All right, same concept for ventricular arrhythmias. They're bad and you want to approach them the same way as SVTs. If the patient is basically coding, you want to follow the algorithm and get them out of it as fast as possible. But if not, then you have time to think about determining the cause because you want to get them out of it. In the ICU setting, the five ones that I tend to see are patients who have electrolyte abnormalities and that's been talked about earlier, like patients with potassium abnormalities or magnesium or calcium. MI could do this frequently, cardiac ischemia or history of myocardial infarction. Cardiomyopathies, basically having heart failure due to another cause. Mechanical irritation, central lines that are in too deep, or maybe they've had tamponade from whatever or trauma. And toxins and medications. Those are basically the causes of fast heart rhythms in the ventricles. So here's one. Here's a patient, comes in, in your ICU, develops this rhythm. So what's the difference between this one and the other ones I showed you? It's wide, right? All right, so how do you define this, number one? So basically, is the QRS complex wider than 120 milliseconds? And the second thing is the patient's aortic. If you meet those two criteria, you have a wide complex tachycardia, right? And if that's the case, there's only two possibilities for this, right? Either they have ventricular tachycardia, so the beats are originating in the ventricle, or it's a supraventricular tachycardia with a wide QRS complex. So something's delaying depolarization of the ventricles. But either way, if the patient's hypotensive, or they're in shock, or they're coding, you don't care. Just get them out of it, right? And then you can figure out a diagnosis later. The converse is also true. If the patient's stable with a wide complex tachycardia, it does not mean that they don't have VTAC. If you take, let's say, a 25-year-old gentleman who's walking around in VTAC with a structurally normal heart, they will walk around with VTAC for weeks before their heart starts failing, right? They'll say, maybe I have palpitations, or shortness of breath, or I can't run a marathon now, but they'll be fine. Now, it's the patients, of course, that have EFs that are 30% who have developed VTAC. Those patients will collapse much quicker. But even then, you might have some time, and they might be hemodynamically stable earlier on. So clinical stability does not mean that you don't have VTAC. The other thing is that most wide complex tachycardias are VT, and your bias should be that this is VT. If you have a history of heart disease, it's almost always VT, right? It's greater than 95%. And if you're older than 35, which some of us in this room are, you're more likely to have VT. And if you can't figure it out, well, guess what you're treated as? VT. All right. I think I've drawn this home, right? All right. All right. So how do you figure out if it's VT if you're not sure between the two? What I use is the scan and zoom criteria, which is kind of a combination of Marriott, Brugada, and a few other references. But it's basically, you scan the whole ECG looking for these four criteria, and then you zoom to the precorial leads. I'm going to go over this quickly in the next 10 minutes, but I'll explain each one. So the first one is to look for precorial concordance. Why? Because this is 100% specific. If you see precorial concordance, it means you're in VT. What is precorial concordance? Your P waves are marching at a rate, and your ventricles are marching at a different rate, and there's no relationship between the two of them. That's it. So here's an example of it. I put arrows on it where you see the P waves basically just marching along with no relationship to the QRS complexes. This is impossible to happen unless you have something beating in the ventricle. It must be VT. That's why it's always the first criteria. Now the issue is once the heart rate starts getting higher, it's hard to see those P waves. So it's only present in about 20, 30% of patients. So it's less specific. Excuse me. It's 100% specific. I have to pay attention to John's lecture better from the morning. It's 100% specific, but it's only 20 to 30% sensitive. Here's another thing. What about this one here? How do you know this is VT? There's a funny beat here that are there. It's called capture and fusion beats. So basically what this is is you have a VT beat, a VT beat, a VT beat, and then a normal beat goes through. So that must be coming from the top chambers. Then VT, VT, VT, and then another one is kind of a fusion between the two beats, between a normal beat and between a VT beat. And then you see another one a few beats later. This is pathomimonic for VT. So the first criteria is what is it? So AV association. The second and third one is capture beat and fusion beat. If you see this, it's pathomimonic for it, 100% specific. Here's another example of capture and fusion beats. But is this a ventricular tachycardia? It's a wide complex rhythm, but it's not fast enough. This is actually a slow ventricular rhythm. It's called accelerated ventricular rhythm. And often you see this in patients who've had MIs and have had a successful reperfusion. They'll oftentimes have this slow ventricular rhythm for a few hours afterwards. You should celebrate this because it's reperfusion. The ventricle is basically happy to be having oxygen again. All right. All right, what about this one? This is the last scan criteria. So we've looked at AV association, capture beats, fusion beats. This is the last one, which is you have extreme axis deviation. Your axis, instead of being leftward or inferior, which is the way the heart normally conducts, is rightward and superior. So if it's rightward and superior, where must it be coming from? The ventricle must be coming from the apex of the heart, right? So this is the criteria for it. If you have extreme axis deviation and you have an initial R wave and AVR, pathomimonic for VT. It's more than 97% specific. All right, so what are the four criteria? AV association, capture, and then extreme axis deviation. All right, awesome. So you guys are doing great. So now, let's say the scanning criteria is not there. Then you start looking and focusing on the precorial leads. And so this is the first one here. The reason why this is VT is because you have precorial concordance. Notice V1 and all through V6. What is the direction? Which way are they deflecting? They're all positive. That is impossible unless it's coming from the ventricle, right? Because in a normal heart, V1, it should be down. And in V6, it should be positive. But in this case, they're all positive, in which case they must be coming from the ventricle. Here's another example. The opposite. It's called negative concordance, right? They're all negative, right? And so again, it must be coming from the ventricle. The next criteria is to look at the QRS, having a wide RS interval. I don't have a good way of remembering this, other than just saying you have to memorize it. This is part of the Brugada criteria. If your RS, in other words, the beginning of the R wave to the bottom to the most negative deflection in any of the precorial leads is more than 100 milliseconds, that means the conduction is really, really prolonged and it must be going through myocardial tissue and it must be starting in the ventricle. So if it's more than 100 milliseconds, it's consistent with VT. And that's the case here. Here's another example. This is, in this case, the third criteria, which is a wide QRS complex. There's a caveat to this, is that if you already have a wide bundle branch block, it's going to be wide anyway. So this is in patients who don't have wide QRS complexes. And the criteria here, again, you have to memorize it. QRS complex greater than 160 milliseconds for left bundle, or greater than 140. And then the last one is, does it look like a bundle branch block or not? Does this one look like a bundle branch block? No, because V1 looks funny, right? It doesn't look like a right bundle, it doesn't look like a left bundle. So that's actually, I don't know how sensitive or specific it is, but I find that electrophysiologists use this criteria a lot. All right. We'll just skip this stuff. So here are the criteria. So let's say them all together. So for the scan criteria, what are the four? A of association. All right. So then you zoom to the precorial leads. And what's the first criteria there? Precorial concordance. Then you look, and this is the Brugada one, the wide RS. You don't have to memorize 100 milliseconds, I hope. But I do. And it's greater than 100 milliseconds. The wide QRS complex, and then the atypical bundle branch block pattern. All right. You did it. So just a reminder, the reason why I went in this specific order is they're an order of specificity. If you have AV dissociation, you don't need to go through any of the other criteria because you already know you have VT. The same thing goes if you have capture or fusion beads. All right. All right. What if there's no scan and zoom? What if none of the criteria are positive? Well, it still could be VT, or it might be an SVT with a wide QRS complex, like somebody with a preexisting bundle branch block or a rate-related bundle branch block. I'm just, in the interest of time, I'm just going to skip all this stuff. But this is a patient, for example, that we weren't sure what it was, and it turned out they just had a typical right bundle branch block. Here's another example. In this case, this patient had a typical left bundle branch block. All right. I'm going to skip all this stuff here. Here's an example where it's coming from the ventricle. It looks like VT, right? But in this case, it's basically pacemaker. The pacemaker is pacing at a rate of 120. I'm just going to skip all this stuff. This one here is just an example of hyperkalemia causing a wide complex rhythm. And it's not VT, technically, it's just the conduction is so slow because of the too much potassium that it's widening. And this is another example. Instead of potassium, it's really flecainide-induced. All right. This is the same ECG I showed before, the 25-year-old with WPW. WPW, all bets are off. You can't interpret it anyway, so you can't tell if it's VT or not. All right. What's this one? This one's not like any other ECG I showed before. Are you brushing your teeth? Or it could be torsades, right? So this is torsades. So when you see this, the differential is basically there's two options. One is if to call it torsades, it basically requires a polymorphic VT, and you have to have a long QT interval before that. If you don't have a long QT interval, you can't call it torsades. You just call it polymorphic VT. That is most often seen in patients with acute MI. So if you see somebody with a normal QT interval, and then they go into polymorphic VT, that's acute MI. All right. If you have torsades, in other words, a long QT interval before the polymorphic VT, the causes are astronomical, right? I mean, there's a whole websites that are devoted to the medications that could cause long QT intervals, right? Basic ones are antiarrhythmics, some antibiotics, antidepressants, antipsychotics. But in my world, heart disease is a big one. So patients with heart disease have problems with conduction. Electrodyte disorders are also notorious for doing this in illicit drugs as well. People with brain injury also get long QT intervals. All right. This is a true ECG, by the way. This is a patient who... What rhythm is this one? How they got this ECG, I don't know. This is V-fib. So the patient had V-fib while they're in the middle of getting ECG, which is amazing. He did fine. He got shocked out of it, then went to the cath lab. So this is V-fib. All right. So obviously, this is unsustainable. So for any one of these Y complex rhythms, if it's ventricular in origin, whether it's VT, polymorphic VT, or VF, you want to determine the urgency of it. Obviously, all V-fib is emergent. You want to code them, right? If they're unstable, go along the ACLS and cardioversion pathway, and then you want to follow up with anti-rhythmic therapy, right? But if you're stable, then you have time to think, okay, should I cardiovert them right now or should I figure out the cause of it or admit them to ICU and consider other interventions? So you have some time. And you want to go basically through this algorithm here, basically look through the causes and find out what was the potential cause for their VT or VF. Here are the pharmacologic therapies for VT and VF. A lot of us use amiodarone just because we're all familiar. It's good for lots of different arrhythmias. And basically, for unstable patients, you could do 150 milligrams over 10 minutes. But if they're coding, you need to give them 300 milligrams push, right? And then afterwards, with either situation, you want to put them on an IV infusion afterwards. An alternative is to use lidocaine, and that's especially helpful for acute MI-associated ventricular arrhythmias. And it's in the guidelines. You could use that as a medication, although I feel like it's less commonly used now than it used to be. If you have hemodynamically stable VT, so if you're not unstable, you could use procainamide instead of amiodarone or lidocaine. And actually, procainamide is actually a better drug and works faster than amiodarone. There's a big caveat. You have to be hemodynamically stable. If you're not stable, you can't use it. What about beta blockers? Beta blockers are the number one medicine to prevent VT and VF. Number one prevention drug. The issue with them is that they don't treat it. So if you're already in VT, you can't get out of it with giving metoprolol, but you could prevent future episodes by giving it. And then the only indication for giving magnesium is for patients with torsades de poids. And you could give as much magnesium as you want. I know we had a thing about hypermagnesemia. You're going to be fine. You could give as much as you want. All right. So that's really the causes for the Y-complex tachycardia.

ventricular arrhythmias

supraventricular tachycardias

electrocardiogram

antiarrhythmics

defibrillation