Ringer Simone K, Clausen Nicola G, Spielmann Nelly, Weiss Markus
Department of Clinical Diagnostics and Services, Section Anaesthesiology, Vetsuisse Faculty University of Zurich, Zurich, Switzerland.
Department of Anaesthesiology, University Children's Hospital Zurich, Zurich, Switzerland.
Paediatr Anaesth. 2020 Sep;30(9):970-976. doi: 10.1111/pan.13943. Epub 2020 Jun 25.
Hypothermia and its combination with hypocapnia are frequently associated with anesthesia.
The goal was to investigate the effects of hypothermia and hypothermia combined with hypocapnia (hypothermia-hypocapnia) on cerebral tissue oxygenation in anesthetized piglets.
Twenty anesthetized piglets were randomly allocated to hypothermia (n = 10) or hypothermia-hypocapnia (n = 10). Cerebral monitoring comprised a tissue oxygen partial pressure (PtO ), a laser Doppler probe, and a near-infrared spectroscopy sensor, measuring regional oxygen saturation (rSO ). After baseline recordings, hypothermia (35.5-36.0°C) with or without hypocapnia (target PaCO : 28-30 mm Hg) was induced. Once treatment goals were achieved (Tr0), they were maintained for 30 minutes (Tr30).
No changes in PtO but a significant increase in rSO (Tr0 (mean difference 8.9[95% CI for difference3.99 to 13.81], P < .001); Tr30 (10.8[6.20 to 15.40], P < .001)) were detected during hypothermia. With hypothermia-hypocapnia, a decrease in PtO (Tr0 (-3.2[-6.01 to -0.39], P = .021; Tr30 (-3.3[-5.8 to -0.80], P = .006)) and no significant changes in rSO occurred. Cerebral blood flow decreased significantly from baseline to Tr0 independently of treatment (-0.89[-0.18 to -0.002], P = .042), but this was more consistently observed with hypothermia-hypocapnia.
The hypothermia-induced reduction in oxygen delivery was compensated by lowered metabolic demand. However, hypothermia was not able to compensate for an additional reduction in oxygen delivery caused by simultaneous hypocapnia. This resulted in a PtO drop, which was not reflected by a downshift in rSO .
体温过低及其与低碳酸血症的联合情况常与麻醉相关。
本研究旨在探究体温过低以及体温过低合并低碳酸血症(低温 - 低碳酸血症)对麻醉仔猪脑组织氧合的影响。
将20只麻醉仔猪随机分为体温过低组(n = 10)和低温 - 低碳酸血症组(n = 10)。脑部监测包括组织氧分压(PtO₂)、激光多普勒探头和近红外光谱传感器,用于测量局部氧饱和度(rSO₂)。在进行基线记录后,诱导体温过低(35.5 - 36.0°C),同时伴有或不伴有低碳酸血症(目标动脉血二氧化碳分压(PaCO₂):28 - 30 mmHg)。一旦达到治疗目标(Tr0),则维持30分钟(Tr30)。
在体温过低期间,未检测到PtO₂有变化,但rSO₂显著增加(Tr0时(平均差值8.9[差值的95%置信区间为3.99至13.81],P <.001);Tr30时(10.8[6.20至15.40],P <.001))。在低温 - 低碳酸血症时,PtO₂降低(Tr0时(-3.2[-6.01至 -0.39],P = 0.021;Tr30时(-3.3[-5.8至 -0.80],P = 0.006)),而rSO₂未发生显著变化。与治疗方式无关,脑血流量从基线到Tr0均显著降低(-0.89[-0.18至 -0.002],P = 0.042),但在低温 - 低碳酸血症时这种情况更为常见。
体温过低引起的氧输送减少通过代谢需求降低得到了补偿。然而,体温过低无法补偿同时存在的低碳酸血症导致的额外氧输送减少。这导致了PtO₂下降,而rSO₂并未相应降低。