Procainamide cardiovascular effects

The place of the dmg in dentistry [153 4] and in electro-convulsive therapy [ 154] (with a description of a technique to surmount difficulties arising from the concurrent use ot suxamethonium) has been evaluated. A refined radio telemetric technique has enabled a detailed study [155] of the cardiovascular effects of propanidid to be made, resulting in strong evidence for a transient procainamide- or quinidine-like depression of myocardial conductive tissue. The above publications [150-5] quote a large number of relevant references. 

Pharmacodynamic interactions. Many TCAs cause sedation and therefore co-prescription with other sedative agents such as opioid analgesics, antihistamines, anxiolytics, hypnotics and alcohol may lead to excessive drowsiness and daytime somnolence. The majority of TCAs can have undesirable cardiovascular effects, in particular prolongation of the QT interval. A similar risk of QT prolongation arises with many other cardiovascular drugs including amiodarone, disopyramide, procainamide, propa-... 

The hemodynamic alterations produced by procainamide are similar to those of quinidine but are not as intense. Alterations in circulatory dynamics vary according to the cardiovascular state of the individual. The hypotensive effects of procainamide are less pronounced after intramuscular administration and seldom occur after oral administration. 

Cardiovascular Intravenous procainamide had a prodysrhythmic effect when it was given as a single 1000 mg bolus during an electrophysiological study in a patient with myotonic dystrophy type 1 [SO J. During ventricular pacing, ventricular tachycardia and fibrillation occurred and required DC cardioversion. By slowing cardiac conduction, procainamide, as do other sodium channel blockers, worsens abnormalities already present in the hearts of patients with myotonic dystrophy t)q)e 1. 

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