This paper is an attempt to provide an exhaustive review of work in the area of automatic control of depth of anaesthesia. It includes systems using both open and closed-loop control and describes 37 papers from 1949 through 1980.
A control system was used to bring the tension of anaesthetic in the brain to any value specified (in MAC units) by the anaesthetist and then maintain it constant until a new value was specified. The control was applied to a volatile agent but allowance was automatically made for the anaesthetic effect of any nitrous oxide concomitantly administered by the anaesthetist. The inspired concentration required to achieve the desired brain tension was calculated from a model of the patient and set automatically on the vaporizer. The quantification of the model was matched to the patient on the basis mainly of body mass and periodic non-invasive measurements of alveolar ventilation and cardiac output. In order to adapt the model to the patient an arterial blood sample was taken every 30 min to obtain the arterial tension of halothane for use as feedback. The system has been tested on eight Alsatian dogs. After omitting results affected by avoidable errors, the SD of the measured-to-computed arterial tension ratio was less than 10%.
Seven Alsatian dogs were anaesthetized with thiopentone, paralysed with pancuronium, and ventilated with 1% halothane in a mixture of air and oxygen in such a way as to maintain Paco2 at 40 mm Hg and Pao2 at 150 mm Hg. From various respiratory and circulatory measurementts the following variables were determined: physiologicaldeadspace, cardiac output, venous admixture, respiratory compliance and resistance, and oxygen and carbondioxide exchcnage. After a controlseries of measurements at a ventilator frequency of was doubled to 50/min and adjustments to tidal volume and inspired oxygen concentration made to maintain constancy of blood gas tensions. The same procedure was followed again at 25/min, l/min and finally at 25/min. At each frequency the I:E ratio was kept at 1/2, the shape of the inspiratory flow waveform was kept constant (a rapid increase followed by a steady decline to zero) and expiration was passive to atmosphere. Mean results showed that physiological deadspace changed relatively little with frequency so that the deadspace:tidal volume ratio increased significantly on changing to 50/min (by 24%) and decreased significantly on changing to 6/min (by 46%). Changes of cardiac output and venous admixture were either not significant or on the borderline of significance and the 95% confidence limits of these changes were within +14%, --12% for cardiac outpur and within plus or minus1.4% of cardiac output for venous admixture. Tt is concluded that, provided Paco2 and Pa02 and mean air way pressure are kept constant, the frequency of ventilation is not important, even over a wide range of values.
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