Metabolic Alkalosis

Saline-responsive metabolic alkalosis  (urine Cl < 10 mMol/L)

  • Metabolic alkalosis:
    • Signs/symptoms:  muscle cramps, tetany, hyperreflexia, seizures, hypercapnia (increased pCO2), decreased serum & urine chloride concentrations, hypokalemia/hypocalcemia, mental confusion, increased susceptibility to tachyarrhythmias, increased risk of digoxin toxicity
    • Causes:
      • Contraction (diuretics cause loss of volume—pull out chloride, bicarb accumulates)
      • Licorice*
      • Endo (Cushing’s*)
      • Vomiting
      • Excess alkali*
      • Refeeding alkalosis*
      • Post-hypercapnia
      • Diuretics
  • Signs/symptoms:  muscle cramps, tetany, hyperreflexia, seizures, hypercapnia (increased pCO2), decreased serum & urine chloride concentrations, hypokalemia/hypocalcemia, mental confusion, increased susceptibility to tachyarrhythmias, increased risk of digoxin toxicity
  • Causes:
    • Loss of Cl-rich, bicarb-poor fluid
    • Chloride loss
    • Gastric acid loss (vomiting, NG suctioning)
    • Excessive diuresis (contraction alkalosis)
  • Response: pCO2 increases [from 40] by 0.6 – 0.7 mmHg for every 1 mEq rise (in bicarb) in HCO3-
    • Body responses less than is the case with metabolic acidosis
  • Treatment: remove the underlying cause
    • H2 antagonist/PPI’s if patient has increased upper GI fluid losses
    • Discontinue NG suction treatment
    • NS & monitor pH &/or [Chloride] in urine

Saline-resistant metabolic alkalosis  (urine Cl > 20 mMol/L)

  • Signs/symptoms:  muscle cramps, tetany, hyperreflexia, seizures, hypercapnia (increased pCO2), decreased serum & urine chloride concentrations, hypokalemia/hypocalcemia, mental confusion, increased susceptibility to tachyarrhythmias, increased risk of digoxin toxicity
  • Causes:
    • Potassium depletion
    • Hypercalcemia
    • Mineralocorticoid excess (hyperaldosteronism, black licorice)
  • Response: pCO2 increases [from 40] by 0.6 – 0.7 mmHg for every 1 mEq rise (in bicarb) in HCO3-
    • Body responses less than is the case with metabolic acidosis
  • Treatment: remove the underlying cause
    • H2 antagonist/PPI’s if patient has increased upper GI fluid losses
    • Discontinue NG suction treatment
    • Remove source of excess mineralocorticoid activity and give spironolactone (b/c saline-resistant MA is usually associated w/ volume expanded hypertension)
      • Spironolactone also helps with the potassium deficit (also need to do volume replacement)
    • Acetazolamide
      • Carbonic anhydrase inhibitor that induces metabolic acidosis & still causes volume loss
      • Consider in patients w/ CHF & renal failure (can’t handle high Na loads)
    • Sub chloride salts for acetate or lactate salts in TPNs
    • Calculate chloride deficit & consider acid replacement if pH > 7.6 or cardiac arrhythmias are present
      • Could use HCl or Ammonium choride or Arginine HCL
        • Ammonium chloride is associated with severe CNS toxicity however & is also contraindicated in patients with either severe liver or kidney impairment
        • Arginine chloride is used for severe metabolic acidosis due to it’s high chloride content.  Avoid in patients with kidney dysfunction
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