Abstract
This study svas 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 5 mg·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\(Pa_{CO_2 } \) 3.33 kPa (25 mm Hg) while blood pressure was kept at baseline levels (hyperventilation alone), and 10 dogs were hyperventilated to\(Pa_{CO_2 } \) 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/l 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.
Résumé
Cette étude a pour objectif ľévaluation de ľoxygénation cérébrale du chien hyperventilé et hypotendu sous anesthésie générale. La tension en oxygène cérébral et musculaire, le lactate, pyruvate et la créatine-phosphokinase (CPK) du liquide céphalo-rachidien ont servis de tests de mesure de ľhypoxie cérébrale.
Vingt chiens ont été anesthésiés au thiopentone 5 mg · kg-1 et intubés. Ľanesthésie a été maintenue au protoxyde-oxygène (50/50), à ľhalothane 0.5 pour cent et au pancuronium 0.1 mg · kg-1 pendant une période ďune à deux heures sous ventilation contrôlée. Cinq chiens ont été maintenus en normocapnie et normotension, cinq furent hyperventilés à une\(Pa_{CO_2 } \) de 3.33 kPa (25 mmHg) tout en maintenant la pression artérielle à la valeur initiale de base (hyperventilation seule), et 10 chiens furent hyperventilés à une\(Pa_{CO_2 } \) de 3.33 kPa (25 mmHg) après quoi on a produit une hypotension artérielle jusqu’à une valeur moyenne de 6.65 kPa (50 mmHg) avec du nitroprussiate de soude et de ľhalothane (hyperventilation et hypotension).
Pendant ľhyperventilation seule, le lactate céphalo-rachidien a augmenté de façon significative comparativement au contrôle; cette augmentation s’est accrue jusqu’à plus de 4 mmol/l lorsque ľhyperventilation a été associée à ľhypotension. Cet accroissement progressif du lactate lors de ľassociation hyperventilation-hypotension a été significative à la fin de la deuxième heure ďhypotension. Le rapport lactate-pyruvate du liquide céphalorachidien et la CPK n’ont augmenté de façon significative que lors de ľassociation hyperventilation-hypotension.
La tension en oxygène du muscle et du cerveau a diminué comparativement à la valeur initiale de base de façon significative avec ľhyperventilation seule, alors que la chute atteignait 2.66 kPa (20 mmHg) avec ľassociation hyperventilation-hypotension. On a trouvé une bonne corrélation entre les changements de tension en oxygène musculairee et cérébral pour les trois groupes (r - 0.914, p < 0.05 et r - 0.908, p < 0.05) respectivement et pour tous les groupes réunis.
Ces données prouvent que ľassociation hyperventilation-hypotension à des niveaux généralement acceptés cause une insuffisance de ľapport ďoxygène cérébral chez le chien anesthésié. Bien que les tensions en oxygène du muscle et du cerveau réflètent le degré ďhypoxie, leur utilité comme moniteurs clinique est probablement limitée.
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References
Eckenhoff, J.E. Deliberate hypotension. Anesthesiology48: 87 (1978).
Michenfelder, J.D., Gronert, G.A. &Rehder, K. Neuroanesthesia. Anesthesiology30: 65(1969).
Sugioka, K. &Davis, D.A. Hyperventilation with oxygen — a possible cause of cerebral hypoxia. Anesthesiology21: 135 (1960).
McDowall. D.G. Monitoring the brain. Anesthesiology45: 117 (1976).
Nilsson. L. &Siesjö. B.K. The effect of deep halothane hypotension upon labile phosphates and upon extra-and intracellular lactate and pyruvate concentrations in the rat brain. Acta Physiol. Scand.81: 508 (1971).
Smith, A.L. Barbiturate protection in cerebral hypoxia. Anesthesiology47: 285 (1977).
Michenfelder, J.D. &Theye, R.A. Canine systemic and cerebral effects of hypotension induced by hemorrhage, trimetaphan, halothane or nitroprusside. Anesthesiology46: 188 (1977).
Harper. A.M. &Glass, H.I. Effect of alterations in the arterial carbon dioxide tension on the blood flow through the cerebral cortex at normal and low arterial blood pressures. J. Neurol. Neurosurg. Psychiat.28: 449 (1965).
Okuda. Y. McDowall. D.G., Ali, M.M.,et al. Changes in CO2 responsiveness and in autoregulation of the cerebral circulation during and after halothane-induced hypotension. J. Neurol. Neurosurg. Psychiat.39: 221 (1976).
Harp, J.R. &Wollman, H. Cerebral metabolic effects of hyperventilation and deliberate hypotension. Brit. J. Anesth.45: 256 (1973).
Shenkin, H.A. &Bouzarth, W.F. Clinical methods of reducing intracranial pressure. New Eng. J. Med.282: 1465 (1970).
Salem, M.R., Wong, A.Y., Bennett, E.J.,et al. Deliberate hypotension in infants and children. Anesth. and Anal.53: 975 (1974).
Thompson, G.E., Miller, R.D., Stevens. W.C.,et al. Hypotensive anesthesia for total hip arthroplasty: a study of blood loss and organ function (brain, heart, liverand kidney). Anesthesiology48: 91 (1978).
Marbach. E.P. &Weil, M.H. Rapid enzymatic measurement of blood lactate and pyruvate. Clinical Chem.13: 314 (1967).
Rosalki, S.B. An improved procedure for serum CPK determination. J. Lab. Clin. Med.69: 696 (1967).
Dean, R.B. &Dixon, W.J. Simplified statistics for small number of observations. Analytical Chem.23: 636 (1951).
SIEGEL, S. Nonparametric Statistics for the Behavioral Sciences. New York: McGraw-Hill (1956), pp. 202–213.
Siesjö, B.K. Brain Energy Metabolism. New York: John Wiley and Sons (1978), pp. 417–428.
Plum, F., Posner, J.B. &Smith, W.W. Effect of hyperbaric-hyperoxic hyperventilation on blood, brain, and CSF lactate. Am. J. Physiol.215: 1240 (1968).
Cohen, R.D. &Simpson, R. Lactate metabolism. Anesthesiology43: 661 (1975).
Siesjo, B.K. The influence of respiratory disturbances on acid-base and energy metabolism of the brain. Intens. Care Med.3: 245 (1977).
Maas, A.I.R. Cerebrospinal fluid enzymes in acute brain injury 2. Relation of CSF enzyme activity to extent of brain injury. J. Neurol., Neurosurg. and Psychiat.40: 666 (1977).
Sherwin, A.L., Norris, J.W. &Bulcke, J.A. Spinal fluid creatine kinase in neurological disease. Neurology19: 993 (1969).
Wolintz, A.H., Jacobs, L.D., Christoff. N.,et al. Serum and cerebrospinal fluid enzymes in cerebrovascular disease. Arch. Neurol.20: 54 (1969).
Furuse, A., Brawley. R.K., Struve, E.,et al. Skeletal muscle gas tension: Indicator of cardiac output and peripheral tissue perfusion. Surgery74: 214 (1973).
McHugh, R.D., Epstein. R.M. &Longnecker, D.E. Halothane mimics oxygen in oxygen micro-electrodes. Anesthesiology50: 47 (1979).
Eckenhoff, J.E., Hale Enderby, G.E., Larson, A.,et al. Human cerebral circulation during deliberate hypotension and head-up tilt. J. Appl. Physiol.18: 1130 (1963).
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Levin, R.M., Zadigian, M.E. & Hall, S.C. The combined effect of hyperventilation and hypotension on cerebral oxygenation in anaesthetized dogs. Canad. Anaesth. Soc. J. 27, 264–273 (1980). https://doi.org/10.1007/BF03007438
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DOI: https://doi.org/10.1007/BF03007438