Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model

被引：0
作者：
Mypinder S. Sekhon
Philip N. Ainslie
Donald E. Griesdale
机构：
[1] Vancouver General Hospital,Division of Critical Care Medicine, Department of Medicine
[2] University of British Columbia,Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences
[3] University of British Columbia Okanagan,Department of Anaesthesiology, Pharmacology and Therapeutics
[4] Vancouver General Hospital,Centre for Clinical Epidemiology and Evaluation, Vancouver Coastal Health Research Institute
[5] University of British Columbia,undefined
[6] University of British Columbia,undefined
来源：
Critical Care | / 21卷
关键词：
Hypoxic ischemic brain injury; Cardiac arrest; Cerebral oxygen delivery; Targeted temperature management; Cerebral edema; Carbon dioxide; Anemia; Hypothermia; Normobaric hyperoxia;
D O I：
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学科分类号：
摘要：
Hypoxic ischemic brain injury (HIBI) after cardiac arrest (CA) is a leading cause of mortality and long-term neurologic disability in survivors. The pathophysiology of HIBI encompasses a heterogeneous cascade that culminates in secondary brain injury and neuronal cell death. This begins with primary injury to the brain caused by the immediate cessation of cerebral blood flow following CA. Thereafter, the secondary injury of HIBI takes place in the hours and days following the initial CA and reperfusion. Among factors that may be implicated in this secondary injury include reperfusion injury, microcirculatory dysfunction, impaired cerebral autoregulation, hypoxemia, hyperoxia, hyperthermia, fluctuations in arterial carbon dioxide, and concomitant anemia.
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