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Abstract：
Introduction: Potential detrimental effects of hyperoxemia on outcomes have been reported in critically ill patients. Little evidence exists on the effects of hyperoxygenation and hyperoxemia on cerebral physiology. The primary aim of this study is to assess the effect of hyperoxygenation and hyperoxemia on cerebral autoregulation in acute brain injured patients. We further evaluated potential links between hyperoxemia, cerebral oxygenation and intracranial pressure (ICP). Methods: This is a single center, observational, prospective study. Acute brain injured patients [traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), intracranial hemorrhage (ICH)] undergoing multimodal brain monitoring through a software platform (ICM+) were included. Multimodal monitoring consisted of invasive ICP, arterial blood pressure (ABP) and near infrared spectrometry (NIRS). Derived parameters of ICP and ABP monitoring included the pressure reactivity index (PRx) to assess cerebral autoregulation. ICP, PRx, and NIRS-derived parameters (cerebral regional saturation of oxygen, changes in concentration of regional oxy- and deoxy-hemoglobin), were evaluated at baseline and after 10 min of hyperoxygenation with a fraction of inspired oxygen (FiO2) of 100% using repeated measures t-test or paired Wilcoxon signed-rank test. Continuous variables are reported as median (interquartile range). Results: Twenty-five patients were included. The median age was 64.7 years (45.9-73.2), and 60% were male. Thirteen patients (52%) were admitted for TBI, 7 (28%) for SAH, and 5 (20%) patients for ICH. The median value of systemic oxygenation (partial pressure of oxygen-PaO2) significantly increased after FiO2 test, from 97 (90-101) mm Hg to 197 (189-202) mm Hg, p < 0.0001. After FiO2 test, no changes were observed in PRx values (from 0.21 (0.10-0.43) to 0.22 (0.15-0.36), p = 0.68), nor in ICP values (from 13.42 (9.12-17.34) mm Hg to 13.34 (8.85-17.56) mm Hg, p = 0.90). All NIRS-derived parameters reacted positively to hyperoxygenation as expected. Changes in systemic oxygenation and the arterial component of cerebral oxygenation were significantly correlated (respectively ΔPaO2 and ΔO2Hbi; r = 0.49 (95% CI = 0.17-0.80). Conclusion: Short-term hyperoxygenation does not seem to critically affect cerebral autoregulation.
摘要：
简介：已经报道了危重患者高氧血症对预后的潜在有害影响。关于高氧合和高氧血症对脑生理的影响的证据很少。这项研究的主要目的是评估高氧合和高氧血症对急性脑损伤患者脑自动调节的影响。我们进一步评估了高氧血症，脑氧合和颅内压（ICP）。方法：这是一个单一的中心，观察,前瞻性研究。急性脑损伤患者[创伤性脑损伤（TBI），蛛网膜下腔出血(SAH),颅内出血(ICH)]通过软件平台(ICM+)接受多模式脑监测.多模式监测包括侵入性ICP，动脉血压（ABP）和近红外光谱（NIRS）。ICP和ABP监测的衍生参数包括压力反应指数（PRx）以评估脑自动调节。ICP,PRx,和NIRS推导的参数(大脑区域氧饱和度，区域氧合和脱氧血红蛋白浓度的变化)，使用重复测量t检验或配对Wilcoxon符号秩检验，在基线和超氧氧氧合10分钟后进行评估，其中吸入氧气（FiO2）的分数为100％。连续变量报告为中值(四分位数间距)。结果：纳入25例患者。中位年龄为64.7岁（45.9-73.2），60%是男性。13例患者（52%）因TBI入院，7（28%）的SAH，和5（20％）的ICH患者。FiO2测试后，全身氧合（氧分压-PaO2）的中位数显着增加，从97（90-101）mmHg到197（189-202）mmHg，p<0.0001。FiO2测试后,没有观察到PRx值的变化（从0.21（0.10-0.43）到0.22（0.15-0.36），p=0.68),在ICP值（从13.42（9.12-17.34）mmHg到13.34（8.85-17.56）mmHg，p=0.90）。所有NIRS衍生的参数都如预期的那样对超氧反应积极。全身氧合的变化与脑氧合的动脉成分显着相关（分别为ΔPaO2和ΔO2Hbi；r=0.49（95％CI=0.17-0.80）。结论：短期的高氧合似乎不会严重影响大脑的自动调节。
