All inhalational agents, including isoflurane, decrease cerebral metabolic rate of oxygen (CMRO2). It is known that isoflurane can cause burst-suppression as well. The CMRO2-decreasing effect does not seem to be significantly different between isoflurane, sevoflurane, and desflurane.
All intravenous induction agents, except ketamine, decrease CMRO2 but preserve CMRO2 – cerebral blood flow (CBF) coupling such that a decrease in CMRO2 is matched by a decrease in CBF. They also tend to decrease CBF (CBF-CMRO2 coupling mechanism) due to their suppressive effect on CMRO2. However, even though both inhalational and most intravenous agents decrease CMRO2, their effects on CBF are distinct. Inhalational agents have intrinsic cerebral vasodilating effect, which causes an increase in CBF. The net result is a balance of these two counteracting effects. Generally speaking, when the gas level is above 1 MAC, inhalational agents cause a dose-dependent increase in CBF (intrinsic vasodilating effect wins). In contrast, intravenous agents do not possess this intrinsic cerebral vasodilating ability. Therefore, they cause a decrease in CBF due to their suppressive effect on CMRO2.
In summary, inhalational agents cause a decrease in CMRO2 and a dose-dependent increase in CBF, which varies from agent to agent. Intravenous agents (except ketamine) cause decrease in both CMRO2 and CBF. The opposite changes in CMRO2 and CBF caused by inhalational agents do not mean that the flow-metabolism mechanism is decoupled; rather, it implies that this coupling mechanism moves to a new CBF level and continues.