Hypothermia for cardiac arrest

Abstract

Therapeutic hypothermia for cardiac arrest survivors has emerged as a highly effective means of improving neurologic outcome. There are a number of purported mechanisms by which it is felt to be effective, but the exact mechanism is unknown. This article reviews the biochemical mechanisms of injury occurring in cardiac arrest, as well as the avenues that hypothermia takes to combat this injury. It also reviews the animal model data in support of this, as well as the newer animal studies that may help to improve the field. Several human studies of hypothermia in cardiac arrest have been performed, and this article reviews these for their methods and shortcomings. Our currently recommended guidelines for performing therapeutic hypothermia are presented. With therapeutic hypothermia comes potential risks to the patient, primarily affecting cardiac, metabolic, and hematologic systems, and these risks and their management are discussed. Multiple methods of cooling exist, including selective cranial as well as systemic cooling by internal or external approaches. Finally, the article discusses the current research in the field of hypothermia for cardiac arrest and implications for future practice.

Therapeutic Hypothermia Following Emergent Coronary Artery Bypass Grafting After Failed Percutaneous Coronary Intervention in a Comatose Post-Cardiac Arrest Patient

“…However, when PCI fails, the safety of hypothermia after emergent CABG has not been demonstrated in post-cardiac arrest patients. CABG may be a relative contraindication for TH because hypothermia may increase the risk of infection and bleeding (5). …”

“…Emergent coronary artery bypass grafting (CABG) after failed PCI is required in less than 1% of cases in institutes with a high case volume (4). Emergent CABG may be a relative contraindication for therapeutic hypothermia (TH) in post-cardiac arrest patients because hypothermia may increase the risk of infection and bleeding (5). However, recent studies have shown the successful application of TH in post-cardiac arrest patients with recent major surgery (6, 7) and pregnancy (8, 9), although they are relative contraindications.…”

Cognitive and Functional Consequence of Cardiac Arrest

“…Excessive release of glutamate activates N-methyl-Da s p a r t a t e ( N M D A ) , 2 -a m i n o -3 -( 3 -h y d r o x y -5 -methylisoxazol-4-yl) proprionate (AMPA), and kainate receptors, leading to a destructive and dysregulated increase in intracellular calcium that causes cell death [22]. Hypothermia may ameliorate many of these changes: it may potentiate cell membrane stabilization, decrease metabolic rate, and suppress the release of destructive enzymes and glutamate, in addition to decreasing inflammation [23].…”

CTL-Derived Granzyme B Participates in Hippocampal Neuronal Apoptosis Induced by Cardiac Arrest and Resuscitation in Rats

“…Despite the application of cardiopulmonary resuscitation (CPR) to reduce the mortality from CA, brain ischemia remains a devastating complication of CA/CPR, with considerable neuronal apoptosis and cognitive deficits within the initial 3 months after CPR in ∼70% of the survivors (2,3). To date, there is a paucity of approaches with clinical efficacy, reliability, and validity to prevent brain injury following CA/CPR (4).…”