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Causes of metabolic acidosis in canine hemorrhagic shock: role of unmeasured ions

Dirk Bruegger email, Gregor I Kemming email, Matthias Jacob email, Franz G Meisner email, Christoph J Wojtczyk email, Kristian B Packert email, Peter E Keipert email, N Simon Faithfull email, Oliver P Habler email, Bernhard F Becker email and Markus Rehm email

Critical Care 2007, 11:R130doi:10.1186/cc6200



See related commentary by Venkatesh and Morgan, http://ccforum.com/content/12/1/113

Previous studies on hemorrhage using the physicochemical approach

VICENTE ALFARO   (07 January 2008)  Department of Physiology, Faculty of Biology, University of Barcelona (Spain) email

I miss in this article a mention to a previously published study evaluating acid-base status in rats during hemorrhage (Alfaro et al. J. Appl. Physiol 86:1617-1625, 1999). This article was the first to use the Stewart’s physicochemical approach to evaluate contributions other than lactate to the development of metabolic acidosis during hemorrhagic shock. In contrast to that reported in the current work, we found an early imbalance in the main strong inorganic ions (decrease in the sodium/chloride ratio) that contributed significantly to the strong ion decrease associated with metabolic acidosis in hemorrhage. However, at later hemorrhagic phases (with decreases in mean arterial pressure similar to those maintained in dogs in the current study, 45 mmHg) the contribution of lactate to metabolic acidosis increased but, certainly, did not account for the whole pH decrease. Therefore, the current study has the interest in defining which other anions (citrate and acetate, as defended by the authors) contribute to metabolic acidosis in hemorrhage animals. I think both studies should be considered as complementary.

Competing interests

No competing interest are declared.

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