Potassium Channel Blockers are easy! Check it out!
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This is Dr. Joel with MedImmersion.
You are watching a flash flood review series video where I review the highest yield stuff for your board exams in as little time as possible.
In this video, I'm going to be talking about the potassium channel blockers, which are a class of the antiarrhythmic agents.
I'll cover some general principles about the class as a whole, and then a few specific drugs in that category, or in this class.
It's gonna be awesome, so stick around.
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Let's jump into it.
This lecture is going to cover a subset of the antiarrhythmics, the potassium channel blockers.
I'll give you an introduction as to what they are.
Then, talk about some general principles that will include the mechanism of action, clinical uses, adverse or side effects, and then I will cover a couple of the highest yield examples in this class.
First of all, if you need to review the entire topic of the antiarrhythmics, with a little bit of cardiac physiology, you should really go over and watch The Antiarrhythmic Agents Lecture first.
This lecture, right now, is a little bit more focused, and I assume that you know a couple of things about antiarrhythmics.
So, the potassium channel blockers, in the Vaughn Williams Antiarrhythmic Agent Classification, are the Class III antiarrhythmics.
You should know that.
And we use the potassium channel blockers and the Class I, or sodium channel blockers, for rhythm control.
The Class IIs and Class IVs are more rate control.
Four drugs that we're gonna talk about amiodarone, ibutilide, dofetilide, and sotalol, which you can remember by the mnemonic AIDS.
As for the mechanism of action, these block myocardial potassium channels, and that has its primary effect on the specific potassium channels that are responsible for the delayed rectifier current, which have a very important contribution on the length of the action potential, and thus, the effective refractory period of cardiac myocytes.
And to explain that a little bit further.
Have you ever wondered why exactly the action potential of a neuron through the spinal cord or a peripheral neuron looks different than the action potential in myocardium.
Well, it's built that way on purpose.
The plateau phase, or the prolongation of the action potential, or the refractory period, gives cardiac tissue special properties that prevent it or contribute to prevention of arrhythmias.
So, the picture on the left is what maybe a bland neuron action potential might look like in the peripheral nervous system.
On the right, we have a cardiac action potential.
And both of these are pretty bland images.
They're not exactly right.
But the point here is that there's a plateau where the cell stays in its non-polarized state for a little bit longer, for a period of time.
Potassium plays a big part in that.
The initial depolarization is caused by a rapid influx of sodium.
And then, it's maintained in that depolarized state by both calcium and potassium trading places across the cell membrane in relatively small amounts.
In phase three, which is the repolarization phase, finally there's a delayed switch, or a delayed rectifier current of potassium, which finally turns on and allows an efflux of positive ions, allowing the membrane potential to come back down to a very negative number.
So, hopefully you can see why if we mess around with the potassium channels that contribute to phase three, we prolong or at least change the shape of the cardiac action potential, which, of course, would have an effect on some kinds of arrhythmias.
So, it was pretty easy to see, I think, from that previous picture that delaying the potassium efflux during the repolarization phases increases or stretches out the action potential duration and also the effective refractory period.
Also, these do not have any effect on the sodium channels, meaning that the conduction velocity, or phase zero, wouldn't be affected or decreased.
And visually, it looks like this, the action potential stretched out and the effective refractory period is increased.
Also, that means that the QT interval is prolonged.
Does that make sense? We use the Class III antiarrhythmic agents for rhythm control.
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