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Procainamide is an antiarrhythmic agent that is used intravenously and orally. It is classified as a type IA antiarrhythmic agent and can be used for the treatment of supraventricular or ventricular arrhythmias.1,2 It is a drug of choice for the treatment of stable sustained monomorphic ventricular tachycardia.3 Procainamide is a useful agent in the treatment of idiopathic repetitive polymorphic ventricular tachycardia in patients with coronary heart disease. It can also be used to treat incessant or recurrent polymorphic ventricular tachycardia secondary to acute myocardial ischemia after revasculariztion has been performed and β-blockers have been administered.3

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The primary treatment for ventricular fibrillation is direct-current cardioversion. Procainamide can be used as an antiarrhythmic for patients that are not converted using electrical shock and intravenous epinephrine or vasopressin. The use of procainamide in this situation is limited due to the long time needed to administer loading doses and lack of evidence-based studies.4 Given orally, procainamide is used for long-term suppression of ventricular arrhythmias.

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Procainamide can be administered for the long-term prevention of chronic supraventricular arrhythmias such as supraventricular tachycardia, atrial flutter, and atrial fibrillation. Ventricular rate control during atrial fibrillation can be accomplished using intravenous procainamide for hemodynamically stable patients with an accessory pathway.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 is an active metabolite of procainamide that has type III antiarrhythmic effects.1,2 A common characteristic of type III antiarrhythmic agents (bretylium, aminodarone, sotalol) is prolongation of the duration of the action potential resulting in an increased absolute refractory period.

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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).7–11

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Figure 8-1
Graphic Jump Location

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 ...

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