Document Detail


Myocardial dysfunction in septic shock.
MedLine Citation:
PMID:  10768082     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
A Kumar; C Haery; J E Parrillo
Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Critical care clinics     Volume:  16     ISSN:  0749-0704     ISO Abbreviation:  Crit Care Clin     Publication Date:  2000 Apr 
Date Detail:
Created Date:  2000-05-31     Completed Date:  2000-05-31     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8507720     Medline TA:  Crit Care Clin     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  251-87     Citation Subset:  IM    
Affiliation:
Section of Critical Care Medicine, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois, USA. akumar@rush.edu
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MeSH Terms
Descriptor/Qualifier:
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:
0/Tumor Necrosis Factor-alpha

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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