Intravenous clonidine decreases minimum end-tidal isoflurane for induction of electroencephalographic burst suppression

The aim of this study was to determine the individual end-tidal isoflurane (ET ISO) threshold concentration for the induction of electroencephalographic (EEG) burst suppression with and without intravenous (IV) clonidine and to evaluate the EEG and cardiovascular response to skin incision during isoflurane/N2O anesthesia. Thirty-nine patients (ASA physical status I or II, 20-68 yr of age) undergoing orthopedic surgery were randomly assigned to receive IV saline (n = 20) or IV clonidine (3 mu g/kg, n = 19). After detection of isoflurane-induced burst suppression, ET ISO was decreased in 0.1% ET steps until burst suppression diminished. Median minimum ET ISO for induction of burst suppression was 1.4% in the saline group and 0.9% in the clonidine group (P < 0.05). Before skin incision, EEG alpha 2 activity was significantly higher in the clonidine group compared with saline group. Fourteen patients (70%) in the saline group and 12 patients (63%) in the clonidine group showed a cardiovascular response to skin incision. After skin incision, EEG alpha 2 power was significantly decreased in both groups. A significant increase of delta activity was only found in the saline group. We conclude that the known minimum alveolar anesthetic concentration reduction of clonidine seems to be due to a direct cerebral action.