Metabolic alkalosis

Metabolic alkalosis is characterized by an increase in the concentration of standard bicarbonates. In principle, this may be due to:
 * losses of an anion, usually chlorides or proteins, which are compensated in the ionogram by the addition of bicarbonates;
 * an increase in the concentration of a cation, most often sodium.

Alkalosis from anion losses

 * Hypochloraemic alkalosis
 * It is accompanied, for example, by prolonged vomiting, in which a large amount of chloride anion is lost through vomiting gastric juice. Diuretics may be another cause of hypochloraemic alkalosis.


 * Hypoproteinemia
 * Proteins behave like polyanions, so the decrease in their concentration is also compensated by the addition of bicarbonates. Typical examples may be liver proteosynthesis failure, protein loss in nephrotic syndrome, or malnutrition.

Hypernatremic alkalosis
It is most often the result of hyperaldosteronism. Some adrenal tumors or other tumors producing this hormone lead to primary hyperaldosteronism. Secondary hyperaldosteronism is more common as a consequence of liver failure, as aldosterone is broken down in the liver. Another cause of secondary hyperaldosteronism may be overactivation of the renin-angiotensin-aldosterone system.

Elevated aldosterone levels cause the kidneys to retain more sodium, which is compensated in the ionogram by the addition of bicarbonate anion. In addition, sodium is being saved at the expense of increased urinary potassium and proton losses, leading to further deepening of alkalosis.

Sodium retention is also caused by corticosteroids, so metabolic alkalosis is accompanied by Cushing's syndrome.

Alkalosis from an excess of other cations
Rarely, metabolic alkalosis can be caused by an excess of another cation, such as ionized calcium. It occurs, for example, in bone tumors (multiple myeloma, metastases of breast cancer, prostate cancer, etc.). During the breakdown of bone tissue, a large amount of Ca2 + as well as HCO3- is released.

Liver failure
Liver failure is typically accompanied by metabolic alkalosis. Its causes are:
 * hypoproteinemia in proteosynthesis failure;
 * secondary hyperaldosteronism with sodium retention - aldosterone is normally broken down by the liver;
 * slowing down the ureasynthetic cycle - a metabolic process that produces a proton for each molecule of urea formed.

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