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==See also==
==See also==
* [[hypokalemia]]
* [[hypokalemia]]
==External links==
==References==
* {{FPnotebook|REN7}}
{{Reflist|2}}


[[Category:Nephrology]]
[[Category:Electrolyte disturbance]]
[[Category:Electrolyte disturbance]]
[[Category:Inborn errors of metabolism]]
[[Category:Inborn errors of metabolism]]
[[Category:Signs and symptoms]]


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Revision as of 17:25, 2 September 2012

Metabolic alkalosis
ICD-10 E87.3
ICD-9 276.3
DiseasesDB 402

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Metabolic alkalosis results from altered metabolism. It is the most common acid-base disorder seen in hospital in the United States.

Is a result of decreased hydrogen ion concentration leading to increased bicarbonate and carbon dioxide concentrations, or alternatively a direct result of increased bicarbonate concentrations.

Causes

Loss of hydrogen ions

GI loss

Renal

  • Hyperaldosteronism causing retention of sodium followed with compensatory excretion of hydrogen
  • Over-diuresis
  • Administration of non-resorbable anions such as, penicillin, carbenicillin, which complexs with positively-charged hydrogen ions in the renal tubules.

Increase in the serum bicarbonate

Shift of hydrogen ions into intracellular space

  • Seen in hypokalemia. Due to a low extracellular potassium concentration, potassium shifts out of the cells, and in order to maintain electrical neutrality, hydrogen shifts into the cells, leaving behind bicarbonate.

Contraction alkalosis

  • This results from a loss of water in the extracellular space which is poor in bicarbonate, typically from diuretic use. Since water is lost while bicarbonate is retained, the concentration of bicarbonate increases.

Compensation

The body attempts to compensate for the increase in pH by retaining carbon dioxide (CO2) through hypoventilation (respiratory compensation). CO2 combines with elements in the bloodstream to form carbonic acid, thus decreasing pH.

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

See also

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