Metabolic Alkalosis: what’s your framework?

Metabolic Alkalosis: a framework
GI hydrogen loss

  1. Removal of gastric secretions
    1. Vomiting
    2. NG tube suctioning
    3. Antacids in advanced renal failure
  2. Loss of intestinal secretions
    1. Rare secretory diarrheas (diarrhea usually results in metabolic acidosis)

Excessive renal hydrogen loss

  1. Primary mineralocorticoid excess
  2. Loop/thiazide diuretics
  3. Bartter and Gitelman syndromes
  4. Posthypercapnic alkalosis
  5. Hypercalcemia with the milk-alkali syndrome

Intracellular hydrogen shift:

  1. Most often occurs in patients with hypokalemia; a contributor in many common causes of metabolic alkalosis (vomiting, diuretics, mineralocorticoid excess)

 Alkali administration

  1. It is difficult to produce significant increase in plasma bicarbonate with chronic alkali therapy in normal individuals
  2. However, alkali loads given to a patient with an impaired renal capacity to excrete the bicarbonate (low effective arterial blood volumes, chloride depletion, hypokalemia, or intrinsic renal disease) may produce metabolic alkalosis

A word on contraction alkalosis:
Contraction alkalosis occurs when there is loss of relatively large volumes of low-bicarbonate, sodium-containing fluid. The alkalosis occurs because the extracellular volume contracts around a constant quantity of extracellular bicarbonate. The most common cause of contraction alkalosis is rapid fluid removal with IV loop diuretics.

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