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

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...

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Autores principales: Sekhon, Mypinder S., Ainslie, Philip N., Griesdale, Donald E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5390465/
https://www.ncbi.nlm.nih.gov/pubmed/28403909
http://dx.doi.org/10.1186/s13054-017-1670-9
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author Sekhon, Mypinder S.
Ainslie, Philip N.
Griesdale, Donald E.
author_facet Sekhon, Mypinder S.
Ainslie, Philip N.
Griesdale, Donald E.
author_sort Sekhon, Mypinder S.
collection PubMed
description 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. Clarifying the underlying pathophysiology of HIBI is imperative and has been the focus of considerable research to identify therapeutic targets. Most notably, targeted temperature management has been studied rigorously in preventing secondary injury after HIBI and is associated with improved outcome compared with hyperthermia. Recent advances point to important roles of anemia, carbon dioxide perturbations, hypoxemia, hyperoxia, and cerebral edema as contributing to secondary injury after HIBI and adverse outcomes. Furthermore, breakthroughs in the individualization of perfusion targets for patients with HIBI using cerebral autoregulation monitoring represent an attractive area of future work with therapeutic implications. We provide an in-depth review of the pathophysiology of HIBI to critically evaluate current approaches for the early treatment of HIBI secondary to CA. Potential therapeutic targets and future research directions are summarized.
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spelling pubmed-53904652017-04-14 Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model Sekhon, Mypinder S. Ainslie, Philip N. Griesdale, Donald E. Crit Care Review 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. Clarifying the underlying pathophysiology of HIBI is imperative and has been the focus of considerable research to identify therapeutic targets. Most notably, targeted temperature management has been studied rigorously in preventing secondary injury after HIBI and is associated with improved outcome compared with hyperthermia. Recent advances point to important roles of anemia, carbon dioxide perturbations, hypoxemia, hyperoxia, and cerebral edema as contributing to secondary injury after HIBI and adverse outcomes. Furthermore, breakthroughs in the individualization of perfusion targets for patients with HIBI using cerebral autoregulation monitoring represent an attractive area of future work with therapeutic implications. We provide an in-depth review of the pathophysiology of HIBI to critically evaluate current approaches for the early treatment of HIBI secondary to CA. Potential therapeutic targets and future research directions are summarized. BioMed Central 2017-04-13 /pmc/articles/PMC5390465/ /pubmed/28403909 http://dx.doi.org/10.1186/s13054-017-1670-9 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Review
Sekhon, Mypinder S.
Ainslie, Philip N.
Griesdale, Donald E.
Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model
title Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model
title_full Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model
title_fullStr Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model
title_full_unstemmed Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model
title_short Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model
title_sort clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5390465/
https://www.ncbi.nlm.nih.gov/pubmed/28403909
http://dx.doi.org/10.1186/s13054-017-1670-9
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