Hypokalemia in rats produces resistance to dysrhythmias under halothane anesthesia.

The arrhythmogenic threshold was investigated during acute and chronic hypokalemia under halothane anesthesia with an epinephrine challenge in the rat model. It was hypothesized that in the setting of severe hypokalemia, general anesthesia would be arrhythmogenic and would be exaggerated with increased levels of catecholamines. Rats were divided into four groups as follows: normokalemic control (group I, n = 10), acute hypokalemia with furosemide (group II, n = 16), acute hypokalemia with hyperventilation (group III, n = 18), and chronic hypokalemia induced by a low potassium (K+) diet (group IV, n = 22). There were no significant differences (P less than .05) in baseline K+ and arterial blood gases among the four groups. There was a significant difference between groups I and II and groups I and IV (P less than 0.05) in serum K+ values after the low K+ diet, but no differences were observed between groups II and IV or groups I and III in serum K+ levels. There was no significant difference in myocardial tissue K+ among the four groups. There was a significant difference in the arrhythmic dose of epinephrine among the four groups (P less than 0.05). Acute hypokalemia was more prone to dysrhythmias than chronic hypokalemia. However, compared with control, acute and chronic hypokalemia groups were resistant to dysrhythmias is probably based on compensatory mechanisms. The heart seems more resistant to K+ changes than skeletal muscle. This resistance is associated with compensation by the cardiac muscle sodium pump in the face of K+ depletion. Hypokalemia per se did not increase the incidence of dysrhythmias under halothane anesthesia in rats.