Our next module is atrial tachyarrhythmias. We have several topics we're going to cover in this one, and I have a few readings here for you to check out. Most of this centers upon guidelines for atrial fibrillation management and some other things related to the other types of supraventricular tachycardias that we're going to talk about. As always, you can read more about these things in the textbook Bronwald's Heart Disease. Our focus today is going to be PACs, atrial arrhythmias such as AFib, AFlutter, PSVT. We'll talk about the CHADS2-VASc score and how you decide on anticoagulation, as well as the significance of the delta wave on an EKG, which we've touched on already in our EKG lecture. Let's start with premature atrial contractions. When we think about atrial arrhythmias, I like to think about these on a continuum. At the first end of that continuum, we have premature atrial contractions. If we string together PACs, we have atrial tachycardia, and then we can have a degeneration of impulses where we have atrial fibrillation. There's a continuum there that when you see people with PACs, most of the time that ends up being completely benign, but there are some things to look for that might make you think, maybe this is someone I need to monitor a little more closely for a progression of these atrial arrhythmias. PACs are extremely common. The epidemiology, the etiology epidemiology, we see these in a lot of different patient types. This is related to excess sympathetic stimulation. It could be from ischemia, valvular heart disease, and the patients when they present with this, they may have things like palpitations or fatigue or dyspnea, so there's a wide range of how people can present depending on how often they're having PACs. When we're evaluating this, we can do things like a Holter monitor or more extensive monitoring like an event recorder. A 12-weight EKG can help us gain a little bit more information about the patient. Echocardiograms can also be done if we want to do a bit more of a workup for that patient depending on what we're considering. The management is generally going to be rate-slowing medications. However, there's a bit more to the story here. This strip is showing you what PACs look like. If you follow my mouse along, we see this is a normal beat, and then this looks pretty normal too, and then this beat here comes in early. One of the most important things you want to do is differentiate between PACs and PVCs, which are premature ventricular contractions. As you've heard me say a lot in this series, the diagnosis frequently lies within your evaluation of the P-wave. With PACs, you'll see there's a narrow complex QRS, and oftentimes, you won't even be able to see a P-wave coming in early. We know that this is atrial in origin in part because of that narrow QRS, and then another thing you can look for is because the P-wave is buried in the preceding T-wave, it'll often look a little bit different than the surrounding T-waves. Sometimes there'll be a little pause after that ectopic focus quiets down, and then you may have a few normal beats before it starts again. Reasons to treat PACs are twofold. They may cause lifestyle-limiting symptoms, and they may progress to more sustained atrial arrhythmias. Of course, the most concerning of that would be atrial fibrillation and atrial flutter. A higher PAC burden is associated with an increased incidence of atrial fibrillation in general. If patients have frequent PACs, or maybe it's suggested by history along with routine EKGs, maybe you might consider additional testing to quantify the PACs. This is where a 24-hour Holter monitor comes in, both for PACs and PVCs. The nice thing about that is I can count how many PACs there are over the course of 24 hours, and you can get a percentage of their total beats. Avoid medical conditions such as structural heart disease or diabetes, hypertension. Those are also shown to have an increased incidence of atrial fibrillation. Let's talk a bit more then, progress into atrial fibrillation, the most common sustained arrhythmia worldwide. The risk increases with age, sleep apnea, hypertension, obesity, diabetes, and there's a number of other things. But we know that when patients have these medical conditions, they are more likely to develop atrial fibrillation at some point during their life. Clinical presentation is often things like palpitations or chest pain, fatigue, dyspnea. They can even progress to heart failure. A lot of their presentation depends on how fast their ventricular rate is. To evaluate patients with AFib, we get a 12-lead EKG for documentation. Rehalter monitoring is typically done to see how often they're in atrial fibrillation. Are they in it all the time? Do they go in and out of it? Other things I'll look for on a monitor is evidence of tachybrady syndrome. Maybe they have really fast heart rates with AFib or accelerated ventricular response, and then that may alternate with periods of bradycardia. Another thing to evaluate for is conversion pauses. Sometimes people, when they convert from atrial fibrillation back to sinus rhythm, may have a pause associated with that. All of those things may help you make better clinical decisions on how to manage that. Certain medications you might use or other more invasive procedures that you may choose to do. Echocardiograms can be done to evaluate things like left atrial size, or if you have someone where you're concerned potentially about a tachycardia-induced cardiomyopathy, you can evaluate that. Baseline blood work is typically ordered to look for things that might be reversible. Maybe the patient has hyper or even hypothyroidism, or they have anemia, they have abnormal electrolyte balance. Those are things that you would consider as being potentially reversible. When you diagnose someone with atrial fibrillation, you should define that as either paroxysmal, which means it's recurrent, that terminates spontaneously, lasting possibly up to seven days, but usually less than 48 hours, or persistent atrial fibrillation. That means it's sustained for at least seven days, or it requires termination by cardioversion. We say a patient has permanent atrial fibrillation when the patient and the provider agree to stop additional attempts to restore normal sinus rhythm. When you're evaluating the patient, we talked a bit about things we might look for like reversible causes with a comprehensive metabolic panel or thyroid function test. We should take a very good history. I like to think about the evaluation of AFib centering around a few things. We think about why did this happen? Is there anything I can do to make this less likely to progress and less likely to happen again? Identify any type of risk factors that might be there. Next is think about how can I make this patient feel better? Patients come and see you because they don't feel well. If they have palpitations and fatigue and dyspnea, think about how you're going to manage that. Are we going to choose a hormonal medication or are we going to choose a rhythm control approach? You always want to think of ways that you can prevent a stroke. Anticoagulation is the other thing that you think about for these patients. We choose a novel oral anticoagulant drug, and that's what we use to minimize the risk of a stroke. We talked about diagnostic testing. If patients have symptoms on a daily basis, a 24-hour Holter monitor is a great place to start. However, if their symptoms are more intermittent, you may choose to do something like a two-week event recorder or even a four-week event recorder. Always think about the hemodynamic stability of the patient that has atrial fibrillation. If someone has underlying ischemic heart disease or they have underlying heart failure, that patient's probably not going to do well if you leave them in atrial fibrillation for long periods of time because you lose your atrial kick and that affects your cardiac output. Our goals ultimately are to control the ventricular response, determine their stroke risk, and relieve their symptoms. Now remember, the fastest way to achieve rate control is to convert them to normal sinus rhythm. So acutely, if the patient is hypotensive, if they're highly symptomatic, think about whether or not you can do a cardioversion. When normal sinus rhythm is restored within 48 hours, the embolic risk is low and anticoagulation is not required prior to doing that. However, if you are not sure how long they've been in AFib or if you know it's been longer than 48 hours, the patient must be anticoagulated for at least three weeks before and four weeks after you do that cardioversion. For rhythm control acutely, you can attempt something like flecainide or maybe propathinone or dofetilide, and sometimes giving them that medication acutely may convert them to sinus rhythm. Long term, it's a bit more complex, and we'll get into more details about this on our next slide. In general, you think about a rate control strategy versus a rhythm control strategy, and you have to consider the individual patient and their clinical situation. Do they have risk factors for stroke? How fast is their ventricular rate? Do they have hemodynamic compromise, and what are their symptoms? If patients are highly symptomatic, they're probably going to do better if we can get them back in normal sinus rhythm, and we talked about the anticoagulation for these patients acutely, and we'll go into more detail about that in the long term as well. Long term management, we can divide this into a rate control strategy and a rhythm control strategy, and in general, we said for years and years that if a patient is asymptomatic and they have atrial fibrillation, there's probably not a big difference in how they're going to do in the long run if you choose rate control versus rhythm control. Now, there's more data that comes out all the time that is very useful in helping us decide how we might manage these patients, so if we choose a rate control strategy, we can use things like beta blockers, non-dihydropurity and calcium channel blockers, or digoxin. When the atrial fibrillation is persistent, it's reasonable to restore sinus rhythm with antiarrhythmic drug therapy or a cardioversion at least once in patients who are younger than 65 and in patients who are 65 or older who are symptomatic from AFib despite adequate heart rate control, so that's another thing to think about. Talk to your patient and figure out how they're feeling. If they're highly symptomatic, if they don't feel well, or if they're suffering from some type of hemodynamic compromise from the atrial fibrillation, that patient should be targeted for rhythm control unless there's contraindications, so rhythm control patients in general will do better with rhythm control if they have a left atrial size that's a bit closer to normal, if they're symptomatic despite rate control, if they're a younger patient, and if they've spent less time in AFib, so the longer amount of time a patient spends in atrial fibrillation, the more adverse electrical remodeling that takes place within the atrium, and that's something, it's essentially a fibrotic process, and the longer they stay in AFib, the more the cardiac conduction system thinks that that's normal, and it's harder to get them back out of rhythm and into normal sinus rhythm, and that's why we think about those younger patients. If you've got someone who's, say, 55 years old and this is their first episode of atrial fibrillation, even if they're asymptomatic, think about it a little bit. Does this person deserve a shot at normal sinus rhythm? What if they come back a year or two down the road and now they're symptomatic? It's going to be harder to get them back into normal sinus rhythm, so we can achieve rhythm control with antiarrhythmic medications as well as radiofrequency ablation, which is an excellent option for a lot of patients that works very, very well. All of these things are going to be more successful with risk factor modification, so I hope that you take from this lecture the importance of targeting risk factors and trying to modify those because that's something that will have a significant effect on their arrhythmia load. You can get up to a 50% reduction in arrhythmia load when we control things like blood pressure, glucose, weight, sleep apnea. Before you talk to a patient about a radiofrequency ablation, for example, we should try to make sure that they have things that are under reasonable control, like sleep apnea. A lot of the studies that have been done show that patients are going to do much better from an arrhythmia standpoint after an ablation if these sorts of risk factors are better controlled before you go ahead with that procedure. Regardless of which pillar you choose, rate control or rhythm control, don't forget about that other pillar, which is risk factor modification. The fourth thing we would add to this slide would be anticoagulation, so those are all the things that we want to consider. You really have to think about the individual patient characteristics because you have a lot of options for what you can use. Most of these drugs are excreted either through the kidneys or through the liver, so think about their renal function and their baseline liver function. Think about what other medications they're taking that maybe might overload one of those pathways. Presence of coronary artery disease limits the use of some medications, in particular flecainide. If they have a depressed LV function, that makes things like Sotolol less desirable. If they have severe hypertension with marked LV hypertrophy, that also puts the patient at a slightly increased risk of proarrhythmia when antiarrhythmic drugs are used. These are all the things to think about, some patient scenario examples. If they have no structural heart disease and they're not hypertensive, they don't have hypertensive heart disease, then things like flecainide, grapaphenone, Sotolol are good choices. With significant LVH, amiodarone is a good choice. Patients with coronary disease, dofetilide and Sotolol, you can also use amiodarone. Patients with heart failure, do a bit better with dofetilide or amiodarone. And then if you're going to attempt a pharmacologic conversion of atrial fibrillation, most commonly we use things like flecainide, you can also use Sotolol and amiodarone. So those are some options for you for antiarrhythmic therapy. We always have to be cognizant of the side effects of these medications. So antiarrhythmic medications, as we've discussed in previous modules, they alter the influx and efflux of intracellular ions that are responsible for depolarization and repolarization. So we're trying to reduce the ability of reentry mechanisms to happen within the heart. But in doing that, sometimes we can go a bit too far. Most of these drugs will prevent or terminate AFib by altering the function of potassium or sodium channels, which as we've learned are very important in our cardiac action potential. There's a fine line often between therapeutic and detrimental effects, and these drugs work really well, but we just have to make sure that we're monitoring the patients regularly. So every six months, and you may have some different protocols depending on where you're working, but think about routinely monitoring an EKG for things like PR interval, QRS, QTC, because those are the things that are going to be affected because of these medications. And then monitoring renal and liver function as well to make sure that you're dosing these medications appropriately. Let's talk a bit more about ablation because this is something that we're going to see used more and more in the management of our atrial fibrillation patients. With a radiofrequency ablation, we use energy to produce small homogenous necrotic lesions by heating up that tissue, and there are clear indications for this. There's class one indications for a catheter ablation for things like SVT that's mentioned here, unifocal atrial tachycardia, atrial flutter, and then for atrial fibrillation, we think about this for patients with lifestyle-limiting symptoms, or maybe they have an intolerance of antiarrhythmic agents. So there are clear indications there, including some for atrial fibrillation. There are also absolute contraindications if the patient has a known atrial thrombus, a mobile left ventricular thrombus, mechanical prosthetic heart valve, or pregnancy. The success rates for atrial fibrillation will vary depending on if it's permanent or chronic AFib or if it's more paroxysmal, whereas things like SVT, a very, very high success rate with a low complication rate, success rates usually anywhere from 90 to 95% for something like that. When you talk about atrial fibrillation ablation, what we do is we target those pulmonary veins, as I'll talk about next, and so that's a more involved procedure because there's more things that we're going to have to target for ablation, more areas there. So catheter ablation can be used for patients with AFib and heart failure in particular. That's another subset of patients that tends to do quite well with this. So ablation for AFib, electrical isolation of the pulmonary veins, and we target areas that have sustained focal impulses, and it's often paired with an antiarrhythmic medication for a period of time. There's a three-month post-RFA radiofrequency ablation blanking period where patients may have some periods of atrial fibrillation as that inflammation and irritation kind of subsides there. So we give people a period of time where we say, we don't call this a failure. This is just a period of time where you're a little bit more likely to have a recurrence, and that's why oftentimes we pair this with an antiarrhythmic medication to allow for a reduction in that adverse atrial remodeling. So variable success rates, but pretty good for patients with paroxysmal atrial fibrillation in particular. Remember, we want to pair this with strict risk factor modification for the best results in symptomatic patients with heart failure and a reduced ejection fraction. Those patients do quite well in the long term with this. So there's many different studies you can read about. There's the CASEL trial, CABANA, and most recently East AFibNet, where patients have some, in general, good outcomes with greater frequency ablation. But one of the things that makes this a little challenging is that there's crossover from some of these trials from a rate control strategy to a rhythm control or ablation arm. But in general, the take-home point you can make from these is that the quality of life in general is improved for patients that have ablation. So that's why we want to consider this in our treatment strategy options. So a few fast facts from the ACC, AHA, AFib, ablation improves quality of life, LB function in heart failure patients. It can be performed in symptomatic persistent AFib, whether or not the patient has been on a rhythm control drug. And it can even be considered in an asymptomatic patient. I put a little asterisk there because we want to make sure we have that discussion with the patient and say, here's what the data shows. So it's certainly something that's an option, but we don't have as much data in those patients. Anticoagulation should be recommended for at least two months after ablation. And we want to monitor for recurrent AFib if that anticoagulation is discontinued post AFib ablation. All right, let's talk a bit more about anticoagulation because there's a lot of interesting things to consider here. Our goal with anticoagulation, we want to reduce the risk of stroke. So we have patients with AFib. One of our treatment pillars is anticoagulation. So we want to evaluate each individual patient's stroke risk. Then we want to evaluate their risk of bleeding, decide on the best choice of anticoagulation, and then set up a monitoring plan so we can follow these patients for adverse events. Certain risk factors we know adjust their stroke risk, things like age, gender, rheumatic valvular disease, if they've had a history of stroke. And so we can use what's called the CHADS-2-VASc score to really assign a risk factor to each individual patient. So here's the CHADS-2-VASc score and the acronym components. So in general, we have to always use our clinical judgment. All major studies have concluded that the benefit from anticoagulation significantly exceeds the risk for almost everybody with AFib with a chance to VASc score of at least two. If a score is one, it generally depends on what that risk factor is. So we always want to consider the individual patient. So you can see there, the higher the number, the higher their chance of having a stroke. So when you evaluate a patient with AFib, always assign them a chance to VASc score. And this will allow you to make the best clinical decision for your patient. There's something called a Hasblood score. Now I'll point out here that the Hasblood score is not quite like the chance to VASc. And you can't compare the two directly and say, this is their chance to VASc score and this is their Hasblood score. But rather the Hasblood score was developed as a way for us to identify potentially reversible risk factors. So we're saying, here's a patient who I think needs anticoagulation. Let me weigh the benefit of anticoagulation against the bleeding risk associated with that. And that's the Hasblood score. So let's say you have a patient who has hypertension or maybe they're on some other medications that may increase their risk of bleeding or they drink a lot of alcohol. Well, those are things we can target and say, let's try and reduce this and take this risk factor away. And then your risk of bleeding hopefully will go down. So that's the main utility of a Hasblood score will help us identify what are the major risk factors that I need to consider in making this decision. So then we have to think what to choose. There's all kinds of medications now that we have to choose from. And so in January of 2019, AHA, ACC and HRS came out with some revised guidelines to say that a novel oral anticoagulant is first line over Warfarin when there's no major contraindication except in patients with moderate to severe mitral stenosis or a prosthetic heart valve. Data from meta-analyses have showed that there's a significant reduction in major bleeding in patients treated with these medications, the NOACs compared with Warfarin. So those are things like Dabigatran, Rivaroxaban. So all those medications are, we classify those as the novel oral anticoagulants. We want to make sure we check renal and hepatic function before initiating one of these medications and at least annually. So as I mentioned, there's several different options for what we can use for these medications. So we start by considering the patient scenario. If we have an additional use of antiplatelet, so maybe someone's had coronary stenting, then something like low dose Rivaroxaban might be our best option. You can also use Dabigatran if you're going to combine that with an antiplatelet like Clopidogrel. Someone with a CHA2-VASc score that's high and they have a reduction in their creatinine clearance, then maybe Warfarin or Apixaban might be a better choice. So consider the medication, think about the potential side effects of that medication and try and do some research to see if there is any data out there showing a reduction in bleeding in certain patient populations. But this is another thing where we have to use our own clinical decision-making to make that choice. Question we get asked a lot by patients is, well, when can I use aspirin? Why can't I just use aspirin? Or maybe I can combine aspirin and Clopidogrel instead of using an anticoagulant, which is a great thought. But we can provide excellent patient education and develop a nice trust and rapport with our patients by having this conversation. So aspirin is consistently and substantially less effective in reducing thromboembolic risk compared to Warfarin in all AFib patients with at least one stroke risk factor. Dual antiplatelet therapy and oral anticoagulation have similar bleeding risks. So when the patient says, well, maybe I can just take my aspirin and my Clopidogrel, then we can say, well, you're not really reducing your risk of bleeding. And we are putting you at a little bit higher risk of stroke as a result of that choice. Aspirin plus Clopidogrel is somewhat more effective than aspirin alone in preventing stroke, but almost twice the major bleeding rate. So that's really our concern with these patients is we don't want to increase their bleeding risk anymore. And we certainly don't want to have a trade-off there where we're reducing the effectiveness of our stroke risk reduction as a result. What about your patient who just can't take oral anticoagulation, but they really have a higher risk of stroke? Well, the left atrial appendage occlusion is an option for these people. So the key point here is they have to have a CHA2DS2 VASc for at least two. So we want to make sure that their benefit from something like this outweighs any potential risk. So we know that there's a fair amount of people that have a contraindication to anticoagulation, but they're still at risk of having a stroke. So this is an option here. The left atrial appendage is a part of the left atrium, and it's kind of like this finger-like projection, and clots can gather there, and then that can predispose to strokes. We can have cardiac emboli that originate there in that left atrial appendage, and that can go on to cause a stroke. So left atrial appendage is this, it's like a frame that gets placed in that left atrial appendage, and there are fixation barbs that anchor that device into the left atrial appendage. And so in doing that, we can close off that area so that those clots, if they do form, they don't get into the circulation. So with this one, we have to make sure the patient is on anticoagulation for a period of time. There are several studies that have been done looking at what is the best way to do this. The PREVAIL trial is probably one of the most widely used regimens post-procedure, which says warfarin 45 days post-operatively, or until you confirm there's been a complete closure by a transesophageal echo, then clopidogrel plus aspirin for four and a half months, then aspirin indefinitely after that. So it's an alternative for non-valvular AFib who is not a candidate for long-term oral anticoagulation. Atrial flutter. So this is often more difficult to rate control than atrial fibrillation. And we want to consider the potential of a reversible cause just like we do with AFib. So think about thyroid function, anemia, are always things you think about, but then also maybe things like pulmonary disease that can predispose to this as well for putting a strain there on those pulmonary veins. Consider other reversible causes as necessary depending on your individual patient. So for atrial flutter, a couple of different options we can use. We can treat it the same way that we treat atrial fibrillation. We mentioned in our EKG lecture about typical versus atypical flutter. Patients that have typical flutter are generally, they do very well with an ablation. So there's one macro-reentrant circuit that's predominant and you do an ablation to disrupt that circuit, prevent reentry, and those people do quite well. If it's atypical flutter, you're more likely to have multiple areas of excitability and irritability. And that gets to be a bit more involved for an ablation, kind of like atrial fibrillation. So we can use ablation if it's typical atrial flutter. If it's not, we can do a cardioversion. We can attempt rate control and we can also use antiarrhythmic drugs. If you have a patient with a rapid atrial flutter and it looks like an SVT, then we can also use adenosine to try and see what's going on. So remember with adenosine, we're going to block within the AV node. And so then you can see really nice flutter waves just continue on while there's a period of ventricular standstill. And that can help you diagnose this if you're not sure what type of SVT it is. Paroxysmal supraventricular tachycardia. Another thing that we discussed in the EKG lecture, but we'll talk about this in terms of treatment in a bit more detail. So the driving circuit of a focus lies in tissue that is above the ventricles. And there's a bimodal age distribution with a variable presentation. Generally what people will say is they feel their heart racing very, very fast and it starts suddenly and it stops suddenly. So that's an important question when you feel your heart racing, do you feel like it happens all of a sudden or does it gradually increase? And so these people with true PSVT will say, no, it just starts and stops just like that, like snapping your fingers. So patients may have simple tachy palpitations and if their heart rate is very fast, they may even present with near syncope or even syncope. So 12 lead EKG is really vital. We want to try and see, get every angle of the heart rate and make sure that it's not too high. Get every camera angle we can into the electrical conduction system of the heart. So by definition, this is going to have a narrow complex QRS. The QRSs will be very regular and we want to try if we can to see the P wave and its relationship to the QRS. There are a few different things that can occur with PSVT. So in general, we can classify this as ectopic atrial tachycardia, AV node reentrant tachycardia or AV reentrant tachycardia. So with atrial tachycardia, there's three or more PACs and it's defined as sustained if it lasts longer than 30 seconds. So in general, this atrial tachycardia occurs via three mechanisms. There's enhanced automaticity or extreme excitability of atrial tissue. It can be triggered like a catecholamine surge or it can be micro reentry where there's a localized area of excitable tissue that causes those premature beats to initiate a tachycardia. With an AV node reentrant tachycardia, we have two limbs in the AV node where there should only be one creating a circuit there. With AV reentrant tachycardia, it's the same concept except now the accessory pathway is between the atria and the ventricle and it's outside of the AV node. All of these things are termed reentrant because there's unidirectional blocks somewhere, a slow conduction of an impulse and a recovery at the block site. So most of the time when we see PSVT, we're gonna think about AV node reentrant tachycardia as our classic one. But atrial tachycardia is something that occurs quite frequently. And make sure you identify if this is focal where there's just one area that's firing off rapidly. Do all the P waves look the same or is it multifocal? So multifocal atrial tachycardia will be an increased heart rate. But the key with this one is all the P waves will look a little bit different. And with multifocal atrial tachycardia, it even can have a slightly irregular appearance because of that. You see someone with multifocal atrial tachycardia, they may have some underlying pulmonary disease that's commonly seen. So if you're in the hospital and you're treating someone with COPD exacerbation or pneumonia, you may notice that they've got multifocal atrial tachycardia intermittently on telemetry. Otherwise we think about atrial tachycardia with things like atrial enlargement and any type of cardiac disease can predispose to this. Certainly things like stimulants can create an increase in that ectopic firing rate. Presentation, tachypalpitations, dyspnea, fatigue are all possibilities. And like everything else we've talked about, it depends on their ventricular rate and also the underlying substrate. So what other conditions do they have? A lot of people with underlying cardiac disease will have decreased physiologic reserve to tolerate those rapid rates. Evaluation, it can look very much like a rapid atrial flutter if you don't see any P waves. So anytime we can, we wanna really look back through telemetry to see, can I see how this initiates and how it terminates? And what you'll see is a PAC come in, a gradual slight lengthening of a PR interval before that P wave often disappears. And that can take place over just a couple of beats. And then as it slows down to terminate, you'll see that P wave poke through again before there's a termination and resumption of potentially sinus rhythm. So management, another one that can be somewhat difficult to rate control depending on what the underlying cause is. So we can try to rate control them with medications. Rhythm control is an option for these people along with potentially an ablation, which is gonna be better suited for someone with a unifocal versus a multifocal. AVNRT and AVRT, we did discuss in our EKG lecture, but for this, for AV node reentrant tachycardia, this is gonna be one of the most common things that you'll see. And it's a reentrant pathway within the AV node where we have a fast and a slow limb. So one of those will be activated. So we have a normal impulse going down the fast pathway, a PAC comes in and blocks at that fast pathway, shoots down the slow pathway of the AV node, and then goes right back up the fast pathway once it is electrically recovered, and that creates our reentrant circuit. So sometimes you won't see anything at all in those QRSs as is the case here when it's really rapid. And that's because that atrial and ventricular activation are occurring almost simultaneously. But sometimes you'll get lucky and you can see a little P wave, their retrograde P wave come through at the end of that QRS telling us about that retrograde conduction up to the atria. So AV reentrant tachycardia, this is what we call accessory pathway SVT. So with AV node reentrant tachycardia as well as AV reentrant tachycardia, ablation is an excellent treatment option for these patients. So they're gonna come in and tell you they're very, very symptomatic, especially with the, we talk about AV node reentrant tachycardia being very common. Those patients, let me go back to that slide here. So these patients with AV node reentrant tachycardia, what we can do is go in and ablate that pathway that shouldn't be there anyways. And in doing that, it's a fairly simple procedure. Now we're left with just that one pathway through the AV node. So another thing as to kind of a clinical pearl I'll mention with this is I'll always tell patients, you may still feel skip beats now and then because we know that it's usually that PAC that comes in and initiates this loop tachycardia. Well, we're not doing anything to fix that. All we're doing is taking out that extra pathway. So that PAC doesn't go down and then come back up and initiate our tachycardia. So I'll always tell patients, you may still feel palpitations. You may still feel an occasional skip beat, but what you shouldn't feel is that followed by a rapid regular sustained tachycardia. So ablation is an excellent option for AV node reentrant tachycardia. We can also give them medications like beta blockers or calcium channel blockers to try and suppress that, but quite patient dependent depending on what they want, but an ablation procedure is an excellent option for that because of the high success rate and the low complication rate. So with AV reentrant tachycardia, another one we treat with ablation, but this one that pathways outside of the AV node. And as a result of that, we see pre-excitation and recall that that is a short PR interval and a slurring in the upstroke of the QRS called a delta wave. So that's what we will look for on baseline EKG for these patients. And you can see there, the delta wave is marked and you can see in every lead, the PR interval is a bit short. So that happens because we are shooting around the AV node outside and that accessory pathway and going down to the ventricles. And that's what creates that slurring in the upstroke because the ventricles are being stimulated outside of the AV node. So if this is their baseline EKG and you see this in a patient who has tachy palpitations or near syncope, that's concerning because that means that patient has the potential to conduct very, very fast outside of the AV node. And so when they actually, they may never manifest an arrhythmia at all. So when you see a delta wave, that just means you need to ask more questions to make sure that they're not having tachy palpitations and they're already manifesting an arrhythmia. But these pathways just depends on which way they go through to the ventricles. So with what we call orthopedromic tachycardia, they're going to go through the AV node and then back up the accessory pathway to the atria. And that's why we see those retrograde P waves in the inferior leads. So conduction occurs integrated via the AV node and retrograde via the accessory pathway. That's gonna be the typical scenario that you'll see with AVRT. Now the other type is much less common that can look a whole lot like VT because it's a wide complex, it looks wide complex. And that occurs because now we're stimulating the ventricles from outside of the AV node through that accessory pathway. We have, and then we're going back up through the AV node. And so remember this is the one that we get a little bit more concerned about because now they're showing that they can conduct fairly quickly down that accessory pathway. So the concern here is really if that person were to develop atrial fibrillation or atrial flutter, where now the atrial rate is extremely high, where they're having some type of a one-to-one conduction that's gonna happen where we have atrial rates of 250 beats per minute, there's the potential for that connection, for that pathway to conduct very quickly. And that's when people can go into ventricular fibrillation and have sudden cardiac death. So those are the people, that's why we care about a delta wave. So evaluation and management, get a 12 lead EKG if you can while they're in the arrhythmia and evaluate the P wave in relationship to the QRS. For anybody with these types of PSVTs, get a Holter monitor, consider the potential for an electrophysiology study to better document what's going on. Radiofrequency ablation is going to be curative for these patients. You can consider rate control management for them. If someone has a delta wave, that warrants closer evaluation. So let's talk about what we do there. So there's two types. So there's with Wolf-Parkinson-White, which is that pre-excitation on EKG, we see that delta wave short PR interval. We call it a pattern if they have pre-excitation without symptomatic arrhythmias. So those are patients where you would do usually a non-invasive management risk stratification approach. So for instance, you might put that patient on a treadmill and hook them up to an EKG and then see what happens as you increase their rates. So remember from our very first lecture about this chain of command within the conduction system, the fastest pacemaker will win. And then as we move through our conduction system, if there's extra pathways, they don't, for instance, like this, in this case, our AV accessory pathway, the bundle of Kent, we don't know how fast that's going to conduct. And so sometimes when you make it go faster, it just kind of stops conducting and everything shunts back to the AV node. So you have someone with pre-excitation, you put them on a treadmill and then you see at faster rates, gradually faster rates, if you see that pre-excitation go away, that means that pathway probably can't conduct very fast for a long period of time. And now you see them shut down the AV node where everything just kind of goes back to normal. So that makes you feel pretty good about it. But if you do that same thing, and then you see that they're able to conduct very, very fast through that accessory pathway, that's someone where you might want to start thinking about, hmm, maybe I need to do something else to see what's going on. So options, an exercise treadmill test, like I mentioned, you can also give the patient an ambulatory monitor for maybe two or three days and just see if they've got any fast rates associated with that. Now, if they have WPW syndrome, this one means they have pre-excitation on EKG in addition to symptomatic arrhythmias involving an accessory pathway. In general, these people are usually recommended for an electrophysiology study and possible ablation. Most people with WPW pattern remain asymptomatic, but AFib can occur in anywhere from 10 to 30% of patients with WPW syndrome. And that's why those people are generally referred to electrophysiology. So I hope you found this discussion on atrial tachyarrhythmias helpful, and I hope you learned some tips that you can incorporate into your own clinical practice. Thank you.

atrial tachyarrhythmias

premature atrial contractions

atrial fibrillation

atrial flutter

paroxysmal supraventricular tachycardia

CHADS2-VASc score

delta wave

electrocardiogram