• H J Woehlck, M N Vicenzi, Z J Bosnjak, and J L Atlee.
• Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226.
• Anesthesiology. 1993 Dec 1; 79 (6): 1304-15.

BackgroundSupraventricular dysrhythmias are common during anesthesia, but have been incompletely investigated. Mechanisms may involve altered automaticity of subsidiary pacemakers and participation of vagal reflexes. The following hypotheses were tested: (1) shifts from the sinoatrial (SA) node to subsidiary pacemakers require intact vagal reflexes and (2) halothane sensitizes the heart to epinephrine-induced atrial pacemaker shifts.MethodsEpicardial electrodes were implanted in eight dogs on both atrial appendages, the right ventricle, along the sulcus terminalis, and at the His bundle. Weekly testing awake (control), awake with atropine methylnitrate, with 1 and 2 micrograms epinephrine.kg-1.min-1 (3 min-infusions), and under 1.25 and 2 MAC halothane was performed. Electrograms were analyzed for the site of earliest activation (SEA), which was scored 1-6 depending on the distance from the SA node, and expressed as the SEA value.ResultsIn conscious dogs (control) and at 1.25 MAC halothane, epinephrine increased the SEA values (shifted activation from SA node) and blood pressure, and decreased heart rate; however, with atropine, SEA values were unaffected by epinephrine, although blood pressure and heart rate were elevated. At 2 MAC, atropine did not affect the epinephrine-induced increase in SEA values. Halothane increased SEA values when combined with 1 micrograms epinephrine.kg-1.min-1.ConclusionsPacemaker shifts account for atrial dysrhythmias in the conscious state and during 1.25 MAC halothane with epinephrine, and require vagal participation. Halothane sensitizes the heart to epinephrine-induced atrial dysrhythmias. Atropine and halothane facilitate His bundle beats during exposure to epinephrine.

27 keywords...

hide…