All right you guys welcome back to another video lesson from ICU Advantage and in this lesson we're going to continue this collection of lessons where we're talking about ICU drips and this is actually going to be Part two, really, in our discussion of our antiarrhythmic medications. The last lesson was covering all that basic foundational information, and in this lesson, we're going to talk about those different classes of medications. But before we begin, if this is your first time to this channel and watching one of our videos, then I do invite you guys to subscribe to our channel below.
Make sure you hit that bell icon, that way you'll be notified as soon as our new lessons become available to you guys. As always, I truly value the subscriptions, the likes, and the comments that you guys leave for us. It really goes a long way to help support this channel, and for that, I do want to thank you guys. Alright, so let's go ahead and get into talking about these different class of medications within this category of antiarrhythmic medications. At the end of the last lesson, we talked about all the different classes, from class 1 being subdivided into the three parts 1A, 1B, and 1C, as well as class 2, class 3, class 4, and either class 5 slash other antiarrhythmics, depending how you might see it referred to.
And so in this lesson, we're going to take a much deeper dive and actually talk about why we have these different classes, how these medications work within each class, and then we are going to cover those specific ICU drip medications that you're going to find within each of these classes. These medications are medications that you're going to come across pretty frequently, especially in the ICU, and so it's going to be really important that you guys do have an understanding of these meds. All right, and so with that said, let's go ahead and start with our class 1 agents.
So these class 1 agents are a group of medications that work to block our sodium channels, specifically within the myocardium. This is going to inhibit potassium repolarizing currents, and thus... prolonging repolarization.
Now I am going to put up here a quick example of what a normal myocyte action potential looks like. Because again, as we talked about, these agents are going to be further divided up into the three subclasses. And each subclass is going to be a little bit different.
And I'm going to show you those effects on how it changes the myocyte action potential. So like I mentioned in the last lesson, this class is going to be divided up into those three subclasses. The first one is Class Ia, then we have Class Ib, and finally Class Ic.
So for our Class Ia agents, these are going to be drugs that inhibit the fast sodium channel. So essentially it's going to be inhibiting phase zero of the action potential. And so when we have elevated serum levels of these drugs, we're going to see slowed conduction, And it's going to prolong the duration and the repolarization of the action potential.
Important to know, though, that these agents can actually cause complications such as prolonging the QT interval or depressing conduction and really promoting re-entry. So the length of the QT interval or having a prolonged QT interval, basically greater than 500 milliseconds, increases the risk of R on T events. which can ultimately lead to either torsades, so which is that form of polymorphic VTAC, or other potentially deadly arrhythmias. And reentry is basically when a previous depolarizing stimulation actually triggers the abnormal impulse generation and sort of propagates or sort of cycles itself back through without being initiated by a pacemaker cell.
And so when giving these medications, really all of these medications, it's going to be important to monitor an ECG. But we're going to be particularly looking for our QRS complexes, our QT interval, and the frequency of any arrhythmias. And essentially the indications for the class 1A agents are going to be for AFib, AFlutter, SVT, and VTAC.
Now let me go ahead and put up here what... the action potential of a myocyte would look like when our patients are on these medications, as you can see here in red. And so here you can see it has a pretty moderate effect on those fast sodium channels, and this is going to increase that absolute refractory period, so that time in which another action potential cannot be propagated.
So here you can see the slope of phase 0 going up is not as steep as it normally would be, and it doesn't go quite as high, and in the end, the action potential goes on longer than it normally would. Now, for our class 1a medications, there are non-IV drip medications such as quinidine and disopiramide, but the one medication that does come in an IV form that I do want to talk about is something called procanamide. So this isn't a medication that's really commonly used so much anymore, but if you do come across it, you'll see it usually with a loading dose of 15 to 18 milligrams per kilogram given over 30 minutes.
And then the typical infusion dose is going to be one to four milligrams per minute. And this isn't a medication that you're typically going to titrate. You'll usually put it on at a particular ordered rate, and they may order changes in that rate depending on the impact that the drug is having.
Alright, so let's move on to our class 1b medications. And the medications in this class actually have a limited effect on our phase 0 depolarization and conduction velocity. These medications, though, are actually going to shorten our action potential duration and repolarization.
Nice thing with these medications is they usually don't prolong that QT interval. As always important to monitor your ECG, we do want to watch for QT interval because they... can have this effect, but usually not often, as well as our arrhythmia frequency.
And our indication for our class 1b agents is going to be for VTAC. So let me go ahead and show you guys here what a class 1b action potential would look like. And so here you can see it does have some effect on those sodium channels, although a pretty weak blocking of those channels.
But interestingly, you do see a decrease in that absolute refractory period. So here you can see that our action potential is actually going to be slightly shorter than it would be if we had just a normal myocyte. Now within this class, we do have other medications that we're going to give that aren't IV drip medications.
These include medications like toconide and mexalatine. But the one medication that I do want to talk about, and this is one that you probably will see pretty frequently, is a medication called lidocaine. Now like I said, you're going to be using this for VTAC.
or if you're having frequent and many runs of PVCs, but it's going to have no benefit in any atrial arrhythmias. Now for lidocaine, you're usually going to find this in a pre-mixed bag of 1,000 milligrams or 1 gram in 250 mLs. And you can start them off with a bolus of 1 to 1.5 milligrams per kilogram, given over 2 to 3 minutes. And you can repeat this in 3 to 5 minutes for... a maximum of three boluses.
Now our typical dose for the infusion is going to be one to four milligrams per minute. And this one has a pretty quick onset of about two minutes. And once again, this isn't going to be one that we typically titrate.
So again, you're going to usually have an ordered dose and then changes to that dose are going to be ordered for you as well. All right, so lastly, let's move on to our class one C agents. And so for the medications in this class, these are actually going to be the strongest medications when it comes to inhibiting fast sodium channels.
So again, this is our phase zero of the action potential. This is also going to significantly slow our conduction. It has a very minimal effect on the repolarization, but with these medications, you can see significant proarrhythmic complications as a result.
So again, when we're monitoring our patient's ECG, we are going to be wanting to check their PR interval, QRS complex, and arrhythmia frequency. And really our indications for these class 1C medications are going to be either life-threatening SVT or VTAC. So once again, let's take a look at how these medications are going to impact our action potential.
And so here you can see the effect of that strong inhibition of those fast sodium channels because the slope... of phase zero going up is significantly reduced, as well as the peak of that is significantly reduced as well. But ultimately, the overall effect on repolarization is pretty minimal, and therefore our action potential duration is about the same that it would be otherwise.
So it is just interesting to visualize and see how these different medications have a different effect on these action potentials. Now when it comes to medications within this class, there actually aren't any that you're going to be giving via IV drip, but some of them are and can be administered via IV, and in some places this may be something that you're doing within the ICU. But examples of some of these other medications are flecainide, propafenone, and myricazine. All right, so that covers our class one agents.
So now let's move on and talk about our class two agents. And these medications are going to be our beta adrenergic antagonist, or what we often call our beta blockers. So these agents are going to work to competitively antagonize and essentially block epinephrine and norepinephrine from binding to beta receptors. So by blocking these beta receptors, they're actually going to inactivate sodium channels. And this is also going to depress phase 4 of depolarization.
And so this is ultimately going to increase the refractory period of the AV node. And so this means we're going to have less transmission onto our ventricles. And these medications are really going to have no effect on repolarization.
When we do talk about these medications, we can classify them as either selective or non-selective. The non-selective medications are really the first generation of these class 2 agents. And these really will bind to both the beta 1 receptors in the heart and the beta 2 receptors in bronchial and skeletal smooth muscle.
The selective antagonists were really our second generation medications. And in lower moderate doses, they're going to be more selective for our beta-1 receptors. But as the doses get higher and higher, they become less and less selective. Now for these patients, again, important to monitor the ECG. We really want to be watching for heart rate, PR interval, and arrhythmia frequency.
But because of the different location of these different receptor sites, We have a couple different effects that we also want to be watching for. So some of the cardiac effects that we want to watch for are going to be things like bradycardia, hypotension, heart failure, or AV node conduction block. And really these medications are going to be contraindicated then in patients who are in a sinus bradycardia or have already a partial AV block.
Now we also want to be monitoring for respiratory effects. And the main thing we're going to be watching out for here is bronchoconstriction. And this is especially important with those non-selective medications due to their blocking of those beta-2 receptor sites.
And so these are going to be then contraindicated in patients with either asthma or COPD. Now our indications, though, for our class 2 medications are going to cover a lot of things. It's going to cover things like SVT.
to catecholamine excess-related arrhythmias, slow ventricular rate AFib, hypertension, tachycardia, and even just to decrease ischemia. And so when we talk about the different medications in this class, these are really all those medications that end in lull. All of those beta blockers, this is usually the one class of medication that people can identify pretty quickly based on the name of the medication. Now there are a lot of medications within this class.
Some that are just of note that we're not going to talk about in terms of an IV drip are going to be our metoprolol, which is a medication that we usually will give either PO or IV push. And this one is cardio selective at low doses, or another medication called propanolol. Again, not common to see this one in an IV drip, typically given PO or IV push again.
This one is non-selective though. And it does have some class one effects as well, so an interesting thing about that medication. But the main medication that I really want to talk about here is a medication called Esmolol. Now Esmolol is cardioselective at low doses, and we're usually going to find this mixed up with 2,500 milligrams or 2.5 grams in 250 mLs. And this one you can give a bolus dose of 500 micrograms per kilogram over one minute.
And our typical infusion is going to be 50 to 300 micrograms per kilogram per minute. Now important to know that we usually don't want to use this medication any longer than 48 hours though. It does have a quick onset of 2 to 10 minutes. And this medication we're going to titrate every 3 to 5 minutes. Alright, and so that'll wrap up our class 2 agents.
So next let's move on and talk about our class 3 agents. So now again for these ones, I am going to put up another example of an action potential here, and we'll talk about how these medications change that. But essentially, the medications in this class are going to be our potassium channel blockers.
And so what this is going to do is this is going to prolong that phase 3 repolarization. As a result, this is going to lengthen the duration of the action potential and ultimately that effective refractory or that absolute refractory period. And so if we take a look at how that action potential looks, you can see here in the beginning it is exactly like as if there was no medication at all. But where we begin to see the effect is once those voltage-gated potassium channels would normally be opening, we have that inhibition going on.
causing that plateau to last longer and ultimately leading to the longer duration of this action potential. Again, as a result, that effective refractory or that absolute refractory period is going to be longer. This is going to extend the amount of time in which the cell is not going to be able to propagate a new action potential.
So it is a common effect, though, of these medications to prolong the QT interval. Now again, we do have medications within this class that we're not going to see in IV drip form. These are going to be things like Brotilium, Sotolol, and Defetilide. But the one that I do want to mention here, and is going to be a medication that you are going to see all the time, is a medication called Amiodarone. So this is one of the most commonly used antiarrhythmic drugs that are out there.
You can also get this in a PO form, but we are going to specifically talk about... the IV form of this medication. And really our indications for this are going to be for VTAC, V-fib, A-fib, and A-flutter. Now a very interesting fact with this medication is in patients who have a new A-fib, so they've been in it less than 48 hours, it's really been shown that the use of amiodarone can restore normal sinus rhythm in these patients in eight hours. for about 60 to 70% of the patients.
So very effective drug. Another interesting thing about amiodarone is it actually has effects that mimic class 1, class 2, obviously class 3, as well as class 4 actions. And so because of this, it does have alpha and beta adrenergic blocking properties. And so in particular with this medication is it can result in bradycardia, AV blocks.
hypotension, and even torsades. Now for this medication in the IV form, we're usually going to find this in a concentration of 900 milligrams in 500 mLs. Make sure though, very important, that you must use an inline filter. Now we're often going to give these patients a loading dose, and this loading dose is usually 150 milligrams given over 10 minutes. So really important that you don't do a rapid bolus with this medication because this can result in...
bradycardia and hypotension in your patient. Definitely have seen it a million times, so make sure you're giving that bolus over at least 10 minutes. Now from there, the dose that we're going to be giving our patient is a set dose.
It's one milligram per minute for six hours, and then we move on to 0.5 milligrams per minute for 18 hours. Now you can continue past the 18-hour point, and certainly if your patient has... issues with arrhythmias.
Again, while we're still at the 0.5, you can re-increase that rate to 1, but this is the typical guidelines. Now as a quick aside, this medication is within your ACLS algorithm, and here we're going to be giving them 300 milligrams IV push, and if needed, a repeat 150 milligram IV push dose. Again, this is solely for our coding patients, but It is important to know this medication here as well. So really good to know is that this medication is rapidly taken up into the myocardium, and usually in a couple hours it's going to be clinically relevant for you. Now like we had mentioned with the other medications, it is important to monitor your ECG.
You want to be watching your PR and QT interval, your QRS complex, and arrhythmia frequency. Alright, so that's going to wrap up our class 3 agents. Now let's go ahead and move on to class four agents.
So now the drugs in this class are going to be our calcium channel blockers. So these medications are going to inhibit the calcium channels in the SA and AV nodes. And as a result, this is going to prolong that conduction through those nodes. This also prolongs that refractory period of the node and ultimately depresses phase four depolarization.
Now indications for these medications are going to be superventricular arrhythmias, slow ventricular response, AFib, AFlutter, or atrial tachycardia. And for these patients, again, important to monitor your ECG. And here you want to be watching your PR interval and your arrhythmia frequency.
So when we talk about our class 4 agents, they're actually divided into three different classifications. And this is really based on their chemical structure, as well as their affinity to either the cardiac or smooth muscle cell calcium channels. One group of these medications is more selective towards those smooth muscle cells, and these are the drugs ending in p-i-n-e, peen.
These ones are typically going to be used as vasodilators for hypertension. An example of this would be nicardipine. And you can actually watch one of our previous lessons, which I'm going to link to up above, covering vasodilators, to see the discussion on nicardipine.
But the remaining two classifications within this class are really only comprised of two drugs. So both of these drugs are going to be more selective for the cardiac muscle cells. And it is important to keep an eye out because these medications can cause bradycardia, conduction blocks, and depressed contractility.
Now, these two medications that make these last two categories, the first one is called verapamil, and the other one is called diltiazem. or cardizem. Now to talk about verapamil, this one's relatively selective for cardiac muscle and really less effective as a vasodilator, although it does have effects on coronary vasodilation, negative chronotropy, and decreased sympathetic activity. Now one important thing to know though is this medication can also have an effect on the slow calcium channels that we find in our pancreatic beta cells.
And this can ultimately lead to hyperglycemia in your patient. So important to keep an eye out for that. And this verapamil is something that we're going to be using for patients who either have angina or really any arrhythmias. So AFib, intraventricular tachycardia, SVT, any of those medications that can have an effect on.
Now for verapamil, this isn't common to see this as an IV drip. But if you do, you might be giving a bolus dose of 0.075 to 0.15 milligrams per kilogram given over two minutes. And then you could see this at a set infusion rate of 0.005 milligrams per kilogram. Now for deltiazem, this one falls in the middle ground between verapamil and the pine medications. So this one has an effect on both cardiac and smooth muscle calcium channels.
This one is a very potent coronary artery vasodilator. And it is a negative inotrope and a negative chronotrope. Indication for diltiazem's use is going to be our atrial arrhythmias, hypertension, SVT, and chronic but stable angina.
This medication we're usually going to find in either 100 to 125 milligrams in 100 mLs. Initial bolus dose is 0.25 milligrams per kilogram, given over two minutes. And you can repeat with 0.35 milligrams per kilogram after about 15 minutes. The infusion dose can be anywhere from 5 to 20 milligrams per hour, although usually 15 is a max, and a max of 24 hours.
And this medication will usually titrate every 15 to 30 minutes. All right, so that finishes up our class 4 agents. And so now we'll move on to our final class, what we call our class 5 agents. or what you'll also hear referred to as other agents. So really the drugs in this class have really different pharmacological properties, but ultimately they have an effect on either the SA or the AV node.
So just to knock this out of the way early, we obviously want to be monitoring our patient's ECG, but here we're checking for heart rate, PR interval, ST segment, T wave. and arrhythmia frequency. Now here within this class, there are three drugs that I am going to talk about.
None of these are ones that you're going to see in continuous IV drips, but at least two of the three are going to be ones that you're going to see pretty commonly in the ICU as well. The first one is medication called adenosine, and this medication depresses our SA node automaticity. It also depresses the AV node conduction, and so ultimately this one's going to be used to treat our tachyarrhythmias. at either the AV node or above. So the common case that you're going to see this is very fast rate SVT.
You give them the adenosine, it pretty much stops everything for a second or two, causes you to really hold your breath, and then slowly the rhythm starts coming back. And for a brief little window, a brief period of time, you're able to often see what the underlying rhythm is. The next medication in this class is a medication called atropine. And atropine is actually a medication that is a muscarinic receptor antagonist.
So these muscarinic receptors are usually found primarily in the SA and AV node. And so by blocking these receptors, we're actually going to be reducing vagal activation at these nodes. In addition to this, it also increases the rate of the SA node. It decreases the AV node conduction and the absolute refractory period. And so ultimately, we're going to be using this one to treat our sinus bradycardias or our second degree type 1 AV block.
Important to know if your patient has any other block, like for instance, a complete heart block, atropine is going to be completely ineffective for them. Now, the last medication I want to talk about in this class is a medication called digoxin or digitalis. And this medication will slow the rate of the SA node and and the conduction through the AV node, and this is primarily due to vagal stimulating effects.
A nice thing about this medication is it actually can increase contraction in cardiac muscle. It does this by inhibiting sodium and potassium ATPase, so basically the sodium-potassium pump. And so this medication is going to be used to treat heart failure, as well as controlling the ventricular response with AFib, AFlutter, and SVT.
Now, the last two agents that I really want to talk about within this class include our magnesium and our potassium supplement. Now, magnesium plays a very important role in many enzymatic reactions, including one that's responsible for the sodium-potassium pump. And so hypomagnesemia can really lead to early cellular depolarization. Potassium, as we know, plays an important role in that membrane potential. And it also plays an important role in the repolarization of the action potential.
And so as a result, either hypomagnesemia or hypokalemia can really precipitate these cardiac arrhythmias, including PVCs, AFib, AFlutter, even VTAC and VFib. And so while this supplementation is something that we can give, PO oftentimes, or more commonly in the ICU, the IV medications. These electrolyte replacements are going to be a constant presence in the care that you provide in the ICU, and they can have very significant impacts on arrhythmias for your patient. So I felt it was very important to include them in here. All right, so that is going to finish up our class five agents.
As well as this lesson covering the classes of antiarrhythmics. Hopefully after watching the lesson on the foundational information, as well as now this lesson where we really did a deep dive into each of the classes, how they work and what those IV drip medications are going to be within each of those classes, hopefully you'll have a better understanding of what these medications are doing, how they're working to help your patient when they're having these different arrhythmias, as well as why you might or might not use a particular medication in certain circumstances. And so with that said, I do want to thank you guys so much for watching. I really hope that you found this lesson and the previous lesson to be of benefit to you guys.
If you did, please go down below, hit that like button, leave us a comment, let us know what you thought. As well as if you haven't already, please subscribe to our channel. We still have a couple lessons left in this collection covering ICU drips, so make sure and keep an eye out for that.
for the next lesson here. As well as in the meantime, head on over and check out the last series of lessons that we did in which we took a look at the endocrine system. As always, thank you guys so much for watching and have a great day!