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Canadian Journal of Anesthesia, Vol 27, 264-273, Copyright © 1980 by Canadian Anesthesiologists' Society
1 Northwestern University and Children's Memorial Hospital, Chicago, II-linois 60614 U.S.A.
This study was done to evaluate cerebral oxygenation in dogs under general anaesthesia with combined hyperventilation and hypotension. Cerebral and muscle oxygen tensions, cerebrospinal fluid lactate, pyruvate, and creatine phosphokinase (CPK) were measured to test for cerebral hypoxia.
Twenty dogs were anaesthetized with thiopentone 5mg·kg-1 and their tracheae were intubated. Anaesthesia was maintained with nitrous oxide and oxygen (50/50), halothane 0.5 per cent, pancuronium 0.1 mg·kg-1 per 1-2 hours and ventilation was controlled. Five dogs were maintained at normocapnia and normotension, five dogs were hyperventilated to PaCOCO2 3.33 kPa (25 mm Hg) while blood pressure was kept at baseline levels (hyperventilation alone), and 10 dogs were hyperventilated to PaCOCO2 3.33 kPa(25 mm Hg) followed by deliberate hypotension to a mean arterial pressure of 6.65 kPa (50 mm Hg) with the use of nitroprusside and halothane (combined hyperventilation and hypotension).
Cerebrospinal fluid lactate increased significantly from control during hyperventilation alone, with an even greater increase to above 4 mmol/1 during combined hyperventilation and hypertension. The incremental rise of lactate with combined hyperventilation and hypotension was significant at the end of the second hour of hypotension. Cerebrospinal fluid lactate/pyruvate ratios and CPK increased significantly above control only with combined hyperventilation and hypotension.
Oxygen tension of muscle and brain decreased from baseline with hyperventilation alone and decreased further to 2.66 kPa (20 mm Hg) after combined hyperventilation and hypotension. Good correlation was found between changes in oxygen tension of muscle and brain in the three groups (r - 0.914, p < 0.05 and r - 0.908, p < 0.05), respectively, for all groups combined.
Evidence is thus presented that the combination of hyperventilation and hypotension to accepted levels causes inadequate cerebral oxygen supply in anaesthetized dogs. Although muscle and brain oxygen tensions reflected the degree of cerebral hypoxia, their usefulness as clinical monitors is likely to be limited.
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