The Alfred Hospital, Melbourne, VIC, Australia.
Crit Care Resusc. 2013 Sep;15(3):186-90.
Laboratory and clinical studies have suggested that hyperoxia early after resuscitation from cardiac arrest may increase neurological injury and worsen outcome. Previous clinical studies have been small or have not included relevant prehospital data. We aimed to determine in a larger cohort of patients whether hyperoxia in the intensive care unit in patients admitted after out-of-hospital cardiac arrest (OHCA) was associated with increased mortality rate after correction for prehospital variables.
Data from the Victorian Ambulance Cardiac Arrest Registry (VACAR) of patients transported to hospital after resuscitation from OHCA and an initial cardiac rhythm of ventricular fibrillation between January 2007 and December 2011 were linked to the Australian and New Zealand Intensive Care Society Adult Patient Database (ANZICS-APD). Patients were allocated into three groups (hypoxia [PaO2<60mmHg], normoxia [PaO2,60-299mmHg] or hyperoxia [PaO2≥300mmHg]) according to their most abnormal PaO2 level in the first 24 hours of ICU stay. The relationship between PaO2 and hospital mortality was investigated using multivariate logistic regression analysis to adjust for confounding prehospital and ICU factors.
There were 957 patients identified on the VACAR database who met inclusion criteria. Of these, 584 (61%) were matched to the ANZICS-APD and had hospital mortality and oxygen data available. The unadjusted hospital mortality was 51% in the hypoxia patients, 41% in the normoxia patients and 47% in the hyperoxia patients (P=0.28). After adjustment for cardiopulmonary resuscitation by a bystander, patient age and cardiac arrest duration, hyperoxia in the ICU was not associated with increased hospital mortality (OR, 1.2; 95% CI, 0.51-2.82; P=0.83).
Hyperoxia within the first 24 hours was not associated with increased hospital mortality in patients admitted to ICU following out-of-hospital ventricular fibrillation cardiac arrest.
实验室和临床研究表明,心肺复苏后早期的高氧可能会增加神经损伤并使预后恶化。先前的临床研究规模较小,或未纳入相关的院前数据。我们旨在更大的患者队列中确定,在纠正院前变量后,接受院外心脏骤停(OHCA)复苏的患者在重症监护病房(ICU)中接受高氧治疗是否与死亡率增加有关。
将 2007 年 1 月至 2011 年 12 月期间从 OHCA 复苏并初始心脏节律为室颤的患者的维多利亚救护车心脏骤停登记处(VACAR)的数据与澳大利亚和新西兰重症监护学会成人患者数据库(ANZICS-APD)进行了关联。患者根据 ICU 入住的前 24 小时内最异常的 PaO2 水平被分配到三组(低氧血症[PaO2<60mmHg]、正常氧血症[PaO2,60-299mmHg]或高氧血症[PaO2≥300mmHg])。使用多变量逻辑回归分析来调整混杂的院前和 ICU 因素,研究 PaO2 与医院死亡率之间的关系。
在 VACAR 数据库中确定了 957 名符合纳入标准的患者。其中,584 名(61%)与 ANZICS-APD 相匹配,且有医院死亡率和氧气数据。低氧血症患者的未调整医院死亡率为 51%,正常氧血症患者的医院死亡率为 41%,高氧血症患者的医院死亡率为 47%(P=0.28)。在校正旁观者心肺复苏、患者年龄和心脏骤停持续时间后,ICU 中的高氧血症与增加的医院死亡率无关(OR,1.2;95%CI,0.51-2.82;P=0.83)。
在院外室颤性心脏骤停后入住 ICU 的患者中,前 24 小时内的高氧血症与医院死亡率增加无关。