Metabolic alkalosis
Metabolic alkalosis | |
Davenport diagram | |
ICD-10 | E87.3 |
ICD-9 | 276.3 |
DiseasesDB | 402 |
eMedicine | med/1459 |
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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 alkylosis[1]:
1. Loss of hydrogen ions Most often occurs via two mechanisms, either vomiting or renally. Vomiting results in the excretion hydrogen ions and the retention of bicarbonate. Renal losses of hydrogen occur when excess aldosterone induces the retention of sodium and hence the excretion of hydrogen.
2. 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.
3. Alkalotic agents Alkalotic agents, such as bicarbonate, administered in excess of excretion capabilities by the kidney can lead to an alkylosis.
4. 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.
(See also loop diuretics and hyperaldosteronism.)
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.