In this talk, I'll be discussing the analysis and therapy of ventricular arrhythmias. My name is Sammy Zachary. I'm a cardiologist and critical care physician at Johns Hopkins in Baltimore, Maryland. This talk has four major objectives. The first is to learn epidemiology and significance of ventricular arrhythmias in the ICU environment. Then we'll focus on differentiating and recognizing ventricular tachycardias and differentiating monomorphic ventricular tachycardia from supraventricular tachycardias. We'll also spend some time discussing polymorphic ventricular tachycardia and ventricular fibrillation. Then we'll transition to learning the etiologies for ventricular arrhythmias, and then finally discuss therapies for ventricular tachycardia and ventricular fibrillation. In the ICU environment, ventricular arrhythmias are a big issue, and they are found in 2.2% of all ICU patients. If they do occur, they're very bad, and then they're associated with an increased mortality rate. So 66% to 73% of patients who have malignant ventricular arrhythmias end up dying. In general, when I evaluate a patient with ventricular arrhythmias in the ICU environment, I have a diagnostic and management approach similar to patients with supraventricular tachyarrhythmias. I want to first determine how much of a problem this ventricular arrhythmia is. If there's signs of shock present, then this patient should be treated emergently. And obviously, if the patient has no pulse, then you want to be performing ACLS as well. If the patient is more stable but has signs of cardiac hypoperfusion, or if there's signs of hypotension, then you want to be treating this patient urgently as well and figure out and treat the underlying cause. In many cases, ventricular arrhythmias can result from cardiac ischemia, so it's also important to have that at the forefront of the management approach and to rule out any inciting causes for cardiac ischemia. In addition to cardiac ischemia, there are a number of etiologies for ventricular arrhythmias. They could occur as a result of hypoxia, changes in intravascular volume, acid-base status, or other causes. I've also bolded the ones that I think are more relevant in the ICU environment. I feel that patients with electrolyte abnormalities are much more likely to develop ventricular arrhythmias, and so it's important to make sure that electrolytes are within the normal ranges. Similarly, patients with cardiac disease or cardiomyopathies tend to have more ventricular arrhythmias, so those should be aggressively treated as well. Many patients in the ICU environment have central lines or other hardware inside their heart, and so it's common to have irritation and ventricular arrhythmias from central lines or from right heart catheters or other devices. Finally, many patients in the ICU environment have a number of medications that are being administered or may have taken substances that could predispose to ventricular arrhythmias, so it's important to also recognize that these could be causes for ventricular arrhythmias. Okay, let's go over our case. This is a 52-year-old man with recent GI bleeding, COPD, CAD, and heart failure who presented with pneumonia and ARDS. On telemetry, his heart rate was noted to be 160. He had a number of abnormal physical exam findings, and his labs are also abnormal. An ECG was performed. Here's his ECG, so what is this Y complex tachycardia? Is it ventricular tachycardia, or is it some other type of tachycardia, and how do you figure that out? Let's get back to that. First of all, let's define what is a Y complex tachycardia. You have to have two conditions. Number one, the QRS complex must be greater than 120 milliseconds in width, and the ventricular rate must be greater than 100 beats per minute. Once these two conditions are satisfied, then basically you have two conditions that could cause this. Number one, and the most common reason, is that the patient has ventricular tachycardia, and this is a rhythm that originates at the ventricle. The second reason is a supraventricular tachycardia with a Y QRS complex, and so what's going on here is that there's a super nodal rhythm, and then you have an abnormality or delayed depolarization of the ventricles. Here are a few general rules for managing patients with Y complex tachycardia and determining if they have ventricular tachycardia or not. In general, any patient with a wide and fast heart rhythm whose hypotensive should be treated as ventricular tachycardia. It's much more important to initially manage the patient than to figure out the diagnosis. Number two, I don't use any clinical stability to differentiate between ventricular tachycardia and supraventricular tachycardia. In fact, I've seen many, many patients who have ventricular tachycardia who are able to maintain adequate cardiac perfusion for at least a few hours. Third is I have a strong bias toward ventricular tachycardia, and that's because most patients with Y complex tachycardia have ventricular tachycardia. In fact, if a patient has heart disease, they have a greater than 95% chance for having VT if they have a Y complex tachycardia. Also, older adults, and that's defined as patients older than the age of 35, have a higher chance of having ventricular tachycardia. So in general, error on the side of ventricular tachycardia. Finally, if you don't really know what's going on, just treat the patient as if they have ventricular tachycardia. Ventricular tachycardia treatments tend to be successful in patients with supraventricular tachycardia, at least initially, and it's much more important to manage the patient and make sure that they're stable before figuring out the diagnosis. Eventually, it's important to figure out if the patient has ventricular tachycardia or not, because that'll be important to prevent recurrences in the future. Okay, so when I look at ECG, how do I figure out if the patient has ventricular tachycardia or not? For me, I use the scan and zoom method. I scan the entire ECG for four different criteria. Number one, do they have AV dissociation? Number two, do they have any capture beats? Number three, do they have any fusion beats? Finally, do they have extreme axis deviation? And that also needs to have an initial R-wave and AVR. Once I finish scanning through the ECG, I then zoom and focus more on the precordial leads. Here, I want to ask myself four new questions. Number one, does the patient have precordial concordance? Number two, does the patient have a wide RS interval, and that means the interval from the beginning of the R-wave to the nadir of the S-wave is more than 100 milliseconds? Number three, does the patient have a new wide QRS complex? And this depends on what type of pattern the patient has. Is it greater than 160 milliseconds for those with a left bundle branch block pattern, or is it greater than 140 milliseconds for a right bundle branch block pattern? And the final question is, does the patient have an atypical right or left bundle branch block pattern? If they have a typical pattern, then this is less likely to be a VT. But if it's atypical, then it's more likely to be a VT. On the right-hand side of this slide, I have in gray font some specific factors that favor VT in patients with atypical right or left bundle branch block patterns. They're here more for your reference, but feel free to review them. All right. So in the next few ECGs, I'll be using the scan and zoom criteria to determine if the patient has ventricular tachycardia. In this ECG, I'll first use the first scan criteria, which is looking for AV dissociation. I'm looking especially at the rhythm strip, so that's lead V1, and notice there's deflections that may reflect atrial activity, which I've highlighted with the blue lines. Since the P-waves are marching at a rate different than the QRS complexes, and there's no relationship between the two, it means that there must be two independent foci for depolarization. This means that the patient must have ventricular tachycardia. And so if you see AV dissociation on an ECG, it's pathobomonic for ventricular tachycardia. Unfortunately, this finding is not often seen, and it's only 21% sensitive. But if you see it, it's 100% specific for ventricular tachycardia. Here's another example of an AV dissociation. If you look especially at the beginning of the strip, I use the black arrows to highlight where I think P-waves are marching through the strip. And notice that they're marching at a rate different than the QRS complexes. For some of the beats, it's hard for me to see any atrial activity because they're buried within the QRS complexes. But overall, I'm pretty confident this ECG shows AV dissociation. All right, so let's take a look at another ECG. This ECG was obtained from a 70-year-old man who was recovering in a surgical ICU after an exploratory laparotomy. His nurses noticed that he had significant ectopy on telemetry, and so they performed this ECG. And they came to the cardiology team to ask if this is ventricular tachycardia or not. So using the scan criteria, the first criteria is AV dissociation, and it's hard for me to see if there's P-waves marching through the strip or not, although it's possible that you could see such activity in lead V1. Even more prominent, though, is the fact that you see capture and infusion beats, as highlighted by the arrows here. Look at the fourth beat, which shows a capture beat. A capture beat essentially is a normal QRS complex that's interspersed among ventricular beats. This means that you see a breakthrough of normal depolarization occurring in between each ventricular beat and its path of mounting for ventricular tachycardia. The dotted lines, dotted arrows, indicate fusion beats, and what's happening here is that this beat kind of looks like a combination of a ventricular beat and a regular QRS complex. When that happens, it means that part of the ventricle is captured from the depolarization through the AV node, and part of it is through ventricular depolarization. So it looks like a hybrid beat in between a normal QRS complex and a ventricular beat. If you see a capture beat or a fusion beat, it's path of mounting for ventricular tachycardia. Here's an even better example of capture and fusion beats. This CCG was obtained from a 50-year-old woman who came in with an anterior ST segment elevation MI, underwent successful cardiac reperfusion, and then showed up in the cardiac intensive care unit for further monitoring. Because she also was noted to have significant activity, she had this ECG performed. Notice here the examples of fusion beats, which I've highlighted with the solid arrow. Notice that these beats look like a combination of a ventricular beat, as shown in the first three beats, and a normal beat, which is the QRS complex in between each one of the fusion beats. This is path of monic for ventricular tachycardia. I should note that this ECG actually doesn't show ventricular tachycardia, and the reason is that the ventricular rate is too slow. It's below 100. But this ECG does show that the patient has a ventricular rhythm. So what this rhythm is actually called is accelerated idioventricular rhythm, and it's often seen in hours following successful PCI of an artery. It's a reperfusion arrhythmia. So if you see a slow ventricular arrhythmia that's regular, you should celebrate, because it means that the patient has been successfully reperfused after a myocardial infarction. It needs no specific treatment. All right, so moving on to this ECG, you'll notice this patient has no AV dissociation and also has no capture or fusion beats. Therefore, you want to move on to the last scan criteria, which is looking for extreme axis deviation and a initial R wave and lead AVR. And in this case, this patient has this. So this is a pathomonic for ventricular tachycardia, and that's what this patient ended up having. So if none of the scan criteria are positive, then it's important to move on to the zoom criteria and focus on the precordial leads. So let's take a look at this ECG. Is this VT? So if you look carefully at lead V1 through V6, you'll notice that all of them are positive. So this is pathomonic for precordial concordance, and it's also pathomonic for ventricular tachycardia. Take a look at this ECG, and again, focus on the precordial leads. What you'll notice is that all of these leads show precordial concordance as well, except this is in the opposite direction. They're all negative. Once again, this is pathomonic for ventricular tachycardia since it's 100% specific for it. Let's move on to this ECG. This patient doesn't meet any scan criteria, and there's no evidence of precordial concordance. So we want to move on to the next zoom criteria, which is looking at the RS interval. Focusing especially on lead V5 here, you'll notice that the beginning of the R wave to the nadir of the S wave is greater than 100%. So this is 66% sensitive and 98% specific for ventricular tachycardia. Note that you could use any RS interval as long as it comes from one of the six precordial leads. I should also note that the patient has other criteria for VT here, including a YQRS complex and an atypical bundle branch block pattern. But the thing that cinches it early on is that the fact that the RS interval is greater than 100 milliseconds. So this ECG was obtained from a 63-year-old man with shortness of breath and chest pain. He already has a known history of ischemic cardiomyopathy with an EF of 10%. While he was transferred to the cardiac intensive care unit, multiple salvos of tachycardia were noted. Then he had this ECG performed. I don't see any evidence of obvious scan criteria, so then I wanted to move on to zoom criteria. What's most striking is that he has a wide QRS interval, which was 162 milliseconds. And since he has a right bundle branch block pattern, when you look at lead V1, this is more suspicious for VT. So he meets this criteria and this ECG shows that he has ventricular tachycardia. Here's another example of ventricular tachycardia. In this case, this is in a patient with a left bundle branch block pattern on his ECG. Notice for here that the QRS duration has to be greater than 160 milliseconds. In this case, this patient's QRS interval was 176. So this is highly suspicious for VT. All right, so let's take a look at this ECG. We've gone through basically all the scan criteria, and now we've gone through all the zoom criteria except for the last one, which is looking to see if the patient has a typical or atypical bundle branch block pattern. So when you look at lead V1 and V6, this patient doesn't have a typical bundle branch block pattern. When you see that, then that's more concerning for ventricular origin. And so that's what this patient had. The patient had basically essentially a ventricular tachycardia because he met this criteria. So just as a reminder, a typical right bundle branch block morphology looks as follows. You want to first look at lead V1. You want to first determine does the patient have a wide QRS complex, and if that's the case, then it should be greater than 120 milliseconds. When looking at lead 1, you tend to see either a rabbit ear pattern, so an RSR pattern or a QR pattern. And then when you look at lead V6 and lead 1, you'll see a slurred S wave. For left bundle branch block morphology, you would see a QRS duration that's typically greater than or equal to 140 milliseconds. And in lead V1, there would be a negative deflection there. Looking at V6 and lead 1, you'd see more of a monomorphic R wave pattern and no Q waves. So those are your typical left bundle branch block morphology and typical right bundle branch block morphologies. If you see a Y complex tachycardia that doesn't have either one of these typical morphologies, then it's highly suspicious for ventricular tachycardia. So just to review, when you're looking at a patient with a Y complex tachycardia, you want to use the scan and zoom criteria to determine if the patient has ventricular tachycardia or not. Using the scan criteria, you want to look at the entire ECG for evidence of AV dissociation, capture beats, fusion beats, or extreme axis deviation with an initial R wave and AVR. If the patient doesn't meet any scan criteria, then I zoom to the precordial leads and see if the patient has precordial concordance, a wide RS interval, a wide QRS complex, or an atypical right or left bundle branch block pattern. If the patient meets any one of these criteria, then the patient most likely has ventricular tachycardia. And these criteria have a sensitivity and specificity that are greater than 90% for detection of ventricular tachycardia. What if the patient with a Y complex tachycardia doesn't meet any of the scan and zoom criteria, but you're still suspicious for ventricular tachycardia? What are the possibilities then? Well, the first thing is that the rhythm might still be ventricular tachycardia, and this can occur in less than 5% of patients. The other possibility is that the rhythm is a variant of supraventricular tachycardia associated with a wide QRS complex. In most cases, this is due to a preexisting bundle branch block. So it's very important to obtain a baseline ECG to compare QRS complexes. The other possibility is the patient has a rate-related bundle branch block. Take a look at this ECG. This was obtained in a 54-year-old man with COPD and respiratory failure. So because it's a Y complex tachycardia, you want to ask yourself, is this VT? So this patient doesn't meet any of the scan and zoom criteria. The patient doesn't have AV dissociation. I can't see any capture or fusion beats. And there's no evidence of extreme axis deviation. Focusing on the precordial leads, there's no precordial concordance. The RS interval appears to be less than 100 milliseconds, and it's actually only really present in lead V6. And the QRS complex is slightly less than 140 milliseconds. So the last criteria is looking to see if this is a typical or atypical bundle branch block. And this looks like a typical right bundle branch block, so it doesn't meet that criteria either. So when we were evaluating this patient, we were highly suspicious that this patient might have a supraventricular arrhythmia. In any case, because we weren't 100% sure, we treated the patient with amiodarone therapy, which slowed down the heart rate. And notice here that you might be able to see the beginnings of flutter waves in lead 2, 3, and AVF. This was even more obvious a few minutes later when the rate slowed even further, and it was obvious to see the typical atrial flutter pattern. So this patient had atrial flutter with a preexisting right bundle branch block. So this ECG was obtained in a 64-year-old woman with seizures and persistent altered mental status. And because it's a wide complex tachycardia, we were suspicious for ventricular tachycardia. However, this patient also had no scan or zoom criteria. She had no AV dissociation. She had no capture or fusion beats. And she had no extreme axis deviation. The zoom criteria were also negative. She didn't have precorial concordance. Her RRS interval could only really be checked in lead V4 and was less than 100 milliseconds. And her QRS complex was in the high side, but it was 144 milliseconds, which is not diagnostic in patients with a left bundle branch block. Finally, when interpreting the QRS complexes, this patient has a typical left bundle branch block pattern. So that's also not consistent with ventricular tachycardia. Nonetheless, this patient was also treated with ambioterone, which slowed down the heart rate. And notice when the heart rate was a little bit slower that you could start to see P waves at the tail end of each T wave. And then a few hours later, the heart rate's even further slowed. This becomes especially obvious that this patient has a preexisting left bundle branch block. So what was that initial ECG? It basically showed that the patient was in sinus tachycardia with a preexisting left bundle branch block. So for this ECG, it was obtained from an 80-year-old woman with hypercapnic respiratory failure and pneumonia. And this patient didn't meet any scan and zoom criteria, but was treated with ambioterone because there was concerns that this patient could be having a supraventricular tachycardia with aberrancy. This is what happened with amiodarone administration. Take a look at the rhythm strips carefully, and I've highlighted the normal beats with the solid arrows. Essentially, what the patient has is narrow QRS complexes when the RR interval increases. And then as the heart rate speeds up, then the patient develops a rate-related right bundle branch block. So this is basically showing—the previous strip basically showed a rate-related right bundle branch block due to a supraventricular tachycardia. So just to summarize, patients can have supraventricular tachycardia with rate-related bundle branch blocks. These typically occur at higher heart rates, and they're most commonly seen in patients with atrial fibrillation with rapid ventricular response, where it's described as Ashman's phenomenon. In most cases, the bundle branch block that tends to occur is a right bundle branch block, and that's because the right bundle has a longer refractory time. If a patient has a rate-related left bundle branch block, that's extremely unusual, and it usually implies infrahissian conduction system disease. Most of these patients eventually will need a pacemaker. So just to review, patients who don't meet any scan or zoom criteria can have—or uncommonly can have—ventricular tachycardia, or they could have a supraventricular tachycardia with a pre-existing bundle branch block or a rate-related bundle branch block. For these reasons, it's critically important to obtain a baseline ECG when the patient is not having the arrhythmia. So it's important to keep a few caveats in mind when using the scan and zoom criteria. With some conditions, the scan and zoom criteria could be positive in the presence of electrolyte abnormalities or ingestion of toxic substances. They're also often positive with ventricular pacing, which makes sense since the pacer is pacing the actual ventricular tissue, or if an accessory pathway is present. In many cases, patients with accessory pathways can have very wide QRS complexes, and it can be hard to differentiate if the patient has a supraventricular or ventricular arrhythmia. So in these cases, it's important to treat the underlying tissue—to treat the underlying issue and treat the patient as if they have ventricular tachycardia until more information is obtained. So here's an example of this. So when you're looking at this ECG, you see multiple scan and zoom criteria for ventricular tachycardia. There's a fusion complex in the middle of the ECG. There's extreme axis deviation with initial R wave and AVR, and there's a wide QRS complex. However, this patient doesn't have ventricular tachycardia. Instead, they have pacemaker-mediated tachycardia, and if you notice here that the pacemaker is firing at about 120 or 130 beats per minute. This is especially obvious if you take a look at each QRS complex, and you'll notice a small pacemaker spike in front of each one of these things. So let's take a look at this ECG. In this case, you see multiple scan and zoom criteria with extreme axis deviation with initial R wave and AVR, evidence for precordial concordance, a wide QRS complex, and an atypical bundle branch block pattern. So it's highly suspicious for ventricular tachycardia. However, you also see these ventricular pacer spikes, especially in the beginning of the strip. But notice that these ventricular pacer spikes are not capturing the ventricle. They're occurring at a different rate, and they're much slower than the ventricular rhythm. So in this case, this is ventricular tachycardia, and the only caveat is that the ventricular pacer is also trying to pace the ventricle. So for this ECG, it was obtained in a 42-year-old abounded man with end-stage renal disease and intermittent dialysis. So when you look at this ECG, you want to determine if this patient has VT. With this history alone, you know that this patient probably has hyperkalemia, and hyperkalemia could significantly lead to QRS widening. And that's probably the most likely explanation for his wide QRS rhythm. And so even though he meets multiple scan and zoom criteria, including a wide RS interval, a wide QRS interval, and atypical bundle branch block, the treatment of choice for him would probably be dialysis. Here's an ECG that was obtained after emergent dialysis was performed, and if you notice, the QRS complexes are now much narrower, and it's a much more normal-looking ECG. So this ECG was obtained from a 45-year-old woman with a history of paroxysmal atrial fibrillation who was treated with rhythm control therapy with flecainide, who developed severe dyspnea and palpitations. She had this ECG. So is this VT? Notice that the patient has a wide complex tachycardia with extreme axis deviation, wide RS complex, a wide QRS complex, and an atypical bundle branch block. However, this is not VT. It's actually due to a sodium channel blockade from the flecainide, and it's basically a wide complex tachycardia for a minute. When this happens, it's basically a toxic ingestion of flecainide. You can often see B2B variability in the QRS complexes, and I've seen that with a number of different toxic ingestions, but it's not present in this case. For this patient, we allowed the flecainide to wash out of her system, and this is her ECG 36 hours after stopping it. Notice how the QRS complexes are now narrower than they were before, and she has a more normal-looking ECG. This ECG was obtained from a 25-year-old man with sudden onset of palpitations, dyspnea, and presyncope. Because of his palpitations, he also had an ECG drawn which showed this wide complex tachycardia. So is this VT? In his case, it looks like VT. He had multiple scan and zoom criteria, including a wide RS interval and a wide QRS complex, and because of that, he underwent urgent cardioversion. This is the ECG after cardioversion. Although the patient now is in sinus rhythm, notice that his QRS complexes are not normal. He has a short PR interval and a wide QRS complex with a delta wave at the beginning of each QRS complex. This is consistent with him having an accessory pathway, and this is diagnostic for Wolff-Parkinson-White syndrome. Now that we know this information, the preceding ECG differential diagnosis changes. Ventricular tachycardia becomes much less likely, and it's much more possible that the patient had antedromic AV-reciprocating tachycardia. In other words, there's a reentry tachycardia that goes down the bundle of Kent or the accessory pathway and goes up the AV node. For these patients, prompt cardioversion is necessary, and you could even block the circuit by blocking the AV node. However, he's likely to go into the rhythm again, so definitive treatment should be considered by ablating the accessory pathway. For this particular patient, he was discharged from the hospital after this arrhythmia, and then had a follow-up electrophysiology ablation a few months later. Since then, he's been doing fine with no cardiovascular issues. Let's take a look at another patient with WPW syndrome. This ECG was obtained in a 27-year-old man with palpitations, dyspnea, and hypotension. And so the main question here is whether this patient had polymorphic ventricular tachycardia or not. And notice that he has multiple scan and zoom criteria for ventricular tachycardia, including precordial concordance, a wide QRS complex, at least for most beats, and an atypical bundle bench block pattern. However, we already know that patients with WPW have accessory pathway, and that could affect ventricular depolarization and repolarization. So these criteria may not be as valid. Some things to make you suspicious of that this is super ventricular in origin is the fact that this is an irregular rhythm, that there are varying QRS morphologies, and that there's a clear delta wave, at least in lead V5 and V4. So the constellation of these findings are most consistent with atrial fibrillation with accessory pathway present. Knowing this information, you can understand why the QRS morphology varies in width and appearance. The reason is because there's intermittent conduction or depolarization of the bundle of KENT and of the AV node due to the inherent chaotic nature of atrial fibrillation. Thus, you have variable depolarization of the ventricle, depending on when impulses are transmitted in those two areas. When you see a patient with this type of arrhythmia, you want to focus on blocking depolarization down the bundle of KENT and favor conduction down the AV node. Thus, the treatment of choice would be treating with procainamide, which slows down atrial and ventricular depolarization, as well as in the bundle of KENT. Interestingly enough, it also doesn't really block the AV node, which is good. You really want to avoid using drugs that preferentially block the AV node, such as beta blockers, calcium channel blockers, and other medications, because that would lead to unopposed depolarization of the bundle of KENT. This could lead to a paradoxical increase in the ventricular rate and predispose the patient to ventricular fibrillation. This was the ECG that was obtained a few minutes after starting procainamide therapy. Although the patient still has evidence of an accessory pathway and a wide QRS complex, notice that the rate is now slower, which is probably due to slowing of conduction down the bundle of KENT and in the ventricles. So you could say that the procainamide made a difference in this patient's condition. In addition, it's probable that the patient's risk of ventricular fibrillation dropped with this type of therapy. Definitive treatment for this patient likely requires an electrophysiology procedure, because he would need ablation of accessory pathways and also cardioversion to restore sinus rhythm. Here's a more contemporary example of atrial fibrillation with WPW that was published in New England Journal of Medicine. Take a look at panel A, which shows a wide complex tachycardia that's irregular and has QRS morphologies that vary in appearance and width. Notice also the QRS complexes highlighted by the small black arrows, which show a clear delta wave at the first part of the QRS complex. The constellation of these findings is characteristic of atrial fibrillation with WPW. In this patient's case, they received procainamide therapy, and then the second ECG was obtained. Procainamide was able to convert the rhythm back into sinus rhythm, and then it's obvious that the delta wave remains present since you could see it in lead V4 and in lead I. For this particular patient, they subsequently underwent an electrophysiology study and ablation of the accessory pathway, and did fine afterwards with no complaints for at least 18 months afterwards. Let's move on to another condition. This ECG was obtained in a 65-year-old woman with chronic pain and opioid abuse who presented with pneumonia and altered mental status. This ECG was obtained after significant ectopy was noted in her telemetry monitoring. Notice that this patient had a wide complex tachycardia with QRS complexes that varied in morphology, amplitude, and axis. This is essentially diagnostic of polymorphic ventricular tachycardia. There are two types of polymorphic ventricular tachycardia. For this particular patient, the patient had torsades des points, which is a polymorphic ventricular tachycardia associated with characteristic twisting of QRS axis and amplitude. It also requires that the patient have a long QT interval prior to developing the ventricular tachycardia. In other patients, they just have polymorphic ventricular tachycardia without a long QT interval. This is typically associated with acute myocardial infarction. And it's not classified as torsades des points. And either type of arrhythmia is inherently unstable and should be aggressively treated. You should probably know that there's many causes for QT prolongation that could lead to torsades des points. In an ICU setting, patients who have electrolyte disorders or menomalic derangements are more likely to develop QT prolongation. In addition, there's a ton of medications that could lead to a prolonged QT interval, especially antibiotics such as for quinolones and macrolides or antifungal agents, antipsychotics, methadone. Illicit drugs could do this as well. And we shouldn't overlook that patients could also have intrinsic abnormalities in their heart, whether it's due to coronary disease, infarction, myocarditis, et cetera, or electrophysiologic causes, all of which could cause prolonged QT interval and then subsequent polymorphic VT and otherwise known as torsades. We've already discussed ventricular tachycardia, polymorphic ventricular tachycardia. I also want to briefly mention ventricular fibrillation, which was found in this patient who had chest pain and shortness of breath. Obviously, you don't have much time when you develop ventricular fibrillation, and you should perform immediate ACLS and synchronized cardioversion. This is another example that was not captured on electrocardiography, but rather on telemetry monitor. Notice the telemetry tracings on top, which showed the patient has an irregular, chaotic, coarse ventricular fibrillation. Also notice that the patient still has atrial activity as demonstrated by the A waves in the CVP tracing. In either situation, you want to aggressively resuscitate the patient by cardioverting the patient and performing CPR. We spent a lot of time discussing how to diagnose ventricular tachycardias and spent a few slides discussing ventricular fibrillation. Let's now focus on management of these ventricular arrhythmias. In most cases, ventricular tachycardia, and for all cases of ventricular fibrillation, these rhythms are inherently unstable and require ACLS and cardioversion, followed by antiarrhythmic therapy. For some patients with ventricular tachycardia, you have a little bit more time, but you should still consider cardioversion expeditiously and consider antiarrhythmic therapy. Once that's been stabilized, once the ventricular arrhythmia has been addressed, it's also important to determine and treat the underlying causes. On the right-hand side is a list of all the arrhythmia causes, which we've discussed before, and I'm just putting it here for your reference. These conditions should be identified and addressed. In patients who have had their underlying causes managed well, but still have episodes of ventricular tachycardia or ventricular fibrillation, they often need expert opinion and management by an electrophysiologist. In some cases, performing an electrophysiology study and ablating the foci causing ventricular tachycardia could be curative. These same electrophysiologists could also consider whether the patient is a candidate for an implantable cardioverter defibrillator, since most patients who have had episodes of ventricular tachycardia or ventricular fibrillation are also predisposed to redeveloping this condition. So, placing an implantable cardioverter defibrillator is critically important to prevent further episodes of sudden death. I want to briefly discuss the pharmacologic therapies for ventricular arrhythmias. For hemodynamically unstable ventricular tachycardia or ventricular fibrillation, there's really only two important therapies. The first is amiodarone. For unstable patients, you'd want to give 150 mg over 10 minutes, but for those who need CPR, you'd want to give a 300 mg bolus of this medication. If the patient is then able to be stabilized, then you'd want to consider this initial therapy with an IV infusion, starting at a rate of 1 mg per minute for 6 hours, then decreasing the rate to 0.5 mg per minute for 18 hours. An alternative therapy to amiodarone is lidocaine, which is especially useful in patients who have ischemic cardiomyopathy. If you decide to use this medication, you initially want to give a bolus of 1 to 1.5 mg per kilogram, which may be repeated. Following this initial therapy, then you'd want to have an IV maintenance therapy starting at 20 mg per kilogram per minute as an infusion. For patients with hemodynamically stable VTA, you could consider prokaryotomyotherapy instead. This medication tends to be safer and associated with less major adverse cardiac events than amiodarone, and actually may cause faster pharmacologic termination of stable ventricular tachycardia than amiodarone. For me, it's becoming a much more popular option for those who have hemodynamically stable ventricular tachycardia. If you decide to use this medication, you want to administer 10 mg per kilogram over a 20-minute period, then decrease the infusion rate to 2 to 3 mg per kilogram during the next 24 hours. I should note that, as I mentioned earlier, that prokaryotomy is probably the treatment of choice for WPW-associated Y-complex tachycardias as well, since it's the best medication to decrease conduction down the bundle of CANT. In addition to amiodarone, lidocaine, and prokaryotomy therapy, you could also consider a beta blocker or metoprolol for managing ventricular arrhythmias. It's not all that useful for managing acute episodes of ventricular arrhythmias, but it's one of the best medications for suppressing future ventricular tachycardia or future ventricular fibrillation episodes. Finally, you could also consider using magnesium therapy. This has been evaluated in a number of different case scenarios, and it's only been found to be useful in patients with torsades de pointes. If the patient does have this type of arrhythmia, then you want to give a 2-gram bolus, which should be repeated as needed, followed by an infusion of 2 to 4 mg per minute. Note that magnesium is ineffective for any other type of arrhythmia. Thank you for listening to this talk. I want to leave you with a few concluding thoughts. First, I hope the scan and zoom criteria is simple and could be incorporated into your practice. For me, it's offered a relatively straightforward framework for differentiating Y-complex tachycardias and for diagnosing ventricular tachycardia. That being said, I wouldn't spend too much time poring over an ECG to determine if it's ventricular tachycardia. If a patient is not doing well, treat the patient as if they have ventricular tachycardia and then figure out the diagnosis later. The second point is that even if you expeditiously treat ventricular arrhythmia, make sure that you look for and treat the inciting cause for the arrhythmia, since the arrhythmia may come back if you don't do that. My third point is that if you see an irregular rhythm and varied QRS beats, you have to rule out two conditions. The first is torsades de poids or polymorphic ventricular tachycardia, and the second, much more rare, is atrial fibrillation or WPW. Both of these conditions require a specific treatment, so it's best to recognize this early. Finally, even in patients who seem relatively straightforward, there's nothing wrong with asking for help in diagnosing and differentiating a Y-complex arrhythmia. That being said, you want to do this after stabilizing the patient. Thanks again for listening to this webinar. Thanks again for listening to this webinar. I know we went over a lot of material, so feel free to email me at the email listed on this slide if you have any further questions or want clarifications on anything I said. I'd be happy to answer any of your questions. In the following two slides, I've also provided a list of references that I thought were useful in preparing this talk. The ones with three asterisks indicate the highest yield of references. Thank you.

ventricular arrhythmias

ICU environment

ventricular tachycardias

supraventricular tachycardias

monomorphic ventricular tachycardia

polymorphic ventricular tachycardia

treatment approach

electrophysiologist