Arterial hyperoxia and in-hospital mortality after resuscitation from cardiac arrest.

Arterial hyperoxia and in-hospital mortality after resuscitation from cardiac arrest.
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DOI:
10.1186/cc10090
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发表时间:
2011
期刊:
Critical care (London, England)
影响因子:
--
通讯作者:
Study of Oxygen in Critical Care (SOCC) Group
Study of Oxygen in Critical Care (SOCC) Group
中科院分区:
其他
文献类型:
--
作者:
Bellomo R;Bailey M;Eastwood GM;Nichol A;Pilcher D;Hart GK;Reade MC;Egi M;Cooper DJ;Study of Oxygen in Critical Care (SOCC) Group

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高氧最近被报道为心脏骤停复苏患者死亡的独立危险因素。我们研究了高氧与此类患者预后之间的独立关系。我们将125个重症监护病房(ICU)的非创伤性心脏骤停复苏患者根据入院后24小时内最差PaO 2水平或肺泡-动脉O2梯度分为三组。我们将“高氧”定义为PaO 2 300 mmHg或更高,“缺氧/氧传递不良”定义为PaO 2 < 60 mmHg或PaO 2与吸入氧分数(FiO 2)的比值< 300,“常氧”定义为缺氧和高氧之间的任何值,“孤立性低氧血症”定义为PaO 2 < 60 mmHg,无论FiO 2如何。出院时的死亡率是主要的结局指标。在总共12,108例患者中,1,285例(10.6%)有高氧,8,904例(73.5%)有缺氧/氧转移不良,1,919例(15.9%)有正常氧,1,168例(9.7%)有孤立性低氧血症(PaO 2 < 60 mmHg)。高氧组死亡率高(1,285例患者中的754例(59%); 95%置信区间(95% CI),56%至61%)(911例(47%); 95% CI,45%-50%),比例差异为11%(95% CI,8%至15%),但不高于缺氧组(5,303(60%)/8,904例患者; 95% CI,59%至61%)。在控制一些潜在混杂因素(包括疾病严重程度)的多变量模型中,高氧导致住院死亡的比值比为1.2(95% CI,1.1 - 1.6)。然而,一旦我们应用考克斯比例风险模型的生存,敏感性分析使用低氧血症的十分位数,时间段匹配和高氧定义为PaO 2> 400 mmHg,高氧与死亡率没有独立的关联。重要的是,在调整FiO 2和相关协变量后,PaO 2不再预测住院死亡率(P = 0.21)。在心脏骤停后入住ICU的患者中,高氧与死亡率之间没有强有力的或可重复的相关性。我们敦促谨慎执行政策,故意降低这些患者的FiO 2。
Hyperoxia has recently been reported as an independent risk factor for mortality in patients resuscitated from cardiac arrest. We examined the independent relationship between hyperoxia and outcomes in such patients. We divided patients resuscitated from nontraumatic cardiac arrest from 125 intensive care units (ICUs) into three groups according to worst PaO2 level or alveolar-arterial O2 gradient in the first 24 hours after admission. We defined 'hyperoxia' as PaO2 of 300 mmHg or greater, 'hypoxia/poor O2 transfer' as either PaO2 < 60 mmHg or ratio of PaO2 to fraction of inspired oxygen (FiO2 ) < 300, 'normoxia' as any value between hypoxia and hyperoxia and 'isolated hypoxemia' as PaO2 < 60 mmHg regardless of FiO2. Mortality at hospital discharge was the main outcome measure. Of 12,108 total patients, 1,285 (10.6%) had hyperoxia, 8,904 (73.5%) had hypoxia/poor O2 transfer, 1,919 (15.9%) had normoxia and 1,168 (9.7%) had isolated hypoxemia (PaO2 < 60 mmHg). The hyperoxia group had higher mortality (754 (59%) of 1,285 patients; 95% confidence interval (95% CI), 56% to 61%) than the normoxia group (911 (47%) of 1,919 patients; 95% CI, 45% to 50%) with a proportional difference of 11% (95% CI, 8% to 15%), but not higher than the hypoxia group (5,303 (60%) of 8,904 patients; 95% CI, 59% to 61%). In a multivariable model controlling for some potential confounders, including illness severity, hyperoxia had an odds ratio for hospital death of 1.2 (95% CI, 1.1 to 1.6). However, once we applied Cox proportional hazards modelling of survival, sensitivity analyses using deciles of hypoxemia, time period matching and hyperoxia defined as PaO2 > 400 mmHg, hyperoxia had no independent association with mortality. Importantly, after adjustment for FiO2 and the relevant covariates, PaO2 was no longer predictive of hospital mortality (P = 0.21). Among patients admitted to the ICU after cardiac arrest, hyperoxia did not have a robust or consistently reproducible association with mortality. We urge caution in implementing policies of deliberate decreases in FiO2 in these patients.
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