, intrinsic sympathomimetic activity. It has a labeled indication for the management of ventricular arrhythmias. Beta-blocker therapy should be tapered gradually rather than withdrawn abruptly, to avoid acute tachycardia, hypertension, and/or ischemia.
Beta-Blockers, Beta-1 Selective
Beta-blockers are effective for reducing the frequency and severity of episodes, via control of the ventricular response during tachycardia, and for reducing the frequency of episodes in a subgroup of patients whose tachycardia is sensitive to catecholamine. Beta-1 selective drugs are also known as cardioselective agents, because they act on beta-1 receptors on the myocardium.
Atenolol selectively blocks beta-1 receptors, with little or no effect on beta-2 receptors except at high doses. It has an off-label indication for supraventricular and ventricular arrhythmias. Beta-blocker therapy should be tapered gradually to avoid the acute tachycardia, hypertension, and/or ischemia that may occur with abrupt withdrawal.
Because of its brief duration of action (10-30 minutes), esmolol is an excellent drug for use in patients at risk of 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. It has a labeled indication for the treatment of supraventricular tachycardia (SVT). Beta-blocker therapy should be tapered gradually, to avoid the acute tachycardia, hypertension, and/or ischemia that may occur with abrupt withdrawal.
Metoprolol is a selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions. During IV administration, carefully monitor blood pressure, heart rate, and ECG. Metoprolol has an off-label indication for MAT. Beta-blocker therapy should be tapered gradually, to avoid the acute tachycardia, hypertension, and/or ischemia that may occur with abrupt withdrawal.
Beta Blockers, Nonselective
Beta-blockers reduce the frequency and severity of episodes via control of ventricular response during tachycardia and by reduction of frequency in a subgroup of patients in whom tachycardia is sensitive to catecholamine. Nonselective agents block beta-1 and beta-2 receptors.
Propranolol is a class II antiarrhythmic. It is a nonselective beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions. Do not administer an IV dose faster than 1 mg/min.
Many class III antidysrhythmic agents have been shown to be effective in maintaining sinus rhythm after conversion from atrial tachycardia.
Amiodarone has antiarrhythmic effects that overlap all 4 Vaughn-Williams antiarrhythmic classes. It may inhibit atrioventricular (AV) conduction and sinus node function. It prolongs action potential and the 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, this agent noncompetitively blocks alpha- and beta-adrenergic receptors.
Amiodarone has a labeled indication for the management of life-threatening recurrent ventricular fibrillation and hemodynamically-unstable ventricular tachycardia (VT) refractory to other antiarrhythmic agents. It is very effective in converting atrial fibrillation and flutter to sinus rhythm and in suppressing recurrence of these arrhythmias.
Amiodarone is the only agent proven to reduce the incidence and risk of cardiac sudden death, with or without obstruction to left ventricular outflow. With exception of disorders of prolonged repolarization (eg, long QT syndrome), amiodarone may be the drug of choice for life-threatening ventricular arrhythmias refractory to beta blockade and initial therapy with other agents.
Before administering amiodarone, control the ventricular rate and congestive heart failure (if present) with digoxin or calcium channel blockers. Most clinicians are comfortable with inpatient or outpatient loading with 400 mg orally 3 times a day for 1 week, because of low proarrhythmic effect, followed by weekly reductions with the goal of the lowest dose with the desired therapeutic benefit. During loading, patients must be monitored for bradyarrhythmias. With oral dosing, achieving efficacy may take weeks.
This class III antiarrhythmic agent blocks K+ channels, prolongs action potential duration, and lengthens the QT interval. It is a non–cardiac-selective beta-adrenergic blocker. Sotalol is effective in the maintenance of sinus rhythm, even in patients with underlying structural heart disease. Class III effects are seen only at oral doses of 160mg/day or higher.
Dofetilide is a class III antiarrhythmic 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.
Dofetilide blocks delayed rectifier current and prolongs action potential duration; indeed, even at higher doses it has no effect on other depolarizing potassium currents. It terminates induced reentrant tachyarrhythmias (atrial fibrillation/flutter and VT) 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 electrocardiographic (ECG) monitoring and monitoring must be continued for 6 doses of the medication. The dose must be individualized according to creatinine clearance (CrCl) and the corrected QT interval (QTc; use the QT interval if the heart rate is less than 60 bpm). There is no information on the use of this drug for heart rates below 50 bpm.
Ibutilide can terminate some atria tachycardias. Ibutilide works by increasing the action potential duration and, thereby, changing atrial cycle-length variability.
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.
Class Ia drugs, which are proarrhythmic, are effective only approximately 50% of the time. Therefore, the use of these agents is limited. In particular, quinidine has been replaced with more effective and safer antiarrhythmic agents and nonpharmacologic therapies.
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. Procainamide has a labeled indication for the treatment of life-threatening ventricular arrhythmias. It is indicated in recurrent VT not responsive to lidocaine, refractory SVT, refractory ventricular fibrillation, pulseless VT, and atrial fibrillation with rapid rate in Wolff-Parkinson-White syndrome.
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 blocks sodium channels, producing a dose-related decrease in intracardiac conduction in all parts of the heart. This agent increases electrical stimulation of the threshold of the ventricle and His-Purkinje system, and by shortening phase 2 and 3 repolarization, it decreases action potential duration and effective refractory periods.
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 VT). It is not recommended in less severe ventricular arrhythmias, even if patients are symptomatic.
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, and it may increase the diastolic excitability threshold and prolong the effective refractory period. Propafenone reduces spontaneous automaticity and depresses triggered activity.
This agent is indicated for the treatment of documented life-threatening ventricular arrhythmias (eg, sustained VT). 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.
Calcium Channel Blockers
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.
During depolarization, diltiazem inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium. Diltiazem injection has a labeled indication for the conversion of paroxysmal SVT and control of rapid ventricular rate in patients with atrial fibrillation and atrial flutter.
During depolarization, verapamil inhibits calcium ions from entering slow channels or voltage-sensitive areas of vascular smooth muscle and myocardium. It has a labeled indication for the treatment of ST.
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 diagnosing SVTs of unknown origin, in terminating SVTs that are dependent on the AV junction, and in some focal atrial tachycardias. If adenosine successfully terminates an atrial tachycardia, the patient may respond to beta-blockers or calcium channel blockers.
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. In a small number of patients with normal potassium levels, high-dose magnesium levels cause a significant decrease in the patient's heart rate and conversion to normal sinus rhythm.
Magnesium is the drug of choice for torsade de pointes and also may be useful for treating conventional VT, especially when hypomagnesemia is confirmed. When administering treatment with magnesium sulfate, monitor for hypermagnesemia because overdose can cause cardiorespiratory collapse and paralysis.
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.
To achieve a total digitalizing dose, initially administer 50% of the dose. Then administer the remaining two 25% portions at 6- to 12-hour intervals (ie, 1/2, 1/4, 1/4).
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.
Adenosine is a first-line medical treatment for termination of paroxysmal SVT. It is effective in terminating AV nodal reentrant tachycardia and AV reciprocating tachycardia. More than 90% of patients convert to sinus rhythm with adenosine 12 mg.
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