Abnormal automaticity is the spontaneous beating of cardiac cells with abnormally depolarized resting membrane potentials. The effects of
halothane on
cardiac arrhythmias caused by abnormal automaticity are controversial, with either antiarrhythmic effects or enhancement of abnormal automaticity reported by different authors. The goal of the present investigation was to clarify the effects of
halothane on abnormal automaticity induced by superfusing excised canine Purkinje fibers (PF) with
barium chloride. Intracellular
microelectrodes recorded action potentials from fibers superfused with
buffer solution in a tissue bath.
Barium chloride 0.25 mM reduced maximal diastolic potential from -82.1 +/- 5.6 mV to -67.4 +/- 9.4 mV (mean +/- SD, P < 0.05). Fibers developed abnormal automatic rhythms at a rate of 47.1 +/- 5.9 bpm.
Halothane, 0.5%-4%, was added to the superfusate.
Halothane reduced the rate of firing in a dose-dependent manner, so that abnormal automaticity was abolished by 4%
halothane and reduced by lesser concentrations. Serendipitously, during
barium superfusion, two additional fibers developed early afterdepolarizations, a cause of triggered arrhythmias in patients with long Q-T syndrome.
Halothane abolished early afterdepolarizations in each. In this model of
barium toxicity in excised canine PF,
halothane antagonized both abnormal automaticity and early afterdepolarizations.
IMPLICATIONS: Life-threatening
cardiac arrhythmias may occur during
anesthesia. An
arrhythmia called abnormal automaticity occurs after
heart attacks and can be mimicked by adding
barium to small segments of heart tissue.
Halothane abolished abnormal automaticity in these tissues, which suggests that it or similar agents may benefit patients prone to developing such abnormal rhythms during surgery.