**1. Introduction**

Since its introduction, deep hypothermic circulatory arrest has been widely utilized for cerebral protection during aortic arch operations [1]. By inducing hypothermia to the brain and visceral organs, tissue oxygen and metabolic demands are reduced to the extent that the period of ischemia resulting from circulatory arrest can be well withstood [2–5]. Because the brain is particularly sensitive to transient periods of hypoxia, cerebral protection is essential

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

during aortic arch operations. Despite the advancement of surgical techniques, perioperative neurological complications following aortic arch operations are still reported to be as high as 5–8% in the current era [6–8]. Therefore, optimal methods how to induce circulatory arrest safely are still debated.

It has been shown that body temperature measurement is not a sufficient indicator of brain temperature [9]. Stone and colleagues reported that when profound hypothermia is rapidly induced and reversed, temperature measurements made at standard monitoring sites may not reflect cerebral temperature. Although a number of modalities, such as near-infrared spectroscopy and transcranial cerebral oximetry, have been introduced to monitor the brain during aortic arch operations, no single technique has proven to be a perfect monitoring tool. A method of physiological monitoring, intraoperative electroencephalography (EEG), was introduced by Ganzel and colleagues in 1997 [10]. The viewpoint is that maximal cerebral protection is achieved at temperatures sufficient to induce electrocerebral inactivity on EEG, under the assumption that maximal suppression of cerebral metabolic activity is achieved at electrocerebral inactivity [2, 11]. Stecker and colleagues reported that the process of cooling to electrocerebral inactivity produced a uniform degree of cerebral protection, independent of the actual nasopharyngeal temperature [12]. Consequently, many institutions have introduced intraoperative EEG to allow for the identification of electrocerebral inactivity before initiating circulatory arrest [13–16], which leads to average minimum temperatures of less than 16°C [17, 18].
