Procainamide

Classification:

Class IA – Sodium (Na⁺) channel blockers

Procainamide – mainly used in patients with pre-excited atrial fibrillation (AF).
Disopyramide – due to its vagolytic effect, suitable in vagal AF.

$Diagram of the effect of procainamide as a class IA antiarrhythmic illustrating reduced myocardial excitability, prolongation of the effective refractory period of an accessory pathway, and pharmacological cardioversion of preexcited atrial fibrillation to sinus rhythm.$

Mechanism:

Slows conduction velocity and reduces excitability in atrial and ventricular myocardium

Blocks sodium channels

Prolongs the effective refractory period (ERP) in atrial and ventricular myocardium

Its metabolite (NAPA) blocks potassium channels (therefore it also exhibits Class III properties)

Accessory pathway – prolongs ERP and slows conduction
Use-dependent (effect increases at heart rate > 90/min.)

Effect on AF:

Cardioversion of pre-excited atrial fibrillation (AF) to sinus rhythm – restoration of sinus rhythm

Procainamide and atrial fibrillation (AF)
Brand names
Procainamid, Pronestyl, Procan, Procanbid, Novocainamid, Novocamid
Indications
Acute cardioversion of pre-excited AF to sinus rhythm
Dosing
Acute cardioversion of pre-excited AF (intravenous) 20–50 mg/min administered up to a maximum total dose of 17 mg/kg Administer until conversion to sinus rhythm or until a total dose of 1.5 g is reached Maintenance infusion (intravenous) 1–4 mg/min for a maximum of 12 hours
Onset of action
< 30 minutes
Effect
Time to conversion to sinus rhythm and success rate < 30 minutes – success rate 50–75 % (intravenous)
Duration of action
2–4 hours (intravenous)
Contraindications
Second- or third-degree AV block (without pacemaker) Prolonged QTc interval ≥ 500 ms Systemic lupus erythematosus History of torsades de pointes Myasthenia gravis Severe heart failure Allergy to procainamide

Patient monitoring during procainamide administration:

Stop administration if a reason for infusion discontinuation occurs (see table below).

Patient monitoring during procainamide administration
Monitoring period	What to monitor	Reason for discontinuation
During infusion	ECG (QRS, QTc interval, rhythm) Blood pressure Clinical status (dizziness, weakness)	QRS widening > 25% QTc > 500 ms Bradycardia < 40/min Hypotension < 90/60 mmHg Ventricular arrhythmia
30–120 minutes after administration	ECG (QRS, QTc interval, rhythm) Blood pressure Clinical status (dizziness, weakness)	QRS widening > 25% QTc > 500 ms Bradycardia < 40/min Hypotension < 90/60 mmHg Ventricular arrhythmia

Adverse effects:

Very common (>10%):

Drug-induced lupus erythematosus – up to 20–30 % (with long-term oral use)

Common (1–10%)

Hypotension
Bradycardia
QRS widening
QT interval prolongation
AV block
Ventricular arrhythmias (mainly extrasystoles)
Haematological disorders, e.g. agranulocytosis (with long-term oral use)

Less common (< 1%)

Flushing, dizziness – due to transient hypotension
Nausea or gastrointestinal discomfort

For pharmacological cardioversion of pre-excited AF, both procainamide and ibutilide may be used.

Procainamide is preferred, but ibutilide is also a suitable alternative.

Procainamide vs Ibutilide and atrial fibrillation
Property	Procainamide	Ibutilide
Class	IA (Na⁺ channel blocker, minimal K⁺ blockade)	III (K⁺ channel blocker)
Cardioversion of pre-excited AF	Yes – first-line drug	Yes – possible, but less preferred
Indication in AF	Acute cardioversion of pre-excited AF	Acute cardioversion of AF or atrial flutter
Conversion success rate to SR	50–75 % (within 30 minutes)	~30–50 % in AF, 60–75 % in atrial flutter
Use in atrial flutter	No	Yes
Main risks	Hypotension, proarrhythmia (torsades de pointes), lupus-like syndrome	QT prolongation, torsades de pointes
Typical patient	Younger patient with AF and WPW (delta wave on ECG)	Patient with AF or atrial flutter without WPW, for urgent conversion