Effect of halothane on the ischemia-induced conduction delay in canine myocardium and the action of norepinephrine
Gotoh, Y.; Tsujinaga, H.; Yokota, S.; Harada, K.; Tamamura, T.; Furukawa, K.
Masui. Japanese Journal of Anesthesiology 33(12): 1317-1322
1984
ISSN/ISBN: 0021-4892 PMID: 6530733 Document Number: 235431
The changes of conduction time in the normal and ischemic myocardium before and after administration of halothane in dogs was studied. The time intervals from the V wave of His bundle ECG to the major deflection of the bipolar electrogram recorded within the normal and ischemic myocardial zones were measured at cycle length of 333 ms. Occlusion of the left anterior descending coronary artery produced conduction delay in the ischemic zone. Before administration of halothane, when mean arterial pressure (MAP) was 75 .apprx. 90 mm Hg, conduction delay increased about 50% above the control value. After administration of 2 MAC halothane, MAP was lowered to 35 .apprx. 50 mm Hg and conduction time was prolonged more than 120% above the control value. When MAP remained at the normal level by infusion of norepinephrine with halothane, the ischemia-induced conduction delay was reduced. The marked conduction delay after administration of halothane occurred due to the combined effect of coronary artery occlusion and hypotension. Even in deep halothane anesthesia, conduction in ischemic myocardium may remain unchanged if blood pressure is maintained with normal limits.