Coles Jonathan P, Fryer Tim D, Coleman Martin R, Smielewski Peter, Gupta Arun K, Minhas Pawan S, Aigbirhio Franklin, Chatfield Doris A, Williams Guy B, Boniface Simon, Carpenter T Adrian, Clark John C, Pickard John D, Menon David K
Division of Anaesthesia, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK.
Crit Care Med. 2007 Feb;35(2):568-78. doi: 10.1097/01.CCM.0000254066.37187.88.
To determine whether hyperventilation exacerbates cerebral ischemia and compromises oxygen metabolism (CMRO2) following closed head injury.
A prospective interventional study.
A specialist neurocritical care unit.
Ten healthy volunteers and 30 patients within 10 days of closed head injury.
Subjects underwent oxygen-15 positron emission tomography imaging of cerebral blood flow, cerebral blood volume, CMRO2, and oxygen extraction fraction. In patients, positron emission tomography studies, somatosensory evoked potentials, and jugular venous saturation (SjO2) measurements were obtained at Paco2 levels of 36+/-3 and 29+/-2 torr.
We estimated the volume of ischemic brain and examined the efficiency of coupling between oxygen delivery and utilization using the sd of the oxygen extraction fraction distribution. We correlated CMRO2 to cerebral electrophysiology and examined the effects of hyperventilation on the amplitude of the cortical somatosensory evoked potential response. Patients showed higher ischemic brain volume than controls (17+/-22 vs. 2+/-3 mL; p<or=.05), with worse matching of oxygen delivery to demand (p<.001). Hyperventilation consistently reduced cerebral blood flow (p<.001) and resulted in increases in oxygen extraction fraction and ischemic brain volume (17+/-22 vs. 88+/-66 mL; p<.0001), which were undetected by SjO2 monitoring. Mean CMRO2 was slightly increased following hyperventilation, but responses were extremely variable, with 28% of patients demonstrating a decrease in CMRO2 that exceeded 95% prediction intervals for zero change in one or more regions. CMRO2 correlated with cerebral electrophysiology, and cortical somatosensory evoked potential amplitudes were significantly increased by hyperventilation.
The acute cerebral blood flow reduction and increase in CMRO2 secondary to hyperventilation represent physiologic challenges to the traumatized brain. These challenges exhaust physiologic reserves in a proportion of brain regions in many subjects and compromise oxidative metabolism. Such ischemia is underestimated by common bedside monitoring tools and may represent a significant mechanism of avoidable neuronal injury following head trauma.
确定过度换气是否会加重闭合性颅脑损伤后的脑缺血并损害氧代谢（CMRO2）。
前瞻性干预性研究。
专业神经重症监护病房。
10名健康志愿者和30名闭合性颅脑损伤后10天内的患者。
受试者接受了氧-15正电子发射断层扫描成像，以测量脑血流量、脑血容量、CMRO2和氧摄取分数。对于患者，在动脉二氧化碳分压（Paco2）水平为36±3和29±2托时，进行正电子发射断层扫描研究、体感诱发电位和颈静脉血氧饱和度（SjO2）测量。
我们估计了缺血性脑体积，并使用氧摄取分数分布的标准差来检查氧输送与利用之间的耦合效率。我们将CMRO2与脑电生理进行关联，并研究过度换气对皮质体感诱发电位反应幅度的影响。患者的缺血性脑体积高于对照组（17±22 vs. 2±3 mL；p≤0.05），氧输送与需求的匹配更差（p<0.001）。过度换气持续降低脑血流量（p<0.001），并导致氧摄取分数和缺血性脑体积增加（17±22 vs. 88±66 mL；p<0.0001），而SjO2监测未检测到这些变化。过度换气后平均CMRO2略有增加，但反应差异极大，28%的患者在一个或多个区域的CMRO2下降超过了零变化的95%预测区间。CMRO2与脑电生理相关，过度换气使皮质体感诱发电位幅度显著增加。
过度换气继发的急性脑血流量减少和CMRO2增加对受伤的大脑构成生理挑战。这些挑战耗尽了许多受试者部分脑区的生理储备，损害了氧化代谢。这种缺血被常见的床边监测工具低估，可能是头部创伤后可避免的神经元损伤的重要机制。
