Quinidine electrophysiological propertie

The electrophysiological properties of lidocaine in atrial muscle resemble those produced by quinidine. Membrane responsiveness, action potential amplitude, and atrial muscle excitability are all decreased. These changes result in a decrease in conduction velocity. However, the depression of conduction velocity is less marked than that caused by quinidine or procainamide. Action potential duration of atrial muscle fibers is not altered by lidocaine at either normal or subnormal extracellular K+ levels. The ERP of atrial myocardium either remains the same or increases slightly after lidocaine administration. 

Therapeutic plasma concentrations of TCAs have clinically significant antiarrhythmic activity (420). Imipramine and nortriptyline (and probably other TCAs) share electrophysiological properties characteristic of type I (A, B) compounds (e.g., quinidine, procainamide, disopyramide) and can even be used in cardiac patients free from depression, exclusively for the control of arrhythmia (421). 

Type I antiarrhythmics appear to share a single receptor site in the sodium channel. It should be noted, however, that a number of type I drugs have other electrophysiologic properties. For instance, quinidine has potent potassium channel blocking activity (manifest predominantly at low concentrations), as does A-acetylprocainamide (manifest predominantly at high concentrations), the primary metabolite of procainamide. Additionally, propafenone has /3-blocking actions. 

Quinidine s effect on the electrical properties of a particular cardiac tissue depends on the extent of parasympathetic innervation, the level of parasympathetic tone, and the dose. The anticholinergic actions of quinidine predominate at lower plasma concentrations. Later, when steady-state therapeutic plasma concentrations have been achieved, the drug s direct electrophysiological actions predominate. The direct and indirect electrophysiological actions are summarized in Table 16.2. 

Both the direct and indirect actions of quinidine are important in determining its ultimate effect on A-V conduction. The indirect (anticholinergic) properties of quinidine prevent both vagally mediated prolongation of the A-V node refractory period and depression of conduction velocity these effects lead to enhancement of A-V transmission. Quinidine s direct electrophysiological actions on the A-V node are to decrease conduction velocity and increase the ERP. 

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