Biomedical subjects

P Ammendrup

Publications and source records attributed to P Ammendrup.

2 recordsLinked to original sources

PubMed1981

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.

Animals↗

PubMed1980

Mechanical hyperventilation: effect on specialized atrioventricular conduction, supraventricular refractoriness, and experimental atrial arrhythmias in dogs anesthetized with pentobarbital or pentobarbital-halothane.

The effect of hypocapnia (PCO2ET 25 vs 40 torr) on specialized atrioventricular (AV) conduction, supraventricular refractory periods, and experimental atrial arrhythmias provoked by premature atrial stimulation (atrial echoes-echoes, repetitive atrial firing (RAF)) was assessed in dogs anesthetized with pentobarbital or pentobarbital-halothane (1.0% end-tidal). Catheter His bundle electrocardiography was used. Both hypocapnia and halothane prolonged AV nodal conduction, but the effect of halothane was more pronounced. Halothane prolonged the atrial functional (AtFRP), atrial effective (AtERP), and AV nodal functional refractory (AVFRP) periods. These effects of halothane were linked to an increased incidence of RAF but not to echoes. Hypocapnia prolonged the AVFRP (less than halothane), had no effect on the AtFRP and shortened the AtERP. These effects of hypocapnia were associated with an increased incidence of echoes, but not with RAF. Echoes and RAF are thought to be caused by reentry within the sinus node, atria, and AV node. The differing effects of halothane and hypocapnia on the incidence of these arrhythmias may be due to differning effects on supraventricular refractoriness.

Anesthesia↗