How does excessive vomiting cause metabolic alkalosis?

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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:

  1. Correction of Volume Depletion:

    • Isotonic saline (0.9% NaCl) administration to restore intravascular volume
    • Addresses both hypovolemia and chloride deficiency
  2. Electrolyte Replacement:

    • Potassium chloride supplementation to correct hypokalemia
    • Chloride replacement to enable renal bicarbonate excretion 1
  3. Treatment of Underlying Cause:

    • Address the cause of vomiting (e.g., antiemetics for nausea, treatment of pyloric stenosis)
  4. 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.

References

Research

The patient with metabolic alkalosis.

Acta clinica Belgica, 2019

Research

Metabolic Alkalosis Pathogenesis, Diagnosis, and Treatment: Core Curriculum 2022.

American journal of kidney diseases : the official journal of the National Kidney Foundation, 2022

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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