Metabolic alkalosis is a metabolic condition in which the pH of the blood is elevated beyond the normal range. This is usually the result of decreased hydrogen ion concentration, leading to increased bicarbonate, or alternatively a direct result of increased bicarbonate concentrations.
There are five main causes of metabolic alkalosis:
1. Loss of hydrogen ions - Most often occurs via two mechanisms, either vomiting or renally. Vomiting results in the loss of hydrochloric acid with the stomach content, which consumes hydrogen ions, raising the pH of the blood. Renal losses of hydrogen ions occurs when excess aldosterone induces the retention of sodium and hence the excretion of hydrogen.
2. Retention of bicarbonate - As a compensatory mechanism for respiratory acidosis, the kidneys will increase their retention of bicarbonate in order to raise blood pH. If respiratory acidosis is prolonged, due to impaired pulmonary function, the resulting excess of bicarbonate can then raise blood pH too high, causing metabolic alkalosis.
3. 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.
4. Alkalotic agents - Alkalotic agents, such as bicarbonate or antacids, administered in excess can lead to an alkalosis.
5. 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.
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.
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.