Document Detail


Myocardial dysfunction in sepsis: clinical and experimental investigations.
MedLine Citation:
PMID:  9793163     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: To review the clinical manifestations and mechanisms of cardiac dysfunction in septic shock. METHODS: Literature review of selected clinical studies and animal models. RESULTS: Depressed myocardial contractile function is a common consequence of severe infections. Bacterial factors, in conjunction with host inflammatory mediators, produce a profile of reversible cardiac dysfunction manifested by a decrease in ventricular ejection fraction, ventricular dilatation, and increased cardiac output. Global ischemia is not the major mechanism that mediates cardiac dysfunction during sepsis. Inflammatory mediators contribute to myocardial dysfunction by damaging the coronary microcirculation and contributing to myocardial edema and cardiocyte damage. However, trials of anti-inflammatory agents have not prevented or increased the rate of reversal of septic shock or improved survival. The link between nitric oxide and clinical myocardial depression remains unclear, as nonselective nitric oxide synthase inhibition does not block the development of ventricular dysfunction. CONCLUSIONS: Serious bacterial infections result in inflammatory injury to the heart manifested by a common profile of cardiac dysfunction. Therapy remains limited to treatment of the infection with antibiotics and supportive care, with fluid resuscitation and selective use of inotropes and vasopressors. Experimental models suggest that new anti-inflammatory strategies (e.g. tyrosine kinase inhibitors) may offer some advantages over those that target a single mediator; these agents remain to be clinically evaluated.
Authors:
A F Suffredini
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Schweizerische medizinische Wochenschrift     Volume:  128     ISSN:  0036-7672     ISO Abbreviation:  Schweiz Med Wochenschr     Publication Date:  1998 Sep 
Date Detail:
Created Date:  1999-01-14     Completed Date:  1999-01-14     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  0404401     Medline TA:  Schweiz Med Wochenschr     Country:  SWITZERLAND    
Other Details:
Languages:  eng     Pagination:  1444-52     Citation Subset:  IM    
Affiliation:
Critical Care Medicine Department, Warren G. Magnuson Clinical Center, National Institutes of Health, Bethesda, MD 20892-1662, USA. anthony_suffredini@nih.gov
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MeSH Terms
Descriptor/Qualifier:
Animals
Humans
Inflammation Mediators / physiology
Myocardial Contraction / physiology*
Nitric Oxide / physiology
Shock, Septic / physiopathology*,  therapy
Ventricular Dysfunction / physiopathology,  therapy
Chemical
Reg. No./Substance:
0/Inflammation Mediators; 10102-43-9/Nitric Oxide

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