Abstract
Intramucosal-to-arterial carbon dioxide difference (the so-called PCO2 [partial carbon dioxide tension] gap) remains largely unaltered during decreased oxygen delivery, if the latter is reduced as flow is maintained. In this condition (hypoxic hypoxia or anaemic hypoxia), the PCO2 gap fails to mirror intestinal tissue dysoxia. Results from several experiments have demonstrated that blood flow is the main determinant of PCO2 gap. Gastrointestinal tonometry is clearly a useful indirect method for monitoring perfusion, but it has rather limited value in detecting anaerobic metabolism when blood flow is preserved. These considerations render it very unlikely that PCO2 may dramatically increase (or that intramucosal pH may decrease) in any hypoxic state with preserved flow.
Highlights
In the present issue of Critical Care, Dubin and collaborators [1] report the results of a study in which they tested the hypothesis that intramucosal-to-arterial carbon dioxide difference may remain unaltered during dysoxia because DO2 is reduced when flow is maintained
The PCO2 gap obtained in this condition was compared with that obtained in ischaemic hypoxia (IH)
This work conducted in sheep is an important confirmatory study of our previous studies that dealt with differential effects of IH and HH on PCO2 gap [2,3]
Summary
In the present issue of Critical Care, Dubin and collaborators [1] report the results of a study in which they tested the hypothesis that intramucosal-to-arterial carbon dioxide difference (the so-called PCO2 [partial carbon dioxide tension] gap) may remain unaltered during dysoxia (a state in which oxygen delivery [DO2] is insufficient to sustain oxygen demand) because DO2 is reduced when flow is maintained. In the range of DO2 values below the critical level, increases in PCO2 gap were smaller in HH than in IH, similar decreases in DO2 were achieved.
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