Augustus Sams

There is a multitude of disease states that induce metabolic alkalosis. In general, the causes can be narrowed down to an intracellular shift of hydrogen ions, gastrointestinal (GI) loss of hydrogen ions, excessive renal hydrogen ion loss, retention or addition of bicarbonate ions, or volume contraction around a constant amount of extracellular bicarbonate known as contraction alkalosis. All of which leads to the net result of increased levels of bicarbonate in the blood. As long as renal function is maintained, excess bicarbonate is excreted in the urine fairly rapidly. As a result, metabolic alkalosis will persevere if the ability to eliminate bicarbonate is impaired due to one of the following causes: hypovolemia, reduced effective arterial blood volume, chloride depletion, hypokalemia, reduced glomerular filtration rate, and/or hyperaldosteronism.

Intracellular Shift of Hydrogen

Anytime that hydrogen ions are shifted intracellularly, this imbalance in the buffer system has a relative increase in bicarbonate. Processes that drive hydrogen intracellularly include hypokalemia.

Gastrointestinal Loss of Hydrogen

Stomach fluids are highly acidic at a pH of approximately 1.5 to 3.5.  Hydrogen secretion is accomplished via parietal cells in the gastric mucosa. Therefore, the large volume loss of gastric secretions will correlate as a loss of hydrogen chloride, an acidic substance, leading to a relative increase in bicarbonate in the blood, thus driving alkalosis.  Losses can occur pathologically via vomitus or nasogastric suctioning.

Renal Loss of Hydrogen

Hydrogen is used within the kidneys are an antiporter energy gradient to retain a multitude of other elements. Of interest here, sodium is reabsorbed through an exchange for hydrogen in the renal collecting ducts under the influence of aldosterone. Therefore, pathologies that increase the levels of mineralocorticoids or increase the effect of aldosterone, such as Conn syndrome will lead to hypernatremia, hypokalemia, and hydrogen loss in the urine. In a similar vein of thought, loop and thiazide diuretics are capable of inducing secondary hyperaldosteronism by increasing sodium and fluid load to the distal nephron, which encourages the renin-angiotensin-aldosterone system.  Genetic defects that lead to decreased expression of ion transporters in the Loop of Henle are possible but less common. These syndromes are known as Bartter and Gitelman disease. The net effect of these genetic defects is akin to the action of loop diuretics.

Retention/Addition of Bicarbonate

Several etiologies lead to increases in bicarbonate within the blood. The simplest of which is an overdose of exogenous sodium bicarbonate in a medical setting. Milk-alkali syndrome is a pathology where the patient consumes excessive quantities of oral calcium antacids, which leads to hypercalcemia and varying degrees of renal failure. Additionally, since antacids are neutralizing agents, they add alkaline substances to the body while reducing acid levels thus increasing pH. A pathology that is in line with normal physiology is the body’s natural compensation mechanism for hypercarbia. When a patient hypoventilates, CO2 retention occurs in the lungs and subsequently reduces pH.  Over time, the renal system compensates by retaining bicarbonate to balance pH. This is a slower process.  Once the hypoventilation is corrected, such as with a ventilator-assisted respiratory failure patient CO2 levels will quickly decrease, but bicarbonate levels will lag in reducing. This causes post-hypercapnia metabolic alkalosis, which is self-correcting. It is possible to calculate the expected pCO2 in the setting of metabolic alkalosis to determine if it is a compensatory increase in bicarbonate, or if there is an underlying pathology driving alkalosis using the following equation:

If the expected pCO2 does not match the measured value, an underlying metabolic alkalosis is a likely present.

Contraction Alkalosis

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