We performed experiments to study the effects of acutely increased intracranial ´ pressure on cerebral gas metabolism. The results and findings were reported to The Journal of Catholic Medical College, (Vol. 24) 1973.
We thereafter evaluated cerebral gas metabolism of fifty patients with Acute cerebral lesions. Cerebral gas metabolism was measured by determining the pO2, PCO2, and. pH values of arterial and venous blood and of the cerebrospinal fluid. Samplings of venous blood were obtained from the internal jugular vein. In the. determination of the p11, p02. and pCO2 of arteria_+ and venous blood and cerebro-spinal fluid, the "Radiometer BMS 3b with Digital Acid-Base Analyser PHM 72" was used. These 50 patients ha4 their gas metabolism measured at interval of 2 or 3 days, from the time of their admission to the time of either their recovery or death.
The following observations were made
1. The 50 patients studied and observed included.
a) Brain contusion 13 cases
b) Epidural or subdural hematoma, 11 cases
c) Skull fracture 10 cases
d) Intracerebral hemorrhage 5 cases
e) Scalp laceration 1 cases
f) Arteriovenous malformation or cerebral rete 5 cases
g) Traumatic subarachnoid hemorrhage 1 cases
h) Intracranial aneurysm 4 cases
2. These 50 patients have been subdivided according to level of consciousness as follows:
a) Group A-Those who were alert with no neurological deficit.
b) Group B-Those who were drowsy with mild neurological deficit.
c) Group C-Those who were stuporous with severe neurological deficit.
d) Group D-Those who were in coma.
3. It was observed that the pH, 102, and pC02. content of the arterial and venous blood and cerebrospinal fluid of those in Group A were within normal ranges.
4. Many cases classified under Group B had respiratory alkalosis of the arterial blood. However those who recovered or became worse revealed no noticeable changes in the cerebral gas metabolism studies.
5. Many cases classified under Group C had respiratory "alkalosis in their arterial blood but only a few showed metabolic acidosis in the cerebrospinal fluid. However the patients who became worse manifested a marked metabolic acidosis in the corebrospinal fluid.
6. Several patients in Group D had severe respiratory alkalosis as well as metabolic alkalosis in their arterial blood and marked metabolic acidosis ih the their cerebrospinal fluid.
7. "Luxury perfusion syndrome" was not seen in any of the fifty cases studied.
8. Only a few cases manifested arterial hypoxemia in the all group.
We believe this was due to the fact that tracheostomy and hyperventilation were done in the early stages with the aim of reducing the raised intracranial pressure.
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