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.

Pathophysiology

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+-eflux and K+ influx from cells through the K+-H+ exchanger, which could be a possible mechanism for the development of hypokalemia.

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

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

References

  1. ↑ "Acid-Base Tutorial - Metabolic Acidosis and Alkalosis". Acid-base.com. 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. doi:10.1038/ki.1975.114. PMID 536.
  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. doi:10.1681/ASN.2011070720. PMC 3269186Freely accessible. PMID 22223876.
This article is issued from Wikipedia - version of the 7/17/2016. The text is available under the Creative Commons Attribution/Share Alike but additional terms may apply for the media files.