Metabolic alkalosis

Background

• 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

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)

DDX

1. Chloride-Responsive (urine Cl < 20 mEq/L)
   1. Loss of gastric secretions
      1. vomiting
      2. NG suction
      3. bulemia
   2. Loss of colonic secretions
      1. congenital chloridorrhea
      2. villous adenoma
   3. Thiazides/loop after D/C
   4. Post hypercapnia
   5. Cystic fibrosis
2. Chloride-resistant (urine Cl > 20 mEq/L)
   1. With HTN
      1. Primary hyperaldo
         1. adrenal adenoma
         2. bilateral adrenal
         3. hyperplasia
         4. adrenal carcinoma
      2. 11B-HSD2
         1. genetic, licorice
         2. chewing tobacco
         3. carbenoxolone
      3. CAH (11-Hydroxylase or 17-hydroxylase deficiency)
      4. Current diuretics + HTN
      5. Cushing syndrome
      6. Exogenous steroids
      7. Liddle syndrome
      8. Renovascular HTN
   2. Without HTN
      1. Bartter syndrome^
      2. Gitelman syndrome^
      3. Severe K+ depletion
      4. Current thiazides/loop
      5. Hypomagnesemia
3. Other causes
   1. Exogenous alkali (Nabicarb + renal failure, metabolism of lactic acid, or ketoacids)
   2. Milk alkali syndrome
   3. Hypercalcemia (inability to concentrate urine leads to hypovolemia)
   4. Intravenous penicillin
   5. Refeeding alkalosis
   6. Massive blood transfusion

^in children

Treatment

1. Correct volume depletion
   1. Normal Saline
      1. Repletion of extracellular volume decr need for Na reaborption
      2. Delivery of Cl to distal tubule increases Cl/bicarb exchange
2. Correct potassium depletion
   1. Giving K+ leads to movement of H+ out of cells -> acidosis
   2. Giving K+ stops hypokalemia-induced distal H+/K+ pump
3. Correct chloride depletion
   1. Must give a reabsorbable anion to replace HCO3
4. Correct mineralocorticoid excess
   1. 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