Halothane and hypocapnia: effects on electrically stimulated atrial arrhythmias in digitalized dogs.

To assess the effectiveness of halothane as an antiarrhythmic agent against atrial arrhythmias brought about by hyperventilation of digitalized subjects, the effects of halothane end-tidal (ET) = 1.0% and hypocapnia (PCO2ET = 25 vs 40 torr) on stimulated atrial arrhythmias (atrial echoes [echoes]; repetitive atrial firing [RAF]) and supraventricular conduction and refractoriness were assessed digitalized dogs. Ten dogs received low dose (LD, 22 microgram/kg/day X 7 days) and nine dogs received high dose (HD, 44 microgram/kg/day X 7 days) digoxin. Serum digoxin levels following LD were 0.5 to 1.8 ng/ml (mean +/- 1 SD = 1.16 +/- 0.31) and following HD were 2.0 to 4.0 ng/ml (3.06 +/- 0.71 ng/ml). High right atrial pacing and extrastimulation and catheter His bundle electrocardiography were used. Spontaneous arrhythmias or conduction disturbances were not observed. Halothane enhanced RAF but not echoes in dogs given LD and HD. It also increased supraventricular conduction time and refractoriness. Hypocapnia had no effect on echoes or RAF and minimal effects on conduction and refractoriness. By analysis of variance, digoxin had no effects on echoes, RAF, refractory periods, or conduction. It is concluded that halothane affords no protection against stimulated arrhythmias in hypocapneic or eucapneic, nontoxic digitalized dogs.