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procainamide

Na+ Channel Blocker (Class IA), K+ Channel Blocker · Antiarrhythmic

Na+ Channel Blocker (Class IA), K+ Channel BlockerAntiarrhythmicATC C01BA02
CDSCO approvedATC C01BA02
EXCRETION
not curated
INTERACTIONS
12 major
SEVERE in our sources
PREGNANCY
not curated
Top interactionssee all 12
  • QuinolonesSevereTextbookG&G 14e · p1144
  • AbarelixSevereDatabaseDDInter
  • AbirateroneSevereDatabaseDDInter
  • AdenosineSevereDatabaseDDInter

Mechanism

Procainamide blocks open Na+ channels (with intermediate τrecovery) and prolongs cardiac action potentials in most tissues, probably by blocking outward K+ current(s). It decreases automaticity, increases refractory periods, and slows conduction.

Indications

Acute therapy of many supraventricular arrhythmiasAcute therapy of many ventricular arrhythmiasTermination of monomorphic ventricular tachycardia (VT)Termination of some supraventricular arrhythmiasWPW reciprocal ventricular tachycardiasPrevention of recurrences of ventricular fibrillation (VF)Alternative regimen for sustained ventricular tachycardia

Dosing

Adult
Loading: 10–17 mg/kg (IV) at a rate of 20 mg/min. Maintenance: 1–4 mg/min (IV); 250–750 mg q3h; 500–1000 mg q6h (slow-release).
Renal adjustment
Reduction of dose and dosing frequency, and monitoring of plasma concentrations required in renal failure.

Pharmacokinetics

Half-life
3–4 h (parent drug); 6–10 h (N-acetyl procainamide)
Bioavailability
>80%
Protein binding
Not specified
Metabolism
Hepatic by N-acetyl transferase to N-acetyl procainamide (active metabolite)
Excretion
67 ± 8%

Contraindications

  • Infranodal conduction disease
  • Arthritis (due to chronic procainamide use)

Side effects

Common
Nausea (dose-related with oral therapy)RashSmall-joint arthralgias (early symptom of lupus syndrome)NauseaVomitingWeaknessMental confusionHallucinations (at higher doses)Flushing (on rapid i.v. injection)Hypotension (on rapid i.v. injection)Rashes (hypersensitivity)Fever (hypersensitivity)Angioedema (hypersensitivity)
Serious
  • Hypotension (at high concentrations, especially during acute IV loading)
  • Marked slowing of conduction (at high concentrations)
  • Torsades de pointes (particularly when N-acetyl procainamide >30 μg/mL)
  • Bone marrow aplasia (0.2% of patients)
  • Drug-induced lupus syndrome (25% to 50% with chronic use, may include pericarditis with tamponade, renal involvement is unusual)
  • haemolysis (in G-6PD deficient individuals)
  • lupus (mainly in slow acetylators)
  • Cardiac toxicity
  • Torsades de pointes
  • Agranulocytosis (rare)
  • Aplastic anaemia (rare)
  • Systemic lupus erythematosus (SLE) (with long-term high dose, especially in slow acetylators)

Drug interactions

Quinolones
Severe
Textbook

Increased risk of QT interval prolongation and torsades de pointes arrhythmias.

Quinolones should be used with caution in patients on class IA antiarrhythmics.

Source: G&G 14e · p1144

Abarelix
Severe
Database

Drug interaction classified as: synergy

Source: DDInter

Abiraterone
Severe
Database

Drug interaction classified as: synergy

Source: DDInter

Adenosine
Severe
Database

Drug interaction classified as: synergy

Source: DDInter

Alfuzosin
Severe
Database

Drug interaction classified as: synergy

Source: DDInter

Alimemazine
Severe
Database

Drug interaction classified as: synergy

Source: DDInter

Amiodarone
Severe
Database

Increased plasma concentrations of procainamide.

Dosages of other antiarrhythmics usually require reduction during amiodarone therapy.

Source: DDInter

Amisulpride
Severe
Database

Drug interaction classified as: synergy

Source: DDInter

Amitriptyline
Severe
Database

Drug interaction classified as: synergy

Source: DDInter

Amoxapine
Severe
Database

Drug interaction classified as: synergy

Source: DDInter

Anagrelide
Severe
Database

Drug interaction classified as: synergy

Source: DDInter

Apalutamide
Severe
Database

Drug interaction classified as: synergy

Source: DDInter

Related guidelines

Ask House about procainamide

Continue into a citation-backed clinical answer with the drug context already attached.

Sources: KD Tripathi 7e, Goodman & Gilman 14e, Harrison 22e·Verified: 2026-05-10 · House clinical team