| Myocardial dysfunction in septic shock. | |
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MedLine Citation:
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PMID: 10768082 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Over the last decade, it has become clear that myocardial depression, like vascular dysfunction, is typical of human septic shock. Human septic myocardial depression is characterized by reversible biventricular dilatation, decreased ejection fraction, and decreased response to fluid resuscitation and catecholamine stimulation (in the presence of overall hyperdynamic circulation). A circulating myocardial depressant substance, not myocardial hypoperfusion, is responsible for this phenomenon. This substance has been shown to represent low concentrations of TNF-alpha and IL-1 beta acting in synergy on the myocardium through mechanisms that include NO and cGMP generation. Despite major advances in our understanding of the hemodynamics and pathogenesis of cardiac dysfunction in sepsis, successful attempts to modulate these mechanisms to improve clinical outcomes in human trials have not been demonstrated to date. For the moment, the therapeutic approach to the patient with cardiac dysfunction in distributive or septic shock must be primarily aimed at reestablishing adequate organ perfusion and oxygen delivery by vigorous fluid resuscitation and vasopressor or inotropic support. In the long term, however, only continued research regarding the cellular mechanisms of organ dysfunction, including septic myocardial depression, will lead to successful therapeutic strategies. These strategies will likely involve direct manipulation of intracellular signaling processes that lead to organ dysfunction as manifested by septic myocardial dysfunction and septic shock. |
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Authors:
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A Kumar; C Haery; J E Parrillo |
Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Critical care clinics Volume: 16 ISSN: 0749-0704 ISO Abbreviation: Crit Care Clin Publication Date: 2000 Apr |
Date Detail:
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Created Date: 2000-05-31 Completed Date: 2000-05-31 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8507720 Medline TA: Crit Care Clin Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 251-87 Citation Subset: IM |
Affiliation:
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Section of Critical Care Medicine, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois, USA. akumar@rush.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Heart / physiopathology* Hemodynamics Humans Sepsis / physiopathology Shock, Septic / mortality, physiopathology* Tumor Necrosis Factor-alpha / physiology Ventricular Dysfunction, Left / physiopathology* Ventricular Function, Right / physiology |
| Chemical | |
Reg. No./Substance:
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0/Tumor Necrosis Factor-alpha |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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