Metabolic Alkalosis

Aka: Metabolic Alkalosis, Chloride Depletion Metabolic Alkalosis

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II. Types

  1. Chloride responsive Metabolic Alkalosis
    1. Loss of body acids (e.g. Vomiting, nasogastric suction)
    2. Extracellular fluid contraction
    3. Saline responsive
  2. Chloride-resistant Metabolic Alkalosis
    1. Increased body buffers
      1. Bicarbonate administration
      2. Renal reabsorption due to excess Mineralocorticoid
    2. Associated with Hypokalemia
    3. Saline unresponsive

III. Causes: Low Urine Chloride <10 meq/L (Chloride Depletion Metabolic Alkalosis)

  1. Gastrointestinal causes
    1. Vomiting
    2. Nasogastric suction
    3. Chloride-wasting Diarrhea
    4. Villous adenoma of colon
  2. Renal Causes
    1. Diuretic use (Urine Chloride >10 meq/L)
    2. Poorly reabsorbable anion
      1. Carbenicillin
      2. Penicillin
      3. Sulfate
      4. Phsophate
    3. Post-Hypercapnia
  3. Exogenous alkali
    1. Sodium Bicarbonate (Baking Soda)
    2. Sodium Citrate
    3. Lactate
    4. Gluconate
    5. Acetate
    6. Transfusion
    7. Antacid
  4. Other causes
    1. Cystic Fibrosis
    2. Achlorhydria
    3. Contraction alkalosis (Dehydration)

IV. Causes: Normal or High Urine Chloride >20 meq/L

  1. Hypertensive Patient
    1. Adrenal Disease (distinguish with plasma renin and serum Aldosterone, see below)
      1. Primary Hyperaldosteronism
      2. Cushing's Syndrome (Pituitary, Adrenal or ectopic)
      3. Liddle Syndrome
    2. Exogenous steroids
      1. Excess Mineralocorticoid intake
      2. Excess Glucocorticoid intake
      3. Excessive licorice intake
      4. Carbenoxalone
      5. Glycyrrhizic acid
      6. Chewing Tobacco
  2. Normotensive Patient
    1. Bartter Syndrome or Gitelman Syndrome
    2. Hypokalemia
    3. Excessive alkali administration
    4. Milk-Alkali Syndrome
    5. Refeeding alkalosis
    6. Diuretics (may cause variable Urine Chloride)
    7. Overcompensation for chronic Respiratory Acidosis (esp. chronic COPD with hypercapnia)
    8. Excessive Mechanical Ventilation (excess bicarbonate is typically slow to correct)

V. Labs

  1. Arterial Blood Gas or Venous Blood Gas
    1. Arterial pH increased
    2. Serum bicarbonate increased
    3. PaCO2 increased (due to compensatory hypoventilation)
      1. PaCO2 = 0.7 x HCO3 + 20 (+/- 1.5)
      2. PaCO2 rises 6 mmHg per 10 meq/L bicarbonate rise
        1. PaCO2 rise is not uniform and roughly increases 1 mmHg for each 1 meq/L Bicarbonate
    4. Excess Anion Gap (EAG) >30 mEq/L
  2. Urine Chloride
    1. See Above
  3. Plasma Renin and Aldosterone
    1. Indicated in Non-chloride Depletion Metabolic Acidosis in a hypertensive patient
      1. Evaluates for causes of high mineralcorticoid activity (adrenal disease)
    2. Plasma Renin decreased and Aldosterone increased
      1. Primary Hyperaldosteronism
    3. Plasma Renin decreased and Aldosterone decreased
      1. Cushing's Syndrome (Pituitary, Adrenal or ectopic)
      2. Liddle Syndrome
    4. Plasma Renin increased and Aldosterone increased
      1. Renal Artery Stenosis
      2. Malignant Hypertension
      3. Renin-producing tumors

VI. References

  1. Morikawa (2025) Am Fam Physician 111(2): 148-55 [PubMed]
  2. Arieff (1993) J Crit Illn 8(2): 224-46 [PubMed]
  3. Narins (1982) Am J Med 72:496 [PubMed]
  4. Narins (1980) Medicine 59:161-95 [PubMed]
  5. Ghosh (2000) Fed Pract p. 23-33
  6. Rutecki (Dec 1997) Consultant, p. 3067-74
  7. Rutecki (Jan 1998) Consultant, p. 131-42

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