Saturday, March 5, 2011


It is a derivative of procaine which is a local anesthetic.

Mechanism of action:
Same as that of quinidine

Cardiac effects:

Almost similar to quinidine.

It decreases ectopic pacemaker rate, conduction velocity (negative dromotropism) and excitability especially in depolarized tissue. By decreasing conduction velocity (negatively dromotropic) it causes a promoted effective refractory period in atrial, ventricular and Purkinje fibers.

However unlike quinidine it has less effecient antimuscarinic action.

Due to its ganglionic receptor blocking properties, it results in more pronounced negative inotropic effects than quinidine.

It instigates serious CCF in patients with already ventricular dysfunction.

Other effects:
It reduces peripheral vascular resistance and may cause hypotension due to its ganglionic blocking properties.


Procainamide is well-absorbed orally.

Its half life is 2 – 3 hours. Some of the procainamide is metabolized in the liver into N-acetylprocainamide (NAPA). NAPA has the same properties as that of class III agents as it prolongs the duration of action potential.
Therapeutic uses:

It is used in atrial and ventricular arrhythmias and ventricular arrhythmias which comes with acute myocardial infarction.

Adverse effects:
It may cause mental confusion, anorexia, nausea, urinary retention and hepatitis. After prolonged use, it may cause reversible form of lupus erythematosus like syndrome in 20-30 percent of patients. Its toxic dose may cause asystole or instigation of ventricular arrhythmias.

Its effects on CNS include depression, hallucination and psychosis.

It is contraindicated in patients with AV block or systemic lupus erythematosus.

It is given up to 50 mg/kg daily in divided doses every 3 to 6 hours.
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