Inhalation anesthetic agents induce anesthesia by depressing brain function via a dose-dependent reversible mechanism that is associated with alterations in cerebral metabolic rate (CMR), in cerebral blood flow (CBF), of the electroencephalogram (EEG), and of evoked potentials. The alterations in CMR and CBF can be attenuated to some extent, but not completely, and therefore can adversely affect outcome in patients with neurologic diseases and in patients undergoing neurosurgical procedures.

Flow-metabolism coupling is defined as a matching of O₂ and glucose delivery to metabolic demand; CBF increases or decreases in concordance with changes in CMR. A misconception about the inhalation anesthetic agents is that, because they increase CBF and decrease CMR, they “uncouple” flow and metabolism. In fact, although increasing concentrations of inhalation anesthetic agents result in a higher CBF for a given CMR, a coupled relationship between these variables persists (Figure 67-1).

This relationship between CMR and CBF is apparent only if adequate blood pressure is maintained; if blood pressure is allowed to decrease, the increase in CBF will be attenuated or abolished because inhalation anesthesia agents inhibit autoregulation in a dose-dependent fashion (Figure 67-2). However, inhalation anesthetic agents do not inhibit CO₂ reactivity and, if anything, may actually exaggerate the response. Thus, in the normal brain, the cerebral vasodilation that occurs in response to an inhalation anesthetic agent can be blunted, abolished, or reversed by decreasing CO₂ levels; however, these responses may not apply in the presence of abnormal intracranial anatomy or physiology.

Because the inhalation agents cause an increase in CBF (and in cerebral blood volume [CBV]), the use of these anesthetics in patients at risk for developing or who have increased intracranial pressure (ICP) is a concern. However, numerous studies have confirmed that hypocapnia attenuates or blocks the increase in ICP that otherwise would occur in at-risk patients.

Anesthesia-induced EEG changes follow a common pattern. When anesthesia is induced with an inhalation agent, the frequency and amplitude of the EEG waveforms increase, and the measurements throughout the cortex are more uniform, such that waveforms measured on the EEG appear to synchronize. At about 1 minimum alveolar concentration (MAC), the EEG slows progressively; depending on the anesthetic agent, burst suppression, an isoelectric pattern, or seizures may evolve as the anesthetic concentration increases.

Michenfelder defined critical regional CBF as “that flow below which the majority of subjects develop ipsilateral EEG changes indicative of ischemia within 3 min following carotid occlusion.” Table 67-1 lists the critical CBF rates of various inhalation anesthetic agents.

The inhalation agents also affect evoked potentials, but only minimally so at concentrations below 1 MAC. All anesthetic agents tend to increase latencies and decrease amplitudes of evoked potentials at concentrations greater than 1 MAC. Evoked potentials of cortical origin are particularly sensitive to the effects of inhalation anesthetic agents; brainstem auditory evoked potentials are the most resistant. Although more sensitive to the effects of inhalation anesthetic agents, somatosensory evoked potentials can be adequately monitored at less than 1 MAC of the inhalation anesthetic agent.