How Excessive Vomiting Causes Metabolic Alkalosis
Excessive vomiting causes metabolic alkalosis primarily through the loss of hydrochloric acid from the stomach, leading to a decrease in hydrogen ions and chloride, which results in increased serum bicarbonate levels and blood pH. 1
Pathophysiological Mechanism
The development of metabolic alkalosis from vomiting involves two key phases:
1. Generation Phase
- Loss of Gastric Acid: Vomiting expels gastric contents containing hydrochloric acid (HCl), resulting in:
- Depletion of hydrogen ions (H+)
- Loss of chloride ions (Cl-)
- Relative increase in bicarbonate concentration in the blood
2. Maintenance Phase
Several factors contribute to sustaining the alkalotic state:
Volume Depletion: Leads to:
- Increased proximal tubular reabsorption of sodium and bicarbonate
- Reduced glomerular filtration rate (GFR)
- Activation of the renin-angiotensin-aldosterone system
Chloride Depletion: Critical factor that:
- Impairs the kidney's ability to excrete excess bicarbonate
- Creates "chloride-depletion alkalosis" 2
Hypokalemia: Commonly occurs with vomiting and:
- Promotes intracellular shift of H+ ions
- Stimulates renal ammoniagenesis
- Enhances bicarbonate reabsorption in the kidney
Secondary Hyperaldosteronism: Develops due to volume depletion and:
- Increases H+ secretion in distal tubule
- Enhances sodium reabsorption and potassium excretion
- Further worsens hypokalemia
Laboratory Findings
Typical laboratory abnormalities in vomiting-induced metabolic alkalosis include:
- Elevated serum bicarbonate (>26 mmol/L)
- Elevated arterial pH (>7.43)
- Hypochloremia (decreased serum chloride)
- Hypokalemia
- Increased blood urea nitrogen (BUN) due to volume depletion
- Compensatory increase in PaCO₂ due to hypoventilation
- Paradoxical aciduria (despite systemic alkalosis)
Clinical Manifestations
Metabolic alkalosis from excessive vomiting may present with:
- Lethargy and confusion
- Muscle weakness and cramps
- Cardiac arrhythmias (especially with hypokalemia)
- Hypotension (due to volume depletion)
- Tetany (in severe cases)
- Respiratory depression (compensatory hypoventilation)
Treatment Approach
The cornerstone of treatment for vomiting-induced metabolic alkalosis is:
Correction of Volume Depletion:
- Isotonic saline (0.9% NaCl) administration to restore intravascular volume
- Addresses both hypovolemia and chloride deficiency
Electrolyte Replacement:
- Potassium chloride supplementation to correct hypokalemia
- Chloride replacement to enable renal bicarbonate excretion 1
Treatment of Underlying Cause:
- Address the cause of vomiting (e.g., antiemetics for nausea, treatment of pyloric stenosis)
Monitoring:
- Serial assessment of acid-base status and electrolytes
- Careful attention to fluid status
Special Considerations
- In cases of severe alkalosis (pH >7.55), more aggressive correction may be required due to associated increased mortality 3
- High cation-gap amino acid solutions may be beneficial in treating chloride-depletion alkalosis with hyponatremia 2
- Paradoxical metabolic acidosis can rarely occur with severe vomiting due to other concurrent processes 4
Understanding this pathophysiological sequence is crucial for appropriate management of patients with vomiting-induced metabolic alkalosis, as addressing both the generation and maintenance factors is essential for successful treatment.