see also:

• acid-base physiology
• arterial and venous blood gases (ABGs/VBGs)

• 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:
  • renal failure
  • dehydration
  • hyperaldosteronism
  • potassium depletion
  • chloride depletion
• 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.

• 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

• 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:
  • diuretics - usually mild, pH rarely > 7.5
• 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

• tend to be oedematous and not responsive to normal saline

• hyperaldosteronism (hypokalaemia + aldosterone ⇒ XS urine H+ secretion & bicarbonate reabsorption):
  • primary
  • secondary:
    • cirrhosis, congestive cardiac failure, renal failure,
    • Bartter's syndrome
    • exogenous mineralocorticoids (licorice; tobacco chewing)
• Cushing's syndrome/steroids
• severe potassium depletion
• adrenogenital syndrome

• 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