title: [Physiology and clinical aspects of the extracellular bicarbonate pool: plea for cognizant use of HCO3-].
abstract: OBJECTIVE
  Derived from literature data the function of bicarbonate (HCO3-) is described together with its extracellular pool, the regulating organs, and the clinical variations.
  
  
  METHODS
  The medical German and English literature was reviewed. No special literature retrieval was performed. Results from measurements at the author's laboratory were used.
  
  
  RESULTS
  HCO3- may be described as the most potential nonrespiratory buffer base. For a 65 kg patient, the extracellular HCO3- pool amounts to approximately 350 mmol with a maximum tolerance limit of +/- 200 mmol. An influx of H+ ions (acidosis) and/or a reduction in the pCO2 (hyperventilation) will reduce this pool, whereas alkalosis and hypoventilation will enlarge it. The lungs (in close cooperation with the erythrocytes), liver and kidneys all contribute to the regulation of this HCO3- pool. The paramount organ for this regulation seems to be the liver, since it is able, even within a period of only a few hours, to eliminate much larger amounts of H+ ions (and correspondingly release HCO3-) than the kidneys are able to eliminate even under extreme conditions. It is primarily the liver which regulates the size of the HCO3- pool through the metabolism of the so-called metabolizable anions (bases) such as acetate, lactate, malate and citrate. The metabolism of these anions in the form of acetic, lactic, malic or citric acid requires (per mol) 1 mol H+ (acetate, lactate), 2 mol H+ (malate) or even 3 mol H+ (citrate), with the corresponding release of HCO3-. Iatrogenic alterations in the HCO3- pool occur more frequently than previously assumed. Infusion solutions may lead to a dilution acidosis (dilution of HCO3-), an infusion acidosis (addition of H+) or an infusion alkalosis (administration of metabolizable anions).
  
  
  CONCLUSIONS
  An improvement in the declaration accompanying infusion solutions is recommended according to their actual pH-dependent composition. In particular, the concepts of base excess (BE, mmol/l) and BE pot. (mmol/l) should be introduced, in order to give an indication of potential alterations in the HCO3- pool after infusion and metabolism. This also applies to blood derivatives, where transfusion acidosis as well as alkalosis may occur, and in hemodialysis and peritoneal dialysis where the occurrence of acidosis and alkalosis during therapy need to be reckoned with.
authors.affiliation: Institut für Physiologie und Pathophysiologie, Universität Mainz.
authors.forename: R
authors.initials: R
authors.lastname: Zander
mesh_terms: D000137:Acid-Base Imbalance / Q000503:physiopathology*; D001639:Bicarbonates / Q000008:administration & dosage / Q000378:metabolism*; D005110:Extracellular Space / Q000502:physiology*; D006706:Homeostasis / Q000502:physiology; D006801:Humans
chemical_list: D001639:Bicarbonates
vernacular_title: Physiologie und Klinik des extrazellulären Bikarbonat-Pools: Plädoyer für einen bewussten Umgang mit HCO3-.