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KMID : 0377519840090040623
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Chung-Ang Journal of Medicine
1984 Volume.9 No. 4 p.623 ~ p.631
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Effect of Hyperventilation on Cerbral Blood Flow, Cerebral Metabolic Rate and Cerebral Vascular Resistance in Enflurane Anesthesia
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Kim Dong-Soo
Cho Hyung-Sang
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Abstract
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It is generally presumed that halothane and enflurane anesthesia impair the cerebral authoregulatory mechanism. Autoregulation of cerebral blood flow may be described as the ability of the brain to maintain an adequate blood flow consistent with its metabolic needs; independent of changes in peripheral hemodynamics. So that increasing the depth of anesthesia to 1 MAC at normocarbia totally eliminates effective cerebral autoregulation. It is documented well that the effect of 1 MAC anesthesia on cerebral autoregulation of blood flow is potentiated by hypercarbia and antagonized by hypocarbia, indicating that the vascular response to PCO_2 fluctuations remains intact. This experiment was designed for the observation of the effect of hyperventilation followed by hypocarbia under enflurane anesthesia on the cerebral blood flow, cerebral metabolic rate and cerebral vascular resistance from the argon desaturation technique by mass spectrometer. Seven unpremedicated, fasted, dogs were anesthetized with enflurane(2 vol%) in oxygen and ventilation was controlled with a anesthesia ventilator. Teflon catheters of mass spectrometer were inserted into the femoral artery and the jugular bulb for pressure monitoring. The mass spectrometer continuously and simultaneously analyzed the partial pressure of oxygen, carbon dioxide and argon in the internal jugular vein and the femoral artery for both saturation and desaturation phases. These were simultaneously recorded on a polygraphy. The following results were obtained: 1. Mean cerebral blood flow of control group under normal ventilation was 51.0±8.3ml/100g/min and it was reduced by 22% by hyperventilation (p＜0.05). 2. Mean cerebral blood flow of enflurane group under normal ventilation was increased by 18%, 59.5±6.0ml/100g/min, in comparison with control group (p＜0.05) and it was reduced by 14% by hyperventilation (p＜0.02). 3. Mean cerebral metabolic rate for oxygen of control group under normal ventilation was 2.8±0.3ml/100g/min and it was reduced by 21% by hyperventilation (p＜0.05). 4. Mean cerebral metabolic rate for oxygen of enflurane group under normal ventilation was decreased by 32%, 1.9±0.2ml/100g/min, in comparison with control group (p＜0.001) and it was reduced by 14% by hyperventilation (p＜0.05). 5. Mean cerebral vascular resistance of control group under normal ventilation was 2.6±0.4㎜Hg/ml/100g/min and it was increased by 30% by hyperventilation (p＜0.05). 6. Mean cerebral vascular resistance of enflurane group under normal ventilation was decreased by 43%, 1.4±0.1㎜Hg/ml/100g/min, in comparison with control group (p＜0.005) and it was increased by 8% by hyperventilation (p＜0.05). 7. Mean cerebral blood flow of enflurane group under hyperventilation was not different statistically from that of control group; however mean cerebral metabolic rate for oxygen and cerebral vascular resistance of enflurane group under hyperventilation were reduced significantly in comparison with control group (p＜0.001 and p＜0.005). 8. Mean arterial pressure of enflurane group under normal ventilation was decreased by 34%, 87±5㎜Hg, in comparison with control group (p＜0.01) and it was reduced by 7% by hyperventilation (p＜0.05).
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