Reperfusion Hyperoxia in Brain after Circulatory Arrest in Humans

Abstract

Changes in the electroencephalogram (EEG), mean arterial blood pressure (MABP), and hemoglobin saturation in brain vasculature of lightly anesthetized normothermic humans undergoing induced circulatory arrest for implantation of an automatic internal cardioverting defibrillator were studied. EEG was measured using a four-channel bipolar montage and hemoglobin saturation was measured transcranially using reflectance spectroscopy at 760 nm with an isosbestic reference at 800 nm. Hemoglobin saturation of blood in the quadriceps muscle was also measured. Thirty-two episodes of hypotension due to ventricular fibrillation were studied along with 31 episodes of hypotension related to ventricular tachycardia and rapid ventricular pacing. In a typical fibrillatory event there was a decrease in MABP followed almost immediately by changes in hemoglobin saturation of blood in the brain vasculature. The first changes in EEG were detected an average of 6.5 s (P < 0.001, paired t test) after the beginning of change of brain vascular hemoglobin. In some cases changes in hemoglobin saturation could be detected without changes in EEG. Desaturation curves from muscle and brain were significantly different, suggesting that the brain probe was measuring hemoglobin change in a rapidly metabolizing volume of tissue that was dissimilar to the skin, muscle, and bone monitored by the probe over the quadriceps muscle. Examination of the 32 episodes of circulatory arrest revealed a marked response that began immediately with recirculation characterized by an increase of the hemoglobin saturation signal from brain vasculature to above baseline as the duration of circulatory arrest exceeded 37 s, this response is termed reperfusion hyperoxia. When the duration of circulatory arrest was less than 37 s, hemoglobin saturation returned to baseline without a period of reperfusion hyperoxia. An early response to reperfusion after cardiac arrest characterized by a marked increase in brain vascular hemoglobin saturation was identified. This event may have significance in understanding the events leading to brain failure.