Metabolic alkalosis

Background

Pathophysiology

• Chloride-Responsive (volume depletion)
  • Condition that produces chloride loss also tends to reduce extracellular volume
    • Reduction in extracellular volume increases mineralocorticoid activity
      • Enhances Na reabsorption and K+/H+ secretion in renal tubule
        • K/H+ secretion -> HCO3 generation
          • Resulting urine is alkaline with little chloride (<10)
• Chloride-Resistant
  • Excess mineralocorticoid activity leads to same cascade as above
    • No hypovolemia so urine chloride is generally normal (>10)

Differential Diagnosis

• Chloride-Responsive (urine Cl < 20 mEq/L)
  • Loss of gastric secretions
    • vomiting
    • NG suction
    • bulemia
  • Loss of colonic secretions
    • congenital chloridorrhea
    • villous adenoma
  • Thiazides/loop after D/C
  • Post hypercapnia
  • Cystic fibrosis
• Chloride-resistant (urine Cl > 20 mEq/L)
  • With HTN
    • Primary hyperaldo
      • adrenal adenoma
      • bilateral adrenal
      • hyperplasia
      • adrenal carcinoma
    • 11B-HSD2
      • genetic, licorice
      • chewing tobacco
      • carbenoxolone
    • CAH (11-Hydroxylase or 17-hydroxylase deficiency)
    • Current diuretics + HTN
    • Cushing syndrome
    • Exogenous steroids
    • Liddle syndrome
    • Renovascular HTN
  • Without HTN
    • Bartter syndrome^
    • Gitelman syndrome^
    • Severe K+ depletion
    • Current thiazides/loop
    • Hypomagnesemia
• Other causes
  • Exogenous alkali (Nabicarb + renal failure, metabolism of lactic acid, or ketoacids)
  • Milk alkali syndrome
  • Hypercalcemia (inability to concentrate urine leads to hypovolemia)
  • Intravenous penicillin
  • Refeeding alkalosis
  • Massive blood transfusion

^in children

Diagnosis

• pH > 7.42 = alkalemia
• HCO3 > 28 = metabolic alkalosis
• Always determine if there is also a concurrent primary respiratory process
  • expected pCO2 = 40 + 0.6(measured HCO3 - 24)
  • if pCO2>pCO2 expected, then there is also a primary respiratory acidosis
  • if pCO2<pCO2 expected, then there is also primary respiratory alkalosis
• Always calculate AG to determine if concurrent primary metabolic acidosis

Treatment

• Correct volume depletion
  • Normal Saline
    • Repletion of extracellular volume decr need for Na reaborption
    • Delivery of Cl to distal tubule increases Cl/bicarb exchange
• Correct potassium depletion
  • Giving K+ leads to movement of H+ out of cells -> acidosis
  • Giving K+ stops hypokalemia-induced distal H+/K+ pump
• Correct chloride depletion
  • Must give a reabsorbable anion to replace HCO3
• Correct mineralocorticoid excess
  • Aldostorone antagonists if indicated (i.e. spironolactone)

• Note: if pt is edematous (CHF, cirrhosis), do NOT give NS
  • If pt is hypokalemic KCl will correct both hypoK AND alkalosis

See Also

Acid-Base

Source

Emedicine, Tintinalli, UpToDate, Kaji 2011