So welcome back to the Internet Book of Critical Care podcast. I'm here with Adam Thomas, and we're going to talk about meth hemoglobinemia.

This is going to be one of those fun clinical pearl podcasts where you're going to understand whole physiology.

And then you're going to be able to bust out some knowledge for your learners around and round.

So Josh, let's get straight into it.

We're going to talk about the physiology of oxidizing hemoglobin in where it can go wrong.

So met hemoglobinemia.

Think about it like that friend that comes over to your house and never leaves.

It doesn't do anything for you.

Normally, hemoglobin's in its reduced state.

FE2 plus.

Things that oxidize it, turn it into a pharic state, FE3 plus.

That includes oxygen. That's the normal thing we want to happen. So to convert FE2 plus to

F3 plus when the oxygen binds to your hemoglol. Now, when other bad things show up and oxidize

that hemoglobin to the ferric state, it can no longer transport O2 or pick up carbon dioxide in the tissues. This is a

major problem. Exactly. That's perfect. So Josh, let's talk about the epidemiology and the major

drugs and toxins that people get exposed to cause or when we should think about methemoglobinemia

in these patients. So rarely this can be genetic and we're not going to focus on that because it's pretty

rare, and patients may present with a history of that.

But most commonly, this is going to be caused by various medications.

The major offenders here are local anesthetics.

The classic would be the benzocaine spray that folks get for transosophageal echo.

Less commonly...

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