Why the study?
Does halothane anesthesia alter ventricular cardiac conduction and refractory periods in a canine model?
Does halothane anesthesia alter ventricular cardiac conduction and refractory periods in a canine model?
Higher concentrations of halothane depress ventricular conduction and shorten refractory periods in the ventricular conduction system in vivo, consistent with its known in vitro effects.
Extends in vitro halothane effects to an in vivo canine model; leaves open any relevance to human arrhythmia risk or anesthetic selection.
Changes in the ventricular conduction system associated with halothane anesthesia were investigated by direct methods of His bundle recording, pacing, and premature stimulation in a canine model. In eight animals a change from 1.5% to 2.4% halothane concentrations was associated with significant prolongation of epicardial activation times by an average of 2.4 and 2.9 msec during atrial and His bundle paced rhythms, respectively. Ventricular functional refractory periods decreased significantly by an average of 7.3 msec, the effective refractory period of the ventricular conduction system did not system did not change, and epicardial conduction delays at the effective refractory period decreased. In six other animals the addition of 1.5% halothane to basal thipental anesthesia was not associated with prolongation of epicardial activation times or decreased ventricular functional refractory periods. However, the effective refractory period of the ventricular conduction system significantly decreased by an average of 9.1 msec, and epicardial conduction delays at the effective refractory period significantly increased by an average of 9.6 msec. A change in halothane concentrations from 1.5% to 2.4% is associated with depression of ventricular conduction and shortened duration of refractory periods in the ventricular conduction system in vivo in a manner consistent with the reported actions of halothane on Purkinje fibers in vitro.
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Turner et al. (1980) studied this question.
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