Abnormal automaticity is the spontaneous beating of cardiac cells with
abnormally depolarized resting membrane potentials. The effects of ha
lothane on cardiac arrhythmias caused by abnormal automaticity are con
troversial, with either antiarrhythmic effects or enhancement of abnor
mal automaticity reported by different authors. The goal of the presen
t investigation was to clarify the effects of halothane on abnormal au
tomaticity induced by superfusing excised canine Purkinje fibers (PF)
with barium chloride. Intracellular microelectrodes recorded action po
tentials 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 +/- so, P < 0.05). Fibers devel
oped abnormal automatic rhythms at a rate of 47.1 +/- 5.9 bpm. Halotha
ne, 0.5%-4%, was added to the superfusate. Halothane reduced the rate
of firing in a dose-dependent manner, so that abnormal automaticity wa
s abolished by 4% halothane and reduced by lesser concentrations. Sere
ndipitously, during barium superfusion, two additional fibers develope
d early afterdepolarizations, a cause of triggered arrhythmias in pati
ents with long Q-T syndrome. Halothane abolished early afterdepolariza
tions in each. In this model of barium toxicity in excised canine PF,
halothane antagonized both abnormal automaticity and early afterdepola
rizations. Implications: Life-threatening cardiac arrhythmias may occu
r during anesthesia. An arrhythmia called abnormal automaticity occurs
after heart attacks and can be mimicked by adding barium to small seg
ments of heart tissue. Halothane abolished abnormal automaticity in th
ese tissues, which suggests that it or similar agents may benefit pati
ents prone to developing such abnormal rhythms during surgery.