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The significance of the potassium ion concentrations inside and outside the cardiac cell membrane was discussed earlier. The effects of increasing serum K+ can be summarized as (1) a resting potential depolarizing action and (2) a membrane potential stabilizing action, the latter caused by increased potassium permea-bility. Hypokalemia results in an increased risk of early and delayed afterdepolarizations, and ectopic pacemaker activity, especially in the presence of digitalis. Hyperkalemia depresses ectopic pacemakers (severe hyperkalemia is required to suppress the SA node) and slows conduction. Because both insufficient and excess potassium is poten-tially arrhythmogenic, potassium therapy is directed toward normal-izing potassium gradients and pools in the body.
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