Monitoring level of sedation with bispectral EEG analysis: comparison between hypothermic and normothermic cardiopulmonary bypass.

The level of sedation of 28 patients undergoing elective coronary artery bypass grafting with fentanyl-propofol anaesthesia was monitored with bispectral analysis (BIS), spectral edge frequency, and band power of the electroencephalogram. Fourteen patients underwent hypothermic cardiopulmonary bypass (CPB) (32 degrees C, group H), and 14 normothermic CPB (group N). The level of sedation was measured with Observer's Assessment of Alertness/Sedation Score and with Ramsay Sedation Score. BIS was the only EEG measurement that paralleled the clinical course of the patients' sedation level. Values (median, 95% confidence intervals (CI)) changed significantly over time in both groups (P<0.0001). In group H, BIS decreased from 97 (95, 99) the day before surgery to 48 (44, 52) after tracheal intubation, to 46 (41, 52) before going off CPB, to 91 (85, 97) immediately before extubation. In group N, values were 93 (91, 97) the day before surgery, 53 (47, 59) after tracheal intubation, 48 (43, 53) before going off CPB, and 90 (84, 96) before extubation. During CPB, BIS values were significantly different between the two groups. Group H had a median of 41 (95% CI, 39, 42), and group N had a median of 49 (95% CI, 48, 51, P<0.0001). Peak values of all other processed EEG parameters during anaesthesia and surgery overlapped with values from the day before, when patients had no sedating medication, and these values did not correlate to the patients' course of sedation during the study. There was no explicit recall of the surgery in either group. During the phases of anaesthesia and surgery without CPB, the progression of BIS levels was comparable with previously published data for non-cardiac surgery. During normothermic CPB, the highest BIS values were close to values representing insufficient depth of sedation. It remains to be elucidated whether the much lower BIS values in the hypothermic group were solely a result of brain cooling or if increased serum propofol concentrations, because of slowed pharmacodynamics during hypothermia, also contributed.