National Institutes of Health Acute Respiratory Distress Syndrome Network (ARDS Network) Investigators, Pulmonary and Critical Care Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.
Crit Care Med. 2011 Sep;39(9):2025-30. doi: 10.1097/CCM.0b013e31821cb774.
The criteria that define acute lung injury and the acute respiratory distress syndrome include PaO₂/Fio₂ but not positive end-expiratory pressure or Fio2. PaO2/Fio2 ratios of some patients increase substantially after mechanical ventilation with positive end-expiratory pressure of 5-10 cm H₂O, and the mortality of these patients may be lower than those whose PaO₂/Fio₂ratios remain <200. Also, PaO₂/Fio₂ may increase when Fio2 is raised from moderate to high levels, suggesting that patients with similar PaO₂/Fio₂ ratios but different Fio₂ levels have different risks of mortality. The primary purpose of this study was to assess the value of adding baseline positive end-expiratory pressure and Fio₂ to PaO₂/Fio₂ for predicting mortality of acute lung injury/acute respiratory distress syndrome patients enrolled in Acute Respiratory Distress Syndrome Network clinical trials. We also assessed effects of two study interventions on clinical outcomes in subsets of patients with mild and severe hypoxemia as defined by PaO₂/Fio₂.
Analysis of baseline physiologic data and outcomes of patients previously enrolled in clinical trials conducted by the National Institutes of Health Acute Respiratory Distress Syndrome Network.
Intensive care units of 40 hospitals in North America.
Two thousand three hundred and twelve patients with acute lung injury/acute respiratory distress syndrome.
None.
Only 1.3% of patients enrolled in Acute Respiratory Distress Syndrome Network trials had baseline positive end-expiratory pressure < 5 cm H₂O, and 50% had baseline positive end-expiratory pressure ≥10 cm H₂O. Baseline PaO₂/Fio₂ predicted mortality, but after controlling for PaO₂/Fio₂, baseline positive end-expiratory pressure did not predict mortality. In contrast, after controlling for baseline PaO₂/Fio₂, baseline Fio₂ did predict mortality. Effects of two study interventions (lower tidal volumes and fluid-conservative hemodynamic management) were similar in mild and severe hypoxemia subsets as defined by PaO₂/Fio₂ ratios.
At Acute Respiratory Distress Syndrome Network hospitals, the addition of baseline positive end-expiratory pressure would not have increased the value of PaO₂/Fio₂ for predicting mortality of acute lung injury/acute respiratory distress syndrome patients. In contrast, the addition of baseline Fio2 to PaO₂/Fio₂ could be used to identify subsets of patients with low or high mortality.
定义急性肺损伤和急性呼吸窘迫综合征的标准包括 PaO₂/Fio₂，但不包括呼气末正压或 Fio2。一些患者在接受 5-10cmH₂O 的呼气末正压机械通气后，PaO₂/Fio₂ 比值会大幅升高，这些患者的死亡率可能低于 PaO₂/Fio₂ 比值仍<200 的患者。此外，当 Fio2 从中等水平升高到高水平时，PaO₂/Fio₂ 可能会增加，这表明 PaO₂/Fio₂ 比值相似但 Fio2 水平不同的患者的死亡率风险不同。本研究的主要目的是评估在 PaO₂/Fio₂ 的基础上增加基线呼气末正压和 Fio₂ 是否可预测急性肺损伤/急性呼吸窘迫综合征患者的死亡率。我们还评估了两种研究干预措施对以 PaO₂/Fio₂ 定义的轻度和重度低氧血症亚组患者的临床结局的影响。
对先前参加美国国立卫生研究院急性呼吸窘迫综合征网络临床试验的患者的基线生理数据和结局进行分析。
北美 40 家医院的重症监护病房。
2312 名急性肺损伤/急性呼吸窘迫综合征患者。
无。
仅有 1.3%的急性呼吸窘迫综合征网络试验入组患者的基线呼气末正压<5cmH₂O，50%的患者基线呼气末正压≥10cmH₂O。基线 PaO₂/Fio₂ 预测死亡率，但在校正 PaO₂/Fio₂ 后，基线呼气末正压不再预测死亡率。相反，在校正基线 PaO₂/Fio₂ 后，基线 Fio₂ 可预测死亡率。以 PaO₂/Fio₂ 比值定义的轻度和重度低氧血症亚组中，两种研究干预措施（低潮气量和液体保守性血流动力学管理）的效果相似。
在急性呼吸窘迫综合征网络医院，增加基线呼气末正压不会增加 PaO₂/Fio₂ 预测急性肺损伤/急性呼吸窘迫综合征患者死亡率的价值。相反，将基线 Fio2 添加到 PaO₂/Fio₂ 中可用于识别死亡率低或高的患者亚组。
