Vasoconstriction seen after phenylephrine may cause vasoconstriction of extracranial vessels without causing a decrease in cerebral oxygenation. (Image source: Thinkstock)

Vasoconstriction seen after phenylephrine may cause vasoconstriction of extracranial vessels without causing a decrease in cerebral oxygenation. (Image source: Thinkstock)

To maintain cerebral perfusion during systemic hypotension, it is common clinical practice to raise blood pressure using a vasopressor. Phenylephrine is probably the most frequent choice. Concerns were raised in the past about a possible direct cerebral vasoconstrictive effect, negating the potential benefits from increased systemic blood pressure.  More recent studies using transcranial Doppler have suggested that this is not the case,yet studies on near-infrared brain oximetry (ScO2) have consistently demonstrated a decrease in ScO2 values with phenylephrine administration (one, two).What is the physiologic explanation?

Dr. Shigehiko Ogoh, Department of Biomedical Engineering, Toyo University, Kawagoe-Shi, Saitama, Japan, and colleagues  measured cerebral blood flow (middle cerebral artery mean blood velocity measured by transcranial Doppler), extracranial cerebral blood flow (internal carotid artery flow), external carotid arterial flow, vertebral artery flow, and skin blood flow with and without IV phenylephrine infusion.  Their findings are published in this month’s issue of Anesthesia & Analgesia in the article titled   “A Decrease in Spatially Resolved Near-Infrared Spectroscopy-Determined Frontal Lobe Tissue Oxygenation by Phenylephrine Reflects Reduced Skin Blood Flow.”

The hypothesis is that since ScO2 reflects both intracranial components and extracranial components, vasoconstriction of the extracranial circulation while preserving or increasing intracranial circulation would lead to a decrease in external carotid artery flow corroborated by a decrease in skin blood flow. This would explain the fall in ScO2 with phenylephrine administration.  The authors studied 7 healthy male volunteers with and without phenylephrine infusions. The authors observed no change in middle cerebral artery mean blood velocity , internal carotid arterial flow, or vertebral arterial flow during phenylephrine infusion.   However, there was a decrease in external carotid arterial flow velocity without a change in diameter, resulting in a decrease in flow that did not reach statistical significance (p = 0.073), though the rank correlation between baseline values and changes in external carotid arterial flow was significant.  There was no difference in skin blood flow.  The authors attributed this to a large variation in baseline values.

Do these results prove that the decrease in ScO2 during phenylephrine is a result of extracranial vasoconstriction?  The answer is a “definite maybe.”  In addition to the limitations cited in the article itself, it should be pointed out that Doppler measurements were not measured simultaneously but sequentially since the investigators only had access to one Doppler machine.  It would be interesting to indirectly verify these results in a clinical setting where the potential influence of “extracranial contamination” of ScO2 can be eliminated at baseline (i.e., administration of phenylephrine infusion during carotid endarterectomy after the external carotid artery has been clamped).