Metabolic alkalosis

From Wikipedia, the free encyclopedia - View original article

Metabolic alkalosis
Classification and external resources
Davenport Fig 12.jpg
ICD-10E87.3
ICD-9276.3
DiseasesDB402
eMedicinemed/1459
 
Jump to: navigation, search
Metabolic alkalosis
Classification and external resources
Davenport Fig 12.jpg
ICD-10E87.3
ICD-9276.3
DiseasesDB402
eMedicinemed/1459

Metabolic alkalosis is a metabolic condition in which the pH of tissue is elevated beyond the normal range (7.35-7.45). This is the result of decreased hydrogen ion concentration, leading to increased bicarbonate, or alternatively a direct result of increased bicarbonate concentrations.

Terminology[edit]

Causes[edit]

The causes of metabolic alkalosis can be divided into two categories, depending upon urine chloride levels.[1]

Chloride-responsive (Urine chloride < 20 mEq/L)[edit]

Chloride-resistant (Urine chloride > 20 mEq/L)[edit]

Compensation[edit]

Compensation for metabolic alkalosis occurs mainly in the lungs, which retain carbon dioxide (CO2) through slower breathing, or hypoventilation (respiratory compensation). CO2 is then consumed toward the formation of the carbonic acid intermediate, thus decreasing pH. Respiratory compensation, though, is incomplete. The decrease in [H+] suppresses the peripheral chemoreceptors, which are sensitive to pH. But, because respiration slows, there's an increase in PCO2 which would cause an offset of the depression because of the action of the central chemoreceptors which are sensitive to the partial pressure of CO2[citation needed] in the cerebral spinal fluid. So, because of the central chemoreceptors, respiration rate would be increased.

Renal compensation for metabolic alkalosis, less effective than respiratory compensation, consists of increased excretion of HCO3- (bicarbonate), as the filtered load of HCO3- exceeds the ability of the renal tubule to reabsorb it.

See also[edit]

References[edit]

  1. ^ "Alkalosis, Metabolic: eMedicine Pediatrics: Cardiac Disease and Critical Care Medicine". Retrieved 2009-05-10. 
  2. ^ Hennessey, Iain. Japp, Alan.Arterial Blood Gases Made Easy. Churchill Livingstone 1 edition (18 Sep 2007).
  3. ^ Cho Kerry C, "Chapter 21. Electrolyte & Acid-Base Disorders" (Chapter). McPhee SJ, Papadakis MA: CURRENT Medical Diagnosis & Treatment 2011: http://www.accessmedicine.com/content.aspx?aID=10909.