The issue of cerebral circulation and oxygen delivery to the brain requires constant vigilance for the clinician in the ICU, the trauma unit and the neurosurgical operation suite. These patients are administered anaesthetic medications that affect cerebral physiology by a lot of different and some times unexplored mechanisms. Apart from the electrophysiologic field which will not be discussed herein, Cerebral Blood Flow (CBF) and Cerebral Metabolic Rate of O2 consumption (CMRO2) are mainly affected by the anaesthetics. Meanwhile, these factors dominantly determine the intracranial blood volume (CBV) and hence intracranial pressure (ICP).
Almost all intravenous anaesthetics (barbiturates, propofol, benzodiazepines) decrease CMRO2 and consequently reduce CBF in a more or less analogous form. The same stands for lidocaine. Ketamine is an exception by stimulating NMDA receptors and thus increasing CMRO2, CBF and ICP.
Volatile anaesthetics in clinically useful concentrations produce small decreases or no effect on CBF but reduce CMRO2 considerably and dose-dependently. Nitrous oxide when administered alone stimulates cerebral activity and increases CMRO2, CBF and ICP. When administered simultaneously with intravenous anesthetics these effects are blunted whereas in conjunction with volatile anesthetics they are augmented.
Opioids tend to reduce CBF and CMRO2 and significantly attenuate increases produced by other anesthetics. Neuromuscular blockers exert no direct effect on cerebral hemodynamics and can only affect cerebral physiology by stimulating histamine release (not all on them) or by adrenergic stimulation.
While all these effects are quite strongly proven in clinical trials, it is imperative to keep in mind that interactions of all medications used in anesthesia can present an entirely different pattern of effects in clinical conditions.