Neuro-Intensive Care Unit, Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
Department of Anesthesiology and Critical Care Medicine, Medical University of Innsbruck, Innsbruck, Austria.
Ther Hypothermia Temp Manag. 2020 Jun;10(2):122-127. doi: 10.1089/ther.2019.0009. Epub 2019 Aug 8.
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°C. High-frequency monitoring included brain temperature, mean arterial blood pressure (MAP), intracranial pressure (ICP), brain tissue oxygen tension (PO), and regional oxygen saturation (rSO) 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°C ± 0.8°C to 28.8°C ± 1.0°C within a median 160 minutes (interquartile range 146-191 minutes), reflecting a rapid induction of deep HT (-4°C/h). MAP and cerebral perfusion pressure (CPP) remained stable until a brain temperature of 35°C (69 ± 8 mmHg, 53 ± 7 mmHg) and decreased to 58 ± 17 mmHg and 40 ± 17 mmHg at 28°C ( = 0.031 and = 0.015). Despite the decrease in MAP and CPP, brain oxygenation increased (PO +5 mmHg, = 0.037; rSO: +7.3%, = 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°C (ORx), 33°C (PRx), and 30°C (COx). At lower temperature, AR-indices increased (PRx: < 0.001, ORx: = 0.02, COx: = 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.
脑温调节对脑血流动力学的影响尚不清楚。我们的目的是在模拟临床意外低温情况下的猪模型中,研究深低温(HT)诱导过程中动态脑自动调节(AR)指数的变化。13 头猪通过体表冷却将核心温度降至 28°C。高频监测包括脑温、平均动脉压(MAP)、颅内压(ICP)、脑组织氧张力(PO)和近红外光谱评估的局部氧饱和度(rSO),以计算 AR 指数(压力反应性指数 [PRx]、氧反应性指数 [ORx] 和脑氧合指数 [COx])。脑温中位数在 160 分钟内(四分位距 146-191 分钟)从 39.3°C ± 0.8°C 降至 28.8°C ± 1.0°C,反映了深 HT 的快速诱导(-4°C/h)。MAP 和脑灌注压(CPP)在脑温达到 35°C(69 ± 8mmHg,53 ± 7mmHg)之前保持稳定,降至 28°C 时降至 58 ± 17mmHg 和 40 ± 17mmHg( = 0.031 和 = 0.015)。尽管 MAP 和 CPP 下降,脑氧合增加(PO +5mmHg, = 0.037;rSO:+7.3%, = 0.029)。HT 诱导过程中 ICP 无变化。HT 诱导过程中 ICP 无变化。基线 AR 指数反映了正常的脑 AR,直到脑温降至 34°C(ORx)、33°C(PRx)和 30°C(COx)时才发生变化。在较低的温度下,AR 指数增加(PRx: < 0.001,ORx: = 0.02,COx: = 0.03),反映了脑 AR 的受损。脑血流对较低的脑温水平反应性降低。尽管这些温度在临床常规中通常不是目标,但在治疗意外深低温患者时应牢记这一点。