Department of Emergency Care and Services, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Department of Neurosurgery, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Neurocrit Care. 2021 Apr;34(2):413-422. doi: 10.1007/s12028-020-01178-w. Epub 2021 Jan 5.
In neurocritically ill patients, one early mechanism behind secondary brain injury is low systemic blood pressure resulting in inadequate cerebral perfusion and consequent hypoxia. Intuitively, higher partial pressures of arterial oxygen (PaO) could be protective in case of inadequate cerebral circulation related to hemodynamic instability.
We examined whether the association between PaO and mortality is different in patients with low compared to normal and high mean arterial pressure (MAP) in patients after various types of brain injury.
We screened the Finnish Intensive Care Consortium database for mechanically ventilated adult (≥ 18) brain injury patients treated in several tertiary intensive care units (ICUs) between 2003 and 2013. Admission diagnoses included traumatic brain injury, cardiac arrest, subarachnoid and intracranial hemorrhage, and acute ischemic stroke. The primary exposures of interest were PaO (recorded in connection with the lowest measured PaO/fraction of inspired oxygen ratio) and the lowest MAP, recorded during the first 24 h in the ICU. PaO was grouped as follows: hypoxemia (< 8.2 kPa, the lowest 10th percentile), normoxemia (8.2-18.3 kPa), and hyperoxemia (> 18.3 kPa, the highest 10th percentile), and MAP was divided into equally sized tertiles (< 60, 60-68, and > 68 mmHg). The primary outcome was 1-year mortality. We tested the association between hyperoxemia, MAP, and mortality with a multivariable logistic regression model, including the PaO, MAP, and interaction of PaO*MAP, adjusting for age, admission diagnosis, premorbid physical performance, vasoactive use, intracranial pressure monitoring use, and disease severity. The relationship between predicted 1-year mortality and PaO was visualized with locally weighted scatterplot smoothing curves (Loess) for different MAP levels.
From a total of 8290 patients, 3912 (47%) were dead at 1 year. PaO was not an independent predictor of mortality: the odds ratio (OR) for hyperoxemia was 1.16 (95% CI 0.85-1.59) and for hypoxemia 1.24 (95% CI 0.96-1.61) compared to normoxemia. Higher MAP predicted lower mortality: OR for MAP 60-68 mmHg was 0.73 (95% CI 0.64-0.84) and for MAP > 68 mmHg 0.80 (95% CI 0.69-0.92) compared to MAP < 60 mmHg. The interaction term PaO*MAP was nonsignificant. In Loess visualization, the relationship between PaO and predicted mortality appeared similar in all MAP tertiles.
During the first 24 h of ICU treatment in mechanically ventilated brain injured patients, the association between PaO and mortality was not different in patients with low compared to normal MAP.
在神经危重症患者中，继发性脑损伤的早期机制之一是全身血压低导致脑灌注不足和随后的缺氧。直观地说，在与血流动力学不稳定相关的脑循环不足的情况下，动脉氧分压（PaO）较高可能具有保护作用。
我们研究了在各种类型的脑损伤后，与正常和高平均动脉压（MAP）相比，低 MAP 的患者中 PaO 与死亡率之间的关联是否不同。
我们筛选了芬兰重症监护联合会数据库中 2003 年至 2013 年间在几个三级重症监护病房（ICU）中接受机械通气的成年（≥18 岁）脑损伤患者。入院诊断包括创伤性脑损伤、心脏骤停、蛛网膜下腔和颅内出血以及急性缺血性卒中。主要暴露因素为 PaO（与最低测量的 PaO/吸入氧比相关记录）和 ICU 治疗最初 24 小时内记录的最低 MAP。PaO 分为以下几类：低氧血症（<8.2kPa，最低的 10%）、氧合正常（8.2-18.3kPa）和高氧血症（>18.3kPa，最高的 10%），MAP 分为等份三分位数（<60、60-68 和 >68mmHg）。主要结局为 1 年死亡率。我们使用多变量逻辑回归模型，包括 PaO、MAP 和 PaO*MAP 的交互项，对高氧血症、MAP 和死亡率进行了调整，调整因素包括年龄、入院诊断、发病前身体机能、血管活性药物使用、颅内压监测使用和疾病严重程度。通过局部加权散点平滑曲线（Loess）为不同的 MAP 水平可视化预测的 1 年死亡率与 PaO 的关系。
在总共 8290 名患者中，有 3912 名（47%）在 1 年内死亡。PaO 不是死亡率的独立预测因子：与氧合正常相比，高氧血症的优势比（OR）为 1.16（95%CI 0.85-1.59），低氧血症为 1.24（95%CI 0.96-1.61）。较高的 MAP 预示着较低的死亡率：MAP 60-68mmHg 的 OR 为 0.73（95%CI 0.64-0.84），MAP >68mmHg 的 OR 为 0.80（95%CI 0.69-0.92），而 MAP <60mmHg 的 OR 为 1.00。PaO*MAP 交互项无统计学意义。在 Loess 可视化中，在所有 MAP 三分位数中，PaO 与预测死亡率之间的关系似乎相似。
在机械通气脑损伤患者 ICU 治疗的最初 24 小时内，与正常 MAP 相比，低 MAP 患者的 PaO 与死亡率之间的关联没有差异。
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