World Library  
Flag as Inappropriate
Email this Article

Contraction alkalosis

Article Id: WHEBN0009673529
Reproduction Date:

Title: Contraction alkalosis  
Author: World Heritage Encyclopedia
Language: English
Subject: Metabolic alkalosis, ICD-10 Chapter IV: Endocrine, nutritional and metabolic diseases, Intravascular volume status, Normal anion gap acidosis, Base excess
Publisher: World Heritage Encyclopedia

Contraction alkalosis

Contraction alkalosis refers to the increase in blood pH that occurs as a result of fluid losses (volume contraction). The change in pH is especially pronounced with acidic fluid losses caused by problems like vomiting.


There are several possible explanations for the process of alkalosis observed after volume contraction.

One popular theory is that alkalosis is simply the loss of solvent volume without a proportional loss in bicarbonate concentration or increase in carbon dioxide concentration.[1][2] This explanation may be especially appropriate for the very short term after volume loss.

Another suggests that the alkalosis is due to renal compensatory mechanisms used to correct volume loss. Extracellular fluid (ECF) volume contraction is associated with decreased blood volume and decreased renal perfusion pressure. Three compensation mechanisms engage as a result:

  1. renin secretion is increased,
  2. production of angiotensin II is increased, and
  3. secretion of aldosterone is increased.

Increases in angiotensin II cause increased Na+-H+ exchange in the proximal tubule and increased HCO3 (bicarbonate) reabsorption in the proximal tubule due to increased luminal H+. Increased aldosterone secretion stimulates the H-ATPase of alpha-intercalated cells of the collecting duct, which causes 1) increased distal tubule H+ secretion, worsening the metabolic alkalosis, and 2) increased generation of "new" bicarbonate within these same cells, which will be reabsorbed.

Additionally, increased aldosterone secretion causes increased distal tubule K+ secretion, in turn causing the hypokalemia seen with contraction alkalosis. Aldosterone also induces H+-efflux from cells through the K+-H+ exchanger, which could be a possible mechanism for the development of alkalosis.

Finally, it has been suggested that the term "contraction alkalosis" is actually a misnomer, and that the alkalosis observed during volume contraction is actually attributable entirely to chloride depletion, which leads to a failure of pendrin, a chloride/bicarbonate exchanger in the collecting duct.[3]


Treatment consists of NaCl infusion to correct ECF volume contraction and administration of K+ to replace urinary losses.


  1. ^ "Acid-Base Tutorial - Metabolic Acidosis and Alkalosis". 2004-11-18. Retrieved 2012-02-15. 
  2. ^ Garella, S; Chang, BS; Kahn, SI (Nov 1975). "Dilution acidosis and contraction alkalosis: review of a concept.". Kidney international 8 (5): 279–83.  
  3. ^ Luke, RG; Galla, JH (Feb 2012). "It is chloride depletion alkalosis, not contraction alkalosis.". Journal of the American Society of Nephrology : JASN 23 (2): 204–7.  
This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.

Copyright © World Library Foundation. All rights reserved. eBooks from Project Gutenberg are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.