Neuroprotection after Cardiac Arrest: Reevaluating the Role of Therapeutic Hypothermia - A Narrative Review

Therapeutic hypothermia, defined as lowering the core body temperature to 32°C-34°C, has emerged as a key intervention in postcardiac arrest care, aimed at mitigating brain injury and improving neurological outcomes. The primary pathways underlying the potential neuroprotective effects of therapeutic hypothermia include the reduction of cerebral metabolic demand, the attenuation of excitotoxicity, and the suppression of inflammation. Early clinical studies, including the Hypothermia After Cardiac Arrest (HACA) and the Therapeutic Hypothermia after Cardiac Arrest in Nonshockable Rhythm (HYPERION) trials, showed promising results and led to the endorsement of this approach in the post-cardiac arrest setting. However, more recent trials, such as the Targeted Temperature Management (TTM), the TTM2 and the HACA in-hospital studies, found no significant benefit in all-cause mortality or neurologic outcomes. These findings raised important questions about the ideal temperature range, the optimal timing of initiation, and the duration of cooling. Moreover, this approach is correlated with potential risks, like coagulopathy, increased infection risk, or electrolyte disturbances. The current review aims to present current clinical guidelines and recommendations from key scientific communities, including the European Resuscitation Council, the European Society of Intensive Care Medicine, the American Heart Association, the European Society for Emergency Medicine and the European Society of Anaesthesiology and Intensive Care, on temperature management among comatose survivors of cardiac arrest and evaluate the benefits and risks of therapeutic hypothermia as a neuroprotective strategy for post-cardiac arrest care.