Eastwood Glenn M, Tanaka Aiko, Bellomo Rinaldo
Department of Intensive Care, Austin Hospital, Melbourne, VIC, Australia; Australian and New Zealand Intensive Care Research Centre, Melbourne, VIC, Australia; School of Nursing and Midwifery, Faculty of Health, Deakin University, Melbourne, Australia.
Department of Intensive Care, Austin Hospital, Melbourne, VIC, Australia; Department of Anesthesiology and Intensive Care, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Resuscitation. 2016 May;102:11-6. doi: 10.1016/j.resuscitation.2016.02.009. Epub 2016 Feb 21.
Optimal cerebral oxygenation is considered fundamental to cerebral protection in cardiac arrest (CA) patients. Hypercapnia increases cerebral blood flow and may also improve cerebral oxygenation. It is uncertain, however, whether this effect occurs in mechanically ventilated early survivors of CA.
We enrolled mechanically ventilated resuscitated patients within 36h of their cardiac arrest. We performed a prospective double cross-over physiological study comparing the impact of normocapnia (PaCO2 35-45mmHg) vs. mild hypercapnia (PaCO2 45-55mmHg) on regional cerebral tissue oxygen saturation (SctO2) assessed by near infrared spectroscopy (NIRS).
We studied seven adult CA patients with a median time to return of spontaneous circulation of 28min at a median of 26h and 30min after CA. During normocapnia (median EtCO2 of 32mmHg [30-41mmHg] and PaCO2 of 37mmHg [32-45mmHg]) the median NIRS-derived left frontal SctO2 was 61% [52-65%] and the right frontal SctO2 was 61% [54-68%]. However, during mild hypercapnia (median EtCO2 of 49mmHg [40-57mmHg] and PaCO2 of 52mmHg [43-55mmHg) the median left frontal SctO2 increased to 69% [59-78%] and the right frontal SctO2 increased to 73% [61-76%])(p=0.001, for all comparisons).
During the early post-resuscitation period, in mechanically ventilated CA patients, mild hypercapnia increases cerebral oxygenation as assessed by NIRS. Further investigations of the effect of prolonged mild hypercapnia on cerebral oxygenation and patient outcomes appear justified.
最佳脑氧合被认为是心脏骤停（CA）患者脑保护的基础。高碳酸血症可增加脑血流量，也可能改善脑氧合。然而，这种效应是否发生在机械通气的CA早期幸存者中尚不确定。
我们纳入了心脏骤停后36小时内接受机械通气的复苏患者。我们进行了一项前瞻性双交叉生理学研究，比较了正常碳酸血症（动脉血二氧化碳分压[PaCO2] 35 - 45mmHg）与轻度高碳酸血症（PaCO2 45 - 55mmHg）对通过近红外光谱（NIRS）评估的局部脑组织氧饱和度（SctO2）的影响。
我们研究了7例成年CA患者，自主循环恢复的中位时间为28分钟，CA后中位时间为26小时30分钟。在正常碳酸血症期间（呼气末二氧化碳分压[EtCO2]中位数为32mmHg [30 - 41mmHg]，PaCO2为37mmHg [32 - 45mmHg]），NIRS得出的左额叶SctO2中位数为61% [52 - 65%]，右额叶SctO2为61% [54 - 68%]。然而，在轻度高碳酸血症期间（EtCO2中位数为49mmHg [40 - 57mmHg]，PaCO2为52mmHg [43 - 55mmHg]），左额叶SctO2中位数增加到69% [59 - 78%]，右额叶SctO2增加到73% [61 - 76%]（所有比较p = 0.001）。
在复苏后的早期，对于机械通气的CA患者，轻度高碳酸血症可增加通过NIRS评估的脑氧合。进一步研究延长轻度高碳酸血症对脑氧合和患者预后的影响似乎是合理的。
