Lidocaine reduces action potential amplitude and membrane responsiveness. Significant shortening of the action potential duration and ERP occurs at lower con centrations of lidocaine in Purkinje fibers than in ventricular muscle. Lidocaine in very low concentrations slows phase 4 depolarization in Purkinje fibers and decreases their spontaneous rate of discharge. In higher concentrations, automaticity may be suppressed and phase 4 depolarization eliminated.
It is difficult to suggest a mechanism for lidocaine's antiarrhythmic action on the basis of its effects on normal ventricular myocardial tissue and His-Purkinje tissue.
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