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INTRODUCTION

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Procainamide is an antiarrhythmic agent that is used intravenously and orally. However, an oral dosage form is no longer available in the United States. It is classified as a type IA antiarrhythmic agent and can be used for the treatment of supraventricular or ventricular arrhythmias.1,2 The intravenous form of procainamide is one of the drugs of choice for the treatment of hemodynamically stable monomorphic ventricular tachycardia in patients without a prolonged QT interval or heart failure.3 Given orally, procainamide can be used for long-term suppression of ventricular arrhythmias.4

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Procainamide can be administered orally for the long-term prevention of chronic supraventricular arrhythmias such as supraventricular tachycardia, atrial flutter, and atrial fibrillation.4 Ventricular rate control during atrial fibrillation can be accomplished using intravenous procainamide for hemodynamically stable patients with an accessory pathway.3,5 Procainamide is also one of the possible choices for the pharmacological cardioversion of atrial fibrillation.5

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Procainamide inhibits transmembrane sodium influx into the conduction system of the heart thereby decreasing conduction velocity.1,2 It also increases the duration of the action potential, increases threshold potential toward zero, and decreases the slope of phase 4 of the action potential. Automaticity is decreased during procainamide therapy. The net effect of these cellular changes is that procainamide causes increased refractoriness and decreased conduction in heart conduction tissue, which establishes a bidirectional block in reentrant pathways.

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N-acetyl procainamide (NAPA) is an active metabolite of procainamide that has type III antiarrhythmic effects.2 A common characteristic of type III antiarrhythmic agents (bretylium, amiodarone, sotalol) is prolongation of the duration of the action potential resulting in an increased absolute refractory period.

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THERAPEUTIC AND TOXIC CONCENTRATIONS

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When given intravenously, the serum procainamide concentration-time curve follows a two-compartment model (Figure 8-1).6 If an intravenous loading dose is followed by a continuous infusion, serum concentrations decline rapidly at first due to distribution of the loading dose from blood to tissues (Figure 8-2).6 When oral dosage forms are given, absorption occurs more slowly than distribution so a distribution phase is not seen (Figure 8-3).7,8,9,10, and 11

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FIGURE 8-1

Procainamide serum concentrations initially drop rapidly after an intravenous bolus as drug distributes from blood into the tissues during the distribution phase. During the distribution phase, drug leaves the blood due to tissue distribution and elimination. After 20-30 minutes, an equilibrium is established between the blood and tissues, and serum concentrations drop more slowly since elimination is the primary process removing drug from the blood. A two-compartment model describes this type of serum concentration/time profile.

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FIGURE 8-2

To maintain therapeutic procainamide concentrations, an intravenous loading dose (over 25-30 minutes) of procainamide is followed ...

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