THERAPEUTIC HYPOTHERMIA AFTER CARDIAC ARREST: A SYSTEMATIC REVIEW

Abstract

Cardiac arrest leads to sudden termination of blood flow, leading to a rapid exhaustion of cerebral oxygen and adenosine triphosphate stores and depressed cerebral function. Neuronal damage occurs in the CNS during cardiac arrest (Phase I, "No Flow") and following the return of spontaneous circulation (ROSC) (Phase II, "Low Flow").The survival of neurons differs, depending on the type, site and period of global anoxia. In general, neurons in the cerebral cortex, hippocampus, and basal ganglia are the most susceptible. Therapeutic hypothermia (also called targeted temperature management) refers to deliberate reduction of the core body temperature, typically to a range of about 32° to 34° C in patients who don’t regain consciousness after return of spontaneous circulation following a cardiac arrest. Following are the benefits of therapeutic hypothermia (TH) which are associated with slowing down of cellular cascade after cardiac arrest by slowing down the cerebral metabolism (approximately 6-8% per 1°C) reducing excitatory amino acids (glutamate) release attenuation and/or reversibility of ischemic depolarization of the CNS leading to membrane stabilization, electrolyte redistribution and normalization of intracellular water concentration and intracellular pH (stabilization of the blood-brain barrier), reduction of oxygen free radical production and lipid peroxidation restoration of normal intracellular signaling mechanisms (including calcium modulation) and inhibition of deleterious signaling mechanisms, such as apoptotic signaling, restoration of protein synthesis and gene expression, inhibition of deleterious inflammatory products (i.e., cytokines, interleukins, arachidonic acid cascade end products), attenuation of CSF platelet-activating factor (PAF) and inhibition of cytoskeletal breakdown.