This protocol covers metabolic alkalosis presenting with intravascular volume contraction, where urine chloride is below 20 mmol/L. The biochemical picture is arterial pH above 7.44 and serum bicarbonate above 27 mEq/L. The low urinary chloride places these patients in the chloride-sensitive subgroup, with distinct treatment implications compared with chloride-resistant metabolic alkalosis.
In this sub-population, volume depletion reduces glomerular filtration rate (GFR), chloride deficiency impairs bicarbonate excretion, and concurrent hypokalemia drives continued bicarbonate generation and retention. Together these factors sustain the alkalotic state. Urine electrolytes — particularly urine chloride — distinguish this chloride-sensitive group (urine Cl⁻ < 20 mmol/L) from the chloride-resistant group (urine Cl⁻ > 20 mmol/L), each requiring a different management approach.
Management addresses the factors maintaining the alkalosis. The approach centres on chloride-based intravenous fluid administration to reverse volume depletion and restore GFR, together with correction of the associated potassium deficit. The full sequence, specific agents, and clinical decision points are set out in the complete protocol.
The treatment of metabolic alkalosis with volume contraction (urine Cl⁻ < 20 mmol/L) targets the factors that maintain the alkalotic state: decreased GFR due to volume depletion, Cl⁻ deficiency, and hypokalemia.
Based on the systemic blood pressure and urine electrolytes, patients with metabolic alkalosis are divided into chloride-sensitive (urine Cl⁻ < 20 mmol/L) and chloride-resistant (urine Cl⁻ > 20 mmol/L) groups.
Administration of Cl⁻-based intravenous fluids expands intravascular volume, restores GFR, and disrupts the avid reabsorption of Na⁺, K⁺, HCO₃⁻, Cl⁻, and water, as well as facilitating HCO₃⁻ excretion.
Repletion of K⁺ to address hypokalemia decreases ammoniagenesis and the generation of new HCO₃⁻ as well as reducing the absorption of HCO₃⁻.
DOI: 10.1053/j.ajkd.2021.12.016
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