This is the final video in this 7 video series on antiarrhythmics.
The topic is an overview of drug selection, some classic antiarrhythmic pitfalls, and
a brief summary.
So, I'm going to go through some common scenarios involving arrhythmias and discuss the consideration
one should have when choosing a specific drug.
First up is the most common: how to rate control rapid a-fib or a-flutter.
The first consideration is whether you are dealing with an inpatient who you are just
attempting to stabilize temporarily while figuring out the long-term plan, or if you
are dealing with an outpatient or soon to be discharged inpatient and need to determine
that long-term plan.
For the acute inpatient, ask whether there is evidence of heart failure or LV dysfunction.
If no, then diltiazem, verapamil, and cardioselective beta blockers are all appropriate options.
There is some evidence, which is consistent with my personal experience, that IV diltiazem
may be the most effective med for acute rate control.
Now, if there is heart failure or LV dysfunction, those meds are all relatively contraindicated
because they are negative inotropes.
So options in this case include amiodarone, and digoxin, as well as cardioversion.
Keep in mind that amiodarone carries the risk of pharmacologically cardioverting the patient
back to sinus, which may or may not be desirable, depending on how long the patient has been
in a-fib or a-flutter, and whether they are already adequately anticoagulated.
Also, digoxin has a long onset of action, even when loaded, and it will definitely be
the slowest of any of these options at getting the rate under control.
For outpatients and/or a long-term rate control strategy, once again, consider heart failure
or LV dysfunction.
If there's none, diltiazem, verapamil, and beta blockers are all appropriate options.
If there is heart failure or LV dysfunction, beta blockers are clear first line, with digoxin
and distant second.
Remember that we want to avoid long-term amiodarone due to its toxicity like pulmonary fibrosis.
Okay, the next scenario, how to pick a medication to pharmacologically cardiovert a-fib or a-flutter.
The first question here is whether the patient is hemodynamically unstable.
If yes, then don't mess with drugs - just do an emergent electrical cardioversion.
If they are stable, but you still want to cardiovert them for some reason, such as symptoms
of palpitations or a difficult to control ventricular rate, you need to consider whether
the patient has so-called structural heart disease, which refers primarily to coronary
artery disease and heart failure, but which also is sometimes considered to include moderate
to severe LVH.
If there is no structural heart disease, then the Ic agents of flecainide and propafenone
are options, as well as the class III drug dofetilide.
An important caveat that I'll return to in a few minutes is that patients started on
flecainide or propafenone should be pretreated with a class II or IV antiarrhythmic, in the
event the a-fib converts to a-flutter.
Now, on the other hand, if the patient does have structural heart disease, amiodarone
is the most common option.
Once a patient has cardioverted back to sinus, either electrically, pharmacologically, or
spontaneously, what is the best medication to maintain sinus rhythm?
If there is no other significant cardiac disease at all present, then flecainide, propafenone,
and sotalol are all ok choices.
If significant LVH is present, for example, from poorly controlled hypertension, then
amiodarone is generally used.
If they have CAD, then it's dofetilide or sotalol.
And if heart failure, it's amiodarone or dofetilide.
Now moving away from a-fib and a-flutter, let's talk VT.
How do you pick a med to pharmacologically cardiovert monomorphic VT?
As with a-fib, if the patient is unstable, electrically cardiovert them immediately.
However, if they are stable, amiodarone, lidocaine, and procainamide are all options.
Lidocaine, in particular, is generally used only in situations of VT in the setting of
acute coronary ischemia.
And of course, even with hemodynamically stable VT, electrical cardioversion is absolutely
still an option, but one that caries the downside of requiring anesthesia and sedation.
And to pick a medication in patients at risk of recurrent monomorphic VT, ask if they are
an ICD candidate.
If yes, then an ICD is by far the best option, to which a beta blocker is usually, but not
always added, primarily to prevent VT altogether and to decrease the burden of shocks.
If the patient is not an ICD candidate for some reason, for example, if they have limited
life expectancy, then just a beta blocker.
If the patients in either situation continue to have a significant burden of VT, options
to consider then include adding amiodarone, switching the beta blocker to sotalol, or
more commonly, just adding sotalol to the beta blocker already present.
One thing regarding the use of amio in this situation is that while it decreases the frequency
of VT, it can also slow the rate of the VT when it does recur to below the detection
limit of the ICD, preventing an appropriate shock.
For example, if the ICD is programmed to shock any tachyarrhythmia above a rate of 150 beats
per minute, but amio lowers the rate of a patient's VT from 170 to 140, that's probably
not going to be doing them any favors.
At this point, I'm going to quickly run through a handful of less common situations.
For termination of AVNRT, first try vagal maneuvers such as a Valsalva or carotid sinus
massage, and if they fail, then move next to adenosine.
For termination of orthodromic AVRT, that is AVRT which goes down the AV node and His
bundle and back up an accessory pathway, vagal maneuvers and adenosine are also recommended.
For termination of antidromic AVRT, when the reentrant rhythm goes down the accessory pathway
and back up the AV node in a retrograde direction, procainamide is the favored drug.
Procainamide is also the preferred drug for the pharmacologic cardioversion of a-fib in
the setting of WPW.
Prevention of VT and VF in Brugada syndrome, which is an inherited defect in one of the
cardiac sodium channels, amio or quinidine are preferred.
It�s one of the rare situations where quinidine is actually used.
Prevention of AVRT, either orthodromic or antidromic, metoprolol, or other beta blocker.
And last, for the prevention of preexcited a-fib, 1c agents flecainide or propafenone
are good choices.
Next, I'll move on to discuss 3 classic pitfalls of antiarrhythmic therapy.
The first is the most common of the three - treating an unknown wide-complex tachycardia
as anything other than VT.
So, the problem here is that there are physician who love to attempt to distinguish unknown
wide complex tachycardias that are due to VT from those due to an SVT with abberancy.
The problem here is that the criteria used to do this, isn't perfect, and the risks from
treating a VT as an SVT with abberancy are much greater than the risks from treating
an SVT with abberancy as VT.
So unless you are somehow absolutely positive that the wide complex rhythm is an SVT, choose
drugs or cardioversion strategies that are most appropriate for VT.
The next classic pitfall: treating a-fib in a patient with WPW with a beta blocker or
calcium channel blocker.
So first, here is an example of what this truly ugly rhythm looks like: a wide-complex,
irregularly-irregular rhythm.
There are very few things that cause this type of rhythm, and preexcited a-fib should
be your first consideration.
The problem with using a beta blocker or calcium channel blocker here is that those drugs primarily
affect conduction through the AV node - they have no impact on conduction down the accessory
pathway, which appears to be the primary route for impulses to get to the ventricles, since
all of the complexes are wide.
So in the best case scenario, these drugs won't help the patient at all.
However, it is widely believed that blockade of signal through the AV node only may paradoxically
increase the frequency with which the impulses moving down the accessory pathway can depolarize
the ventricles.
In other words, giving these patients beta blockers or calcium channel blockers may actually
accelerate their heart rate.
So instead, they must be treated with drugs that impact both the AV node and the accessory
pathway, or preferably, be given a drug that can safely cardiovert them and don't even
attempt rate control.
So for example, as mentioned a few minutes ago, procainamide.
The final classic pitfall is treating a-flutter with a sodium channel blocking drug, without
a concurrent beta blocker or calcium channel blocker.
So here, we have atrial flutter with a flutter rate, that is, the frequency of flutter waves
of about 280 waveforms/min.
There is 2:1 AV block, result in a ventricular rate of 140.
What sodium channel blockers can do is to slow the rate at which the wavefronts of depolarization
travel around the reentrant circuit, without impacting the AV node.
This is a problem because the AV node cannot be able to conduct 280 supraventricular impulses
per min, it might be able to conduct 180 or 200 impulses per min.
So this is what can result.
After treatment with a sodium channel blocker, they have slowed the rate of flutter waves
to 200 waveforms per minute, which is the same as 200 impulses hitting the AV node per
min, which in younger patients it actually can conduct.
So instead of have 2:1 A-flutter with an overall ventricular response of 140 beats/min, we
have 1:1 a-flutter with an overall ventricular response of 200 beats/min, and that is most
certainly not an improvement.
So when starting a class I drug in a patient with a-flutter, always put them on a beta
blocker or calcium channel blocker before or at the same time.
I hinted at this problem in lesson 2 when mentioning the so-called pill-in-the-pocket
to paroxysmal a-fib, in which patients take a 1c drug on an as needed basis for palpitations.
These patients should also be concurrently treated with AV blocking drugs as well - in
the event that those palpitations are actually from a-flutter and not a-fib, which frequently
coexist in the same patient at different times, and which may feel identical.
So that's all of the information on antiarrhythmics I'm covering in the series.
Here's a chart that summarizes the most important information that I've presented about each
of the drugs, excluding atropine, isoproterenol, and ivabradine.
Don't worry, I'm not going to read through it, but it's here if you want to pause the
video and take a screen shot or just test your memory.
And finally, these are my 5 main, general takeaways from the whole series.
First, antiarrhythmics are a large, physiologically complex, and pharmacologically diverse collection
of drugs.
The standard classification system is simple and hasn't been improved upon in 50 years,
but it fails to adequately capture this complexity.
All antiarrhythmics are also proarrhythmic, particularly class III drugs and digoxin.
Although appropriate indications for some drugs can be easily deduced from first principles,
you probably have already noticed, that this is not true for all of them.
Unfortunately, many drug-indication pairings just need to memorized.
Last, as a general rule, due to their lower frequency of use and less favorable risk/benefit
ratio, class I and III drugs, excluding short-term amiodarone) should only be prescribed after
consultation with a cardiologist, provided there is time to do so.
That's not to say that there aren't situations in which you should discuss therapy with class
II, IV, or the non-classifiable drugs with a cardiologist.
There are countless situations in which a cardiologist can be helpful at choosing the
most appropriate medication.
It's just that with the class I and III drugs, it's difficult to imagine a scenario in which
a non-cardiologist should take it upon themselves to prescribe on their own.
Even myself as a hospitalist who has a particular interest in electrophysiology, I don't prescribe
drugs like sotalol or flecanide without discussing it with the true experts.
So that concludes this 7 video series on antiarhythmics.
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