Department of Emergency Medicine, Cooper University Hospital, One Cooper Plaza, Camden, NJ 08103, USA.
JAMA. 2010 Jun 2;303(21):2165-71. doi: 10.1001/jama.2010.707.
Laboratory investigations suggest that exposure to hyperoxia after resuscitation from cardiac arrest may worsen anoxic brain injury; however, clinical data are lacking.
To test the hypothesis that postresuscitation hyperoxia is associated with increased mortality.
DESIGN, SETTING, AND PATIENTS: Multicenter cohort study using the Project IMPACT critical care database of intensive care units (ICUs) at 120 US hospitals between 2001 and 2005. Patient inclusion criteria were age older than 17 years, nontraumatic cardiac arrest, cardiopulmonary resuscitation within 24 hours prior to ICU arrival, and arterial blood gas analysis performed within 24 hours following ICU arrival. Patients were divided into 3 groups defined a priori based on PaO(2) on the first arterial blood gas values obtained in the ICU. Hyperoxia was defined as PaO(2) of 300 mm Hg or greater; hypoxia, PaO(2) of less than 60 mm Hg (or ratio of PaO(2) to fraction of inspired oxygen <300); and normoxia, not classified as hyperoxia or hypoxia.
In-hospital mortality.
Of 6326 patients, 1156 had hyperoxia (18%), 3999 had hypoxia (63%), and 1171 had normoxia (19%). The hyperoxia group had significantly higher in-hospital mortality (732/1156 [63%; 95% confidence interval {CI}, 60%-66%]) compared with the normoxia group (532/1171 [45%; 95% CI, 43%-48%]; proportion difference, 18% [95% CI, 14%-22%]) and the hypoxia group (2297/3999 [57%; 95% CI, 56%-59%]; proportion difference, 6% [95% CI, 3%-9%]). In a model controlling for potential confounders (eg, age, preadmission functional status, comorbid conditions, vital signs, and other physiological indices), hyperoxia exposure had an odds ratio for death of 1.8 (95% CI, 1.5-2.2).
Among patients admitted to the ICU following resuscitation from cardiac arrest, arterial hyperoxia was independently associated with increased in-hospital mortality compared with either hypoxia or normoxia.
实验室研究表明，心肺复苏后暴露于高氧可能会加重缺氧性脑损伤；然而，临床数据尚缺乏。
检验复苏后高氧与死亡率增加相关的假说。
设计、地点和患者：使用 2001 年至 2005 年期间 120 家美国医院的项目影响（IMPACT）重症监护病房（ICU）的关键护理数据库进行多中心队列研究。患者入选标准为年龄大于 17 岁、非创伤性心搏骤停、在 ICU 入住前 24 小时内进行心肺复苏、以及在 ICU 入住后 24 小时内进行动脉血气分析。患者根据 ICU 中获得的第一批动脉血气值的 PaO（2）预先分为 3 组。高氧定义为 PaO（2）≥300mmHg；低氧定义为 PaO（2）＜60mmHg（或 PaO（2）与吸入氧分数比值＜300）；正常氧定义为不属于高氧或低氧。
院内死亡率。
在 6326 例患者中，1156 例有高氧血症（18%）、3999 例有低氧血症（63%）和 1171 例有正常氧血症（19%）。高氧血症组的院内死亡率明显高于正常氧血症组（732/1156 [63%；95%置信区间 {CI}，60%-66%]）和低氧血症组（2297/3999 [57%；95% CI，56%-59%]）；差异比例分别为 18%（95% CI，14%-22%）和 6%（95% CI，3%-9%）。在控制潜在混杂因素（如年龄、入院前功能状态、合并症、生命体征和其他生理指标）的模型中，高氧暴露的死亡比值比为 1.8（95% CI，1.5-2.2）。
在心搏骤停复苏后入住 ICU 的患者中，与低氧血症或正常氧血症相比，动脉高氧血症与院内死亡率增加独立相关。
