Document Detail

Septic shock in humans. Advances in the understanding of pathogenesis, cardiovascular dysfunction, and therapy.
MedLine Citation:
PMID:  2197912     Owner:  NLM     Status:  MEDLINE    
Septic shock is the commonest cause of death in intensive care units. Although sepsis usually produces a low systemic vascular resistance and elevated cardiac output, strong evidence (decreased ejection fraction and reduced response to fluid administration) suggests that the ventricular myocardium is depressed and the ventricle dilated. In survivors, these abnormalities are reversible. Failure to develop ventricular dilatation in nonsurvivors suggests that dilatation is a compensatory mechanism needed to maintain adequate cardiac output. With a canine model of septic shock that is very similar to human sepsis, myocardial depression was confirmed using load-independent measures of ventricular performance. Endotoxin administration to humans simulates the qualitative, cardiovascular abnormalities of sepsis. The pathogenesis of septic shock is extraordinarily complex. Diverse microorganisms can generate toxins, stimulating release of potent mediators that act on vasculature and myocardium. A circulating myocardial depressant substance has been closely associated with the myocardial depression of human septic shock. Therapy has emphasized early use of antibiotics, critical care monitoring, aggressive volume resuscitation, and, if shock continues, use of inotropic agents and vasopressors. Pharmacologic or immunologic antagonism of endotoxin or other mediators may prove to enhance survival in this highly lethal syndrome.
J E Parrillo; M M Parker; C Natanson; A F Suffredini; R L Danner; R E Cunnion; F P Ognibene
Publication Detail:
Type:  Consensus Development Conference; Consensus Development Conference, NIH; Journal Article; Review    
Journal Detail:
Title:  Annals of internal medicine     Volume:  113     ISSN:  0003-4819     ISO Abbreviation:  Ann. Intern. Med.     Publication Date:  1990 Aug 
Date Detail:
Created Date:  1990-08-27     Completed Date:  1990-08-27     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  0372351     Medline TA:  Ann Intern Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  227-42     Citation Subset:  AIM; IM    
Rush-Presbyterian-St. Luke's Medical Center, Chicago, IL 60612.
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MeSH Terms
Cardiovascular System / physiopathology
Endotoxins / physiology
Shock, Septic* / etiology,  physiopathology,  therapy
United States
Reg. No./Substance:
Comment In:
Ann Intern Med. 1990 Dec 15;113(12):991-2   [PMID:  2240923 ]

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