Our next arrhythmia module is ventricular tachyarrhythmias. My main goal here is to discuss things like PVCs, ventricular tachycardia, ventricular fibrillation, as well as progression of ventricular fibrillation to asystole. We will focus on things like differentiating between types of ventricular tachycardia, primary mechanisms, as well as some discussion about cardioverter defibrillators. Here's some readings that you can check out. As usual, we have our Braunwald's heart disease text chapters that are there. With our last one, we started with PACs, and we'll do the same thing with this one with PVCs. As I mentioned, you've got to be able to tell the difference between a PVC and a PAC because we tend to think about some different things associated with each of those. With these PVCs, you can see in the top strip there, the one that comes in early, so let me get my mouse and point that out to you. The beat that comes in early right here is slightly wider than the intrinsic beat. Here's a normal beat, and this one comes in early, and you notice that the QRS is wider than usual. Then there's a little pause here before a normal beat comes in, followed by a PVC. When every other beat comes in early, we call that ventricular bigeminy. The other thing you'll notice about this is that all of those PVCs look the same, so we call them monomorphic. That's an important clinical distinction to make because in the bottom strip here, I've got those PVCs labeled. They all look a little bit different from one another. What that means is that there's more than one area of irritability within the ventricle, and that's something that we want to maybe consider and maybe expand our differential diagnosis for that. Make a note if the PVCs are unifocal or multifocal, and are they occurring in any type of a pattern like bigeminy or trigeminy, because that means you're probably going to have a higher PVC load. PVCs, there are certain things that increase the risk, or we see them more frequently in patients who are older in age, male gender, certainly things like hypokalemia predisposed to this, medications, structural heart disease, infiltrative heart disease like amyloidosis, sarcoidosis can be associated with this, genetic disorders like a prolonged QT interval, pulmonary disease as well as endocrine disease can be potential reversible causes of PVCs. Patients may present on a continuum of symptoms. They may have very minor palpitations to actual near syncope associated with PVCs. It depends on how often they're having them, how long they're lasting, and then what is their underlying physiologic reserve. Patients with underlying coronary disease or heart failure may tolerate these less well than an otherwise healthy person. Patients also will have decreased or absent peripheral pulses intermittently. If you think about those PVCs that come in early, the heart hasn't had time to really relax and feel again before it beats. That PVC doesn't get transmitted down peripherally. That's an important thing to think about. If a patient calls you and you know they have PVCs and they say, my heart rate is 30 beats per minute, and they're feeling their radial pulse, well, how do they feel? Well, I feel okay. I just have my heart rate's really slow. Think about the potential there. Maybe they're having bigeminy, or maybe they're just not able to palpate every single pulse at that radial point. Evaluation, we get a 12-lead EKG, and that's going to help us identify and localize those PVCs. For instance, you can actually look at an EKG and tell if it's right ventricular outflow tract, which generally carries a better prognosis, tends to be more benign, or left ventricular outflow tract, or maybe they're multifocal coming from many areas within the heart. A 12-lead EKG is a vital part of the evaluation. You can also do ambulatory monitoring like we talked about with PACs. If they have no structural heart disease, a lot of times these end up being benign. If you put a Holter monitor for 24 hours on a given number of people, most of them are probably going to have a few PVCs here and there. However, if they have a lot of PVCs, even if they're relatively asymptomatic, that can be something that is concerning. Patients that have anywhere from 10% to 20% of their total beats are PVCs, that can predispose to the potential for a cardiomyopathy, and you may want to consider treating those as a result. Echocardiograms should be done in patients if you're concerned about a reduction in their LVEF, and a stress test if you're concerned about the potential for ischemia, if they have additional intermediate or moderate risk for ischemia, you might consider that as well. Stress should be monitored because hypokalemia is a reversible cause of this, and certain medications can predispose as well. You always want to consider the individual patient's symptoms. How many PVCs do they have? What's their burden? Are you concerned about an associated cardiomyopathy occurring as a result of this? Beta blockers are good choices, especially for more the hyperadrenergic PVCs, they work really well. Non-dihydropuridine calcium channel blockers are also considered first line. You can use antirhythmics if other rate-slowing medications don't work, and you could consider radiofrequency ablation if the PVCs are focal, so they're coming just from one area, if they fail pharmacologic therapy, or if there's a decline in their LV function. Ventricular tachycardia, so if you start stringing together a lot of PVCs, then we have ventricular tachycardia, and that is sustained if it's lasting for longer than 30 seconds. Three potential causes of VT, it can be an automatic focus, which is adrenergically mediated, it could be related to triggered activity, we talked about that with an abnormal action potential where you have some prolonged repolarization, that can predispose to abnormal early after depolarizations or delayed after depolarizations, and we think about that with a prolonged QT if you see that on their baseline EKG. Reentry is one that you'll see with structural heart disease, so if you have a bunch of scar tissue in the heart in a particular area, that can create a reentrant pathway where you can have this typically monomorphic ventricular tachycardia. So when patients have VT, whether it's sustained or non-sustained, you have to make a note if it's monomorphic or polymorphic. So in this example, right here, we can see that this would be polymorphic. So torsade de pointe means twisting of the points, and this means that there's more than one area within the ventricular myocardium that's irritable. So we call it twisting of the points because there's one focus that fires off for a few times, and that's why we'll see a predominant axis here, and then another PVC takes over and fires off for a few beats, and then we see the axis twist up because it's coming from a different area, and then it twists back down when another one takes over. Again, that concept of the fastest ectopic pacemaker will win, even if it shouldn't be there. And then this is a great example of monomorphic VT, where every single beat looks just like the other one. So polymorphic VT should bring about, in your mind, a differential diagnosis. Now, there's lots of things that can do this. When I see it, I think about ischemia, hypokalemia, or a prolonged QT interval. So that's where my mind's going to go and look at their electrolytes, look at their medications, evaluate the potential for some underlying ischemia there that we need to do something about. So here's a 12 lead of someone in ventricular tachycardia. There are two things we can look for to really help us nail down this diagnosis of VT. As we've mentioned, if someone has a wide complex tachycardia and they have structural heart disease, you treat it like VT until you prove it's not, because that's more common than an aberrantly conducted SVT. So two key features would be AV dissociation, and that is where you can see P waves and you can see them kind of buried somewhere in that QRS, but they're not associated. A fusion beat is something that is extremely helpful, but you really only see both of these things in slower VT. So fusion beats indicate activation of a ventricle from two different foci. So you've got one of them as the ventricular focus there that's firing off. And then you remember your atria is still beating away. So you've still got those P waves. And if that rate slows a little bit, then one of those P waves can capture there in the ventricle, or you can have a fusion of those two. And that's what happens here. So if we look at a capture beat, so here, well, let's look at this one first. Here's a VT beat right there, looks different from this one, which is a capture beat. And then a fusion beat will look like, as you might suspect, a fusion of those two complexes. And so it looks like kind of a mix of the two of those things. That's a fusion beat generally seen at ventricular rates that are a little slower, but AV dissociation and fusion beats have long been considered a hallmark and diagnostic of ventricular tachycardia. So those are things you want to look for. VT, we see this in patients with ischemic heart disease, cardiomyopathy, channelopathies, or it can also be idiopathic where someone gets it and you wouldn't suspect that. They don't have those classic risk factors for it. The symptoms depend on the ventricular rate. I have seen patients that have had very well tolerated slow VT at 120 beats per minute. And then someone else will have VT at a rate of 130 and feel like they're going to pass out. So it depends on how fast their ventricular rate is and how much physiologic reserve do they have. If someone's got an EF of 20% and they've got ischemic heart disease and they go into VT, they're probably not going to tolerate that very well. So evaluate their underlying, how fast their heart rate is, and then evaluate them for underlying cardiac conditions that might make them more symptomatic. Patients that have short or sustained VT, they may be hemodynamically stable. They may also be hemodynamically unstable. So your first step in evaluating someone with VT is to evaluate their hemodynamic stability. What's their blood pressure, what's their heart rate, and how do they feel? A 12 lead EKG should be done to try and confirm that it's VT and also potentially localize where that's coming from. That could be helpful if you know someone has had a large MI in a particular area of their heart and then you can localize that VT to coming from that area. We're not going to get into the details in this lecture, but I do have an article in one of the early slides there that talks to you a bit more about how you can localize the focus of VT. Think about the possibility of active ischemia. Does that person just need to go for a heart catheterization? Look at their electrolytes, evaluate their QT interval, an echocardiogram can be done to look at their LVEF because we know if their EF is lower, they may not tolerate that as well. And that is an individual risk factor for VT. Electrophysiology study can be done, exercise stress test should not be done in someone who is hemodynamically unstable, of course. And then think about the possibility of outflow tract VT because that tends to have a bit better prognosis, particularly RVOT. So your management really depends on their hemodynamic situation. Are they hemodynamically compromised where they feel like they're going to pass out and their blood pressure and heart rate are low? Well, then that person probably just needs either a cardioversion or a defibrillation depending on if they have a pulse. So acutely, we want to pursue medical management. So someone's in VT and they're stable, you can try to give them IV amiodarone, Sotolol, beta blockers work really well for polymorphic VTs. If someone is not hemodynamically stable, then a cardioversion can be done or defibrillation again, depending if they have a pulse. So if arrhythmia does not respond to medical management and to prevent a recurrence, cardioversion can be done. And then think about electrolyte replacement. Is there something that's reversible? If their potassium is really low, certainly replace their potassium when they're less likely to have a recurrence. Patients that may come in with VT if they've got decompensated heart failure. So managing their heart failure will make them less likely to have a recurrence and then monitor for signs of ischemia that might mean they need to go to the cath lab. So long-term ablation is done if the patient has monomorphic VT, that's a good option, but usually you're going to progress through your other options first. Defibrillator, certainly if this is something that they qualify for, and we'll talk about that in a minute. Beta blockers are great for all your patients with VT and you can consider antiarrhythmic therapy. Another thing to think about in your workup is the potential for some type of an infiltrative cardiac disease, although that's less commonly seen, but think about things like the potential for amyloidosis or sarcoidosis that can start infiltrating into that tissue. So sometimes we'll do cardiac MRIs for something like that. All your patients though should have an echocardiogram to make sure that there's no issues with their LV function that maybe you weren't aware of. So there are recommendations for the treatment of recurrent ventricular arrhythmias for patients with ischemic heart disease from the ACC AHA HRS. So patients with ischemic heart disease and recurrent arrhythmias and they have significant symptoms or if they've got an ICD and they have ICD shocks, despite optimal device programming and ongoing treatment with beta blocker, we can use antiarrhythmics like amiodarone or Sotalol. So there's some good data there to support that. Patients with prior MI and recurrent episodes of symptomatic sustained VT or who present with VT or VF storm and they've failed or intolerant of amiodarone or other antiarrhythmic medications, then those patients you would consider for a catheter ablation. I like this chart also from, so this is a, I've got a citation there that you can read about this in. So I like this chart because it really brings the focus back to preventive care. So when we think about patients that are going to come in with sudden cardiac death, we typically picture the person with a low EF, someone's got coronary disease and that is common, but actually most of the people who come in and the general population, there are people that we just don't know are at high risk. So it really, I think this really brings the focus back to let's try and do a better job with our preventive care for these patients from a cardiovascular standpoint. So of those with sudden cardiac death, about 50% of all of those patients, it's their first cardiac event. And the out of hospital survival is only about 10% in those patients. There are certain things that increase your risk of this age, male gender, ischemic heart disease, LVH. We know those are all things that increase your risk, but in general, it's those people that we didn't know were even at risk in the first place. So always want to bring that focus back to the importance of preventive care for people. We want to, instead of leaving the faucet running, so to speak, and mopping up, turn off the faucet. So that's why I like to think about that. There are clear indications for implantable defibrillators and we divide this into primary versus secondary. So on this chart over here, we have patients with ischemic heart disease with a meaningful survival of at least one year. So do the following apply. They've got a low ejection fraction. They are at least 40 days post MI or at least 90 days post revascularization. EF is at least 35% or less. And they have New York Heart Association class two or three heart failure, despite being on good medical therapy. ICD is recommended for primary prevention. If their EF is less than or equal to 30% and they have class one heart failure, despite guideline directed medical therapy, then they need a defibrillator. So that key point there is that if someone has an MI, then you have to wait 40 days, put them on good medical therapy. So at minimum, they should be on a beta blocker, an ACE or an ARB specific to heart failure and give them 40 days to see if their EF recovers. If they are revascularized, we give them 90 days to see if their EF recovers. That's primary prevention. Secondary prevention. If someone has a sudden cardiac arrest, certainly due to VT or VF, if they have hemodynamically unstable VT, stable VT or unexplained syncope plus inducible sustained monomorphic VT on an EP study, then ICD is recommended for secondary prevention of sudden cardiac death. Okay. So ventricular fibrillation. If someone has VT and they don't spontaneously come out of it, or you don't do something to bring them out of it, it can progress to ventricular fibrillation. This is where there's no meaningful cardiac output. So these patients are usually going to pass out. Their ventricular rate is typically very fast and so fast that eventually you can't really tell what it is because there's no meaningful cardiac output. It occurs most often in association with coronary disease and as a terminal event. The longer time someone spends in VF, the less chance of successful defibrillation. So if you think about this also on a continuum and someone starts off in VT and then they progress, they stay in VT and now they're in VF and you can really kind of pair that with a success rate just going down for cardioversion. So we really want to try and cardiovert those people, defibrillate those people as quickly as we can once we realize this. And then of course, once someone goes into asystole, now that's not a shockable rhythm. So three to five minutes, you can have brain damage unless this is corrected. So the clinical presentation, near syncope, progressing quickly to loss of consciousness. You generally won't be able to palpate a pulse or a blood pressure in these patients. And the management should really follow ACLS guidelines. So we do CPR, defibrillation, and just kind of a little summary there of what we do. So one shock with CPR and you always want to obtain IV access as quickly as possible while you're doing this epinephrine or vasopressin, followed by amiodarone or lidocaine. And then epinephrine, if it's not a shockable rhythm, we're going to continue CPR. So when in doubt, always follow your ACLS guidelines once someone progresses specifically to ventricular fibrillation. That concludes our lecture on ventricular tachyarrhythmias. Thank you so much.

ventricular tachyarrhythmias

PVCs

ventricular tachycardia

ventricular fibrillation

asystole