Reis Cesar, Akyol Onat, Araujo Camila, Huang Lei, Enkhjargal Budbazar, Malaguit Jay, Gospodarev Vadim, Zhang John H
Department of Physiology and Pharmacology, Loma Linda University School of Medicine, 11041 Campus Street, Risley Hall, Room 219, Loma Linda, CA 92354, USA.
Department of Anesthesiology, Loma Linda University Medical Center, Loma Linda, CA 92354, USA.
Int J Mol Sci. 2017 Jan 11;18(1):129. doi: 10.3390/ijms18010129.
Cardiac arrest (CA) is a well-known cause of global brain ischemia. After CA and subsequent loss of consciousness, oxygen tension starts to decline and leads to a series of cellular changes that will lead to cellular death, if not reversed immediately, with brain edema as a result. The electroencephalographic activity starts to change as well. Although increased intracranial pressure (ICP) is not a direct result of cardiac arrest, it can still occur due to hypoxic-ischemic encephalopathy induced changes in brain tissue, and is a measure of brain edema after CA and ischemic brain injury. In this review, we will discuss the pathophysiology of brain edema after CA, some available techniques, and methods to monitor brain oxygen, electroencephalography (EEG), ICP (intracranial pressure), and microdialysis on its measurement of cerebral metabolism and its usefulness both in clinical practice and possible basic science research in development. With this review, we hope to gain knowledge of the more personalized information about patient status and specifics of their brain injury, and thus facilitating the physicians' decision making in terms of which treatments to pursue.
心脏骤停（CA）是全球脑缺血的一个众所周知的原因。在心脏骤停及随后意识丧失后，氧张力开始下降，并导致一系列细胞变化，如果不立即逆转，这些变化将导致细胞死亡，并引发脑水肿。脑电图活动也开始改变。虽然颅内压（ICP）升高不是心脏骤停的直接结果，但它仍可能由于缺氧缺血性脑病引起的脑组织变化而发生，并且是心脏骤停后脑水肿和缺血性脑损伤的一个指标。在这篇综述中，我们将讨论心脏骤停后脑水肿的病理生理学、一些可用的技术以及监测脑氧、脑电图（EEG）、颅内压（ICP）和微透析以测量脑代谢的方法，及其在临床实践和可能的基础科学研究中的应用。通过这篇综述，我们希望获得更多关于患者状态及其脑损伤细节的个性化信息，从而有助于医生在选择治疗方案时做出决策。
