In order to study the relationship between heart rate and depth of anaesthesia, respiratory sinus arrhythmia (RSA) was investigated during enflurane and isoflurane anaesthesia in 28 patients (15-39 years). Positive pressure ventilation (six breaths min-1) was used. Respiratory sinus arrhythmia was evaluated during light anaesthesia, deep anaesthesia (burst suppression in EEG) and light anaesthesia again by using signal averaging technique. In most patients, decrease of the heart rate was seen during inspiration (positive tracheal pressure), and increase during expiration. Respiratory sinus arrhythmia did not disappear in deep anaesthesia. Inter-individual variation in the magnitude and phase relationship of respiratory sinus arrhythmia was considerable, and was not associated to the level of anaesthesia.

We have studied the effects of nitrous oxide on EEG burst suppression patterns during stable isoflurane anaesthesia in 13 ASA I patients. After induction of anaesthesia with propofol, the concentration of isoflurane was increased with continuous EEG monitoring to burst suppression level (mean end-tidal concentration of isoflurane, 1.7 (SD 0.2)%), and kept constant during the study. During surgery, isoflurane in air and oxygen (FIO2 0.35), or isoflurane in 65% nitrous oxide in oxygen were given to each patient for 30 min, in random order. EEG was recorded and digitized off-line. The proportion of EEG suppression time was measured after a washin or washout period of at least 15 min for nitrous oxide. There was a significant decrease in the proportion of EEG suppression time (from 69.5 to 43.7%) when air was replaced by nitrous oxide. We conclude that the EEG effects of isoflurane and nitrous oxide are not additive and that nitrous oxide opposes the depression of isoflurane on the central nervous system.

The results suggest that during isoflurane anaesthesia, nitrous oxide has a different effect on EEG and cortical SEP at the same time. The effects of nitrous oxide may be mediated by cortical and subcortical generators.

EEG burst suppression pattern was recorded during propofol and isoflurane anaesthesia. Using a long time constant, i.e. a high-pass filter with low cut-off frequency, revealed slow potentials, DC shifts, during bursts. These have been extensively studied in conjunction with cognitive-evoked potentials and epileptic discharges, but not previously in burst suppression EEG.

Despite the moderate amplitude changes produced by hypothermia, SEPs can be successfully monitored during hypothermia. Theoretically, the different behaviour of amplitude in peripheral and cranial components of SEP during hypothermia is interesting. Hypothermia has a more profound effect on synaptic transmission, represented by the cortical N20 latency, than on the peripheral nerve conduction velocity. Intraoperative monitoring of temperature is essential whenever SEPs are recorded. The sternal retractors were not responsible for the intraoperative SEP changes.