From the Guidelines
Metabolic alkalosis from vomiting occurs primarily due to the loss of gastric acid and subsequent compensatory mechanisms, leading to a decrease in hydrogen ions in the body and a shift in pH balance toward alkalinity. When a person vomits, hydrochloric acid from the stomach is lost, initiating this process. The kidneys then attempt to maintain the new acid-base balance through several mechanisms, including increased bicarbonate reabsorption in the renal tubules to preserve elevated bicarbonate levels, and activation of the renin-angiotensin-aldosterone system due to hypovolemia from fluid loss, which increases sodium reabsorption and potassium excretion 1. This potassium depletion, defined as K<3.5 mEq/L, further exacerbates the alkalosis as hydrogen ions move into cells to replace the lost potassium. Additionally, chloride depletion from vomiting maintains the alkalosis, as the kidneys require adequate chloride to excrete bicarbonate.
Key factors in the pathophysiology of metabolic alkalosis with vomiting include:
- Loss of gastric acid (hydrochloric acid) from the stomach
- Decrease in hydrogen ions in the body
- Increase in bicarbonate reabsorption by the kidneys
- Activation of the renin-angiotensin-aldosterone system
- Potassium depletion (hypokalemia) due to increased potassium excretion
- Chloride depletion from vomiting, which hinders bicarbonate excretion by the kidneys
Laboratory tests, as mentioned in the evaluation of patients with bowel obstruction and potential vomiting 1, are crucial for identifying electrolyte imbalances, elevated urea nitrogen, and metabolic alkalosis that may occur as a consequence of vomiting and dehydration. Addressing the underlying cause of vomiting, correcting volume depletion with normal saline, and replenishing electrolytes, particularly potassium and chloride, are essential in managing metabolic alkalosis. In severe cases, administration of acetazolamide may be considered to increase bicarbonate excretion, though this is rarely needed once volume and electrolytes are restored.
From the Research
Pathophysiology of Metabolic Alkalosis with Vomiting
The pathophysiology of metabolic alkalosis with vomiting involves several key factors:
- Generation of alkalosis: This can occur due to excessive hydrogen ion loss by the gastrointestinal tract, such as through vomiting 2, 3, 4, 5.
- Maintenance of alkalosis: This 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, 5.
- Role of the kidney: The kidney plays a crucial role in maintaining acid-base balance through bicarbonate reclamation and generation 3, 4, 5.
- Factors affecting bicarbonate reabsorption: These include effective arterial blood volume, glomerular filtration rate, chloride, and potassium 3, 4.
Clinical States Associated with Metabolic Alkalosis
Metabolic alkalosis can be associated with various clinical states, including:
- Vomiting: This is a common cause of metabolic alkalosis, particularly when it leads to chloride depletion 2, 3, 4, 5, 6.
- Mineralocorticoid excess: This can lead to increased bicarbonate reabsorption and contribute to metabolic alkalosis 3, 4, 5.
- Licorice ingestion: This can cause mineralocorticoid excess and lead to metabolic alkalosis 3, 4, 5.
- Diuretic administration: Certain diuretics can lead to hypokalemia and hypochloremia, contributing to metabolic alkalosis 3, 4, 5.
Treatment of Metabolic Alkalosis
Treatment of metabolic alkalosis involves:
- Correcting existing depletions: This includes replenishing potassium, chloride, and other electrolytes as needed 2, 3, 4, 5.
- Preventing further losses: This may involve addressing the underlying cause of vomiting or other factors contributing to metabolic alkalosis 2, 3, 4, 5.
- Administering carbonic anhydrase inhibitors or acid infusion: These may be used in severe cases of metabolic alkalosis 3, 4, 5.