Cerebral Autoregulation is Impaired During Deep Hypothermia-A Porcine Multimodal Neuromonitoring Study.

Effects of brain temperature modulation on cerebral hemodynamics are unclear. We aimed at investigating changes of dynamic cerebral autoregulation (AR) indices during induction of deep hypothermia (HT) in a porcine model mimicking the clinical scenario of accidental HT. Thirteen pigs were surface-cooled to a core temperature of 28 degrees C. High-frequency monitoring included brain temperature, mean arterial blood pressure (MAP), intracranial pressure (ICP), brain tissue oxygen tension (PbtO2), and regional oxygen saturation (rSO(2)) assessed by near-infrared spectroscopy to calculate AR-indices (pressure reactivity index [PRx], oxygen reactivity index [ORx], and cerebral oximetry index [COx]). Brain temperature decreased from 39.3 degrees C +/- 0.8 degrees C to 28.8 degrees C +/- 1.0 degrees C within a median 160 minutes (interquartile range 146-191 minutes), reflecting a rapid induction of deep HT (-4 degrees C/h). MAP and cerebral perfusion pressure (CPP) remained stable until a brain temperature of 35 degrees C (69 +/- 8 mmHg, 53 +/- 7 mmHg) and decreased to 58 +/- 17 mmHg and 40 +/- 17 mmHg at 28 degrees C (p = 0.031 and p = 0.015). Despite the decrease in MAP and CPP, brain oxygenation increased (PbtO2: +5 mmHg, p = 0.037; rSO(2): +7.3%, p = 0.029). There was no change in ICP during HT induction. Baseline AR-indices reflected normal cerebral AR and did not change until a brain temperature of 34 degrees C (ORx), 33 degrees C (PRx), and 30 degrees C (COx). At lower temperature, AR-indices increased (PRx: p < 0.001, ORx: p = 0.02, COx: p = 0.03), reflecting impaired cerebral AR. Cerebrovascular reactivity is impaired at lower brain temperature levels. Although these temperatures are usually not targeted in clinical routine, this should be kept in mind when treating patients with accidental deep HT.