Abstract

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.

Causes

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

Compensation

Compensation for metabolic alkalosis occurs mainly in the lungs, which retain carbon dioxide (CO) through slower breathing, or hypoventilation (respiratory compensation). CO 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 pCO which would cause an offset of the depression because of the action of the central chemoreceptors which are sensitive to the partial pressure of CO 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 HCO (bicarbonate), as the filtered load of HCO exceeds the ability of the renal tubule to reabsorb it.

To calculate the expected pCO2 in the setting of metabolic alkalosis, the following equations are used:

- pCO2 = 0.7 [HCO3] + 20 mmHg +/- 5

- pCO2 = 0.7 [HCO3] + 21 mmHg