The effects of hypoxemia on the cerebral vasculature have been described in animal models, but data from human studies are limited and have often relied on invasive methodology. The ability to detect a threshold for hypoxic vasodilatation in humans may be clinically useful, particularly in patients with impaired intracranial compliance. Because physiology may differ among subjects, it would be advantageous to measure such thresholds using noninvasive bedside techniques that could be readily applied to individual patients. We have attempted to identify thresholds of hypoxic vasodilatation in volunteers using noninvasive methods of measurement. Thirteen healthy volunteers were studied using transcranial Doppler sonography. Time-averaged middle cerebral artery maximal flow velocity (MCA FVx), mean arterial blood pressure, peripheral oxygen saturation (Spo2), and partial pressure of endtidal CO2 were measured at baseline and during graded reduction in arterial Spo2 to 85%, at normocapnia. Flow velocity and estimated cerebrovascular resistance (CVRe) were indexed and plotted against Spo2. There was no significant change in mean arterial pressure during desaturation to 85%, although the mean heart rate increased from 65 to 82 bpm. An increase in MCA FVx and reciprocal decrease in CVRe were observed when Spo2 decreased to below 90%. These results suggest that hypoxemic cerebral vasodilatation may be measured noninvasively and that in normal human volunteers, the threshold is at an Spo2 of 90%, which is greater than that previously reported.
Implications: The ability to detect the point at which cerebral blood vessels dilate using noninvasive techniques is clinically advantageous. We have attempted to do this using transcranial Doppler sonography in volunteers whose inspired oxygen concentrations were gradually decreased. Thresholds of cerebral vasodilatation were found to be higher than those previously reported. These thresholds are important with regard to adequate perfusion in various pathologic states.