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. If you found them to be helpful, please consider
hitting the like button, and sharing these videos with your classmates and colleagues.
