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 lido-caine administration.

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