Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Simple and mixed acid-base disorders

Michael Emmett, MD
Biff F Palmer, MD
Section Editor
Richard H Sterns, MD
Deputy Editor
John P Forman, MD, MSc


Each day, adults generate large amounts of acids that must be expired, excreted, metabolized to non-charged neutral molecules, and/or buffered to avoid fatal acidemia. These acids are of three major classes:

Approximately 15,000 mmol (considerably more with exercise) of carbon dioxide (CO2) is produced each day, which combines with water to form carbonic acid (H2CO3).

Metabolic reactions generate several thousand mmol per day of organic acids, such as lactic acid and citric acid. These acids are metabolized to neutral products (such as glucose) and to CO2 and water. Normally, the generation and utilization rates of these organic acids are equal so that their steady state concentration in the extracellular fluid is relatively low and stable.

Approximately 50 to 100 meq of nonvolatile acid is produced each day (mostly sulfuric acid derived from the metabolism of sulfur-containing amino acids in the diet).

Acid-base balance is maintained by normal pulmonary excretion of carbon dioxide, metabolic utilization of organic acids, and renal excretion of nonvolatile acids.

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:

Subscribers log in here

Literature review current through: Nov 2017. | This topic last updated: Oct 18, 2016.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2017 UpToDate, Inc.
  1. Rose BD, Post TW. Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed, McGraw-Hill, New York 2001. p.328.
  2. Rose BD, Post TW. Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed, McGraw-Hill, New York City 2001. p.307.
  3. Cengiz M, Ulker P, Meiselman HJ, Baskurt OK. Influence of tourniquet application on venous blood sampling for serum chemistry, hematological parameters, leukocyte activation and erythrocyte mechanical properties. Clin Chem Lab Med 2009; 47:769.
  4. Kelly AM, Kyle E, McAlpine R. Venous pCO(2) and pH can be used to screen for significant hypercarbia in emergency patients with acute respiratory disease. J Emerg Med 2002; 22:15.
  5. Malatesha G, Singh NK, Bharija A, et al. Comparison of arterial and venous pH, bicarbonate, PCO2 and PO2 in initial emergency department assessment. Emerg Med J 2007; 24:569.
  6. Chu YC, Chen CZ, Lee CH, et al. Prediction of arterial blood gas values from venous blood gas values in patients with acute respiratory failure receiving mechanical ventilation. J Formos Med Assoc 2003; 102:539.
  7. Malinoski DJ, Todd SR, Slone S, et al. Correlation of central venous and arterial blood gas measurements in mechanically ventilated trauma patients. Arch Surg 2005; 140:1122.
  8. Walkey AJ, Farber HW, O'Donnell C, et al. The accuracy of the central venous blood gas for acid-base monitoring. J Intensive Care Med 2010; 25:104.
  9. Adrogué HJ, Madias NE. Secondary responses to altered acid-base status: the rules of engagement. J Am Soc Nephrol 2010; 21:920.
  10. Wiederseiner JM, Muser J, Lutz T, et al. Acute metabolic acidosis: characterization and diagnosis of the disorder and the plasma potassium response. J Am Soc Nephrol 2004; 15:1589.
  11. Pierce NF, Fedson DS, Brigham KL, et al. The ventilatory response to acute base deficit in humans. Time course during development and correction of metabolic acidosis. Ann Intern Med 1970; 72:633.
  12. Rose BD, Post TW. Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed, McGraw-Hill, New York City 2001. p.542.
  13. Bushinsky DA, Coe FL, Katzenberg C, et al. Arterial PCO2 in chronic metabolic acidosis. Kidney Int 1982; 22:311.
  14. Daniel SR, Morita SY, Yu M, Dzierba A. Uncompensated metabolic acidosis: an underrecognized risk factor for subsequent intubation requirement. J Trauma 2004; 57:993.
  15. Albert MS, Dell RB, Winters RW. Quantitative displacement of acid-base equilibrium in metabolic acidosis. Ann Intern Med 1967; 66:312.
  16. Fulop M. A guide for predicting arterial CO2 tension in metabolic acidosis. Am J Nephrol 1997; 17:421.
  17. Javaheri S, Shore NS, Rose B, Kazemi H. Compensatory hypoventilation in metabolic alkalosis. Chest 1982; 81:296.
  18. Javaheri S, Kazemi H. Metabolic alkalosis and hypoventilation in humans. Am Rev Respir Dis 1987; 136:1011.
  19. POLAK A, HAYNIE GD, HAYS RM, SCHWARTZ WB. Effects of chronic hypercapnia on electrolyte and acid-base equilibrium. I. Adaptation. J Clin Invest 1961; 40:1223.
  20. Van Yperselle de Striho, Brasseur L, De Coninck JD. The "carbon dioxide response curve" for chronic hypercapnia in man. N Engl J Med 1966; 275:117.
  21. VAN YPERSELE DE STRIHOU C, GULYASSY PF, SCHWARTZ WB. Effects of chronic hypercapnia on electrolyte and acid-base equilibrium. III. Characteristics of the adaptive and recovery process as evaluated by provision of alkali. J Clin Invest 1962; 41:2246.
  22. Arbus GS, Herbert LA, Levesque PR, et al. Characterization and clinical application of the "significance band" for acute respiratory alkalosis. N Engl J Med 1969; 280:117.
  23. Brackett NC Jr, Wingo CF, Muren O, Solano JT. Acid-base response to chronic hypercapnia in man. N Engl J Med 1969; 280:124.
  24. Martinu T, Menzies D, Dial S. Re-evaluation of acid-base prediction rules in patients with chronic respiratory acidosis. Can Respir J 2003; 10:311.
  25. Krapf R, Beeler I, Hertner D, Hulter HN. Chronic respiratory alkalosis. The effect of sustained hyperventilation on renal regulation of acid-base equilibrium. N Engl J Med 1991; 324:1394.