Antiarrhythmials

Poking around the Student Doctor Network, I saw a neat question and just decided to have fun with it.  I’m playing with the idea of tackling a few topics in this manner, complete with Podcasts so that you can listen along (and I don’t have to type so much).  If this sound like something you’d use, let me know; Ill let the interest drive it.

To everyone else, sorry to bore you to death.

 

Quote:

Originally Posted by guitarguy09 View Post

I noticed FA 2007 p.255-256 lists “amiodarone” as being both a Class Ia and Class III antiarrhythmic, while Lippinocott’s and Wikipedia list is being solely Class III. Does it act in some other way aside from blocking K+ channel outflow during phase 3 (prolonging the AP and effective refractory period)? Lippincott’s says that it has Class I, II, III, and IV actions, but that it is unlike Class I because it does not prolong the QT interval (although it’s listed with the other Class III antiarrhythmics as increasing QT in FA). What’s up with this??

Awesome question with a cool answer. Unfortunately, it requires some detail to explain. Here’s a table I made when I was sorting it out for myself.

The Na+ channels of the SA and AV nodes are always firing (more or less) and are termed “active”. This is in contrast to the Na+ channels of the ventricles that are usually off or “inactive”. This all makes sense when you remember that the slow depolarization of the SA/AV is via Na+ channel, whereas the Na+ channels of the ventricles are off except for a very brief phase 0 upstroke (not a lot of time for a drug to take effect).

So, what makes a Class I a Class I is its action on these active Na+ channels. From this, you expect their action to be in the nodes and not in the ventricles. What makes Quinidine a Ia is its additional K+ action. In the SA/AV, this would prolong repolarization. In the ventricles, this would also prolong repolarization. Now, the prolonged QT, the slowing HR, etc begin to make sense.

If you can keep the differences between the SA/AV and the Ventricles straight AND commit the table I included to memory, then the effects of these drugs start to come together. Shockingly, more detail up front requires less memorization later on and leads to a real understanding of antiarrhythmials.

So when people say that Amiodarone is also a Class I, they’re missing it! Amiodarone doesn’t have the basic action that makes a Class I a Class I, and instead includes the actions that make a Ia and a Ib different from a standard Class I.

Lot of details, but interesting nonetheless. The only thing I’ll add is that the Na+ channel in the SA/AV is a “funny” channel and that the Ca2+ channel in the SA/AV is an L-type channel. Why do you care? Well, the actions of Beta-Blockers don’t make sense otherwise. Beta-blockers like Propranolol can act at the Funny channel and the L-type channels in the SA/AV, and can also act at the Ca2+ in the ventricle, but you don’t see them affect the Na+ channel in the ventricles.

You should be able to piece together the rest. In the meantime, here are the bullet points.

Block: Effect

K+: Delays repolarization ↑AP duration, ↑ ERP, ↑ QT interval (risk for Torsade de pointes)
Na+ (SA/AV): ↓ automaticity, ↓ slope of phase 4, ↓ cell excitability
Na+ (Vent) : ↓ conduction, ↓ slope of phase 0 depolarization
Ca2+: ↓ conduction (SA/AV), ↓ slope of phase 4, ↓ phase 2 plateau (Vent), ↓ contractility, ↓ QT interval
Beta-receptor: Na+ (SA/AV)-block and Ca2+-block; negative chronotropic, dromotropic, and inotropic

Mg2+: Functional Ca2+ blocker; first line in Torsades de Pointes, Digitoxin toxicity
Adenosine: Receptors on SA and AV node; ↑ K+ and ↓ Ca2+ conductance, hyperpolarizes; may cause AV block; DOC in diagnosing/abolishing AV nodal arrhythmias. Toxicity: flushing, chest burning. t1/2 = 10s.

Hope it helps, topher.

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2 Responses to Antiarrhythmials

  1. nosugrefneb says:

    Duh. I could have recited that in my sleep.
    BAAAAHAHAHAHA. What the hell is a Class III antiarrhythmic? (Kind of joking, kind of not, kind of amused at how little I remember a mere 8 months later.)

  2. in the middle of running a code in the back of a moving ambulance, i was reaching for the amio vials (they only come 150mg per vial, and you need 300mg for a single ACLS dose naturally) and as i’m drawing the meds up, i honestly thought to myself “class III antiarrhythmic”…

    adenosine doens’t just cause chest burning btw, it causes “baseball-bat-to-the-chest-itis”… whenever you give it to someone its always nice to let them know that they’re about to get chemically punched in teh stomach so they won’t get too pissed at you. i didn’t really believe the half life could be that short-lived, but it really just evaporates once it hits the tissues… the best way to give it is to have a 2-way IV port hooked up with a syring of drug and a syring of saline to slam in behind it.

    lidocaine is usually frowned upon nowadays, at least in ems, but the n=1 time i’ve used it, the PVC’s just melt away… (R on T phenomenon is just about the worlds scariest thing when its your patient on the monitor… “just don’t hit, just don’t hit, just don’t…”)

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