Electrophysiologic effects of enflurane and halothane on isolated rabbit hearts in the presence and absence of metabolic acidosis.
Electrophysiologic effects of halothane and enflurane in the presence of a normal pH and during metabolic acidosis were examined in isolated rabbit hearts perfused at a constant rate. During exposure to a normal pH, both halothane and enflurane produced concentration-dependent suppression of sinus node automaticity and atrioventricular conduction. Intraatrial and intraventricular conduction times during constant pacing were slightly but significantly prolonged by these anesthetics at 2 MAC. The magnitudes of these electrophysiologic changes were similar with halothane and enflurane when compared at the same MAC. These electrophysiologic effects became more marked during metabolic acidosis (pH 6.9). These results suggest that enflurane and halothane have direct depressant actions on the cardiac conduction system and that these electrophysiologic effects may be augmented by metabolic acidosis.
D000138:Acidosis / Q000503:physiopathology*; D000818:Animals; D001283:Atrioventricular Node / Q000187:drug effects; D002304:Cardiac Pacing, Artificial; D004594:Electrophysiology; D004737:Enflurane / Q000494:pharmacology*; D005260:Female; D006221:Halothane / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects*; D006325:Heart Atria; D006329:Heart Conduction System / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects; D006352:Heart Ventricles; D066298:In Vitro Techniques; D008297:Male; D011817:Rabbits
D004737:Enflurane; D006221:Halothane