Bimar-Blanc M C, Dejode J M, Bimar J
Département d'Anesthésie-Réanimation, CHU Nord, Marseille.
Ann Fr Anesth Reanim. 1988;7(4):279-88. doi: 10.1016/s0750-7658(88)80029-7.
The effects of isoflurane and halothane anaesthesia on brainstem auditory (BEAR) and somatosensory evoked potentials (SEP) were recorded in 15 patients; eight received isoflurane and seven halothane. Atropine alone was given as premedication. After induction of anaesthesia with thiopentone, it was maintained with 50% nitrous oxide in oxygen. Ventilation was controlled. Isoflurane and halothane concentrations were gradually increased to 3%. Recordings were made at 1%, 2.5% and 3%. There were statistically significant differences in the latencies of SEP and BEAR with increasing concentrations of anaesthetic. The BEAR waves significantly affected were wave V and the latency between peaks I to V (p less than 0.001); for the SEP, it was wave N20. SEP central conduction time was prolonged with both anaesthetics (p less than 0.001). The effects of isoflurane and halothane were similar. These results could not be explained by changes in central body temperature or end-tidal carbon dioxide concentration. The study showed a dose-related direct effect of both anaesthetic agents on the brainstem auditory and somatosensory evoked responses. It may be that the measurement of changes in evoked potentials could be a useful indicator of anaesthetic depth.