Metabolic Alkalosis

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Alkalosis Maintenance Mechanisms

The normal kidney has an extremely high filtration and excretion capacity for bicarbonate, so prolonged elevation of serum bicarbonate requires the mandatory presence of a factor that prevents its normal renal excretion through the proximal or distal convoluted tubule. These factors include hypovolemia, extracellular chloride depletion, and severe hypokalemia.

Classification Based on Response to Urinary Chlorine

To optimally guide the diagnostic approach, analytical determination of urinary chlorine in a simple sample is required:

Chlorine-Responsive Alkalosis (urinary Cl^- < 15 mEq/L)

It occurs secondary to the loss of fluids rich in gastric chloride, inducing depletion of extracellular volume that compensatorily activates the renin-angiotensin-aldosterone system (RAAS):

• Gastric Losses: Prolonged symptoms of profuse vomiting or continuous uninterrupted nasogastric aspiration.
• Use of Diuretics: Loop or thiazide diuretics in late phases after the cessation of their active effect.
• Treatment of choice: Abundant infusion of 0.9% Physiological Saline Solution, which restores intravascular volume by providing the chloride ion necessary to restore normal renal excretion of bicarbonate by intercalated B cells.

Chlorine-Resistant Alkalosis (urinary Cl^- > 20 mEq/L)

Classically associated with states of primary mineralocorticoid excess or deep intracellular potassium depletion:

• Primary hyperaldosteronism: Conn syndrome or bilateral adrenal hyperplasia that promotes uncontrolled secretion of aldosterone, forcing distal reabsorption of sodium and the consequent massive urinary excretion of potassium and hydrogen ions by the apical proton pump.
• Severe hypokalemia: Stimulates cellular K⁺/H⁺ exchange, displacing hydrogen ions to the intracellular cellular space and alkalinizing the extracellular plasma systemically.