SFGH 5.31 pearls: metabolic alkalosis

  • Major causes metabolic alkalosis – Vomiting/NG suction, loop and thiazide diuretics, laxative abuse, mineralocorticoid excess, milk-alkali syndrome.
  • For those with profound alkalosis with hypovolemia, avoid resuscitation with plasmalyte, as it contains bicarb. Better to replete with NS w/K or just NS and replete K separately
  • Profound alkalemia also can cause a left shift of the oxygen dissociation curve, leading to impaired peripheral oxygen unloading and lactate elevation à give supplemental oxygen!
  • An elevated serum pH requires both an initial insult, (usually loss of hydrogen ions in the urine or GI tract) and a maintenance phase that prevents normalization of the pH. The maintenance phase causes include: volume contraction, renal impairment, decreased effective blood volume (CHF, cirrhosis) or a combination of these factors.
  • Remember that alkalemia drives phosphorus and potassium into cells, so labs will often show profound hypoK and hypo phos, but these numbers do not reflect total body stores
  • The lytes abnormalities associated with alkalemia can lead to muscle weakness, decreased cardiac contractility and increased risk for arrhythmia and should be corrected as soon as possible, keeping in mind that their extra-cellular levels will change as your correct the pH
  • Betahydroxy butyrate can be elevated in any ketotic state, not just DKA
  • Severe alkalemia can also cause seizure, agitation/disorientation, and coma due to decreased cerebral blood flow
  • Fun fact – the combination of 3 concomitant acid-base disorders is known as “the triple ripple”!
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