The Effect of Therapeutic Temperature Management on Cell Death and Apoptosis in Resuscitative Attempts

TTM has been historically classified into: mild (34.536.5°C), moderate (34.5-32°C), marked (28-32°C) and profound hypothermia (<28°C) [1,2]. The technique can be separated into three phases: induction, maintenance and rewarming; and each phase produces several changes in normal physiology. Very recent literature data pointed out that in real-world practices without a strictly controlled environment, TTM can improve survival and favorable neurological outcome in post-CA patients independent of initial rhythm [3]. Furthermore, international consensus groups and committees recommended TTM for adults with CA with an initial shockable rhythm at a constant temperature between 32°C and 36°C for at least 24 hours [4]. In the post-resuscitative period, TTM is thought to mitigate neurologic reperfusion injury by decreasing cerebral oxygen consumption and biochemical damage [5]. TTM was postulated to offer an extended therapeutic window to restore the integrity of circulation, with the brain maintained in a protective, hypometabolic state. Prolonged, moderate cerebral hypothermia initiated within a few hours after severe HIE and maintained until resolution of the acute phase of delayed cell death is reported to reduce acute brain injury in term infants and in adults after CA [6]. The specific mechanisms of hypothermic neuroprotection are not yet clear, partly because TTM suppresses a myriad of potential injurious factors. This article is written to review the current literature to summarize data regarding cellular injury following CA and effects attributed to the procedure of TTM in the emergency setting.