SummaryT he objective of the study was to exam ine the changes in central nervous system (CNS) activity and physical behaviour during induction and awakening from CO 2 anaesthesia. Two studies, each using pigs immersed into 90% CO 2 gas for a period of 60 s were performed. In study 1, we monitored middle latency auditory evoked potentials (changes in latencies, amplitudes and a depth of anaesthesia index), electroencephalographic parameters (delta, theta, alpha and beta electroencephalographic power and 95% spectral edge frequency) and heart rate; and in study 2, we monitored body movements and arterial and venous partial pressure of CO 2 and O 2 . No behavioural signs of distress were observed during the early part of the induction. T he swine exhibited muscular activity from 13±30 s after induction-start as well as during awak ening from anaesthesia, possibly because of a transitory weaker suppression of the brain stem than of the cortex. T he CNS and blood gas param eters started to change from the very start of induction. T he CNS suppression lasted only approxim ately one minute after the end of the induction period. T he two studies indicated a good tem poral relationship between changes in amplitude, depth of anaesthesia index, spectral edge frequency, and arterial P CO 2 during the induction period.
The authors conclude that the MLAEP peaks and the AAI correlate well to the MOAAS, whether extracted by MTA or ARX, but the ARX method produced a significantly shorter delay than the MTA.
A method is described for measuring middle-latency auditory evoked potentials (MLAEP) in consciously awake, non-sedated pigs during the induction of thiopentone anaesthesia (0.6 ml/kg, 2.5% thiopentone solution). It was done by using autoregressive modelling with an exogenous input (ARX). The ability to perceive pain during the induction was compared with (1) the changes in latencies and amplitudes of the MLAEP, (2) the change in a depth of anaesthesia index based on the ARX-model and (3) the change in the 95% spectral edge frequency. The pre-induction MLAEP was easily recordable and looked much like the one in man, dogs and rats. The temporal resolution in the ARX method was sufficiently high to describe the fast changes occurring during induction of thiopentone anaesthesia. As previously reported from studies in man, dogs and rats, induction of thiopentone anaesthesia resulted in significantly increased latencies and decreased amplitudes of the MLAEP trace as well as in a significantly reduced depth of anaesthesia index and spectral edge frequency. None of the changes, however, related well to the ability to react to a painful stimulus. Whether an ARX-based depth of anaesthesia index designed especially for pigs might be better than the present index (designed for man) for assessing depth of anaesthesia must await the results of further studies.
Background The objective of this study was to prospectively test the Cerebral State Index designed for measuring the depth of anesthesia. The Cerebral State Index is calculated using a fuzzy logic combination of four subparameters of the electroencephalographic signal. The performance of the Cerebral State Index was compared with that of the Bispectral Index and the A-Line ARX Index. Methods This study applied raw data from two previously published clinical protocols. The patients in protocol 1 were given a continuous propofol infusion, 300 ml/h, until 80% of burst suppression occurred. In protocol 2, a stepwise increased target-controlled infusion of propofol was administered to patients until loss of response to noxious stimuli while the Observer's Assessment of Alertness and Sedation was registered every 4 min. The Cerebral State Index was calculated off-line from the recorded electroencephalographic data. The Spearman rank correlation coefficient between electronic indices and the effect site concentration of propofol was calculated along with the prediction probability of each index to predict the Observer's Assessment of Alertness and Sedation level. Results The Spearman rank correlation coefficients between the Cerebral State Index, Bispectral Index, and A-Line ARX Index and the propofol effect site concentration were -0.94, -0.89, and -0.82, respectively, in protocol 1, whereas the prediction probability values between the Cerebral State Index, Bispectral Index, and A-Line ARX Index and the Observer's Assessment of Alertness and Sedation score in protocol 2 were 0.92, 0.93, and 0.91, respectively. Conclusion The Cerebral State Index detects well the graduated levels of propofol anesthesia when compared with the propofol effect site concentration and the Observer's Assessment of Alertness and Sedation score.
The aim of this study was to assess unconsciousness in pigs during exposure to CO2 through changes in the middle latency auditory evoke potentials (MLAEP) of the central nervous system (CNS), blood parameters (pH, carbon dioxide partial pressure [pCO2], oxygen partial pressure [pO2], oxygen saturation [SatO2] and bicarbonate [HCO−3]), behaviour and the corneal reflex. The MLEAP did not decrease significantly until after 60 s exposure to CO2. The blood parameters (decreased pH, pO2 and SatO2 and increased pCO2 and HCO3) changed 53 s after the onset of immersion. The burst suppression index (BS%) and the A-line ARX index (AAI) from the MLEAP recovered basal levels at 136 and 249 s, respectively. The first blood parameter to return to basal levels was HCO−3 at 76 s of exposure, followed by SatO2 at 180 s, pH and pO2 at 210 s and pCO2 at 240 s. During exposure to the gas, pigs exhibited lateral head movements and sneezing (10.3 s), gasping (23.5 s) and vocalisation (26.1 s). Furthermore, all pigs demonstrated muscular excitation after between 19 and 39 s exposure, when the AAI and BS% values were not significantly different from basal values. It was suggested, therefore, that these excitatory movements represent conscious movement, indicative of aversion to the gas. According to our results, loss of consciousness began, on average, after 60 s inhalation of 90% CO2. During exposure to the gas, decreased brain activity was seen, immediately following the changes in blood parameters. Following exposure, the restoration of blood parameters to basal levels allows a return to normal brain activity.
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