Disopyramide administration reduces membrane responsiveness in Purkinje fibers and ventricular muscle and reduces the action potential amplitude. Even greater depression may occur in damaged or injured myocardial cells. Action potentials are prolonged after disopyramide administration, and this results in an increase in the ERPs of His-Purkinje and ventricular muscle tissue. Unlike procainamide and quinidine, disopyramide does not produce postrepolarization refractoriness.
The effect of disopyramide on conduction velocity depends on extracellular K+ concentrations. Hypo-kalemic patients may respond poorly to the antiar-rhythmic action of disopyramide, whereas hyper-kalemia may accentuate the drug's depressant actions.
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