Document Detail

Mechanisms of tissue hypercarbia in sepsis.
MedLine Citation:
PMID:  17981634     Owner:  NLM     Status:  MEDLINE    
Intramucosal acidosis, that it is to say, an increased intramucosal-arterial PCO2 difference, is a common finding in clinical and experimental sepsis. Nevertheless, the physiologic significance of increases in tissue PCO2 is controversial, since CO2 can be generated by both aerobic and anaerobic biochemical processes. PCO2 can rise after buffering of protons produced in the hydrolysis of high-energy phosphate compounds by bicarbonate, or after the anaerobic production of acids, like lactate. In this case, it could represent tissue dysoxia. Alternatively, an increase in tissue PCO2 could denote hypoperfusion and diminished removal of the CO2 produced during the oxidation of pyruvate. In this last situation, aerobic metabolism might be preserved. In the present review, we discuss the physiologic mechanisms that determine tissue and venous hypercarbia during the three classic forms of hypoxia: stagnant, hypoxic and anemic hypoxia. The results of experimental studies suggest that tissue minus arterial and venoarterial PCO2 gradients primarily reflect alterations in tissue perfusion. These conclusions are further confirmed by a mathematical model of CO2 transport. In sepsis, however, tissue hypercarbia might develop despite normal or high cardiac output. This phenomenon has been initially interpreted as secondary to alterations in energetic metabolism, the so-called cytopathic hypoxia. Yet, new evidences show that the underlying mechanism to tissue hypercarbia in sepsis might be due to severe microcirculatory derangements. In summary, experimental results support the hypothesis that increases in tissue and venous CO2 are insensitive markers of tissue dysoxia, and merely reflect vascular hypoperfusion.
Arnaldo Dubin; Elisa Estenssoro
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Publication Detail:
Type:  Journal Article; Review     Date:  2008-01-01
Journal Detail:
Title:  Frontiers in bioscience : a journal and virtual library     Volume:  13     ISSN:  1093-4715     ISO Abbreviation:  Front. Biosci.     Publication Date:  2008  
Date Detail:
Created Date:  2007-11-05     Completed Date:  2007-12-11     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9709506     Medline TA:  Front Biosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1340-51     Citation Subset:  IM    
Facultad de Ciencias Medicas, Universidad Nacional de La Plata and Sanatorio Otamendi y Miroli, Buenos Aires, Argentina. <>
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MeSH Terms
Acidosis, Respiratory / pathology*
Arteries / metabolism
Carbon Dioxide / metabolism*
Hydrogen-Ion Concentration
Models, Biological
Mucous Membrane / metabolism,  pathology*
Oxygen / metabolism
Oxyhemoglobins / metabolism
Sepsis / metabolism*,  pathology*
Reg. No./Substance:
0/Oxyhemoglobins; 124-38-9/Carbon Dioxide; 7782-44-7/Oxygen

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

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