Adult: In life-threatening cases: 100 mg every 5 minutes as a bolus inj given at a rate not exceeding 50 mg/min. Administer doses until the arrhythmia is controlled or until a total of 500 mg has been given; wait for approx 10 minutes before giving additional doses. Alternatively, a loading dose of 20 mg/mL may be given via infusion at a rate of 1 mL/min over 25-30 minutes to deliver 500-600 mg of procainamide. Max: 1000 mg (given by either method). Maintenance to ensure therapeutic plasma concentrations: 2 mg/mL may be given at a rate of 1-3 mL/min; if total daily fluid intake must be decreased: 4 mg/mL may be given at a rate of 0.5-1.5 mL/min. Maintenance doses are adjusted according to clinical response, weight and age, and the general condition and CV status of the patient. Discontinue treatment if continuous conduction disturbances or hypotension occurs. Elderly: Initiate therapy at the lower end of the dosage range.
Renal Impairment
Dosage adjustment may be needed.
Reconstitution
Direct IV/bolus inj: Dilute vials before administration to enable the control of the dosage rate. IV infusion: Dilute to a concentration of 20 mg/mL (loading dose) or to 2 or 4 mg/mL (maintenance dose) with the appropriate diluent (e.g. 5% dextrose in water).
Contraindications
Complete heart block, 2nd-degree AV block or various types of hemiblock (in the absence of a functional artificial pacemaker), torsade de pointes, SLE, myasthenia gravis.
Special Precautions
Patient with pre-existing marrow failure or cytopenia of any type, atrial fibrillation or flutter (patient should be cardiovert or digitalised prior to administration), CHF, acute ischaemic heart disease, cardiomyopathy, 1st-degree heart block; electrolyte imbalance (e.g. hypokalaemia, hypomagnesaemia), arrhythmias associated with digitalis intoxication. Renal and hepatic impairment. Elderly. Pregnancy and lactation.
Adverse Reactions
Significant: Drug-induced lupus erythematosus-like syndrome with prolonged use, conduction disturbances; proarrhythmic effects (e.g. QTc prolongation), increased A-V conduction leading to ventricular rate acceleration. General disorders and administration site conditions: Weakness. Investigations: Increased serum transaminases. Nervous system disorders: Dizziness. Psychiatric disorders: Depression, psychosis with hallucination. Skin and subcutaneous tissue disorders: Angioneurotic oedema, urticaria, pruritus, maculopapular rash. Vascular disorders: Hypotension, flushing. Potentially Fatal: Blood dyscrasias (e.g. agranulocytosis).
Symptoms: Hypotension, oliguria, lethargy, nausea, vomiting, confusion; continuous widening of the QRS complex, prolonged Q-T and P-R intervals, lowering of the R and T waves; increasing AV block, ventricular extrasystoles, ventricular tachycardia or fibrillation; delayed intraventricular conduction. Management: Symptomatic and supportive treatment. Monitor ECG, blood pressure, and vital signs. Administer vasopressors after adequate fluid volume replacement. Ensure mechanical cardiorespiratory support. May perform haemodialysis to remove from the circulation.
Drug Interactions
May cause a potentiated prolongation of conduction or diminished contractility and hypotension with other group IA antiarrhythmic agents (e.g. quinidine, disopyramide). May cause additive antivagal effects on A-V nodal conduction with anticholinergic agents. May enhance the therapeutic efficacy of neuromuscular blocking agents. Cimetidine or trimethoprim may increase the plasma concentration of procainamide.
Food Interaction
Increased clearance and reduced elimination half-life with alcohol.
Lab Interference
Tests which depend on fluorescence to measure the concentrations of procainamide or its active metabolite may be affected by propranolol or by suprapharmacologic concentrations of lidocaine or meprobamate.
Action
Description: Procainamide is a class 1a antiarrhythmic. Through direct cardiac effects and an increased electrical stimulation threshold of the ventricle and His-Purkinje system, it causes a reduced myocardial excitability and conduction velocity and possibly a decreased myocardial contractility. Pharmacokinetics: Distribution: Widely distributed throughout the body. Crosses the placenta and enters breast milk. Volume of distribution: 2 L/kg. Plasma protein binding: 15-20%. Metabolism: Metabolised in the liver via acetylation to form the active metabolite N-acetyl procainamide (NAPA). Excretion: Mainly via urine (approx 30-60% as unchanged drug; 6-52% as NAPA); faeces (<5% as unchanged drug). Elimination half-life: 2.5-4.7 hours (procainamide); 6-8 hours (NAPA).
Chemical Structure
Procainamide Source: National Center for Biotechnology Information. PubChem Compound Summary for CID 4913, Procainamide. https://pubchem.ncbi.nlm.nih.gov/compound/Procainamide. Accessed Feb. 22, 2022.
Storage
Store between 20-25°C. Diluted solutions: Storage recommendations may vary depending on the diluent used and the resulting final concentration (refer to specific product guidelines).
C01BA02 - procainamide ; Belongs to class Ia antiarrhythmics.
References
Anon. Procainamide. AHFS Clinical Drug Information [online]. Bethesda, MD. American Society of Health-System Pharmacists, Inc. https://www.ahfscdi.com. Accessed 09/12/2021.Anon. Procainamide. Lexicomp Online. Hudson, Ohio. Wolters Kluwer Clinical Drug Information, Inc. https://online.lexi.com. Accessed 09/12/2021.Buckingham R (ed). Procainamide Hydrochloride. Martindale: The Complete Drug Reference [online]. London. Pharmaceutical Press. https://www.medicinescomplete.com. Accessed 09/12/2021.Procainamide Hydrochloride Injection (International Medication Systems, Limited). DailyMed. Source: U.S. National Library of Medicine. https://dailymed.nlm.nih.gov/dailymed. Accessed 09/12/2021.Procainamide Hydrochloride Injection, Solution (Hospira, Inc.). DailyMed. Source: U.S. National Library of Medicine. https://dailymed.nlm.nih.gov/dailymed. Accessed 09/12/2021.
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