Metabolic alkalosis: Difference between revisions
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==Causes== | ==Causes== | ||
There are four mechanisms of metabolic alkalosis: | There are four mechanisms of metabolic alkalosis: | ||
===Loss of hydrogen ions=== | |||
====GI loss==== | |||
** Vomiting | ** Vomiting (excretion hydrogen ions and the retention of bicarbonate) | ||
** Nasogastric tube suction | ** Nasogastric tube suction | ||
** | ====Renal==== | ||
** With excess aldosterone retention of sodium and hence the excretion of hydrogen occurs | |||
* Over-diuresis | |||
* Administration of non-resorbable anions such as, penicillin, carbenicillin, which complex with positively-charged hydrogen ions in the renal tubules. | |||
===Increase in the serum bicarbonate=== | |||
** Ingestion of sodium bicarbonate, baking soda, citrate, lactate, or acetate. | ** Ingestion of sodium bicarbonate, baking soda, citrate, lactate, or acetate. | ||
===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. | * 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. | * 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== | ==Compensation== | ||
Revision as of 17:20, 2 September 2012
| Metabolic alkalosis | |
 | |
|---|---|
| Davenport diagram | |
| ICD-10 | E87.3 |
| ICD-9 | 276.3 |
| DiseasesDB | 402 |
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
There are four mechanisms of metabolic alkalosis:
Loss of hydrogen ions
GI loss
- Vomiting (excretion hydrogen ions and the retention of bicarbonate)
- Nasogastric tube suction
Renal
- With excess aldosterone retention of sodium and hence the excretion of hydrogen occurs
- Over-diuresis
- Administration of non-resorbable anions such as, penicillin, carbenicillin, which complex with positively-charged hydrogen ions in the renal tubules.
Increase in the serum bicarbonate
- Ingestion of sodium bicarbonate, baking soda, citrate, lactate, or acetate.
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.