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Metabolic alkalosis mechanisms and compensation

Metabolic alkalosis mechanisms and compensation

Metabolic alkalosis mechanisms and compensation

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Pathophysiology - The Base Buildup

  • Definition: A primary ↑ in serum $HCO_3^−$, leading to ↑ pH.
  • Mechanism: Involves two distinct phases:
    • Generation: The initial insult causing acid loss or base gain (e.g., vomiting, alkali ingestion).
    • Maintenance: The kidney's failure to excrete the excess $HCO_3^−$. This is the key step and is primarily driven by:
      • Volume depletion (Euvolemia or hypovolemia)
      • Chloride depletion
      • Hypokalemia

Renal tubule bicarbonate reabsorption mechanisms

Contraction Alkalosis: Volume depletion → ↑ Angiotensin II → ↑ Proximal tubule $Na^+-H^+$ exchange → ↑ $HCO_3^−$ reabsorption, thus maintaining the alkalosis.

Etiologies - Acid Out, Bicarb In

  • H⁺ Loss (Acid Out):
    • GI: Vomiting, nasogastric (NG) suction.
    • Renal: Diuretics (loop/thiazide), hyperaldosteronism.
  • HCO₃⁻ Gain (Bicarb In):
    • Exogenous: Citrate from blood transfusions, acetate in TPN, antacid abuse.
CategoryUrine Chloride ($U_{Cl^−}$)Key Causes
Saline-Responsive< 20 mEq/L- Vomiting / NG suction
- Prior diuretic use
Saline-Resistant> 20 mEq/L- Hyperaldosteronism (Conn's)
- Bartter & Gitelman syndromes

📌 Mnemonic: 'VOMIT' (Vomiting, Oversecretion of aldosterone, Mineralocorticoid excess, Iatrogenic, Total parenteral nutrition).

Compensation - The Body's Balancing Act

  • Respiratory Compensation: The lungs hypoventilate to retain acidic $CO_2$ and lower pH.

    • Formula: Expected PaCO₂ = 0.7 * [HCO₃⁻] + 20 (± 5)
  • Renal Compensation: Kidneys try to excrete excess $HCO_3^−$. This is often impaired by volume depletion or hypokalemia, which maintains the alkalosis.

  • Paradoxical Aciduria: Despite systemic alkalosis, urine becomes acidic. This occurs in volume-depleted states (e.g., vomiting).

⭐ A low urine chloride (< 20 mEq/L) strongly suggests a saline-responsive metabolic alkalosis, where correcting the volume deficit is the primary treatment.

Renal tubule ion exchange in metabolic alkalosis

  • Metabolic alkalosis is driven by a primary ↑ in serum HCO₃⁻.
  • Differentiated by urine chloride (UCl⁻) and response to saline.
  • Saline-responsive (UCl⁻ < 20 mEq/L) is caused by volume & Cl⁻ depletion (e.g., vomiting, diuretics) and corrects with IV saline.
  • Saline-resistant (UCl⁻ > 20 mEq/L) is due to mineralocorticoid excess (e.g., Conn's, Cushing's).
  • Respiratory compensation involves hypoventilation, leading to a predictable ↑ in PaCO₂.
  • Often associated with hypokalemia due to intracellular K⁺ shifting.

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