This is a lecture written for medical students getting their first exposure to acid-base physiology.
This is a version for residents where the learners have previous experience with acid base. (Powerpoint | PDF)
Scope:
primary disorder
second primary disorders affecting compensation
anion gap
osmolar gap
bicarbonate before
The presentation depends on a brand new supplemental questions handout (Word, PDF). This is an 11 page book of 67 unique practice questions with answers
In your chloride intoxication group of causes, add TPN
In your GI loss of HCO3, “change HCO3 to HCO3 precursors” since what we lose in diarrhea is not HCO3 per se since pH of the stool is not acidic, we lose citrate, etc which transform into HCO3 eventually
Interesting comment on renal bicarb loss: I would add an extra group and call it decrease renal NH4+ excretion and add distal RTA, renal insufficiency and hypoaldosteronism. You don’t lose HCO3 in distal RTA or hypoaldosteronism. You could argue that NH4+ synthesis in proximal tubule generates “new HCO3” but the student will get lost in that concept
In the renal HCO3 loss group I would add post-treatment of DKA, and post-hypocapnia
Toluene can cause both anion gap and non anion gap metabolic acidosis but the non anion gap is more common because the unmeasured anions are rapidly excreted by the kidneys
Pentamidine also blocks ENaC and can cause hyperkalemia