All right, so welcome back to the Internet Book of Critical Care podcast.

I'm here with Adam Thomas, and we're going to talk about Brash syndrome.

It took us a few years to come around to it, and you've grown up with the brash, haven't you, Josh?

But it was there all along, Adam.

Yeah, I got it.

So we're going to talk about the pathophysiology, who gets this and how to treat it.

It's a lot of fun.

I love when this comes around.

This is the critical care equivalent of the nursemaids elbow jaws.

It's something that you can fix and it's super satisfying.

So let's start off ground floor.

What is Brash syndrome and what is the syndrome made up of?

Yeah. So Brash syndrome stands for bradycardia, renal failure, which is either acute or acute on chronic, avionotal blocker, typically a beta blocker of Vrapnel or deltisome, shock, and hyperchialemia. And the core physiology here is that hyperkelemia and avonotal blockers are both well known to cause

bradycardia.

But they can essentially function synergistically to cause bradycardia.

So you can get pretty substantial bradycardia with relatively mild to moderate hyperkillemia

and like a conservative dose of a beta blocker, calcium channel blocker.

I think that's the most important point to highlight.

Thanks for starting off there, Josh, because if you look at the numbers themselves, they don't really match

the clinical picture, eh? Like, you look at the mar or what meds they're on at home. You realize

they're on these meds. Their renal failure is horrible, but the K's maybe like 5.5 or maybe 6.1,

nothing catastrophic, but they're sick, right?

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