EFFECTS OF ANESTHETIC AGENTS ON INTRACRAN IAL-PRESSURE

Barbiturates, etomidate and propofol decrease cerebral blood flow (CBF ), mediated by a decrease in cerebral metabolism, thus decreasing intr acranial pressure (ICP). As the reduction in CBF is secondary to a dec rease in cerebral metabolism, these agents will have little effect on CBF or ICP in patients without active cerebral metabolic activity. Ket amine is usually not administered for the anaesthetic management of pa tients at risk of intracranial hypertension because of the reported in creases in cerebral metabolism, CBF and ICP. The increase in CBF, howe ver, may be partly mediated by a sympathetically induced increase in b lood pressure and partly by a simultaneous increase in PaCO2 in sponta neously breathing patients. More recent studies report no increase in ICP or flow when ventilation is controlled or when other agents are as sociated. There is renewed interest in ketamine because it blocks exci tatory amino acid receptors in the brain. Synthetic opioids including fentanyl, sufentanil, and alfentanil have been reported to cause an in crease in ICP in patients with various intracranial lesions. When bloo d pressure was supported, no clinically relevant increase in ICP or fl ow velocity with alfentanil or sufentanil was observed. Thus, the incr ease in ICP reported with these agents may be related to the compensat ory autoregulation-mediated vasodilation, underscoring the importance of administratering these agents carefully to avoid systemic hypotensi on. Halothane consistently increases CBF and should not be used in pat ients with increased ICP. In contrast, isoflurane does not cause incre ase in CBF at concentrations below 1 to 1.5 MAC, although the effects on cerebral blood volume are less clear. Desflurane and sevoflurane ha ve similar effects. CO2 reactivity is preserved with all inhaled agent s. In patients with increased ICP however, it would be preferable to a void these agents or to administer very low doses.