Document Detail


The severity of shock is associated with impaired rates of net alveolar fluid clearance in clinical acute lung injury.
MedLine Citation:
PMID:  22821995     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The rate of alveolar fluid clearance (AFC) is associated with mortality in clinical acute lung injury (ALI). Patients with ALI often develop circulatory shock, but how shock affects the rate of AFC is unknown. To determine the effect of circulatory shock on the rate of AFC in patients with ALI, the rate of net AFC was measured in 116 patients with ALI by serial sampling of pulmonary edema fluid. The primary outcome was the rate of AFC in patients with shock compared with those without shock. We also tested the effects of shock severity and bacteremia. Patients with ALI and shock (n = 86) had significantly slower rates of net AFC compared with those without shock (n = 30, P = 0.03), and AFC decreased significantly as the number of vasopressors increased. Patients with positive blood cultures (n = 21) had slower AFC compared with patients with negative blood cultures (n = 96, P = 0.023). In addition, the edema fluid-to-plasma protein ratio, an index of alveolar-capillary barrier permeability, was highest in patients requiring the most vasopressors (P < 0.05). Patients with ALI complicated by circulatory shock and bacteremia had slower rates of AFC compared with patients without shock or bacteremia. An impaired capacity to reabsorb alveolar edema fluid may contribute to high mortality among patients with sepsis-induced ALI. These findings also suggest that vasopressor use may be a marker of alveolar-capillary barrier permeability in ALI and provide justification for new therapies that enhance alveolar epithelial and endothelial barrier integrity in ALI, particularly in patients with shock.
Authors:
Yosaf F Zeyed; Julie A Bastarache; Michael A Matthay; Lorraine B Ware
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Publication Detail:
Type:  Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-07-20
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  303     ISSN:  1522-1504     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-09-17     Completed Date:  2012-11-29     Revised Date:  2013-09-17    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L550-5     Citation Subset:  IM    
Affiliation:
Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
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MeSH Terms
Descriptor/Qualifier:
Acute Lung Injury / complications*,  drug therapy,  physiopathology
Adult
Bacteremia / drug therapy,  etiology,  physiopathology*
Body Fluids / metabolism
Humans
Male
Middle Aged
Prospective Studies
Pulmonary Alveoli / metabolism*
Pulmonary Edema / metabolism
Respiratory Distress Syndrome, Adult / complications,  physiopathology
Shock / etiology,  physiopathology*
Vasoconstrictor Agents / therapeutic use
Grant Support
ID/Acronym/Agency:
HL090785/HL/NHLBI NIH HHS; HL103836/HL/NHLBI NIH HHS; HL51856/HL/NHLBI NIH HHS; K24 HL103836/HL/NHLBI NIH HHS; R37 HL051856/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Vasoconstrictor Agents
Comments/Corrections

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


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