Metabolic alkalosis

Metabolic alkalosis
Classification and external resources
Davenport diagram
ICD-10	E87.3
ICD-9	276.3
DiseasesDB	402
eMedicine	med/1459

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

Causes

There are five main causes of metabolic alkalosis^[1].

These can be divided into two categories, depending upon urine chloride levels.^[2]

Chloride-responsive (<10 mEq/L)

• Loss of hydrogen ions - Most often occurs via two mechanisms, either vomiting or via the kidney.
  • Vomiting results in the loss of hydrochloric acid with the stomach content. To make stomach acid, body moves hydrogen ions from blood to the stomach, causing low hydrogen ions in blood, raising pH of the blood.
  • Renal losses of hydrogen ions occurs when excess aldosterone induces the retention of sodium and hence the excretion of hydrogen from blood to urine, causing low hydrogen ions in blood, raising pH of the blood.

• 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 blood pH.

Chloride-resistant (>20 mEq/L)

• Retention of bicarbonate

• Shift of hydrogen ions into intracellular space - Seen in hypokalemia. Due to a low extracellular potassium concentration, potassium shifts out of the cells. In order to maintain electrical neutrality, hydrogen shifts into the cells, raising blood pH.

• Alkalotic agents - Alkalotic agents, such as bicarbonate (administrated in cases of peptic ulcer or hyperacidity) or antacids, administered in excess can lead to an alkalosis.

Compensation

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 in the blood. 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

• hypokalemia

References

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