• Cesar Reis, Onat Akyol, Camila Araujo, Lei Huang, Budbazar Enkhjargal, Jay Malaguit, Vadim Gospodarev, and John H Zhang.
• Department of Physiology and Pharmacology, Loma Linda University School of Medicine, 11041 Campus Street, Risley Hall, Room 219, Loma Linda, CA 92354, USA. cesarreis@hotmail.com.
• Int J Mol Sci. 2017 Jan 11; 18 (1).

AbstractCardiac 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.

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