| Indication |
For the treatment of life-threatening ventricular arrhythmias. |
| Pharmacodynamics |
Procainamide is an agent indicated for production of local or
regional anesthesia and in the treatment of ventricular tachycardia
occurring during cardiac manipulation, such as surgery or
catheterization, or which may occur during acute myocardial infarction,
digitalis toxicity, or other cardiac diseases. The mode of action of the
antiarrhythmic effect of Procainamide appears to be similar to that of
procaine and quinidine. Ventricular excitability is depressed and the
stimulation threshold of the ventricle is increased during diastole. The
sinoatrial node is, however, unaffected. |
| Mechanism of action |
Procainamide is sodium channel blocker. It stabilizes the neuronal
membrane by inhibiting the ionic fluxes required for the initiation and
conduction of impulses thereby effecting local anesthetic action. |
| Absorption |
75 to 95% |
| Volume of distribution |
|
| Protein binding |
15 to 20% |
| Metabolism |
Hepatic |
| Route of elimination |
Trace amounts may be excreted in the urine as free and conjugated
p-aminobenzoic acid, 30 to 60 percent as unchanged PA, and 6 to 52
percent as the NAPA derivative. |
| Half life |
~2.5-4.5 hours |
| Clearance |
Not Available |
| Toxicity |
LD50=95 mg/kg (rat, IV); LD50=312 mg/kg (mouse, oral); LD50=103 mg/kg (mouse, IV); LD50=250 mg/kg (rabbit, IV) |
