• J Swartz, M Cummings, W Pucci, and D Biehl.
• Can Anaesth Soc J. 1985 Nov 1; 32 (6): 577-82.

AbstractThe effects of anaesthetic agents, per se, on the asphyxiated foetus are difficult to quantitate clinically. Anaesthesia is often necessary in foetal distress, however, to effect a rapid delivery. To investigate the effect of general anaesthetic agents commonly used for Caesarean section we administered these agents to 18 chronically prepared pregnant ewes with asphyxiated foetuses in utero. The foetuses were asphyxiated by partial occlusion of the umbilical cord until foetal arterial pH had decreased from 7.30 to a range of 7.08-7.13. The animals were divided into three groups: Group A which received no anaesthesia and thus served as a control, Group B which received thiopentone (3 mg . kg-1) intravenously followed by 50 per cent nitrous oxide and 0.5 per cent halothane in oxygen for 15 minutes, and Group C which received thiopentone (3 mg . kg-1) followed by one per cent halothane in oxygen for 15 minutes. Foetal cerebral, myocardial, and renal blood flows were measured by injection of radioactive microspheres after production of asphyxia and after 5 and 15 minutes of anaesthesia. General anaesthesia in both groups B and C abolished the hypertension and bradycardia produced by foetal asphyxia secondary to umbilical cord occlusion. There were no significant differences between Groups B and C in foetal pH, PCO2, or PO2. Two foetuses in the nitrous oxide group died after ten minutes of anesthesia, but the aetiology of the sudden demise is unclear. We conclude that general anaesthesia abolishes the foetal response to umbilical cord occlusion and does not improve foetal oxygenation or acid-base status.

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