Nitrous oxide effects on EEG and awareness

Studies of the behavioural and electrophysiological effects of nitrous oxide (N2O) are of importance because of its wide use, occasional abuse and its proposition as a model for studying the effects of sedatives and anaesthetics on memory and cognition. The gas is the first drug whose effects on memory and cognition have been studied, dating from 1799. Its effects on the electroencephalogram (EEG) were also described shortly after the introduction of the EEG. The drug causes a decrease in amplitude and frequency of alpha rhythm and activation of high beta range frequencies. Initiation of inhalation of the gas and its cessation may result in transient high amplitude delta activity, a relatively uncommon phenomenon. When used in combination with other anaesthetic agents, the EEG effects become additive. The gas does not change the bispectral index (BIS) or the early auditory evoked potentials (AEP). However, the somatosensory evoked potentials and the P300 of the AEP are sensitive. Also, when the gas is added to a propofol anaesthetic, it increases the BIS value at which subjects would not respond. N2O in subanaesthetic concentrations produces substantial impairment of learning in humans and animals. Explicit memory may be more impaired than implicit memory. Surgery may enable more learning resulting in a relatively high incidence of recall of intra-operative events when N2O is used as the sole anaesthetic. A relatively high incidence of unpleasant dreams and unconscious memory may also occur under the same conditions. Opioid supplementation of the gas is not adequate to block these sequelae during surgery. The addition of potent volatile agents, in end-tidal concentrations of at least 0•8–1 MAC, or intravenous anaesthetics should obliterate these types of memories.