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Intraoperative Fluid Management

  • M. Rehm
  • U. Finsterer
Conference paper

Abstract

In the perioperative period, large volumes of intravenous infusions (crystalloids and colloids) are often administered to compensate for major surgical blood losses. The occurrence of metabolic acidosis due to administered intravenous infusion solutions has been known since at least the 1940s [1, 2]. To date, however, there is an ongoing controversy about the causes for this acidosis. Advocates of the ’classical’ approach, according to Siggaard- Andersen [3], favor the dilution hypothesis, which was originally proposed by Peters and van Slyke in 1946 [2]. This implies the dilution of the entire extracellular volume (ECV) with different electrolyte solutions that are free of bicarbonate. Since 1983, however, an alternative approach can be used to explain this form of a metabolic acidosis [4]. Stewart’s quantitative approach [4], which is discussed in detail elsewhere [5], defines paCO2, strong ion difference (SID), and the sum of all anionic charges of weak plasma acids ([ATOT]) as independent pH-regulating variables, whereas pH and bicarbonate (Bic) are dependent variables [4]. Stewart’s algorithms explain that a decrease in SID or an increase in [Prot ] will result in a decrease in pH (and vice versa) [4]. Recently, this approach has received much attention mainly because it explains the whole mystery of acid-base chemistry in a relatively simple quantitative manner [6, 7, 8, 9, 10, 11, 12, 13, 14, 15]. Advocates of the Stewart approach argue that the reason for a metabolic acidosis after the administration of intravenous infusions is not the dilution of Bic but the infusion of strong anions.

Keywords

Metabolic Acidosis Saline Group Crystalloid Solution Crystalloid Infusion Acute Normovolemic Hemodilution 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    Shires GT, Holman J (1948) Dilution acidosis. Ann Intern Med 28: 557–559PubMedGoogle Scholar
  2. 2.
    Peters J, van Slyke DD (1946) Quantitative clinical chemistry: Interpretations. Vol I, 1st edn. Williams and Wilkins, BaltimoreGoogle Scholar
  3. 3.
    Sigaard-Andersen O (1976) The acid-base status of the blood, 4th edn. Williams and Wilkins, BaltimoreGoogle Scholar
  4. 4.
    Stewart PA (1983) Modern quantitative acid-base chemistry. Can J Physiol Pharmacol 61: 1444–1461PubMedCrossRefGoogle Scholar
  5. 5.
    Fencl V, Leith DE (1993) Stewart’s quantitative acid-base chemistry: applications in biology and medicine. Respir Physiol 91: 1–16PubMedCrossRefGoogle Scholar
  6. 6.
    Bellomo R, Ronco C (1999) New paradigms in acid-base physiology. Curr Opin Crit Care 5: 427–428CrossRefGoogle Scholar
  7. 7.
    Kellum JA (1999) Acid-base physiology in the post-Copernican era. Curr Opin Crit Care 5: 429–435CrossRefGoogle Scholar
  8. 8.
    Story DA, Bellomo R (1999) The acid-base physiology of crystalloid solutions. Curr Opin Crit Care 5: 436–439CrossRefGoogle Scholar
  9. 9.
    Liskaser, Story DA (1999) The acid-base physiology of colloid solutions. Curr Opin Crit Care 5: 440–442CrossRefGoogle Scholar
  10. 10.
    Tan HK, Bellomo R (1999) The effect of continuous hemofiltration on acid-base physiology. Curr Opin Crit Care 5: 443–447CrossRefGoogle Scholar
  11. 11.
    Feriani M, Dell’Aquila R, Ronco C, La Greca G (1999) The acid-base effects of peritoneal dialysis. Curr Opin Crit Care 5: 448–451CrossRefGoogle Scholar
  12. 12.
    Bellomo R, Ronco C (1999) The pathogenesis of lactic acidosis in sepsis. Curr Opin Crit Care 5: 452–457CrossRefGoogle Scholar
  13. 13.
    Kaplan LJ, Bailey H, Kellum J (1999) The etiology and significance of metabolic acidosis in trauma patients. Curr Opin Crit Care 5: 458–463CrossRefGoogle Scholar
  14. 14.
    Hayhoe M, Bellomo R (1999) The pathogenesis of acid-base changes during cardiopulmonary bypass. Curr Opin Crit Care 5: 464–467CrossRefGoogle Scholar
  15. 15.
    Leblanc M (1999) The acid-base effects of acute hemodialysis. Curr Opin Crit Care 5: 468–478CrossRefGoogle Scholar
  16. 16.
    Scheingraber S, Rehm M, Sehmisch C, Finsterer U (1999) Rapid saline infusion produces hyperchloremic acidosis in patients undergoing gynecologic surgery. Anesthesiology 90: 1265–1270PubMedCrossRefGoogle Scholar
  17. 17.
    Rehm M, Orth V, Scheingraber S, et al (2000) Acid-base changes caused by 5% albumin versus 6% hydroxyethylstarch solution in patients undergoing acute normovolemic hemodilution. Anesthesiology 93: 1174–1183PubMedCrossRefGoogle Scholar
  18. 18.
    Van Slyke DD, Hastings AB, Hiller A, Sendroy J (1928) Studies of gas and electrolyte equibrilia in blood. XIV. Amount of alkali bound by serum albumin and globulin. J Biol Chem 79: 769–780Google Scholar
  19. 19.
    Figge J, Mydosh T, Fencl V (1992) Serum proteins and acid-base equilibria: a follow-up. J Lab Clin Med 120: 713–719PubMedGoogle Scholar

Copyright information

© Springer-Verlag Italia 2002

Authors and Affiliations

  • M. Rehm
    • 1
  • U. Finsterer
    • 1
  1. 1.Department of AnaesthesiologyLudwig-Maximilians UniversityMunichGermany

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