Blood flow, not hypoxia, determines intramucosal PCO2

doi:10.1186/cc3489

Critical Care
Volume 9
Issue 2

Viewing options:

Abstract
Full text
PDF (40KB)

Associated material:

Related literature:

Articles citing this article
on Google Scholar
on ISI Web of Science
on PubMed Central
Other articles by authors
on Google Scholar

Gutierrez G

on PubMed

Gutierrez G
Related articles/pages
on Google

on Google Scholar

on PubMed

Tools:

Post to:

Commentary

Blood flow, not hypoxia, determines intramucosal PCO₂

Guillermo Gutierrez

Pulmonary and Critical Care Medicine Division, Department of Medicine, The George Washington University Medical Center, Washington, DC, USA

author email corresponding author email

Critical Care 2005, 9:149-150doi:10.1186/cc3489


Published:	28 February 2005

See related research article http://ccforum.com/content/9/2/R66

Abstract

Monitoring tissue hypoxia in critically ill patients is a challenging task. Tissue PCO₂has long been proposed as a marker of tissue hypoxia, although there is considerable controversy on whether the rise in CO₂with hypoxia is caused by anaerobic metabolism and excess CO₂production or by the accumulation of aerobically produced CO₂in the setting of blood flow stagnation. The prevention of increases in intestinal PCO₂in aggressively resuscitated septic animals supports the notion that tissue CO₂accumulation is a function of decreases in blood flow, not of tissue hypoxia.