From the Guidelines
Metabolic alkalosis in vomiting is primarily caused by the loss of hydrochloric acid from gastric contents, followed by compensatory mechanisms involving the kidneys, renin-angiotensin-aldosterone system, and electrolyte imbalances, as supported by the understanding of potassium loss in vomiting and diarrhea 1. The process begins with the direct loss of acid from the stomach, which shifts the body's pH toward alkalinity. As the body attempts to compensate for the loss of fluids and maintain blood volume, the kidneys reabsorb sodium, leading to the reabsorption of bicarbonate and excretion of hydrogen ions, further contributing to the alkalosis.
- Key factors involved in the development of metabolic alkalosis during vomiting include:
- Loss of hydrochloric acid from gastric contents
- Renal reabsorption of sodium and bicarbonate
- Activation of the renin-angiotensin-aldosterone system, leading to increased aldosterone secretion
- Aldosterone-mediated sodium reabsorption in exchange for potassium and hydrogen ions
- Hypokalemia, which perpetuates alkalosis through intracellular shift of hydrogen ions and increased renal ammonium excretion
- Hypochloremia, contributing to bicarbonate retention Given the complex interplay of these factors, management of metabolic alkalosis in vomiting should focus on addressing the underlying cause, restoring fluid volume, correcting electrolyte imbalances, particularly hypokalemia and hypochloremia, as indicated by the common electrolyte abnormalities such as hypokalemia 1.
From the Research
Mechanism of Metabolic Alkalosis in Vomiting
The mechanism of metabolic alkalosis in vomiting involves the loss of hydrogen ions and the subsequent increase in plasma bicarbonate levels 2, 3.
- Generation of Alkalosis: Vomiting leads to the excessive loss of hydrogen ions, resulting in an increase in plasma bicarbonate levels 2, 3.
- Maintenance of Alkalosis: The maintenance of metabolic alkalosis is due to the kidney's inability to excrete excess bicarbonate, which can be caused by factors such as hypovolemia, chloride depletion, hypokalemia, hyperaldosteronism, and renal failure 2, 3, 4.
- Pathogenesis: The pathogenesis of metabolic alkalosis involves two derangements: the generation of metabolic alkalosis via gain of alkali or loss of acid, and the maintenance of metabolic alkalosis by increased tubular bicarbonate reabsorption 4.
- Clinical States: Vomiting is a common clinical state associated with metabolic alkalosis, along with other conditions such as mineralocorticoid excess, the adrenogenital syndrome, licorice ingestion, diuretic administration, and Bartter's and Gitelman's syndromes 3, 5.
- Treatment: Treatment of metabolic alkalosis typically involves correcting the underlying cause, such as replenishing lost fluids and electrolytes, and may include the administration of carbonic anhydrase inhibitors, acid infusion, or low bicarbonate dialysis in severe cases 3, 5.