ABSTRACT
The use of controlled hyperventilation during neurosurgical procedures prevents the deleterious effects of hypercarbia on the cerebral blood flow and intracranial pressure. hyperventilation with hypocarbia produces cerebral vasoconstriction, reduced cerebral blood flow and a reduction in brain size in the majority of patients with increased intracranial pressure. But since excessive cerebral vasoconstriction might induce cerebral ischemia, there has been much discussion concerning the optimal level of hypocarbia. Several studies have shown biochemical evidence of a change in cerebral glucose utilization to anaerobic metabolism during hypocarbia. In our investigation, the effect of hyperventilation on 10 neurosurgical patients was evaluated by blood gas analysis and the estimation of lackate and pyruvate in arterial blood and the cerebrospinal fluid. The results were as follows: 1) PaCO2 decreased from a prearesthetic value of 38+/-2.2 mmHg to 22+/-2.1mmHg 1 hour postinduction and 24+/-2.2mmHg at 2 hours due to hyperventilation. pH was 7.58+/-0.047 1 hour postinduction and 7.56+/-0.018 at 2 hours. PaO2 was 251+/-33.0mmHg 1 hour postinduction 1 hour and 215+/-20.9mmHg at 2 hours under a 50% inspired oxygen concentration(FiO2=0.5). 2) The arterial blood lactate value increased statistically significantly from a preanesthetic value of 9.3+/-1.5mg% to 11.8+/-1.47mg% 1 hour postinduction(p<0.01) to 12.5+/-1.53mg% at 2 hours(p<0.005). However all values were within the normal range(4.7+/-15.1mg%), and the lacte/pyruvate ratio did not change. 3) In the cerebrospinal fluid, pH was 7.45+/-0.057, PCO2 was 34+/-3.5mmHg and PO2 was 91+/-6.7mmHg following hyperventilation for 1 hour. The lactate value of the cerebrospinal fluid was 19.2+/-3.14mg%(normal range: 11.0~27.0mg%) and the lactate/pyruvate ration was 14.5+/-2.39. 4) No evidence of an excessive increase in CSF lactate was seen in any case. The above findings suggest that maintenance of an adequate oxygen concentration and a carbon dioxide value over 20mmHg would prevent cerebral ischemia following hypocarbia due to hyperventilation.