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Procainamide (PA) is indicated in the treatment of life-threatening ventricular arrhythmias.
PA is metabolized to an active metabolite, N-acetylprocainamide (NAPA), with metabolism controlled by genetically determined enzymes. In patients with normal renal function, fast metabolizers will have a PA:NAPA ratio less than 1 at 3 hours after the dose is administered. Slow acetylators (PA:NAPA ratio >2 after 3 hours) are more likely to present with systemic lupus erythematosus-like symptoms and may test positive for antinuclear antibodies.
Patients who have prolonged exposure to procainamide levels above 12 mcg/mL or a NAPA concentration of 40.0 mcg/mL or higher are very likely to exhibit symptoms of toxicity, which are characterized by hypotension, ventricular fibrillation, widened QRS complex, junctional tachycardia, oliguria, confusion, nausea, and vomiting.
Renal disease, hepatic disease, cardiac failure, and states of low cardiac output reduce the metabolism and clearance of PA and NAPA.
Coadministration of histamine H2 receptor antagonists, such as cimetidine and ranitidine reduce renal clearance of PA and NAPA resulting in higher plasma concentrations of each.