Regional cerebrovascular oxygen saturation, a quantitative measure of hemoglobin saturation in the combined arterial, venous, and microcirculatory compartments of the brain, can be measured noninvasively with near infrared spectroscopy. We assessed the sensitivity of this aggregate saturation to cerebral hypoxia during transient cerebral hypoxic hypoxia in seven human subjects. Regional cerebrovascular oxygen saturation measured over the middle frontal gyms and analog electroencephalogram were recorded. We compared the time to achieve two end points: the earliest paroxysmal burst of theta-delta background slowing and a cerebrovascular oxygen saturation of <55%. Saturation fell below 55% prior to the electroencephalographic change (/?<0.05). In a related effort, we also compared spectroscopically measured regional cerebrovascular oxygen saturation with an estimate of this value calculated from arterial and cerebral mixed venous saturation in nine patients. A positive linear relation (n=68, /f=0.55, s=4.2) was noted. (Stroke 1991^2:596-602)
Profound hypothermia with circulatory arrest is an important surgical adjuvant that allows protected cessation of cerebral blood flow for a brief period. In seven patients undergoing this procedure, continuous spectroscopic measurement of cerebral hemoglobin oxygen saturation was performed. Circulatory arrest at 18 degrees C was associated with a significant progressive desaturation (p < 0.01) of residual cerebral hemoglobin. Arrest time varied based on operative complexity (range 10 to 65 minutes), and a negative linear correlation between arrest time (y) and oxygen saturation (x) was noted (y = -0.87 x + 64). Five patients whose saturation remained above 35% had no neurological injury attributable to hypoxia. One patient (Hunt and Hess Grade 0) whose saturation fell below 35% had evidence of a global hypoxic injury at postmortem examination. Spectroscopically measured cerebral hemoglobin saturation (cerebral oximetry) may be used to monitor metabolic activity during circulatory arrest. Although the clinical utility of such monitoring cannot be established at this time, the potential may exist to prolong the safe duration of induced circulatory arrest for cerebral protection.
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