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Clinical review: Myocardial depression in sepsis and septic shock
Myocardial dysfunction frequently accompanies severe sepsis and septic shock. Whereas myocardial depression was previously considered a preterminal event, it is now clear that cardiac dysfunction as evidenced by biventricular dilatation and reduced ejection fraction is present in most patients with...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2002
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC153435/ https://www.ncbi.nlm.nih.gov/pubmed/12493071 |
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author | Court, Olivier Kumar, Aseem Parrillo, Joseph E Kumar, Anand |
author_facet | Court, Olivier Kumar, Aseem Parrillo, Joseph E Kumar, Anand |
author_sort | Court, Olivier |
collection | PubMed |
description | Myocardial dysfunction frequently accompanies severe sepsis and septic shock. Whereas myocardial depression was previously considered a preterminal event, it is now clear that cardiac dysfunction as evidenced by biventricular dilatation and reduced ejection fraction is present in most patients with severe sepsis and septic shock. Myocardial depression exists despite a fluid resuscitation-dependent hyperdynamic state that typically persists in septic shock patients until death or recovery. Cardiac function usually recovers within 7–10 days in survivors. Myocardial dysfunction does not appear to be due to myocardial hypoperfusion but due to circulating depressant factors, including the cytokines tumor necrosis factor alpha and IL-1β. At a cellular level, reduced myocardial contractility seems to be induced by both nitric oxide-dependent and nitric oxide-independent mechanisms. The present paper reviews both the clinical manifestations and the molecular/cellular mechanisms of sepsis-induced myocardial depression. |
format | Text |
id | pubmed-153435 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2002 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-1534352003-04-18 Clinical review: Myocardial depression in sepsis and septic shock Court, Olivier Kumar, Aseem Parrillo, Joseph E Kumar, Anand Crit Care Review Myocardial dysfunction frequently accompanies severe sepsis and septic shock. Whereas myocardial depression was previously considered a preterminal event, it is now clear that cardiac dysfunction as evidenced by biventricular dilatation and reduced ejection fraction is present in most patients with severe sepsis and septic shock. Myocardial depression exists despite a fluid resuscitation-dependent hyperdynamic state that typically persists in septic shock patients until death or recovery. Cardiac function usually recovers within 7–10 days in survivors. Myocardial dysfunction does not appear to be due to myocardial hypoperfusion but due to circulating depressant factors, including the cytokines tumor necrosis factor alpha and IL-1β. At a cellular level, reduced myocardial contractility seems to be induced by both nitric oxide-dependent and nitric oxide-independent mechanisms. The present paper reviews both the clinical manifestations and the molecular/cellular mechanisms of sepsis-induced myocardial depression. BioMed Central 2002 2002-09-12 /pmc/articles/PMC153435/ /pubmed/12493071 Text en Copyright © 2002 BioMed Central Ltd |
spellingShingle | Review Court, Olivier Kumar, Aseem Parrillo, Joseph E Kumar, Anand Clinical review: Myocardial depression in sepsis and septic shock |
title | Clinical review: Myocardial depression in sepsis and septic shock |
title_full | Clinical review: Myocardial depression in sepsis and septic shock |
title_fullStr | Clinical review: Myocardial depression in sepsis and septic shock |
title_full_unstemmed | Clinical review: Myocardial depression in sepsis and septic shock |
title_short | Clinical review: Myocardial depression in sepsis and septic shock |
title_sort | clinical review: myocardial depression in sepsis and septic shock |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC153435/ https://www.ncbi.nlm.nih.gov/pubmed/12493071 |
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