Therapeutic Hypothermia After Cardiac Arrest

Abstract

Post cardiac arrest syndrome is a complex pathophysiological state that results after return of spontaneous circulation (ROSC) following a successful cardiopulmonary resuscitation. This term has aptly replaced the previous terminology of post resuscitation syndrome as post resuscitation denotes the end of the act of resuscitation, whereas to achieve increased survival rates with good neurological function, a much more complex and intensive phase of management, has to begin after ROSC Cardiac arrest and ROSC is a case of whole-body ischemia and subsequent reperfusion injury. This injury mechanism along with pre-arrest comorbidities cause enormous biochemical, structural, and functional insults, which in a complex interrelated process leads to progressive cell destruction, multiorgan dysfunction, neuronal apoptosis, and death. Many of these processes are temperature sensitive. Hypothermia has been shown to attenuate or ameliorate many deleterious temperature-sensitive mechanisms, thereby contributing to protection of the brain and heart Therapeutic hypothermia occurs in three phases: cooling (induction), maintenance, and rewarming.Induction: unstable period during which the patient’s core temperature is reduced quickly to target temperature,Maintenance: more stable period during which the patient is maintained at target temperature for 12-24 hours, and Rewarming: relatively unstable period during which the patient is returned to normothermia over the course of 12 to16 hours All patients undergoing TH should receive sedation to decrease metabolic demand, oxygen consumption, and the shivering threshold as well as to help maintain neuroprotective benefits of TH. The most commonly used sedatives are propofol, midazolam, and dexmedetomidine. Evaluating the patient’s neurologic status after TH can be challenging. Drugs used for sedation and shivering suppression may make clinical assessment unreliable. Diagnostic tests used to evaluate the patient’s neurologic status may include magnetic resonance imaging, EEG, and somatosensory evoked potentials. AHA and ILCOR recommend delaying neurologic prognostication for at least 72 hours after the patient has been rewarmed. Signs of poor clinical prognosis include absent corneal, pupillary, and motor responses and extensor posturing after rewarming MTH induced alterations of electrolyte levels strongly correlate with the depth of hypothermia, and are generally well tolerated in post CA patients. Effects on coagulation correlate well with the degree of cooling and do not appear to add additional bleeding complications.