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NEUROSURGICAL ANESTHESIOLOGY AND NEUROSCIENCE

The Effects of Arterial Carbon Dioxide Partial Pressure and Sevoflurane on Capillary Venous Cerebral Blood Flow and Oxygen Saturation During Craniotomy

Klaus Ulrich Klein, MD^*, Martin Glaser, MD, Robert Reisch, MD, PhD, Achim Tresch, MSc, Christian Werner, MD, PhD^*, and Kristin Engelhard, MD, PhD^*

From the Departments of *Anesthesiology, Neurosurgery, Johannes Gutenberg-University, Mainz, Germany; and Department of Chemistry and Biochemistry, Gene Center Munich, Ludwig-Maximilians-University, Munich, Germany.

Address correspondence and reprint requests to Klaus Ulrich Klein, MD, Department of Anesthesiology, Johannes Gutenberg-University, Langenbeckstrasse 1, 55131 Mainz, Germany. Address e-mail to kuklein{at}uni-mainz.de.

Abstract

BACKGROUND: Intraoperative routine monitoring of cerebral blood flow and oxygenation remains a technological challenge. Using the physiological principle of carbon dioxide reactivity of cerebral vasculature, we investigated a recently developed neuromonitoring device (oxygen-to-see, O₂C^TM device) for simultaneous measurements of regional cerebral blood flow (rvCBF), blood flow velocity (rvVelo), oxygen saturation (srvO₂), and hemoglobin amount (rvHb) at the capillary venous level in patients subjected to craniotomy.

METHODS: Twenty-six neurosurgical patients were randomly assigned to anesthesia with 1.4% or 2.0% sevoflurane end-tidal concentration. After craniotomy, a fiberoptic probe was applied on a macroscopically healthy surface of cerebral tissue next to the site of surgery. Simultaneous measurements in 2 and 8 mm cerebral depth were performed in each patient during lower (35 mm Hg) and higher (45 mm Hg) levels (random order) of arterial carbon dioxide partial pressure (Paco₂). The principle of these measurements relies on the combination of laser-Doppler flowmetry (rvCBF, rvVelo) and photo-spectrometry (srvO₂, rvHb). Linear models were fitted to test changes of end points (rvCBF, rvVelo, srvO₂, rvHb) in response to lower and higher levels of Paco₂, 1.4% and 2.0% sevoflurane end-tidal concentration, and 2 and 8 mm cerebral depth.

RESULTS: RvCBF and rvVelo were elevated by Paco₂ independent of sevoflurane concentration in 2 and 8 mm depth of cerebral tissue (P < 0.001). Higher Paco₂ induced an increase in mean srvO₂ from 50% to 68% (P < 0.001). RvVelo (P < 0.001) and srvO₂ (P = 0.007) were higher in 8 compared with 2 mm cerebral depth. RvHb was not influenced by alterations in Paco₂ but positively correlated to sevoflurane concentration (P = 0.005).

CONCLUSIONS: Increases in rvCBF and rvVelo by Paco₂ suggest preserved hypercapnic vasodilation under anesthesia with sevoflurane 1.4% and 2.0% end-tidal concentration. A consecutive increase in srvO₂ implies that cerebral arteriovenous difference in oxygen was decreased by elevated Paco₂. Unchanged levels of rvHb signify that there was no blood loss during measurements. Data suggest that the device allows detection of local changes in blood flow and oxygen saturation in response to different Paco₂ levels in predominant venous cerebral microvessels.