Department of Neurology, Division of Neurocritical Care, Columbia University Medical Center, 177 Fort Washington Avenue, New York, NY 10032, USA.
J Neurol Neurosurg Psychiatry. 2010 Jul;81(7):793-7. doi: 10.1136/jnnp.2009.174425. Epub 2009 Dec 3.
Hyperventilation has been shown to be associated with cerebral vasoconstriction and increased risk of infarction. Our aim was to determine whether spontaneous reduction in end-tidal CO(2) (EtCO(2)) was associated with an increased in brain tissue hypoxia (BTH).
We studied 21 consecutive patients (mean age 50+/-16 years; 15 women) undergoing continuous monitoring for brain tissue oxygenation (PbtO(2)), intracranial pressure (ICP), cerebral perfusion pressure (CPP) and EtCO(2); mean values were recorded hourly BTH was defined as brain tissue oxygen tension (PbtO(2)) <15 mm Hg.
Diagnoses included subarachnoid haemorrhage (67%), intracranial haemorrhage (24%) and traumatic brain injury (10%). Overall, BTH occurred during 22.5% of the study period (490/2179 hourly data). The frequency of BTH increased progressively from 15.7% in patients with normal EtCO(2) (35-44 mm Hg) to 33.9% in patients with EtCO(2)<25 mm Hg (p<0.001). The mean tidal volume and minute ventilation were 7+/-2 ml/kg and 9+/-2 1/min, respectively. Hypocapnia was associated with higher measured-than-set respiratory rates and maximal minute ventilation values, suggestive of spontaneous hyperventilation. Using a generalised estimated equation (GEE) and after adjustment for GCS, ICP and core temperature, the variables independently associated with BTH events were EtCO(2) (OR: 0.94; 95% CI 0.90 to 0.97; p<0.001) and CPP (OR: 0.98; 95% CI 0.97 to 0.99; p=0.004).
The risk of brain tissue hypoxia in critically brain-injured patients increases when EtCO(2) values are reduced. Unintentional spontaneous hyperventilation may be a common and under-recognised cause of brain tissue hypoxia after severe brain injury.
过度通气与脑血管收缩和梗死风险增加有关。我们的目的是确定自主降低呼气末二氧化碳（EtCO2）是否与脑实质缺氧（BTH）增加有关。
我们研究了 21 例连续接受脑氧饱和度（PbtO2）、颅内压（ICP）、脑灌注压（CPP）和 EtCO2 连续监测的患者（平均年龄 50+/-16 岁；15 名女性）；平均每小时记录一次值，BTH 定义为脑氧张力（PbtO2）<15mmHg。
诊断包括蛛网膜下腔出血（67%）、颅内出血（24%）和创伤性脑损伤（10%）。总体而言，BTH 在研究期间的 22.5%（490/2179 小时数据）发生。BTH 的频率从正常 EtCO2（35-44mmHg）患者的 15.7%逐渐增加到 EtCO2<25mmHg 的患者的 33.9%（p<0.001）。潮气量和分钟通气量分别为 7+/-2ml/kg 和 9+/-2 1/min。低碳酸血症与测量的呼吸频率和最大分钟通气量值高于设定值有关，提示自发性过度通气。使用广义估计方程（GEE），并在调整 GCS、ICP 和核心温度后，与 BTH 事件独立相关的变量为 EtCO2（OR：0.94；95%CI 0.90-0.97；p<0.001）和 CPP（OR：0.98；95%CI 0.97-0.99；p=0.004）。
在严重脑损伤患者中，当 EtCO2 值降低时，脑实质缺氧的风险增加。自发性过度通气可能是严重脑损伤后脑实质缺氧的常见且未被认识到的原因。
