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metabolic alkalosis


  • a primary metabolic alkalosis is a derangement of acid-base homeostasis whereby arterial pH and bicarbonate levels are both raised.
  • persistence of a primary metabolic alkalosis usually requires either:
  • the body will try to correct a primary metabolic alkalosis by hypoventilating to create a secondary compensatory respiratory acidosis with expected pCO2 = 0.9 x bicarb + 9, to maximum pCO2 of 60 otherwise hypoxia will result.
  • a compensatory metabolic alkalosis may occur in an attempt to restore homeostasis in response to a primary respiratory acidosis - see acid-base physiology
  • post-hypercapnoeic respiratory alkalosis:
    • an apparent metabolic alkalosis may appear to result in a chronic CO2 retaining patient who is acutely hyperventilated to a CO2 lower than normal for them, as their chronically corrected pH levels rise with the acute hyperventilation as pCO2 falls but still higher than 40, while bicarb. remains high.

alkaline urine

  • indicates cause is exogenous alkali (but rarely a strong alkali) as kidneys attempt to excrete the excess base


  • massive transfusion: citrate blood; plasmanate (if renal failure)
  • milk alkali syndrome
  • urinary alkalisers (eg Ural)
  • carbenicillin
  • metabolism of organic anions (eg. bicarbonate, lactate, citrate)
  • nonparathyroid hypercalcaemia

low urinary chloride (< 10mmol/L) with acidic urine

  • these patients generally have chloride ion loss and are hypovolaemic


  • GIT chloride loss:
    • prolonged loss of gastric fluid (high in Na, HCl) such as vomiting or prolonged nasogastric aspiration
    • congenital chloride wasting diarrhoea
    • villous adenoma
  • renal chloride loss:
  • cutaneous chloride loss:
    • cystic fibrosis (infants)
  • inadequate chloride intake:
    • chloride deficient infant formula


  • iv normal saline with KCl supplement
    • ⇒ volume expansion
    • ⇒ supress renal acid excretion and increases renal bicarbonate excretion
  • if severe volume depleted metabolic alkalosis, consider also:
    • mineral acid Rx:
      • HCl
        • see below
      • arginine HCl:
        • 100g/L = 475mmol H+/L
        • rarely used, must be given via central line
        • can cause serious hyperkalaemia in patients with renal failure particularly if coexistent liver disease

high urinary chloride (> 10mmol/L) +/- hypokalaemia

  • tend to be oedematous and not responsive to normal saline



  • Rx underlying cause
  • KCl replacement Rx:
    • reverses the i/cellular shift of H+, thereby increasing bicarb. excretion
    • if hypovolaemic, may allow saline responsiveness to be regained
  • if indeed pt is oedematous, consider:
    • spironolactone
    • acetazolamide
  • if in renal failure, consider:
    • mineral acid Rx
      • iv HCl:
        • iv 0.1 to 0.2N HCl solution (100-200 mmol/L) via central line diluted in 5% dextrose
        • dose based on bicarbonate space of 50% total body weight
        • to reduce plasma bicarbonate from 50 to 40 mmol/L in a 70kg patient, the estimated amount of HCl required = 10 x 70 x 0.5 = 350 mmol
        • up to 200mmol can be given over 18 hours
        • average dose required is 90mmol
        • max. infusion rate = 0.2 mmol/kg/hr and 1 mEq/min
      • other mineral acids:
        • ammonium chloride:
          • 20g/L = 374mmol H+/L
          • rarely used, must be given via central line
          • can raise ammonia levels in patients with liver failure
    • dialysis
metabolic_alkalosis.txt · Last modified: 2010/01/18 07:05 by

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