On today's episode of real-life pharmacology, I'm going to talk about the anti-arhythmic amyodorone.

Ami-odurone is a class three antihrythmic.

It's got a few different mechanisms of action, including affecting sodium and potassium, as well as potentially calcium channels,

and possibly has some mild beta and alpha blocking activity as well. Amioderone is used to help

with rhythm control in atrophibulation.

Now, if you remember atrophibulation,

the usual first step is to try to do rate control

with beta blockers and calcium channel blockers

like Deltiasm and verapamil.

If that fails, if that's unsuccessful, if patients continue to have symptoms,

amyodorone may be considered in this setting to help with that rhythm control.

Now there are lots of unique clinical pearls with amiodorone.

So first let's kind of talk side effects and pharmacokinetics.

Amioderone, one thing really important to remember is that it has an incredibly long half-life.

So it may take in the ballpark of 40 to 60 days for half of that drug to be

eliminated from the body. And this can play a significant role in complicating things like drug

interactions, which I definitely will talk about drug interactions

coming up a little bit later on here. As far as adverse effects go, you definitely need to

remember thyroid function with amyodorone. So checking that TSA can be very important, making sure that we're maintaining

normal levels there and not having signs or symptoms of hyperthyroid or hypothyroid. I will say in

clinical practice, amyodorone has been associated with hyperthyroidism, but I can tell you that I'm much more commonly

see in practice it cause hypothyroidism. Remember, that's an elevated T.S.H. Another potential

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