Karyn M. Austin, MD, discusses common variants and red flags for pediatric ECGs.
Good afternoon, everyone. Right. That looks good. Great. Um, So, first, thanks for inviting me to speak today. I really wanted this to be an extremely practical um representation of the types of ECGs that you oftentimes come across in the outpatient or primary care setting. And then some of the kind of can't miss things that either, um, you know, definitely need referral to a cardiologist or those that should go straight to an electrophysiologist. So just to start off, I have no financial disclosures in terms of our outline. It's really straightforward today. I'm actually not going to spend a lot of time on sort of how to read EKGs. I think everyone is really at the point that they probably have their own system and it's not really worth trying to undo or redo that. But I did want to bring some attention to a few basics that I think get overlooked, which really help us interpret EKGs, and then a couple features of the quality of the EKG that can allow us to appropriately interpret it. Then we're going to go over the common variants. I think these are things that you folks will see all the time, either coming back on ECG reads or if you have the capability in your office to do an ECG, they might come back on an auto read and kind of what to do about them and if they require referral. And then some of the red flag things, these are things that require a referral to a cardiologist and or an electrophysiologist. And I really wanted this to be an example or to be a talk where we gave examples of each one. And uh very specific guidance about what the recommendations would be. So, in terms of ECG tips, if we think about reading EKGs, it's actually not that hard, but it does take a lot of practice, as is the case with most things in cardiology. Um, and for me, the most important thing is that it requires discipline, and really the goal is not to be able to identify very wild, crazy things on an EKG. It's to feel very confident when it's a normal EKG and to confidently call it normal. So, I always love to bring up this study. This was done, oh gosh, maybe late 90s, early 2000s now, done at Brigham and Women's Hospital where they took a bunch of radiologists and they had them look at CT scans. And essentially, the radiologists all found the nodule in the lower right lung. Every single one of them identified it. But 83% of the radiologists missed the fact that there was a gorilla in the top left lung. And that is because we have a confirmation bias. When we see something that reinforces the, I got it, we very quickly forget to look at all the other features, and we see that. Very commonly with EKG reading. And that's always what I draw your attention to, and that's what I tell my fellows and the residents. Discipline is the single most important thing. Don't start with the obvious thing. Start with the technique that allows you to go through the EKG in a systematic way so you don't miss, um, other important findings. So, when we think about the EKG, I think it's important to have a basic understanding of what the leads are and what they look for. So, we think about this as in limb leads and precordial leads. And the limb leads are really looking at the axial plane or the frontal plane, and they can be broken. Down into two different versions, what we would call bipolar versus unipolar. And bipolar, what that means is the way that I describe it to the fellows is if you can touch both points in that circuit, you can touch the positive pole and the negative pole, then it is a bipolar circuit. And if you think about how the stickers are aligned, it's right arm, left arm, and left leg. As an aside, the right leg is not part of an EKG. It is not part of Eindhoven's triangle. It's actually a ground, and it's used to filter out noise just for those interested. But if we think about the bipolar leads, if I'm traveling, um, electrically speaking from the right arm to the left arm, that is lead one. And so I can touch both the positive and negative poles in those situations. So we would consider that a bipolar lead. Unipolar leads, on the other hand, Are reflective of usually a ground, um, either mathematical ground or real ground, plus a sticker. So in the case of the augmented limb leads, these are using a ground called Wilson Central Terminal, which is again a mathematical ground in the center of a heart. It's actually an average of. All the limb leads. And so, it localizes to the pure center of the heart. And then, basically, from that ground to the right arm, to the left arm, and to the left leg, those are all unipolar. We can only touch the positive pole in that situation, since the negative pole is sort of this ambiguous, amorphous thing. And so, bipolar and unipolar leads are present in the limb lead category or the frontal plane axis. If we kind of put all of these together, this is what gives us our vector coordination or our axis on the EKG. And if there's one thing I would recommend, it's Generally understanding the directionality of how the electricity is moving in the heart, it really helps you interpret EKGs on an entirely different level. And when I first started out, I would literally take this circle, this axis, and I would draw it on every EKG. And I would walk through sort of what is the cure x axis. What is the general direction of the vector depolarization, you know, based off of, um, sort of the, the coordinated vectors through the heart. And so again, if we think about the magenta colors as being the unipolar leads, we are traveling between two stickers, so right arm to left arm, and again, the negative and positive poles are just a historical norm. Technically they could go either direction, but the idea being that if you travel towards a positive pole, that is a positive deflection on the EKG. If you travel away from a positive pole, that is a negative deflection on an EKG. So, again, just generally thinking, if we're trying to say, is this sinus rhythm, it would mean to us that it's coming from the high right atrium. And so in lead one, we would expect it to be going from the right side of the heart towards the left side of the heart, so, i.e., traveling towards the positive pole. Therefore, we would expect That P wave to be upright in lead one. And you can do this with any of the, you know, deflections on an EKG. And it's really this concept of the directionality of the vector of electricity, and it helps us interpret kind of, um, a little bit more physiologically what we're looking at. So the last component of the EKG is the precordial leads. This is where you can get most of the variability because while there are defined places where the limb leads, um, excuse me, the precordial leads go, you can imagine in babies and children with, you know, heart disease or other things going on, maybe they've had surgery, there might not be a lot of real estate, and so you might end up with a little bit of an atypical presentation. So, it is a situation where you have to take that information with a grain of salt and try to understand, um, are the features that concern me in the precordial leads also present in the limb leads? Because if they're not, it might be something that I'm much more willing to kind of dismiss. The limb leads really are the focal, um, component of an EKG and in my opinion, give you the vast majority of the information that you need, especially in the outpatient setting. So the precordial leads that's opposed to giving you the frontal or axial plane, they're giving you the horizontal plane. So they're traveling from Wilson Central Terminal, that's WCT, outward from the chest. And again, they should be going across the chest from the right chest in V1 all the way to V6. And then of course in pediatrics we add 3 additional leads to look at right voltages with them. V3R, V4R, and then we add a V7 as well. So, in general, that information is supposed to augment or to help the limb lead information, but I would say in general is a less reliable source for kind of primary information. So, again, we're not going to go through the details of EKG reading today. I thought it was much more helpful to go through specific examples of things that you see all the time and help you identify them in the primary care setting. Um, so the first, you know, just pick a system and stick with it. Whatever that system is, maybe it's something you learned in medical school, maybe it's something you've developed on your own over time. Just make sure it's something that's systematic so that you don't miss anything. Checking the quality of the EKG. I do want to take a minute to talk about this because I think this doesn't get talked about that often, and there are many things that can be remedied just by either repeating an EKG or being able to appropriately interpret an EKG in the setting of something abnormal or not even abnormal, just something atypical about the quality or, or the technique of how the EKG was obtained. So I do wanna take a minute to talk about calibration, sweep speed, and then artifact, and actually limb lead reversals we're gonna talk about when we actually go through EKGs. So, on the right here, this is an example of an EKG from a newborn. I'm just arbitrarily saying this is a newborn in the newborn nursery. Um, again, we're not gonna go through the actual read on it, but if you kind of just generally look at this, it's relatively normal EKG for a neonate. It's a rightward axis. There's some stronger RV voltages which makes sense in the neonatal period. Um, but the thing that, again, oftentimes gets missed is the calibration, and the calibration can be noted in the box that is either on the left or the right of the screen. And a normally calibrated EKG should be two big boxes tall and one box wide. And what that information is telling us, it's telling us essentially the voltage or the amplitude that is being displayed on the screen. And so if it is not a correctly calibrated EKG, which is very common when it gets printed, So the EKG machines will often force the EKG to fit on a on a page, and they will auto calibrate it. That is not true when we look at things in sort of EKG reading programs. Usually they are kept at standard calibration, but if someone hands you an EKG, it's very easy to over um overstep this this process and to not confirm that the EKG is normally calibrated. So what this certain EKG is suggesting is that in fact all the voltages on the screen are actually been cut in half. And so if we take this EKG and we turn it into a normal calibration EKG, now we see that the voltages are in fact much taller, and this is much more concerning for possible RVH. In fact, there's like no R wave progression. Um, and this child actually is a single right ventricle, not that it necessarily matters for this situation, but it's really to convey the concept that ensuring that the EKG is at the proper calibration, which again, two big boxes tall and one box wide, to allow us to interpret the voltages in order to correctly read the EKG. The next is the sweep speed. Now, in general, again, if you're looking at an EKG reading system, it should always default to a sweep speed of 25 millimeters per second. If you're ever not certain, all of that information should be in the bottom. Usually it's the left hand side of the EKG. Um, and again, it also actually tells you your voltage calibration, which should be 10 millimeters per millivolt. And so a sweep speed of 25 millimeters per second is standard. Sometimes. Let's just say someone's getting an EKG or a rhythm strip because a patient might be an SVT. They might change either accidentally or intentionally, the sweep speed, which can make the EKG, it's essentially the time across the EKG. It can stretch out a QRS and make it look like a bundle branch block or a very slow rhythm, or it can, um, sort of Constantina it down and make it look like a much faster. Them when in fact it is not. So, granted, this is a less common situation, but I was just in the NICU two days ago, and I walked into the room and I looked up at the monitor, and I was like, Oh my God, that's a really fast heart rate. But then I was like, that doesn't make sense because the pulse is actually only like 140 or 150. And what happened is they had adjusted the sweep speed to make it look like it was a heart rate of 300 beats per minute, when in fact it was not. So it's just something to always just get into the practice of doing initially when you get an EKG handed to you is to ensure that it is normal calibration, normal sweep speed. The last is artifact. It's really straightforward. It's actually surprising how much this happens in the hospital. But if it's a crappy EKG, just repeat it. We'd much rather get really high-quality data and be able to give a really good interpretation. Um, many times I'm asked, well, can't you just read it anyway? Can't, you know, can't you just assume that, um, it's normal? And the reality is we really can't, and it wouldn't necessarily be appropriate. In the same way, you wouldn't. Ask, you know, the radiologist to read a KUB and just guess that the lungs also look OK based off the base of the lungs. Um, you know, we wouldn't necessarily be able to do that. So we want to be able to make sure that we can see all of the waves appropriately, that we can see the P wave, even if it's just in portions of the EKG, we know that it's technically challenging and babies and toddlers, they're moving, they're screaming, they're crying. Um, but if we can get at least some portion of each lead that looks OK, that's usually enough to interpret. But if the entire EKG isn't good, just ask them to repeat it. OK. So, now we're really gonna get into the meat of what I was hoping to talk about today, which is going through some of the common variants, what causes them and what to do about them, and then going through some of the more red flag features. So, many of these you'll know, maybe some of them are due. I don't, I, I'm not sure, but I think these are things that come up not infrequently. And in fact, I know we get referrals to the cardiology clinic. Usually, they're not necessarily referred to EP, but we get referrals to the cardiology clin clinic, not infrequently for many of these findings. Um, the First is the absolute most heinously named thing on the planet, sinus arrhythmia. One, because it's named arrhythmia. And so, um, if someone is not familiar with this, or perhaps is new to pediatrics or rotating through, particularly adults, um, rotating through that might not be looking at pediatric EKGs, having the word arrhythmia on an EKG can be very alarming. Also, it can be very alarming to parents. I've gotten, you know, self-referrals where a family comes in because they were like, well, my EKG literally says arrhythmia on it. Like, of course, I need to see a specialist. So, what are we looking at when we think about sinus arrhythmia? Really, what it is called is respirophasic variation in the heart rate. That is the more appropriate name for what it is. It is entirely normal finding, particularly in children and young adults. It is a rhythmic variation in the sinus rate. All of the rates are at physiologic rates. That's important. So, the heart rate, both at slow and slightly faster rates are all physiologically appropriate for the patient's age. At times, you may see a subtle change in the P wave morphology on the slower beats versus the faster beats. Now, the reason for this is that the sinus node is not really a discrete feature in the heart. I always describe it to the fellows as, think of it more like a ladder. And in fact, there are different sort of areas of the sinus node that are responsible. For different heart rates. And because of that, you can get subtle changes in the P wave morphology as a reflection of those changes in heart rate. Now, all of those P waves should still be originating from the high right atrium, which brings us back to ensuring that our axis for the P wave is normal. So, upright in 12 and AVF is pretty typical for a high right atrial. Um, sinus rhythm and a levocardic heart. But if you sort of pick up on subtle variability in the P wave, that doesn't necessarily mean it's abnormal. And in fact, many times that goes with something like sinus arrhythmia. And then most importantly, this is as symptomatic. A patient should never be symptomatic from sinus arrhythmia. So if you feel like they have symptoms that are affiliated with their rhythm, then it's unlikely to be, uh, truly a sinus arrhythmia problem. It could be a different issue. When we think about the actual underlying physiology, what's happening here? So first, again, I said it's very normal in children and young adults. It is due to changes in vagal tone during inspiration and expiration. So during inspiration, you decrease your intrathoracic pressure as your diaphragm goes down. This increases venous return. The venous return then activates the barrow receptors, particularly along the carotid sinus, but other places as well. These barrow receptors inhibit vagal tone. So what that means is that you are inhibiting vagal tone and therefore allowing the heart rate to be elevated slightly during those periods of time. Then of course with expiration, the opposite happens. You have increased intrathoracic pressure as the diaphragm comes up, decreased venous return, the baroreceptives are now inactive, and therefore the vagal tone goes unchecked, and this leads to a slight decrease in the heart rate. And oftentimes you can see this across an EKG as a very rhythmic sort of change that would match a typical respiratory rate for that child. So vagal tone is a common thing we're going to talk about today. Children have a lot of vagal tone, and that manifests in their EKG in a variety of different ways, and nearly all of them are completely normal and a really good sign of cardiovascular health. And so part of the features of, or part of what I'd like to convey to you today is there are some simple things you can even do in the office to sort of reassure yourself that yes, this is just a vagal tone issue and nothing needs to be done. But for pure sinus arrhythmia, again, the pathophysiology is vagal tone that is inhibited during inspiration, leading to an increased heart rate. It is exceedingly common. It can often be very exaggerated, particularly in like the 6 to 10, 6 to 12 year range. It can even bleed into young adulthood and sort of, you know, 20-somethings. Um, as people get older, they develop less and less of this, again, because of an overall decrease in cardiovascular health and decrease of vagal tone. Um, the intervention here is none. If you see this on an EKG, this can be reassuring. In fact, many times what I do nowadays is I actually just take it out and I just say it's a normal EKG because that's what it is. It can sometimes be more alarming to leave the read in as sinus arrhythmia. Other times I'll just put it parenthetically like normal variant. Um, there should be no activity restrictions for these patients, and they do not require a cardiology referral. OK. The next probably most common thing that we see, um, and typically this is a referral for, quote, an abnormal QRS axis or an abnormal EKG is a limb lead reversal. So, limb lead reversals are surprisingly common. The most common one is left arm, right arm, and that's because as the person putting on the stickers, sometimes it's like they're, they're on their right side, they're putting it on the right, which is the patient's left arm and vice versa. So for me, it's not that you should memorize every limb lead reversal. Um, in electrophysiology, we have the vast majority of them memorized, but every now and then I get surprised. I had one the other day where it was like a counterclockwise rotation of all of the leads. Everything was like rotated on one spot to the right. But a left arm, right arm reversal is easy typically to identify and again, it is a really nice thing to be able to quickly see and say to the office or the EKG tech or whatever, um, you know, could we repeat this EKG or could we go double check the lead placement and make sure that everything's plugged in appropriately. So, the giveaway in this scenario is that everything in lead one is negative. So, the P wave is negative, the QRS is negative, and the T wave is negative. That is an extremely uncommon situation in lead one, because again, lead one is basically a right to left lead, and for most normal hearts, the bulk of the electrical impulse is moving from the right side of the heart to the left side. Of the heart. So, typically, everything should be positive in lead one. So, if you ever get an EKG where all of lead one is negative, that should cue you in that potentially this is a limb lead reversal. The other features that we can often see is that, um, the precordial leads do not reflect the limb lead reversal, because there are situations where we have dextrocardia patients, and so you can have negative things, particularly P waves and lead one. But your precordial leads, which again are going from the right chest towards the left chest, should reflect whether or not the voltages, um, uh, basically coincide with that finding of dextrocardia. So, in a typical heart, you should go from V1 to V6. and you should have R wave progression. Meaning that most of the time, you start with more of an S wave, and then as you progress through the EKG, you should develop more of an R wave. That's very typical. It makes sense. You're moving towards the left ventricle, which, again, should be the bulk of the ventricular contraction. These patients, again, will be asymptomatic. They shouldn't really have, um, symptoms related to this since it's a technical feature. Um, there are plenty of places to kind of look on the internet if you're like, hey, is this a limited reversal? You can show up exam or pull up examples and look at those. Um, but on the left here, there's actually just an example of what the EKG looks like and what the lead is supposed to, um, look like on the right. So, in a left arm, right arm reversal, again, everything in lead one is inverted, and actually leads 2 and 3 are. Flip flopped. And so, the other feature that I often look for is that lead two should almost universally always have the biggest P wave. It is literally the axis that sort of the bulk of the P wave is traveling down. And so, it should almost always have the largest P wave. So, if I see a bigger P wave in 3 than in 2, and 1 is inverted, it is literally a 99% chance that this is a limbley reversal. Um, there are some other features too in that AVR and AVL, um, are reversed, and then AVF is typically unchanged. So, for this situation, it's just misplacement of the leads. Left arm, right arm is the single most common one. I probably read a couple of these per day, if I'm honest. It's sadly very common. Um, usually just repeating the EKG and checking the lead placement is enough to do. Obviously, no sports restriction and no cardiology referral is required. But it's a good thing to keep an eye out for. If you ever see everything negative in lead one, that should sort of like, Um, uh, sparkki or spidey sense that maybe something's off. The next one is a low atrial rhythm. Another very common, um, rhythm that we can typically see usually in teenagers, but sometimes younger children as well. So, in this, um, EKG, the defining features are that the inferior leads, which we would consider 23, and AVF. Again, if you think about your circular axis, 23, and AVF are all at the bottom. It's 120, 90, and 60. Um, 23, and AVF are all inverted. They're all negative P waves. And what that tells us, again, is that the bulk of the electrical activity is traveling away from those leads. So, remember what I said in the beginning, if you go towards a positive pole, you're a positive deflection on the EKG. If you go away from the positive pole, it's a negative deflection. So if all of those leads have a negative deflection, what that means is the electrical activity is actually going from inferior atrium to superior atrium, from the bottom of the atrium to the top of the atrium. And so that is telling us that it originates in the bottom of the atrium. Now, in lead one, we're still upright, which tells us our left-right axis. So it still tells us that it's coming from the right atrium, but the bottom of the right atrium. The other feature that we typically see is the PR PR interval is a little short. So say you on your auto read it says something like short PR. This is a feature that you should always check and look for. Is the P wave negative in the inferior leads? And it kind of makes sense geographically. If you're in the bottom of the right atrium, you're technically closer to the AV node, so your PR interval is technically shorter. And so that's really the etiology behind that finding. Now, what makes this normal and not an arrhythmia is the rate. That's important. So you have to think about the context of the patient's age and what they're doing at the time and is the heart rate appropriate for this presentation. Usually these patients are asymptomatic and usually they have resting bradycardia. And the reason for this is because, again, a lot of vagal tone, which inhibits your sinus rate, and your heart has, you know, multiple backup pacemakers, your low atrial rhythm is a very common atrial backup pacemaker. So when the sinus node is slightly suppressed by vagal tone, these other pacemakers can kind of kick in and take over. So, increased vagal tone leads to utilization of these backup pacemakers. The low right atrium is a very, very common one. We see this frequently, again, athletes, teenagers, um, you know, otherwise healthy kids many times as well. A nice intervention to try in the clinic, and you'll see this come up a lot when whenever you think that vagal tone might be contributing, I literally like, take off the lead, keep the stickers on, have the kid do 30 jumping jacks. They think it's hilarious, they have the best time doing it. Put the leads back on and repeat. EKG. If the P wave is now upright, when the heart rate is elevated, you have just proven this, right? It's a poor man's exercise test, essentially. So, if that normalizes after that process, you can feel extra confident in saying, this is a normal variant, this is a completely normal heart. It's doing all the things that it should be doing. Someone with a low right atrial rhythm, it is still an AV synchronous rhythm, right? It is still providing appropriate cardiac output. And like I said, when the heart rate elevates almost universally, it will transition to a, um, high right atrial sinus rhythm. So, no restrictions on activity. And again, you do not need to refer to cardiology unless there's some other feature about their evaluation that is concerning to you. First-degree heart block. Um, we get this one quite a bit in the teenagers as well. Now, granted, on the West Coast, I think about this differently than when I was practicing on the East Coast because on the East Coast, we always have to assume Lyme is kind of in the mix at that point. But out on the West Coast, it's extremely uncommon to sort of be in that situation. So I think it's much more reasonable to um look at the features of the patient and determine whether or not any additional evaluation is warranted. So as a general rule, if the PR is greater than one big box, that's like a nice ballpark that I usually give people, which is 200 milliseconds, which for most people, including like younger children, would be very long. For teenagers, they can oftentimes go up to 200, maybe a little bit beyond that, but I think still a ballpark of one big box is a reasonable place to start. For most situations, again, on the West Coast, this is due to increased vagal tone, as it, as I have been saying repeatedly and repeatedly. Very commonly associated with bradycardia, very commonly associated with teenage males, very active athletes, things like that. The remainder of the EKG should be normal though, meaning that the QRS should be nice and narrow. There should be no T wave abnormalities. And then again, just like we said with the other situation with a low atrial rhythm, the PR should Shorten with an increased heart rate. That is a normal response with exercise. And then finally, the patient should be symptomatic. So, obviously, if they're coming in with another symptom, fatigue, pre-syncope, syncope, you do have to think about some of those other features, like, could there be, you know, a Lyme exposure, and that would need to be worked up. But if it's just an incidental finding on an EKG, that is another situation in which you can almost universally move on and not evaluate it further. In this situation, another example of increased vagal tone, which leads to the PR prolongation, I see it probably most commonly in teenage male athletes. I would say that's probably the biggest cohort of patients where I see this. You can do the same thing as we talked about with the low atrial rhythm, have them do some jumping jacks, and again, the PR should shorten in response to an increased heart rate. If that happens, you can feel very reassured that this is all related to increased vagal tone and that it doesn't require any restriction of sport. And no cardiology referral. Now, of course, if the patient is symptomatic or it doesn't shorten, or even if you're just never sure, there's nothing wrong with sending them to cardiology for an evaluation. But in general, what we're trying to do is to make sure that you guys have the agency to kind of make some of these decisions so that, you know, the family doesn't necessarily have to wait and come in and see another specialists and, you know, sort of be worked up about that if it's not needed. Um, PACs, very, very common thing that we see. So, in terms of what we think about with a PAC, this is a premature atrial contraction. And I always joke with the fellows, like, what does the P stand for in PAC? Because sometimes they, they forget, in fact, it has to come in early, which, which is a defining feature of the um, um, of the ectopy, but sometimes When that doesn't happen, I have to remind them that it's not really a PAC at that point. It's something else that we have to figure out what it is. But a premature atrial contraction. It's an early atrial impulse that still conducts down the typical Hisperkinji system. So what that means is that the QRS on a PAC should be exactly the same as a QRS on a conducted beat. Now, as with every Everything in medicine, are there examples where that's not the case? Yes, and we call that aberration. Those are typically very early PACs, so PACs that aberrantly conduct. But I think a general rule that you can sort of think about is if the QRS looks the same and I can identify another P wave, that that is most consistent with a PAC. The other thing is that PACs typically come from someplace other than near the sinus node, meaning that the P wave axis and shape should be different than the normal beats. And this EKG is a really good example of that. What we can see, and again, lead two is almost universally where I'm looking for a P wave. It's the best lead to see P waves, the vast majority of time. You can see that the P wave is nice and upright, very normal, and then on the extra beat, this P wave is now inverted and You know, one could argue potentially a little bit closer to the, um, the QRS complex, but, you know, that's up for debate, I suppose. But regardless, the axis is very different, and you can see that play out on a few different leads in the rhythm strip here, in that that extra beat has a different P wave morphology, suggesting that that P wave is originating from another location in the heart. We use this strategy all the time in EP when we think about localizing something if we're going to take someone to the electrophysiology lab for an ablation. So let's just say for PACs we wouldn't do it, but let's say they had, you know, tons and tons of PVCs and we wanted to do an ablation. We can localize what ventricle it's in, then we can counsel the family on how we would approach it based off of the morphology of the QRS of the P wave. So you can get an idea of, well, here, um, these P waves are negative in lead 1 and in lead 2, which to me tells me they're coming from the low left atrium. So they're coming from farther down in the left atrium as opposed to the high right atrium for a sinus node B. In this situation, the patient is almost always asymptomatic in terms of like actual, you know, like syncope or chest discomfort. Oftentimes, they may feel palpitations, but frequently they don't even feel these. It sort of depends on the child. Um, in terms of the pathophysiology, this is due to increased automaticity in the atrium. Automaticity infers that there's an area of cells that are just firing off on their own, and this can be due to a number of different reasons, underlying reasons, but it's typically driven by catecholamine or body adrenaline response. So we oftentimes will see this during acute illness. So, I get a lot of referrals from a kid or a teen who came in with flu, and when they were in the hospital. Hospital, Somebody heard an irregular rhythm and then got an EKG and they had PACs. So, periods of illness and high stress, we see this fairly frequently. Um, rarely an intervention needs to be had. So typically, I think it's reasonable, in particular, if they're coming in during a period of stress, allow that period to pass and see if the symptoms are still there and see if the EKG shows still shows PVCs on the follow-up, you know, a week or two later. Um, if again, you're ever not certain or, or you need another set of eyes, it's never wrong to refer to cardiologist for these situations, but it's not, as long as the child is not like overtly symptomatic, it's not inherently dangerous to watch this. We very, very uncommonly treat PACs. I actually can't think of a situation in recent memory where I've put a patient on medication for PACs. Um, there should be no sports restriction activity, and you might be wondering, well, like Karen, you just told us that these are driven by catecholamines. They're going to exercise, their catecholamines are going to go up. True, but the other thing your catecholamines are going to do is that they're going to increase your sinus rate. And when your sinus rate goes up, it's actually going to suppress these extra areas. We call that suppression of automaticity. And that's a feature of ectopy. So, PACs should be suppressed by the sinus rhythm as it goes up. PVCs should be suppressed by the sinus rhythm as it goes up. And we see that on exercise tests. If you exercise these patients as their normal heart rate goes up, they're able to suppress these extra locations in the heart that are firing off. Cardiology referral, again, is only required if the patient is truly symptomatic, it's persistent, it just feels atypical to you or there's some other concerning symptom. PVCs, kind of the other side of the coin. So when we think about PVCs, it's the same idea. They have to be premature, meaning they have to be early. They have to sort of beat the underlying sinus rhythm. These are early ventricular impulse, which usually implies that the QRS would be significant. Significantly wider than a conducted QRS. And the reason for that is that a narrow QRS is the result of traveling down the Hisperkinji system. So just like with a PAC, if you travel down the Hisperkinji system with a sinus beat, it's narrow. When you travel down the Hisperkinji system with a Um, ectopic atrial beta PAC, it's also narrow. But if you are traveling from cell to cell to cell to cell to cell with a PVC, which is what's happening because you are no longer engaging the hyperkinji system, you have to activate much more slowly. You have to activate cell to cell to cell to cell to cell, which takes longer and thus gives you a wide cure. It's the same principle behind why. Um, paced cuss are also wide. We're not using the hyperkinji system. We're actually just activating from a random location in the heart where the pacing lead is. So paced beats are always wide, PVCs are always wide. It's also the reason why pre-excited beats are typically wide because they're also activating outside of the hisperinji system. So, Typically, these can be either in isolation, but sometimes they kind of cluster in patterns. Um, we call those trigemini orbigemini, depending on whether or not they're every other, every third. You can also have this for PACs, so it's not exclusive, that terminology is not exclusive to PVCs. Frequently, there's something called a compensatory pause after the PVC, which is a small pause before the sinus node reengage. Ages. Again, patients can oftentimes be asymptomatic, but may feel palpitations. Another very, uh, common description we hear is a forceful or a powerful beat. So, they don't really describe it as coming early or being irregular, but they feel a very strong beat. And that just, that's due to sort of the filling differences between the early and the, the normal beats. In terms of PVCs, the natural history suggests that these will improve or completely go away over time, usually by the time someone's kind of in their 20s and like young adulthood. So the vast majority of patients we try to drag our feet on, even the ones that have a ton of PVCs, I know it seems crazy sometimes. But there are rare cases where ventricular dysfunction can be a complication, and that is actually true for anything that activates outside of the Hisperkinji system, pacemaker-mediated cardiomyopathy, WPW, all of these at very Low incidence rates but possible to cause ventricular dysfunction over time, which is why these patients, unlike patients with PACs, do need to be referred to cardiology. They need to be regularly evaluated to ensure that 1, their burden improves over time, and 2, that they don't develop dysfunction. There have been some studies. This was a study done at Boston Children's and I was there, where we looked at all of the patients who had PVCs and we sort of looked at their EFs to determine what was the prevalence of developing dysfunction, but then also, is there kind of a cutoff at which we get more concerned. Thankfully, there are actually very few patients who ever developed even Borderline LV dysfunction. So, again, there's only one patient even below 40% here. Um, and the vast majority of these patients are above a PVC burden of 15%. That's not to say that if you have a burden less than 15%, you'll never get dysfunction. We have seen that. So, it doesn't exclude you from being followed, but it can help you counsel the family. And again, this brings me back to the idea that if a patient has frequent PVCs either on an incidental EKG or maybe they'd complain of palpitations and you find them, that does require a referral to cardiology. They don't necessarily have to come see electrophysiology again because rarely we treat them with either medication or catheter ablation. We try to just wait unless they're very symptomatic. This is also due to increased automaticity, but it's automaticity in the ventricle as opposed to in the atrium. The most common location is in the RV outflow tract. Um, they can sort of coalesce into couplets, triplets, and then what we would call non-sustained VT. There are patients that kind of have that as a manifestation. It's overall rare, but you know, of course, I'm sure all of you have seen patients with PVCs, so it's not like you, you know, get one every 5 years. Intervention, usually what we do on the cardiac side is we want to categorize the burden or the percent PVCs. So we do an ambulatory rhythm monitor of some type. Again, if you're referring and you have the capabilities to get some of this data ahead of time, that is always appreciated and helpful. So, you know, if you want to throw on a ZO or you have a Bardi or whatever from your office, you could certainly do that. We recommend at least a yearly echo. Usually, that's plenty. And like I said, I've actually never had a patient who developed dysfunction, but it is possible. Another thing that we can do to kind of ensure that these are typical or normal PVCs is we can do an exercise test to make sure that the PVCs suppress at higher heart rates. That's a little bit up to the cardiologist. I would say probably 75% of cardiologists still do that. Others feel very confident with the look of the PVCs and watching it over time. And then rarely, we recommend medications for patients, and that's only if they're extremely symptomatic. The medications are actually quite good. Um, usually it's starting with a beta blocker and then it progressing to something like flecainide if that doesn't work. And then catheter ablation. Catheter ablation, um, is definitely something we would recommend for anyone who's symptomatic or someone who has non-sustained VT as a component of their PVC burden. The ablation success rates are lower than they would be for accessory pathways or AVNRT, which are, those are usually above 96%. For PVCs, it's usually about 80%. And the reason is because we put children to sleep when we do ablations. And as you can. See up at top, uh, catecholamines and automaticity drive this. And so when they're put to sleep, many times their PVCs go away completely, and then it's really hard to map where they are and get rid of them because they just don't have enough of them during the procedure. That's again, another reason why we prefer to wait if possible. These patients should not be restricted. Again, the vast majority of the time, they will suppress with higher heart rates, and if you're ever not certain, um, or that the patient wants to do sports, that's always a good indication to do an exercise test so that everybody knows that, um, the risk of, uh, an event is, is extremely, extremely low. And then finally, just to reiterate the fact that these patients do require referral to cardiology for follow-up. OK, uh, I think this is the last in this section, um, incomplete red bundle branch block. We get this a lot, um, and I certainly understand because it's kind of a, it, it's, it's a challenging read, and I want to explain why it's read the way it is and what it means and what the sort of the history is it. So, really what it is, is an RSR and V1. And the cure restoration, unlike with a complete right bundle branch block, is less than 110 milliseconds, and actually usually much less than that. Usually it's completely normal. Um, and so in this setting, the reason that incomplete right bundle branch block kind of originated was that You know, years ago, 20 some odd years ago, there was this thought, or there were some early studies that suggested that this finding could be associated with um vol shunts to the right atrium, particularly ASDs, but could be partial veins, things like that too. Um, and that this finding could be a feature of those presentations. Um. That certainly can be possible, but I'm going to show you some data as to the fact that that really is neither sensitive nor specific. If this finding is present in the setting of an otherwise normal EKG and the patient is asymptomatic, i.e., they do not have a murmur, because again, if you have an ASD in volume load, you should have a relative pulmonic stenosis murmur. That's the murmur of an ASD. It's relative PS. If you don't have those findings, essentially at this point, we consider an RSR a completely normal finding in children and young adults. And this again originated or not originated, but was recently looked at in a large paper again out of Boston that essentially looked at what were the features of, you know, how these patients were worked up and how many of them had something positive in terms of being more or less likely to have an ASD. The only thing that they really found was that these patients were much more likely to have an echo, so 12 versus 7%. But they were no more likely to have an ASD, 2.5 versus 3%, so it wasn't even statistically significant. Now, granted, um, if the patient has other features that would make you concerned about an ASD, i.e., a murmur, it would certainly still be indicated to get an echo. But if it's just an isolated RSR or incomplete right bundle branch block, it does not necessarily require additional workup. The other thing that they found is there's a lot of interreader variability, and I've actually gotten to the practice of not even calling it an incomplete right bundle. I just call it an RSR because that is physically what it is. Um, and there really, to my mind is not enough data to support that there's an association with a physiologic or pathophysiologic finding. So it's very common in children, um, and in this situation, I would say unless you have other suspicion, an isolated RSR does not need to be worked out further. So it can be a normal finding. It can be seen in RV conduction disease, but again it's neither specific nor sensitive. Uh, the prevalence is very common, I would say. I see this multiple times a day as I'm reading EKGs. Typically, no intervention is required unless, of course, there's another finding that makes you suspicious for a right atrial volume load, i.e., an ASD murmur. Um, the patient should not be restricted from activity, again, unless there's another symptom that drives you to have them evaluated by cardiology. And so, if it's an isolated finding, doesn't need follow-up. If it's not an isolated finding or you're not sure, it's never wrong to refer. All right. So we're gonna finish out by talking about um red flag EKGs. Um, I think I've actually done some talks where we reviewed some of these features and so many of them will be familiar to, and I'm sure none of them will be a surprise, uh, but it's just helpful to reiterate kind of the rationale behind why they need to be referred. So, WPW, pre-excitation, Delta wave, all different names for the same thing. Um, essentially, this is Pre-excitation of the ventricle due to an accessory pathway. The EKG features can be sort of marked or very, very subtle. And so, this is an example of a very obvious EKG with pre-excitation, but they can be less obvious. And that's why I came up with a couple of kind of smaller features that oftentimes we don't talk about as ways to determine whether someone is pre-excited. So the short PR is the first one that really does have to be a feature of the EKG. Many times, and I shouldn't say many times, but we definitely get referrals for kind of slightly wider curesss or cusses that are a little asymmetric with a concern for, ah, is this a delta wave? But a delta wave implies that basically you're pre-exciting, which means that the PR interval should be very short. So if you have a normal PR interval, Um, and just a delta wave, you know, you, you can feel pretty confident that it's unlikely to be WPW. What I will advocate for though is look at all the leads. For example, if you just looked at lead 3 here, you probably would not think that was a pre-excited QRS. So, it's really got to be something that is present in multiple leads. Um, we just talked about the delta wave. Again, that is ventricular pre-excitation, loss of a septal Q wave. This is actually a really, um, good one to keep in your back pocket and thinking about with WPW. So if we think about how the septum activates, it actually activates from the left ventricle to the right ventricle. That's how the hyperkini system activates the septum. And since it's heading from left to right, it's actually heading away from the bulk of the electrical activity, which means there's a slight negative, iEQ wave in the QRS complex in the lateral precordial leads. So 567, and And then also typically one in AVL, but I usually just focus on 567. You should almost always have a tiny little Q wave in those leads in a normal EKG. So, if you have some features and a lack of a Q wave, that might cue you in, that there could be subtle pre-excitation. We oftentimes see that as one of the best signs for a left lateral pathway, because those EKGs can be very subtle in terms of the delta wave. Um, oftentimes the QRS is wide, slightly, but doesn't necessarily have to mean a bundle branch block, meaning 110 milliseconds. And associated with the abnormal depolarization of the heart, you get abnormal repolarization. So that typically gives you wonky T waves and many times QT prolongation. I've actually had a few. Situations where I've been referred a patient to rule out long QT syndrome, and in fact, they're just pre-excited. And so, if you start to see some of these features, um, you know, putting it together and even, you know, calling our office, asking someone to have a peek at it, calling the fellow, asking someone to look at it, and, you know, let you know if you think it's pre-excited, we're always happy to do that. So, WPW, what does it sort of physiologically represent? It represents the presence of an accessory pathway between the atrium and the ventricle, meaning there's an extra myocardial connection that the patient was born with, typically not something they developed. And it creates a substrate for SVT, which is one type of arrhythmia, and a substrate for what we call pre-excited atrial arrhythmias. Because of the pre-excited atrial arrhythmias, those are actually life-threatening arrhythmias, and I'll explain why. There is an associated associated sudden cardiac death risk with WPW. It's about 0.25% per year, about 3 to 4% over a lifetime. Therefore, because of this, all patients with WPW need to be referred to an electrophysiologist specifically. And that is true regardless of whether or not they've ever had SVT, all right? And let's talk about why. So when we think about activation of the myocardium, typically everything should be going down the Hisperkinji system and through the AV node. Again, this delta wave represents pre-excitation, early excitation of the ventricle down the accessory pathway, because the accessory pathway does not decrement, which is a normal function of the AV node. That's what gives you the pause between the P wave and the QRS. The AV node, I sort of explained to families, it's kind of like a bouncer. It's like quality control between the atrium and the ventricle. It's designed to protect the ventricle from abnormal rhythms. When you add in another connection between the atrium and the ventricle, now you can conduct abnormal rhythms in the atrium to the ventricle without any type of barrier. That's where the problem comes in. So, the accessory pathways themselves are microscopic. Again, something congenital that they were born with. Um, they're also known as bypass tracts because they bypass the AV node. Um, I like to show this picture to families because, you know, for something this small, it's actually annoying how much trouble it can cause. Um, and typically because of the sudden cardiac death risk, we recommend catheter ablation for any patient over the age of 25 with 25 kg. Sorry, not, did I say age? I meant weight. Any patient over 25 kg with WPW. Importantly, there is not compelling data to suggest that there is an increased risk of sudden cardiac death with exercise. And so while it used to be the case that all of these patients were restricted from activity, that is no longer my practice based off the data that we have available to us. So the reason for the sudden cardiac death risk is not because of the SVT. SVT does not kill you, all right? SVT in a structurally normal heart is not a life-threatening arrhythmia. But if you have an atrial arrhythmia, the most common being atrial fibrillation, and I know you're thinking, well, it's a kid, how could he get atrial fibrillation? There is an associated increased risk of Afib in patients with WPW. We don't know why. There's probably some underlying myopathy of some type. But basically, in a normal heart, when you have afib, your atrium is sort of literally vibrating at 500 to 700 beats per minute. It's exceptionally fast. It is not pumping blood at all, right? It is barely sloshing it around the heart. Your AV node does something called decrement. So while it does not let 500 to 700 beats through, maybe it lets 100, maybe 80 beats through. And that is why all the grandparents around there can walk around with Afib all the time, cause they have an AV node plus or minus the medication that blocks the majority of the atrial activity from getting to the ventricle at the AV node. On the flip side, if you have an extra connection, i.e., an accessory pathway, that connection does not decrement. That connection might let 500 beats through. I don't know. Nobody knows. All the pathways are different, and depending on their electrophysiologic properties, they may conduct electrical activity to. The ventricle, meaning that if you've taken atrial fibrillation and now you're conducting it to the ventricle, you've just turned that into ventricular fibrillation, which is a life-threatening arrhythmia. So this is the reason we ablate WPW. It is not the SVT. Yes, that is a benefit if the patient has SVT and it bothers them, but it is because of the sudden cardiac death risk from this particular reason. So again, it's WPW represents antigrade conduction down an accessory pathway from A to B during sinus rhythm. In and of itself, it is not an arrhythmia, but it does have an associated sudden cardiac death risk. It's fairly common in the population, 0.1 to 0.3%, depending on some of the insurance claims that we've looked at. We recommend catheter ablation for any patient over 25 kg. Actually, technically it's 20 kg, but usually once you get to school age, definitely middle and high school, you should be referred for an ablation. Um, my practice is not to restrict these patients. Again, based off the data that we have where we looked at large studies of patients with WPW and when they had events, the vast majority of them were at rest. Um, and then cardiology referral is required, and I would recommend sending directly to an electrophysiologist if possible, if you have one, which would be me? Um, OK. The next couple we can go through relatively quickly. This is another one that requires referral and can be a little bit sneakier. This EKG is very obvious, but there are other ones that are more subtle. T wave inversions in the lateral precordial leads are not common and not necessarily normal at any age. A baby, a toddler, a 10-year-old, a high school student, it doesn't matter. If you have T wave inversions in the lateral precordial leads, that requires evaluation. And the reason is because there is a high association with cardiomyopathies, either hypertrophic cardiomyopathy or some other form of cardiomyopathy. Now, it can be a normal variant, and this is more common in African-American teenage males, um, Hispanic teenage males. We can see T wave inversions in those patients, but they need an evaluation to ensure that they have a normal echo. You can't just assume it's normal. So I would recommend or my recommendation is that any patient with lateral T wave inversions needs to be referred to cardiology. Doesn't have to necessarily come to EP but should go to cardiology. We don't really know the exact pathophysiology of T waves, uh, even still, in 2025. Nobody really knows how T waves are formed. There's lots of thoughts that it's due to a combination of the disordered myocytes from the cardiomyopathy and also the abnormal depolarization that affects the repolarization, and then the concern with chronic ischemia due to the fact that if you had a very thick muscle from hypertrophic cardiomyopathy. This is a rare finding, um, but again, it's another thing where there are very few black and white things in medicine. I think this is one of the ones like WPW that should go to a cardiologist every time. Um, usually just requires an initial evaluation, which is like echo monitor, checking of symptoms. Um, sports and activity, uh, that really needs to be at the discretion of, I would say, the cardiologists they're being referred to. Very, very, very few things require a blanket restriction on exercise these days. Even most of the patients I follow with hypertrophic cardiomyopathy, I allow to exercise. There's A lot of data over the last 10 years that says that the risk associated with an event is not increased even with vigorous exercise in those patients. And so those recommendations are changing over time, and it doesn't necessarily mean that every kid is going to be taken out of sports just because they had either an abnormal EKG or even hypertrophic cardiomyopathy. Um, and then, yes, this requires a referral. Um, heart block. This is an obvious one. You guys see this, um, uh, you know, I, I feel like every year I get one or two of these, where a kid showed up to the clinic and the last PCP visit, the heart rate was normal, and then you notice that the heart rate's, you know, 45, and they get referred for an EKG. EKG and they have heart block of some type. Um, the things that are helpful in thinking about the EKG for approving heart block is that the atrial rate has to be faster than the ventricular rate, because if it's not, it could just be a junctional rhythm, which is not necessarily an abnormality. There should be AV dissociation, and again, oftentimes you have to follow it over maybe a few EKGs to be positive it's not conducting, because sometimes, like in the beginning here, you might look at that first or the second P wave and PR interval and say, yeah, that could conduct, maybe that's a conducted beat. But if you look at the QRS over time, it doesn't vary, meaning that it's never brought in by a P wave. It's just sort of marching along in the background. Symptoms are dependent. I would say most of the patients who show up in the outpatient setting are asymptomatic by definition, right? They haven't presented to an ED with syncope. Um, and it depends mostly on the escape rate and sort of their activity level. I would say the symptom we usually hear most commonly is not so much that I'm like, oh, I passed out. It's like, oh, I'm just not as good in gym class anymore. I can't really keep up. And that's just because they can't augment their cardiac output because they can't increase their heart rate the way that someone else could. Again, not surprising to you, this requires cardiology evaluation. The two most common kinds are congenital, which is an autoimmune mediated phenomenon, usually occurs in fetal life, and so we know about it almost always ahead of time. But there are late onset ones. Those are the ones you guys see in your clinic. And like I said, I probably get one or two a year of last year, this kid was fine, and this year they're in heart block. Um, Prevalence is rare, not surprising. Intervention pacing is not always immediately indicated. Now, eventually, will most people get a pacemaker? Yes, but pacing is really mostly indicated for symptomatic patients and for those in which they're not able to do their daily activities or an activity that they want to do, right? So I still have some patients without a pacemaker. I follow a college kid who does ballet and doesn't have a pacemaker, and she's completely fine. She's able to exercise and do all the normal things. And anytime you can minimize pacing, you should. So just because you have heart block doesn't mean you always get a pacemaker, although the vast majority of time you will. Um, they're not restricted from sports or activity, and they should be referred to an optrophysiologist. Long QT syndrome. So, um, this one's tough because I would say that in general, we require a few EKGs to really diagnose long QT syndrome, but a couple of the EKG features that I think are the most helpful in having a higher sort of positive predictive, uh, value for it is really a QTC greater than 480. I know there's lots of weird published things out there about like 440. I don't know where that came from. It is not based off of anything. But 480 is what most of us use nowadays, pretty much for both genders, but usually we allow it to be a little bit longer for, um, postpubescent females versus males. Um, estrogen prolongs the QT and so as part of that, women on average have a longer QT interval. There may also be T wave abnormalities such as notching, um, that can be a common feature that we see. Uh, the patient usually is asymptomatic. People don't feel a QT being long. The only thing they feel is if they had an arrhythmia associated with their long QT syndrome, which is actually still very uncommon. The family history is really critical here. So almost all forms of long QT are invariably inherited. And so understanding the family history and particularly things like drowning, single car accidents, um, sudden death, things like that are most helpful to know. And of course, if there's any question, it does require a cardiology evaluation. Keeping in mind that all babies and neonates have basically QT prolongation at birth that resolves over the first, usually week or two of life. Um, in general, I will not diagnose long QT syndrome until a baby is about 1 month old. So, if you get a patient who got discharged from the NICU cause they were preemie and maybe their QTC was 475 or something like that, it's definitely worth repeating. If it's normalized, it does not mean they need follow-up. If it's still abnormal or you're not sure, of course, you can always reach out. When we measure the QT interval, it should universally be measured in leads 2 and V5. Um, that's where the normals come from. We do not measure a U wave. A U wave is not part of the T wave. And essentially what you're measuring is the tangent on the downslope of the T wave or the upslope if it's a biphasic T wave, where it intersects with the baseline. That intersection is technically the end of the QT. And then it's normalized to the heart rate, which by definition is the preceding RR interval. So, if you really want to measure a QT interval, pretty much what we do, or what I do when someone sends me to someone for an exercise test is I measure 3 beats in lead 53 beats in lead 2, and then average all of those together. The auto read almost always overestimates the QT interval. Don't rely on that. Don't assume that it's shorter than than what it is. If it's ever borderline or you're not sure, it's best to try to measure it yourself or um refer them for evaluation. In terms of how we think about long QT syndrome, 12, and 3 account for the vast majority of cases. They're way more common than any of the other forms. Um, as I mentioned before, it's nearly always inherited, and so typically there's a family history. There some low penetrance things might not have an obvious one, but usually you can tease out some history that makes sense for long QT. The channels involved here are potassium channels. They're most of what are responsible for the repolarization and the action potential, and then also gain of function mutations in SCN-5A, although that's an uncommon cause. Long QT3 is a less common cause of long QT syndrome. Beta blockers are still the mainstay and work extremely well. If you are compliant with beta blockers, your risk for an event is exceedingly, exceedingly low, to the point where, again, we do not universally restrict patients with long QT syndrome anymore from sports and activity. Um, the only exception to that is a patient who's had an event with long QT1 who wants to do swimming. That's really the one situation where we still feel that the risk outweighs the benefit from an exercise perspective. But in general, we really want these kids to live as normal a life as they can, and, um, my preference is to always advocate for exercise and activity when they're able to. So usually an inherited syndrome that prolongs the repolarization phase, what this does is it leads to vulnerable myocardium that could increase the risk of life threatening arrhythmias. The prevalence is rare. The intervention is beta blockers. Just as an aside, nadolol and propranolol are really the only beta blockers that your long QT patient should be on. If you ever have a patient who's not on one of those two, you should reach out to their cardiologist and ask them why. There is significant, significant data that say that these are, those are far superior to metoprolol, atenolol, any other beta blocker. Um, ICDs should be really uncommon. It shouldn't be a situation where you actually see a lot of patients with ICDs these days and long QT syndrome. It should really be a last resort. Um, sports and activity, I would recommend that this is at the, um, guidance of the electrophysiologist that they're following, and ideally an inherited arrhythmia specialist. But typically, if they're on stable beta-blocker therapy for more than 3 months, then they're allowed to participate, assuming they're other high-risk features. And again, they refer to cardiology in these situations. If you're not certain, they can come directly to EP or inherited arrhythmias clinic with myself, or if they need to see a primary cardiologist first, that's also OK. Uh, last one, SVT. You guys, you know, again, you've got a baby who comes in, maybe they're not feeding as well, but they're here for a well child visit, otherwise doing OK. You hook them up to the pulse ox and you know, the heart rate's 250. So this is a narrow complex tachycardia. SVT should travel down the AV node and then travel back up either an accessory pathway or another pathway in the AV node. Those are the two most common types, AVRT and AVNRT. We typically think of the rates as being more than 220 for babies, about 180 for kids and and teenagers, excuse me. ST changes are really common. Sometimes that freaks people out. Um, there is kind of this sort of low level ischemic, uh, ischemia that is happening on the endocardial surface, um, but it's not a chronic ischemia that we worry about risk of dysfunction for. There are rare circumstances where the SVT is a wide complex tachycardia. We call that aberration or antidromic, um, depending on the etiology, but I, as a rule, I would basically say that the vast majority of SVTs are going to be a narrow complex tachycardia. And then not surprising, we would always recommend that these get referred to an electrophysiologist since we're very comfortable with managing them both from a medication and ablation standpoint. The two most common mechanisms, as I said, are an accessory pathway, so the cousin to WPW, which is also an accessory pathway. If you have SVT with your WPW, you're going down the AV node and up the pathway. That's AVRT. Or you can have re-entry inside the AV node. That's more common with children and teenagers and like college age kids. Um, everyone in the middle, probably 50/50. Uh, these are relatively common. It's probably the most common thing that I manage from an ablation perspective and procedural perspective. Intervention depends on the presence of WPW. So typical treatment, if you do not have WPW we could watch it. You don't have to do anything with SVT if it's rare and well-tolerated. You can do medications, but all the medications are preventative and so there's a downside that you have to take a medication every day. And then ablation. Again, anyone over pretty much 20 or 25 kg, if they want an ablation, it would be safe to do so at that point. That's usually about a 6 or 7 year old for those interested. Um, sports restriction, they should not be restricted from activities. Uh, Obviously, if they feel like every time I go to gym class I get SVT and they don't want to, that's fine. But if they want to do something and they feel OK, they have to know themselves, take breaks when needed, be able to rest when, um, when necessary, but they shouldn't necessarily be restricted. And again, we refer these to electrophysiology. So that kind of brings me to the end in terms of conclusions. Again, I would say the goal is to feel confident calling it normal. You don't have to diagnose every small little thing, but if you can feel confident that the EKG is a normal variant, then, you know, that's really what we're trying to give you the agency to do. If the EKG isn't high quality, just repeat it really easy. It's a cheap test and it gives us a lot of information, and many times it can be really helpful to have a high quality EKG. As we alluded to in the beginning, a lot of what we see in normal variants is related to increased vagal tone in children. So a good kind of like cheap trick is to make the kid do some form of exercise in the room and repeat the EKG. If it got better or quote normalized after that, you can feel really confident that this is still just a normal variant and something that you can watch or do nothing about. Another theme is that very few cardiac disorders actually require exercise restriction nowadays, and that hopefully what you're starting to see is that a lot of these kids are able to participate in things. We know that exercise is so dramatically important for mental health, physical health, reduces your risk of diabetes, Alzheimer's, cancers, congenital or coronary artery disease, like all of these things. And so we need to balance the risk of an actual event based off the data and the benefits of the long term improvement in their general health. And just to like reiterate the things that we talked about at the end, uh, WPW, lateral T wave inversions, heart block, concern for long QT, and SVT should always be referred to cardiology and or electrophysiology depending on who you have available for you. And with that, this is kind of our contact information. You can always get to EP or um cardiology through the access center. And then my contact is actually on the right. You can always email me questions or run through patients with me or ask me to look at an EKG if that's interested. And then Brittany Ojea is our scheduler for electrophysiology. So again, if you had a patient that you wanted to refer, you could also reach out to our office directly. And I'm happy to take any questions.
