Journal of Applied Physiology Add DOIs to your references at manuscript stage!
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Appl Physiol 98: 62-71, 2005; doi:10.1152/japplphysiol.00292.2004
8750-7587/05 $8.00
This Article
Right arrow Full Text Free
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (4)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lang, W.
Right arrow Articles by Zander, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lang, W.
Right arrow Articles by Zander, R.

Prediction of dilutional acidosis based on the revised classical dilution concept for bicarbonate

Werner Lang and Rolf Zander

Institut für Physiologie und Pathophysiologie, Johannes Gutenberg-Universität Mainz, Mainz, Germany

Submitted 18 March 2004 ; accepted in final form 5 August 2004

Due to the controversy surrounding the term dilutional acidosis, the classical dilution concept for bicarbonate has been rigorously revised for the prediction of pH, actual bicarbonate concentration, and base excess. In the algorithms derived for buffer solutions, blood, and whole body (1-, 2-, and 3-fluid compartment), only bicarbonate is considered. On dilution at constant PCO2, the final concentration of bicarbonate is the sum in terms of pH, due to the following processes: dilution, formation from chemical reaction with the nonbicarbonate buffers phosphate, hemoglobin, and plasma proteins, and transfer from erythrocytes and interstitial fluid to plasma. At constant PCO2, the level of carbonic acid is held constant, whereas those of the buffer bases are reduced by dilution, resulting in acidosis. In mixed bicarbonate/phosphate buffer, the final concentration of HCO3 exceeds the diluted value due to additional buffering of H2CO3 by HPO42–. For whole blood in vitro, pH, and actual bicarbonate concentration are predicted from dilution with 0.9% saline from initial Hb (100%) to infinite dilution (pure saline). The acidosis from dilution of plasma bicarbonate is mitigated by contributions from plasma proteins (<1 mmol/l) and from the erythrocytes (~5 mmol/l). Similarly, for whole body, the main contributions to combat primary dilutional acidosis in the range of hemodilution (relative Hb: 100–50%) are from the erythrocytes (1.2–2.2 mmol/l) and from the interstitial fluid (3.3–7.2 mmol/l). Perioperatively measured nonrespiratory acidosis is predictable if caused by hemodilution with fluids containing neither bicarbonate nor its precursors, irrespective of other electrolytes.

volume expansion; volume replacement; acute normovolemic hemodilution; infusion solutions



Address for reprint requests and other correspondence: W. Lang, Institut für Physiologie und Pathophysiologie, Johannes Gutenberg-Universität Mainz, Saarstrasse 21, 55099 Mainz, Germany (E-mail: wlang{at}uni-mainz.de)




This article has been cited by other articles:


Home page
J. Appl. Physiol.Home page
Rebuttal from Drs. Boning and Maassen
J Appl Physiol, July 1, 2008; 105(1): 361 - 361.
[Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2005 by the American Physiological Society.