HYPERVENTILATION ON CEREBRAL BLOOD FLOW/BRAIN OXYGENATION IN BRAIN INJURY

每年约有200万人遭受创伤性脑损伤 (TBI)在美国，大约有10万人死亡，9万人留下 长期残疾。 这些患者的管理进展 降低了死亡率，但对改善脑损伤几乎没有作用。 最近 对严重TBI患者的研究表明， 脑血流量（rCBF）在受伤后的最初几个小时内有助于 继发性脑损伤 此外，使用急性 过度通气（HV）治疗颅内压升高， TBI可能导致或加重缺血，从而增加而不是减少脑缺血。 防止继发性CNS损伤。 为了了解HV的影响， 在脑氧合方面，重要的是要确定 TBI患者的rCBF产生足够严重的脑缺氧 导致缺血性神经损伤 PET扫描仪的存在， 巴恩斯犹太医院的NNICU，结合我们丰富的经验 利用PET检测缺血，我们在临床上的专业知识 TBI患者的管理，以及大量可用的患者人群 给了我们一个独特的机会来解决这些问题。 我们建议 研究急性HV对脑血流和脑的影响 TBI中的氧合。 具体来说，我们将测试的假设，严重 （PaCO 2约为25 mm Hg），但不是中度（PaCO 2约为30 mm Hg） TBI后过度通气可能导致CBF减少， 严重到足以导致脑能量衰竭（定义为CBF， 不足以满足代谢需要）。 我们将研究30名患者， 12小时非穿透性重度头部损伤（GCS小于或等于 8)刚完成PET测量的患者（CBF、CMRO 2、OEF 2 A-VDO 2和CvO 3作为项目1的一部分。 ICP升高的患者（18 - 25 mmHg），将进行重复PET检查 急性脑梗死后再次测量rCBF和CMRO 2、OEF、A-VDO 2和CvO 2， HV，将研究三组，每组10例患者。 第一组 将使PaCPO 2降至30+2 mmHg。 如果没有病人出现脑 缺血可能严重到足以导致能量衰竭， PaCO 2降至25 ± 2 ℃。 否则，第二组 在初始PaCO 2大于 然后或等于35，到35=2，以确定是否有一个安全 阈值HV。 第三组10名患者将作为非- 超通风控制。 这些调查对于确定 正确使用HV治疗急性TBI。

Each year approximately 2 million people suffer traumatic brain injuries (TBI) in the U.S. Of these about 100,000 die and 90,000 are left with long-term disabilities. Advances in the management of these patients have reduced mortality but done little to ameliorate brain injury. Recent studies in severe TBI patients have suggested that reduced regional cerebral blood flow (rCBF) in the first few hours after injury contributes to secondary brain injury. Additionally, the use of acute hyperventilation (HV) to treat elevated intracranial pressure following TBI may led to or exacerbate ischemia thus augmenting rather than preventing secondary CNS injury. In order to understand the impact of HV on brain oxygenation, it is important to determine if the reduction in rCBF seen in TBI patients produces brain oxygen deprivation severe enough to cause ischemic neuronal damage. The presence of a PET scanner in the NNICU at Barnes-Jewish Hospital, combined with our extensive experience with the use of PET to detect ischemia, our expertise in the clinical management of TBI patients, and the large available patient population gives us a unique opportunity to address these issues. We propose to investigate the impact of acute HV on cerebral blood flow and brain oxygenation in TBI. Specifically we will test the hypothesis that severe (PaCO2 of about 25 mm Hg) but not moderate (PaCO2 of about 30 mm Hg) hyperventilation following TBI can produce reduction in CBF potentially severe enough to cause cerebral energy failure (defined as CBF that is insufficient to meet metabolic needs). We will study 30 patients within 12 hours of non-penetrating severe head injury (GCS less then or equal of 8) who have just completed PET measurements of regional (CBF, CMRO2, OEF2 A-VDO2 and CvO3 as part of project 1. Patients with elevated ICP(18 - 25 mm Hg) at the time of the initial PET study will have repeat PET measurements of rCBF and CMRO2, OEF, A-VDO2, and CvO2, again after acute HV, Three groups of 10 patients each will be studied. The first group will have PaCPO2 lowered to 30+2 torr. If no patient develops cerebral ischemia potentially severe enough to cause energy failure the second group will have PaCO2 lowered to 25+2 torr. Otherwise, the second group will have PaCO2 lowered, in those patients with an initial PaCO2 greater then or equal to 35 torr, to 35=2 torr to determine if there is a safe threshold for HV. A third group of ten patients will serve as non- hyprventilated controls. These investigations are critical to determine the proper use of HV in the treatment of acute TBI.