themselves putting the patient into metabolic alkalosis. Cystic fibrosis – excessive loss of sodium chloride in the sweat leads to contraction of the extracellular volume in the same way as contraction alkalosis, as well chloride depletion. 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. Chloride-indeterminate alkalosis Milk alkali syndrome Blood product administration since this contains sodium citrate which is then metabolized into sodium bicarbonate. Typically, this is seen with large volume transfusions such as more than 8 units. Decreases in albumin and phosphate will cause metabolic alkalosis. Chloride-resistant (Urine chloride > 40 mEq/L) Retention of bicarbonate – Retention of bicarbonate would lead to alkalosis. 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. Hyperaldosteronism – Loss of hydrogen ions in the urine occurs when excess aldosterone (Conn's syndrome) increases the activity of a sodium-hydrogen exchange protein in the kidney. This increases the retention of sodium ions whilst pumping hydrogen ions into the renal tubule. Excess sodium increases extracellular volume and the loss of hydrogen ions creates a metabolic alkalosis. Later, the kidney responds through the aldosterone escape to excrete sodium and chloride in urine. Excess glycyrrhizin consumption Low levels of magnesium in the blood Severely high levels of calcium in the blood Bartter syndrome and Gitelman syndrome – syndromes with presentations analogous to taking diuretics characterized with normotensive patients Liddle syndrome – a gain of function mutation in the genes encoding the epithelial sodium channel (ENaC) which is characterized by hypertension and hypoaldosteronism. 11β-hydroxylase deficiency and 17α-hydroxylase deficiency – both characterized by hypertension Aminoglycoside toxicity can induce a hypokalemic metabolic alkalosis via activating the calcium sensing receptor in the thick ascending limb of the nephron, inactivating the NKCC2 cotransporter, creating a Bartter's syndrome like effect. 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 is an increase in pCO2 which would cause