Document Detail


Adult respiratory distress syndrome.
MedLine Citation:
PMID:  425503     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Many causes for the adult respiratory distress syndrome (ARDS) have been reported, all with common pathologic, pathophysiologic and biochemical end results. The final common pathway may involve changes in lung content of a critical enzyme, superoxide dismutase, or alterations in surfactant metabolism, or both. The early assumption that the disorder is partially due to oxygen toxicity from inspired oxygen concentrations greater than 60 percent is consistent with findings of recent biochemical studies. Although the lung normally maintains its alveoli dry, during ARDS increased permeability of small pulmonary vessels results in primary pulmonary edema, in contrast to edema from increased vascular pressure. These data have been obtained mainly in animals; whether they apply to humans with ARDS is not certain. Tissue oxygenation is improved by increasing end-expiratory pressure in an animal model of ARDS, more effectively during spontaneous breathing than during mechanical ventilation. During spontaneous breathing, adverse ventilatory effects were caused by stimulation of pulmonary reflexes.
Authors:
D H Simmons; G Nash; K L Brigham; D F Tierney; D H Simmons
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Western journal of medicine     Volume:  130     ISSN:  0093-0415     ISO Abbreviation:  West. J. Med.     Publication Date:  1979 Mar 
Date Detail:
Created Date:  1979-05-24     Completed Date:  1979-05-24     Revised Date:  2008-11-20    
Medline Journal Info:
Nlm Unique ID:  0410504     Medline TA:  West J Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  218-35     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Humans
Respiratory Distress Syndrome, Adult*

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


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