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Canadian Journal of Anesthesia, Vol 19, 339-350, Copyright © 1972 by Canadian Anesthesiologists' Society
1 Departments of Anaesthesia and Cardiology, The Research Institute, The Hospital for Sick Children and the Departments of Anaesthesia and Paediatrics, University of Toronto, Toronto, Ontario
Beagle dogs were anaesthetised with halothane, trichlorethylene or methoxyflurane, at various end tidal concentrations were ventilated to maintain arterial carbon dioxide tension constant.
Under light anaesthesia, serve arterial hypoxaemia caused significant increases in cardiac output, stroke volume and heart rate and a decrease in total systemic vascular resistance. Oxygen transport values during hypoxaemia remained close to control levels measured when the dogs were breathing air, unless the arterial oxygen tension fell below 25mm Hg. Then the oxygen transport values fell despite significant increases in cardiac output. The clinical signs of hypoxaemia were clear in the lightly anaesthetised dogs.
Under deep anaesthesia, the rise in cardiac output during hypoxaemia was not significant and the total systemic vascular resistance did not fall. Oxygen transport values decreased from the control levels. Some clinical signs of hypoxaemia were less striking than in the lightly anaesthetisted hypoxaemic dogs. Morbidity and mortality rates were high in this group.
We conclude that the cardiovascular response to hypoxaemia was well maintained only in those dogs under light anaesthesia with the agents studied.
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