Mixed acid-base disorders

Epiphany today!

You know how CO2 and bicarbonate levels change together?  Like if CO2 goes up, bicarb goes up, and if CO2 goes down, bicarb goes down?

Well, then: LET ME BLOW YOUR MIND!

In mixed acid-base disorders, there is both a respiratory and a metabolic acid-base disruption.  So the bicarb and CO2 change in opposite directions!


It totally makes sense if you think about it a little bit.  For example, in cardiopulmonary arrest, the patient stops breathing.  They will therefore accumulate CO2 and have a respiratory acidosis.  BUT because they stop breathing (and cause they're ludicrously ischaemic from no heart pumping), they also become hypoxic.  Anaerobic metabolism ensues and lactic acid accumulates.  They will then develop a metabolic acidosis, saturating all the available bicarb with a proton blitz - leading to a mixed acidosis which messes with everyone's minds.

Holy crap! Amazing.

Acid-base: My Achilles' Heel

ACID-BASE BALANCE IS THE BANE OF MY EXISTENCE!!!

There are not very many things in this life that I naturally suck at.  Basically the list just includes team sports and acid-base balance. 

My strategy for overcoming this obstacle has thus far been identical to my strategy for dealing with team sports: complete and utter avoidance.  Unfortunately, acid-base keeps poking its' ugly snout back into my USMLE business, and I realize I must meet this enemy head-on (or risk having my ass handed to me on a platter on test day).

To date, physiology textbooks like Sherwood and Guyton (both my usual favorites) have failed me dismally.  So it is with a heavy heart that I turn to USMLE Step 1 Secrets in the vain hope that somehow this high-yield review source will explain the mysteries of protons and bicarbonate in such a way as my currently feeble mind can unravel.

God's teeth!  What witchery be this?  It is starting to make sense! (Just a little bit.)

Stuff I didn't know until now:
- The kidney is 'better' at excreting bicarbonate than it is at retaining it.  This explains why renal compensation in respiratory alkalosis (compensatory mechanism = excrete bicarb) is faster and more complete than the renal compensation for respiratory acidosis (compensatory mechanism = retain/synthesize bicarb).

- There are a gajillion things that can cause metabolic alkalosis, but they all revolve around a couple of major mechanisms:

1. Hypokalaemia: three main effects ...
   (1) ↓ K+ secretion at distal tubule --> ↑ H+ loss at distal tubule (serum pH ↑s)
   (2) Cells exchange K+ for H+ --> ↓H+ in serum and ↑H+ in cells (serum pH ↑s)
   (3) Proximal tubule cells excrete excess intracellular proton in the form of ammonium ion (serum pH ↑s)
2. Excessive activation of aldosterone receptor - promotes K+ & H+ excretion in exchange for Na+ retention (serum pH ↑s through direct effect of excreting protons and indirect effect of hypokalaemia)
3. Volume depletion - causes ↑ Na+ retention (attempt to maintain plasma volume) --> ↑H+ loss and ↑bicarb retention at proximal tubule; also indirect effects of RAAS --> ↑ aldosterone activity
4. Proton loss to the outside world - loss of acid to outside world --> ↑ serum pH

So, things that cause metabolic alkalosis include:

• Loop & thiazide diuretics - vol depletion & hypokalaemia
• Bartter syndrome - loss of Na+/K+/2Cl- transporter - mimics loop diuretic
• Gitelman's syndrome - loss of Na+/Cl- transporter - mimics thiazide diuretic
• Vomiting & antacid overuse - loss of acid
• Conn's syndrome - primary hyperaldosteronism
• Cushing syndrome - excess glucocorticoid exerts effect on aldosterone receptor
• Liddle's syndrome - mimics hyperaldosteronism
• 11β-hydroxycortisol dehydrogenase deficiency (essential or secondary to licorice) - decreased breakdown of steroids - mimics hyperaldosteronism

I think it's better to learn the mechanisms than to memorize the list.

Metabolic acidosis coming up soon!  Stay tuned ...

Xo --KM <3