Medication Summary
The mechanism of junctional ectopic tachycardia (JET) is not well understood, and identifying a specific pharmacologic agent to target the disorder is difficult. Because some experimental forms of junctional tachycardia exhibit a triggered mechanism induced by digoxin toxicity, avoiding digoxin seems reasonable. Nevertheless, digoxin is frequently used in the treatment of JET without apparent adverse effect but with questionable efficacy. Ventricular dysfunction is often prominent in patients with postoperative and congenital JET; thus, calcium channel blockers are usually avoided because of their negative inotropic effects. One case report has documented use of calcium channel blockers with apparent effectiveness. Drugs effective against automatic tachycardias appear to be effective in the treatment of congenital and postoperative JET.
Congenital JET has been successfully controlled with amiodarone, propafenone, or cautious combinations of both medications. Postoperative JET has been successfully controlled with amiodarone, propafenone, procainamide, or moricizine (discontinued from the market in July 2007). Propranolol or sotalol have also been used in the therapy of these rhythm disorders.
Antiarrhythmic agents
Class Summary
These agents alter the electrophysiologic mechanisms responsible for arrhythmia.
Amiodarone (Cordarone)
May inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation.
Before administration, control the ventricular rate and CHF (if present) with digoxin.
Propafenone (Rythmol)
Treats life-threatening arrhythmias. Possibly works by reducing spontaneous automaticity and prolonging refractory period.
Procainamide (Procan, Pronestyl)
Class IA antiarrhythmic used for PVCs, ventricular tachycardias, and supraventricular tachycardias. Increases refractory period of the atria and ventricles. Myocardiac excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity.
Propranolol (Inderal)
Class II antiarrhythmic nonselective beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions.
Sotalol (Betapace)
Class III antiarrhythmic agent, which blocks potassium channels, prolongs action potential duration (APD), and lengthens QT interval. Noncardiac selective beta-adrenergic blocker.
Atenolol (Tenormin)
Selectively blocks beta1-receptors with little or no effect on beta2 types.
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Lead II rhythm strip of a surface ECG from a patient with postoperative JET. Atrial activity (P) is marked with blue lines and ventricular depolarization (QRS) is marked in red. Note the narrow QRS complexes due to their origin at the AV junction. Also note the dissociation between atrial and ventricular depolarizations where some of the QRS complexes seem to "follow" the P waves. However, this is not possible because the PR intervals are exceedingly short to allow conduction. In addition, some of the P waves fall after the QRS.
