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Acute mechanical circulatory support for cardiogenic shock: the “door to support” time

Cardiogenic shock (CS) remains a major cause of in-hospital mortality in the setting of acute myocardial infarction. CS begins as a hemodynamic problem with impaired cardiac output leading to reduced systemic perfusion, increased residual volume within the left and right ventricles, and increased ca...

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Detalles Bibliográficos
Autores principales: Esposito, Michele L, Kapur, Navin K
Formato: Online Artículo Texto
Lenguaje:English
Publicado: F1000Research 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5443341/
https://www.ncbi.nlm.nih.gov/pubmed/28580136
http://dx.doi.org/10.12688/f1000research.11150.1
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author Esposito, Michele L
Kapur, Navin K
author_facet Esposito, Michele L
Kapur, Navin K
author_sort Esposito, Michele L
collection PubMed
description Cardiogenic shock (CS) remains a major cause of in-hospital mortality in the setting of acute myocardial infarction. CS begins as a hemodynamic problem with impaired cardiac output leading to reduced systemic perfusion, increased residual volume within the left and right ventricles, and increased cardiac filling pressures. A critical step towards the development of future algorithms is a clear understanding of the treatment objectives for CS. In this review, we introduce the “door to support” time as an emerging target of therapy to improve outcomes associated with CS, define four key treatment objectives in the management of CS, discuss the importance of early hemodynamic assessment and appropriate selection of acute mechanical circulatory support (AMCS) devices for CS, and introduce a classification scheme that identifies subtypes of CS based on cardiac filling pressures.
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spelling pubmed-54433412017-06-02 Acute mechanical circulatory support for cardiogenic shock: the “door to support” time Esposito, Michele L Kapur, Navin K F1000Res Review Cardiogenic shock (CS) remains a major cause of in-hospital mortality in the setting of acute myocardial infarction. CS begins as a hemodynamic problem with impaired cardiac output leading to reduced systemic perfusion, increased residual volume within the left and right ventricles, and increased cardiac filling pressures. A critical step towards the development of future algorithms is a clear understanding of the treatment objectives for CS. In this review, we introduce the “door to support” time as an emerging target of therapy to improve outcomes associated with CS, define four key treatment objectives in the management of CS, discuss the importance of early hemodynamic assessment and appropriate selection of acute mechanical circulatory support (AMCS) devices for CS, and introduce a classification scheme that identifies subtypes of CS based on cardiac filling pressures. F1000Research 2017-05-22 /pmc/articles/PMC5443341/ /pubmed/28580136 http://dx.doi.org/10.12688/f1000research.11150.1 Text en Copyright: © 2017 Esposito ML and Kapur NK http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution Licence, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Esposito, Michele L
Kapur, Navin K
Acute mechanical circulatory support for cardiogenic shock: the “door to support” time
title Acute mechanical circulatory support for cardiogenic shock: the “door to support” time
title_full Acute mechanical circulatory support for cardiogenic shock: the “door to support” time
title_fullStr Acute mechanical circulatory support for cardiogenic shock: the “door to support” time
title_full_unstemmed Acute mechanical circulatory support for cardiogenic shock: the “door to support” time
title_short Acute mechanical circulatory support for cardiogenic shock: the “door to support” time
title_sort acute mechanical circulatory support for cardiogenic shock: the “door to support” time
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5443341/
https://www.ncbi.nlm.nih.gov/pubmed/28580136
http://dx.doi.org/10.12688/f1000research.11150.1
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