A New Artificial Respirator

Fig. 5 shows actual changes in blood urea recorded during thiopentone / D-tubocurarine chloride/ nitrous oxide/oxygen anaesthesia with manually controlled respiration. It can be seen from the results of seven cases investigated that the degree of hyperventilation that occurs during manually controlled respiration has a negligible effect on the blood urea, and in only one case was there any possibility of urea being incriminated as a cause of potentiation of thiopentone. It is interesting to note that in the one case in which a rise in urea was noted an excessive degree of hyperventilation wvas produced for investigational purposes. It would seem that with controlled respiration as carried out during anaesthesia there are no deleterious effects on kidney function and no marked rise in blood urea. Loss of consciousness can follow hyperventilation if this is carried to extremes (McCance, 1935; Seevers et al., 1939). A diminution in cerebral blood flow of the order of 30% lpart of a general peripheral vasoconstriction) with an average increase of 15% in cerebral oxygen consumption has been reported (Kety and Schmidt, 1946). These would lead to a certain degree of cerebral anoxia, which may be aggravated by the effects of lowering the C02 tension on the oxygen dissociation curve of blood. While more oxygen can be taken up by the blood in the lungs, less will be given oftto the tissues (Barach et al., 1947). While it is known that potentiation of barbiturate anaesthesia can be accomplished by any means whereby central anoxia is produced (Peterson, Shideman, and Linares, 1950), this could not have played a part in the potentiation of thiopentone observed during manually controlled respiration. In these cases the degree of hyperventilation was so slight that none of the anaesthetists concerned realized that they were in fact hyperventilating the patients until they were told of the pH changes of the blood. Furthermore, using the thiopentone/ D-tubocurarine chloride/nitrous oxide/oxygen sequence with manually controlled respiration of the same degree as in the series of cases referred to earlier, Prime and Gray (1952) found peripheral vasodilatation rather than vasoconstriction. The fact that a patient is not breathing spontaneously will reduce the tone of the intercostals and hence abdominal muscles. If thiopentone/nitrous oxide/oxygen were used without a muscle relaxant, controlled respiration would reduce the amount of barbiturate required to produce satisfactory relaxation. This does not apply directly to the cases described above, but is the probable explanation of the lowered requirements of D-tubocurarine chloride observed at the end of two hours' anaesthesia with manually controlled respiration, as compared with patients who were allowed to breathe spontaneously. All of the arguments quoted above are applicable to the anaesthetic technique described by Brennan (1952). With doses of 500 mg. of thiopentone for a large healthy adult he was able to produce long periods of narcosis. Undoubtedly he used a higher percentage of nitrous oxide (75%,h) to obtain a better analgesia, but it is doubtful if this actually resulted (Seevers et al., 1937). Hyperventilation was purposely carried out from the beginning of the operation, and the changes in pH of the blood must have been greater than those recorded in either Fig. 2 or Fig. 4.