Hypercarbia causes cerebral vasodilation. If you have ever seen an intra- or acute post-op neurosurgical patient, or really any patient about to herniate, you can remember this because they will be hyperventilated to pCO2 around 25-30 to decrease ICP via cerebral vasoconstriction; in this case, we have the opposite. The curve of pCO2 vs cerebral blood flow is quite steep in the physiologic range meaning small changes in ventilation make a significant difference in CBF.

The more general principle: endothelia vasodilate in the presence of high CO2; you gotta get rid of that acid somehow! Can’t let it accumulate, as lower pH within a “micro-environment” affects structure/efficiency of enzymes, proteins, etc. The more acidic a local environment, the more you expect nearby vasculature to dilate (as a means of increasing flow rate, thereby ferrying off accumulate acid).

The anesthesiologist can exploit this mechanism. By hyperventilating (blowing off CO2), the brain vasculature senses a low CO2 / “hunky-dory state,” which requires no vasodilation. In other words, the vasculature does not need to continue the ATP-consuming practice of synthesizing Nitric Oxide (NO).

Hyperventilation causes decreased PaCO2 which subsequently leads to arterial vasoconstriction thus lowering cerebral blood flow (CBF), cerebral blood volume, and ICP.

He wants to increase ICP (cerebral vasodilation) which he can do by decreasing the respiratory rate (hypoventilation).