TOPOGRAPHICAL ELECTROENCEPHALOMETRY DURIN G INDUCTION OF ANESTHESIA WITH KETAMINE AND MIDAZOLAM

The neurophysiological action of ketamine has attracted increasing int erest in recent years, with special interest in receptor action and in neurophysiological differences between and psychomimetic side effects of the two enantiomorphs. Most of the neurophysiological examinations published deal with ketamine as a single anaesthetic agent, although it has been suggested to that psychomimetic side-effects and haemodyna mic deterioration could be avoided by combining ketamine with a sedati ve drug. The primary aim of our study was to examine the combined keta mine-midazolam action on cerebral activity; secondly, we planned to lo ok at these interactions topographically at different points of the co rtex to evaluate topographical differences in the combination's action ; thirdly, the cerebral and haemodynamic reactions to anaesthesiologic al stimuli (intubation, gastric tube) were evaluated and compared. Met hods. Sixteen patients scheduled for elective aortocoronary bypass sur gery were examined. Topographical electroencephalometric data were obt ained by processed EEG with a CATEEM system at 17 recording points ove r the cortex and compared with heart rate and arterial blood pressure during the induction period. After documentation of the baseline data ketamine (3 mg/kg) and midazolam (0.15 mg/kg) were applied within 10 m in by means of an automatic device. At the end of the infusion period patients were intubated, and after a further 10 min a gastric tube was placed. Results. Induction resulted in increases in delta and beta 2 output (P < 0.05) in the early induction period and in significant dec reases (P < 0.05) in alpha 1, alpha 2 and beta 1 activity. No signific ant change in theta activity was observed throughout the observation p eriod. Intubation led to significant increases of power particularly i n the temporal and parietal leads of all frequency bands, but not in t he frontal area. Insertion of the gastric tube did not alter cerebral function. Conclusion. The interaction of ketamine and midazolam leads to increases in beta 2 and delta power and to significant decreases in the alpha bands and beta 1. Increases of theta activity, a typical ef fect of single-agent anaesthesia with ketamine, were not observed. Thu s, the action of combined ketamine and midazolam on cerebral function is not an additive, but an interactive process. Despite a relatively h igh induction dosage, haemodynamic changes during intubation occurred and were accompanied by changes in cerebral activity. This can be rega rded as incomplete cerebral suppression even by these induction dosage s.