B. Zickmann et al., TOPOGRAPHICAL ELECTROENCEPHALOMETRY DURIN G INDUCTION OF ANESTHESIA WITH KETAMINE AND MIDAZOLAM, Anasthesist, 43, 1994, pp. 190000059-190000067
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.