The Efficacy of Therapeutic Hypothermia in Post-Cardiac Arrest Patients

Abstract

The Efficacy of Therapeutic Hypothermia in Post-Cardiac Arrest Patients

Albert D. Panke, RN

Cardiac arrest has proven to be the most clinically significant cause of cerebral hypoxia and ischemic damage, with an estimated 40 to 130 cases per 100,000 people each year. Mild therapeutic hypothermia has been utilized for years as a neuroprotectant in order to reduce cerebral insult after cardiac arrest. By cooling patients to a core temperature range of 32° to 34° Celsius, the metabolic demands of the entire body are drastically decreased. This enables the body to rest more efficiently and makes more oxygen available for the recovering cardiac muscle and cerebral tissue. Mild therapeutic hypothermia may also inhibit the production of free radicals, amino acid production, and calcium shifts, all of which may damage the mitochondria of cells and lead to subsequent cellular death. The aim of this research project is to review the available data regarding the neurological outcome of patients who undergo mild therapeutic hypothermia versus patients who remain normothermic after their initial resuscitation. A search was performed on large databases such as Medline, CINAHL, and ProQuest to access resources. Key terms utilized include therapeutic hypothermia, cardiac arrest, and neurological effects.