Relationship of cerebral blood flow, cerebral metabolism, and electroencephalography to outcome in acute experimental compression ischemia--barbiturate effects on delayed brain swelling.

Acute compression ischemia was induced in 30 cats by progressive inflation of an epidural balloon, followed by rapid decompression. Changes in intracranial pressure, mean arterial blood pressure, cerebral blood flow (CBF), arteriovenous oxygen difference (AVDO2), cerebral metabolic rate of oxygen (CMRO2), and electroencephalography (EEG) were studied in 13 untreated animals and in seven animals receiving barbiturate. Ten cats with cardiovascular or respiratory problems, or intracranial hematoma were excluded from the study. In untreated animals, six (46%) survived with no brain swelling and were classified as the "no swelling group," and seven (56%) died from fatal brain swelling and were classified as the "delayed swelling group." All animals with barbiturate therapy showed no brain swelling. Serial measurement of CBF, AVDO2, and CMRO2 indicated the existence of postischemic delayed hypoperfusion associated with relative hypermetabolism in untreated animals. Good recovery of CBF and CMRO2 was observed in the "no swelling group," and poor recovery in the "delayed swelling group." The time course of the total fast-wave components on EEG was quite similar to that of CMRO2, and the time course of the "CBF index," which is % fast-wave component of EEG divided by AVDO2, was similar to that of CBF. Barbiturates reduced CMRO2 and fast-wave component during administration, possibly improving the relatively hypermetabolic state, and reduced the mortality rate to 0%. The maximum effects of barbiturate could be expected by administering the drug at the stage of delayed hypoperfusion with relative hypermetabolism, indicated by rapid recovery of the % fast-wave component, high AVDO2, and low CBF index.