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Pathophysiology and the Monitoring Methods for Cardiac Arrest Associated Brain Injury

机译:心脏骤停相关脑损伤的病理生理学和监测方法

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摘要

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.
机译:心脏骤停(CA)是全球性脑缺血的众所周知的原因。在CA和随后的意识丧失之后,氧气张力开始下降并导致一系列细胞变化,这些变化将导致细胞死亡,如果不能立即逆转,则会导致脑水肿。脑电图活动也开始改变。尽管颅内压升高(ICP)并非心脏骤停的直接结果,但由于缺氧缺血性脑病引起的脑组织变化,仍可能发生颅内压升高,这是CA和缺血性脑损伤后脑水肿的一种度量。在这篇综述中,我们将讨论CA术后脑水肿的病理生理学,一些可用的监测脑氧的技术和方法,脑电图(EEG),ICP(颅内压)以及微透析对脑代谢的测量及其在脑内的有用性。临床实践和可能的基础科学研究正在发展中。通过这次审查,我们希望获得有关患者状态和脑损伤细节的更多个性化信息的知识,从而有助于医生就采用哪种治疗方法做出决策。

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