title: A critique of Stewart's approach: the chemical mechanism of dilutional acidosis.
abstract: OBJECTIVE
  While Stewart's acid-base approach is increasingly used in clinical practice, it has also led to new controversies. Acid-base disorders can be seen from different viewpoints: on the diagnostic/clinical, quantitative/mathematical, or the mechanistic level. In recent years, confusion in the interpretation and terminology of Stewart's approach has arisen from mixing these different levels. This will be demonstrated on the basis of a detailed analysis of the mechanism of "dilutional acidosis." In the classical dilution concept, metabolic acidosis after resuscitation with large volumes is attributed to the dilution of serum bicarbonate. However, Stewart's approach rejects this explanation and offers an alternative one that is based on a decrease in a "strong ion difference." This mechanistic explanation is questionable for principal chemical reasons. The objective of this study is to clarify the chemical mechanism of dilutional acidosis.
  
  
  METHODS
  Experimental data and simulations of various dilution experiments, as well as theoretical and chemical considerations were used.
  
  
  RESULTS
  1. The key to understanding the mechanism of dilutional acidosis lies in the open CO2/HCO3 (-)-buffer system where the buffer base (HCO3(-)) is diluted whereas the buffer acid is not diluted (constant pCO2). 2. The categorization in independent and dependent variables depends on the system regarded. 3. Neither the principle of electroneutrality, nor a change in [SID], nor increased H2O dissociation plays a mechanistic role.
  
  
  CONCLUSIONS
  Stewart's approach is valid at the mathematical level but does not provide any mechanistic insights. However, the quantification and categorization of acid-base disorders, using Stewart approach, may be helpful in clinical practice.
  
  
  BACKGROUND
  The online version of this article (doi:10.1007/s00134-009-1528-y) contains supplementary material, which is available to authorized users.
authors.affiliation: Department of Clinical Pharmacology, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria. daniel.doberer@meduniwien.ac.at
authors.forename: Daniel
authors.initials: D
authors.lastname: Doberer
authors.forename: Georg-Christian
authors.initials: GC
authors.lastname: Funk
authors.forename: Karl
authors.initials: K
authors.lastname: Kirchner
authors.forename: Bruno
authors.initials: B
authors.lastname: Schneeweiss
mesh_terms: D000136:Acid-Base Equilibrium / Q000502:physiology; D000138:Acidosis / Q000175:diagnosis* / Q000453:epidemiology* / Q000378:metabolism; D001639:Bicarbonates / Q000378:metabolism; D002245:Carbon Dioxide / Q000378:metabolism; D003627:Data Interpretation, Statistical; D004563:Electrochemistry; D004573:Electrolytes / Q000378:metabolism; D006438:Hemodilution; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008962:Models, Theoretical; D015532:Rehydration Solutions
chemical_list: D001639:Bicarbonates; D004573:Electrolytes; D015532:Rehydration Solutions; D002245:Carbon Dioxide