Class Ia drugs quinidine procainamide disopyramide

Quinidine used to be popular as an effective antiarrhythmic agent against both supraventricular and ventricular arrhythmias, but has fallen into disuse after a large meta-analysis suggested excess mortality due to drug-induced torsade de pointes. Quinidine directly suppresses sinus node and atrioventricular node conduction and increases the refractory period of atrial, ventricular, and His-Purkinje tissue, although an anticholinergic action may increase atrioventricular nodal conduction. The most important side-effect is torsade de pointes associated with QT prolongation. Other side-effects are seen in the gastrointestinal system, together with tinnitus, thrombocytopenia, and hypotension. The drug may precipitate digoxin toxicity. The drug is metabolized hepatically and dose reduction is necessary in patients with hepatic disease.

Procainamide has a similar mode of action to quinidine but prolongs the QT interval less. Long-term administration may result in a lupus syndrome. It is generally safe and well tolerated. Torsade de pointes is less common. It is useful in the treatment of sustained monomorphic ventricular tachycardia where it has been shown to be superior to lidocaine (lignocaine) in a small randomized cross-over trial ( Gorgels ela/ 1996). The usual dose is 10 mg/kg body weight at a rate of 100 mg/min. A

maintenance infusion of 2 to 6 mg/min may be required. Oral use is limited by the short plasma half-life, such that even slow-release preparations have to be administered several times daily to maintain antiarrhythmic efficacy. It is useful as a predictor of antiarrhythmic efficacy. Failure of procainamide to suppress inducibilty of ventricular tachycardia by electrophysiological testing indicates that no other single agent is likely to be efficacious.

Disopyramide differs markedly from quinidine in a number of respects. It is profoundly negatively inotropic which makes it particularly unsuitable for use in critically ill patients with impaired myocardial function. Gastrointestinal side-effects are generally less, but anticholinergic side-effects are much more prominent. Such effects may cause acceleration of atrioventricular nodal conduction and may require coadministration of atrioventricular nodal blocking drugs when used for the treatment of supraventricular arrhythmias.

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