Assessment of Cerebral Autoregulation Patterns with Near-infrared Spectroscopy during Pharmacological-induced Pressure Changes.

BACKGROUND Previous work has demonstrated paradoxical increases in cerebral oxygen saturation (ScO2) as blood pressure decreases and paradoxical decreases in ScO2 as blood pressure increases. It has been suggested that these paradoxical responses indicate a functional cerebral autoregulation mechanism. Accordingly, the authors hypothesized that if this suggestion is correct, paradoxical responses will occur exclusively in patients with intact cerebral autoregulation. METHODS Thirty-four patients undergoing elective cardiac surgery were included. Cerebral autoregulation was assessed with the near-infrared spectroscopy-derived cerebral oximetry index (COx), computed by calculating the Spearman correlation coefficient between mean arterial pressure and ScO2. COx less than 0.30 was previously defined as functional autoregulation. During cardiopulmonary bypass, 20% change in blood pressure was accomplished with the use of nitroprusside for decreasing pressure and phenylephrine for increasing pressure. Effects on COx were assessed. Data were analyzed using two-way ANOVA, Kruskal-Wallis test, and Wilcoxon and Mann-Whitney U test. RESULTS Sixty-five percent of patients had a baseline COx less than 0.30, indicating functional baseline autoregulation. In 50% of these patients (n = 10), COx became highly negative after vasoactive drug administration (from -0.04 [-0.25 to 0.16] to -0.63 [-0.83 to -0.26] after administration of phenylephrine, and from -0.05 [-0.19 to 0.17] to -0.55 [-0.94 to -0.35] after administration of nitroprusside). A negative COx implies a decrease in ScO2 with increase in pressure and, conversely, an increase in ScO2 with decrease in pressure. CONCLUSIONS In this study, paradoxical changes in ScO2 after pharmacological-induced pressure changes occurred exclusively in patients with intact cerebral autoregulation, corroborating the hypothesis that these paradoxical responses might be attributable to a functional cerebral autoregulation.