Influence of anesthesia on cerebral blood flow and cerebral metabolism: an overview

Knowledge of the influence of anesthetics on cerebral blood flow and metabolism is the key to both safe neuroanesthesia practice and understanding the possible neuroprotection offered by these agents. In this paper the authors summarize recent data from the literature. All volatile anesthetics (except for nitrous oxide) produce a dose dependent decrease in cerebral metabolism. The changes in cerebral blood flow depend on the changes in cerebral metabolism and on direct vasodilatory effects; frequently volatile anesthetics increase cerebral blood flow. Cerebral autoregulation is dose-dependently altered. While CO2-response is preserved in the normal brain, this is not necessarily the case in injured brain or in presence of brain edema or tumor. Therefore, the volatile anesthetics are probably not the best choice when brain perfusion is impaired. Intravenous anesthetics (except ketamine) cause a dose-dependent decrease in cerebral metabolism and blood flow. Propofol has identical effects as the other intravenous agents. Autoregulation is preserved during the administration of propofol. The effects of narcotic agents depend largely on the background anesthetic. Pathological conditions induced physiologic changes, and coadministration of other drugs can greatly alter the effects of anesthetics on the brain.