Mechanism of action
The drug exerts an electrophysiological effect on the heart similar to quinidine. The main mechanism consists of the blockade of sodium ($Na^+$) and potassium ($K^+$) channels, which prevents cell membrane depolarization. This leads to the prolongation of phase 0 (depolarization), phase 3 (repolarization), and phase 4 of the action potential. Procainamide also possesses moderate ganglion-blocking activity.
Pharmacological effects and differences from quinidine
Compared to quinidine, procainamide has important differences:
- Less depression of myocardial contractility (less pronounced negative inotropic effect).
- Less pronounced anticholinergic (vagolytic) properties.
- Complete absence of $\beta$-adrenoreceptor blocking activity.
Procainamide can concentrate in saliva in amounts exceeding plasma levels (saliva/plasma ratio is 3.5), allowing its use for non-invasive monitoring.
Indications for use
Indications for prescription are identical to quinidine:
- Ventricular and supraventricular tachyarrhythmias;
- Extrasystole.
Dosing regimen: Administered orally in doses from 0.25 to 1.0 g (maximum daily dose is 4.0 g). Administered intravenously as a bolus of 0.1 g; for repeated administration, the total maximum daily dose is 1.0 g.
Side effects
The main side effects include:
- Hemodynamic: marked decrease in blood pressure (hypotension) due to ganglion-blocking action.
- Cardiac: impaired myocardial conduction.
- Extracardiac: gastrointestinal disorders (nausea, vomiting, diarrhea) and neurological disorders (up to convulsions).
An important role is played by genetic polymorphism: the presence of "slow" and "fast" acetylators determines the rate of hepatic metabolism. In patients with N-acetyltransferase deficiency (the "slow acetylator" phenotype, characteristic of up to 50% of the Caucasian population), the risk of adverse reactions increases sharply. In renal failure, there is a high risk of accumulation of the active metabolite (N-acetylprocainamide).
Metabolism and excretion features
Procainamide undergoes hepatic metabolism involving amidase enzymes (hydrolysis of the amide bond). An active metabolite is formed — N-acetylprocainamide, which is excreted by the kidneys more slowly than the parent drug. The drug is also excreted by salivary glands via passive diffusion.
Briefly: answers to topical questions
What side effects does procainamide cause?
Procainamide (Procainamidum) causes hemodynamic, cardiac, extracardiac, and immuno-allergic side effects.
- Hemodynamic — decrease in blood pressure (hypotension) due to ganglion-blocking action.
- Cardiac — conduction disturbances.
- Extracardiac — gastrointestinal disorders (nausea, vomiting, diarrhea) and neurological disorders (convulsions; neuropsychiatric disorders are rare).
- Immuno-allergic — fever, joint and muscle pain, skin rash, agranulocytosis, and lupus-like syndrome.
The frequency of side effects increases sharply in case of hepatic N-acetyltransferase deficiency in "slow acetylators".
What are the contraindications for the use of procainamide?
There are the following contraindications to the intravenous administration of procainamide:
- Severe heart failure.
- Acute myocardial infarction.
- End-stage renal failure. In renal failure, there is also a high risk of accumulation of the active metabolite.
Which drugs does procainamide have clinically significant interactions with?
Procainamide has a clinically significant interaction with atropine: co-administration enhances the anticholinergic effect.
Procainamide — Class IA antiarrhythmic: blocks Na+ channels, causes hypotension due to ganglion blockade, and is metabolized in the liver by slow and fast acetylators.
Class and exam questions
To which class of antiarrhythmic drugs does procainamide belong?
Procainamide belongs to class IA (quinidine-like agents), which block sodium channels.
What causes the drop in blood pressure during procainamide administration?
Arterial hypotension during procainamide administration is due to its moderate ganglion-blocking action.
Which active metabolite is formed during the biotransformation of procainamide?
The active metabolite N-acetylprocainamide is formed in the liver and is excreted by the kidneys more slowly than the parent compound.
What else to study on this topic
- Comparative characteristics of class IA, IB, and IC antiarrhythmics
- Genetic polymorphism of N-acetyltransferase and its clinical consequences
- Pharmacokinetics and metabolite accumulation in renal failure
- Mechanisms of drug monitoring using saliva concentration
- The role of non-microsomal enzymes (amidases) in the hydrolysis of amide compounds
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