Today's topic is electrophysiology for the cardiovascular advanced practice provider. My goal with this presentation is to share with you some pearls that I learned from working for many years in electrophysiology, and I've tried to pick out things that are specific to disease states that you may be encountering in your own clinical practice. Our main objectives are listed here on the screen, but we're going to focus on things like atrial arrhythmias, paroxysmal supraventricular tachycardia, ventricular tachycardia, as well as a few pearls related to pacemakers and defibrillators. By the end of this presentation, I hope you feel confident and comfortable in creating a treatment plan for patients with many different types of arrhythmias. Let's start with premature atrial contractions. Premature atrial contractions, or PACs, are very common. You'll see them a lot in clinical practice. The majority of these patients will end up being fairly benign. However, it's up to us as clinicians to make sure there's not something else going on. PACs, the reasons to treat them are twofold. They may cause lifestyle limiting symptoms, and they may progress to sustained atrial arrhythmias, the most concerning of which would be atrial fibrillation and atrial flutter. A higher PAC burden is associated with an increased incidence of atrial fibrillation. If frequent PACs are suggested by history or by routine monitoring, such as EKGs, consider additional testing to quantify the PACs, such as ambulatory Holter monitoring. Epidemiology includes things like excess sympathetic stimulation, ischemia, or valvular heart disease. Patients may present with symptoms such as palpitations, fatigue, or dyspnea. You can check a 12-lead EKG to try and capture these on monitoring, or maybe you'll evaluate patients via telemetry in the hospital. Your main job with PACs is to differentiate them from other things like premature ventricular contractions, and what's helpful when you're evaluating PACs is that you'll notice that the QRS is narrow, and a P wave will often come early, and so if you can find a P wave, try and evaluate that. You can't always see a P wave, and sometimes it's buried in the preceding T wave. Sometimes PACs will come in pairs, or they may occur every other beat. We call this atrial bigeminy. While there's no consensus information regarding total PAC count that is potentially concerning, a PAC burden approaching or exceeding 10% of total beats in 24 hours may warrant additional follow-up. Sometimes you see PACs in patients that have additional comorbidities that may predispose to additional atrial arrhythmia, such as structural heart disease or diabetes mellitus. Hypertension is also associated with an increased risk of atrial fibrillation, which sometimes can be seen initially with an increased amount of PACs. The majority of the time, though, when you see patients with PACs, they end up being benign, and so we want to look for reversible causes as well. Things like excessive caffeine intake or stress, dehydration, and poor sleep patterns can also predispose to PACs. Try to quantitate them by monitoring, and then for management, there are many different options, but your first option should be a rate-slowing medication. Things like beta blockers work really well for PACs because they suppress hyperadrenergic response as well. Calcium channel blockers are an additional option for management of PACs. Atrial fibrillation. This is the most common sustained arrhythmia worldwide. The risk increases with things like age, sleep apnea, hypertension, obesity, and diabetes. In fact, these are so common that atrial fibrillation increases substantially with age, but then the more of these risk factors that you add together, the more likely your patient is to have atrial fibrillation. Clinical presentation may be things like palpitations or fatigue or dyspnea. Patients may present with signs of ischemia like chest pain or heart failure. Oftentimes this will depend on the ventricular rate. Patients that have an increased heart rate or an accelerated ventricular response with atrial fibrillation are more likely to be symptomatic. When you're evaluating a patient with atrial fibrillation, a 12 lead EKG is the first step followed by ambulatory Holter monitoring to assess total arrhythmia load. You may order an echocardiogram to assess for structural heart disease or the size of the left atrium. An increased left atrial size is associated with atrial fibrillation. Symptoms like valvular heart disease can contribute to this, specifically mitral regurgitation. You may consider an ischemic workup as well, depending on how the patient presents. So the first step is to take a very good history. Evaluate the type and severity of symptoms. When did the symptoms first start? Would you classify this patient as having paroxysmal symptoms where they come and go? Is their atrial fibrillation persistent or chronic? How long do the episodes last? Always look for reversible causes, things like a comprehensive metabolic panel to evaluate for electrolytes, thyroid function tests in case the patient has hyperthyroidism that is undiagnosed, or maybe there's an underlying anemia that's contributing. Diagnostic testing, ambulatory monitoring will help quantify the total amount of atrial fibrillation that's present, and you may consider, as mentioned, an echocardiogram or a stress test. Once you identify that a patient has atrial fibrillation, you should immediately risk stratify that patient. Patients should be evaluated for the risk of a stroke, and that's ultimately your concern with atrial fibrillation. You want to evaluate a patient's CHAD2-VASc score, which we'll talk about in detail here. If symptoms are occurring on a daily basis, a 24-hour Holter monitor is probably the best place to start. However, you may need to order a more extensive monitoring, like a two- to four-week monitor if a patient has symptoms that are occurring maybe only a few times per week. The management, your first step is to figure out how long this has been going on, how bothersome the symptoms are to the patient, and then evaluate their overall heart rates. We want to make sure we control their ventricular response, and the fastest way to achieve rate control is to convert that patient to sinus rhythm. Determine what their stroke risk is, try to control their overall rhythm, and you always want to prevent a recurrence. Atrial fibrillation management can be thought of in terms of acute or more long-term. In the acute phase of managing atrial fibrillation, consider their symptoms. If the patient is hypotensive and they're highly symptomatic, a cardioversion may be attempted. This is where the timing of the symptoms is very important, because if the patient's been in atrial fibrillation for longer than 48 hours, the risk of intracardiac thrombus formation is high, and at that point, we need to anticoagulate the patient for about three weeks before we can attempt a cardioversion. If a patient's been in atrial fibrillation and you're certain of it for less than 48 hours, a cardioversion can be attempted. If you still need to cardiovert the patient, but you think the risk of a thrombus is there, you can also do a transesophageal echocardiogram just prior to cardioverting that patient. For rhythm control, options include flecainide, propafenone, and dofetilide in the acute phase. The long-term management of atrial fibrillation is a lot more complex. In general, we like to think of atrial fibrillation management as a rate control strategy or a rhythm control strategy. If the patient is symptomatic, they probably deserve a shot at maintaining normal sinus rhythm, so you always have to take into account the clinical situation, things like risk factors for stroke, the ventricular rate, and hemodynamic impact of the arrhythmia as well as the patient's symptoms. So we need to pick a strategy, either try to control the rate or try to control the rhythm, and we'll talk about some different options for that. And possibly the most important step in the management of atrial fibrillation is to evaluate the need for anticoagulation because we don't want our patients to have a stroke. For rate control options, we have beta blockers or non-dihydropyridine calcium channel blockers as well as digoxin. Those are all good options for controlling a patient's rate. We tend to choose beta blockers first, but you always have to consider the individual patient scenario and if there are contraindications to certain medications. When atrial fibrillation is more persistent, it's reasonable to restore sinus rhythm with an anti-arrhythmic drug therapy or a cardioversion at least once in patients younger than 65 and in patients 65 or older who are symptomatic despite adequate heart rate control. You can also consider an ablation procedure, which we'll discuss here a little bit later. For rhythm control, patients do a little better if their left atrial size is less than 5 centimeters. Younger patients and those who have less time in atrial fibrillation. The longer time a patient spends in atrial fibrillation, the more likely they are to have adverse electrophore remodeling. So atrial fibrillation can actually cause a fibrotic process within the atria, which makes it very difficult to get the patient back into normal sinus rhythm. So if you choose rhythm control strategy, it's generally a good idea to attempt that as early as possible. Radiofrequency ablation is a great option for a lot of patients, particularly in patients with heart failure with reduced ejection fraction. In general, radiofrequency ablation is associated with an improvement in quality of life. Risk factor modification is an often underappreciated treatment pillar in atrial fibrillation. You can have an up to 50% reduction in arrhythmia load when blood pressure, glucose, weight, and sleep apnea are well controlled. Specifically when it comes to ablation procedures, these patients will do better in the long term if their risk factors are well controlled. Antirhythmic therapy is a little bit complex, though. There's lots of different options that we can choose, and there are certain contraindications to many of these drugs. If patients have renal failure, they should not be given sotolol or difetilide. If patients have liver failure, they shouldn't receive amiodarone. The presence of coronary artery disease can also alter our choice of antirhythmic drug. For example, things like flecainide aren't generally recommended. If someone has a depressed LVEF, you'll want to avoid things like sotolol. And finally, patients with severe hypertension with marked left ventricular hypertrophy, such as a LV wall thickness greater than about a centimeter and a half, there's a slightly increased risk of proarrhythmia when these drugs are used. When you prescribe these medications, you also have to be aware that you need to routinely monitor your patients. In general, we're going to get things like liver or renal function testing regularly to make sure that there's no issues with toxicity, and EKGs are also ordered to monitor things like PR interval, QR restoration, and the QTC. So if you remember back to the days of pathophysiology and physiology, our cardiac action potential, that's really where these drugs work their magic. So antirhythmic medications alter the influx and the efflux of intracellular ions that are responsible for depolarization and repolarization. And they act on different drugs, act on different phases of that action potential in order to exert their desired effect. As a result of this, we can see EKG changes. For instance, with flecainide being a sodium channel blocker, it can affect things like the PR interval or the QR restoration, whereas things like sotolol that are potassium channel blockers, we can start affecting things like the QT interval. So be cognizant of the drug that you choose and what kind of side effects you need to look for and monitor at routine visits, because there's often a fine line between therapeutic and detrimental effects. Atrial fibrillation ablation is a very exciting technology that we have available now. This uses radiofrequency energy to produce small homogenous necrotic lesions by heating tissue in a particular area, and we generally target the pulmonary veins for this. There are clear indications which are set forth by the American College of Cardiology. So class one indications for catheter ablation with regard to atrial fibrillation would be lifestyle limiting symptoms and inefficiency or intolerance of at least one anti-rhythmic agent. We can also do ablations for other things like paroxysmal supraventricular tachycardia or symptomatic ventricular tachycardia. For atrial fibrillation, there are known contraindications as well, such as an atrial thrombus or a mobile left ventricular thrombus. Patients who have mechanical prosthetic heart valves are generally not crossed with ablation catheters in pregnancy. Success rates for curing atrial fibrillation are generally very high. However, patients do a little bit better if the ablation is pursued early in the course of atrial fibrillation, for reasons I already mentioned related to adverse atrial remodeling. Patients also do a little bit better if they have been in atrial fibrillation for less time. Patients who have paroxysmal atrial fibrillation might do a little better than someone who has chronic atrial fibrillation. The procedure involves electrical isolation of the pulmonary veins. Certain things put an increased pressure on this portion of the atria. Things like obstructive sleep apnea or hypertension can contribute to increased pressure and that places a strain and can predispose atrial fibrillation. Atrial fibrillation that is sustained is targeted for radiofrequency ablation. Oftentimes we will pair this procedure with an antiarrhythmic medication for a period of time. Success rates are generally better for paroxysmal atrial fibrillation than for those with persistent or chronic AFib. Studies show that strict risk factor modification has the best results when you pair this with an ablation. Anticoagulation. This is a common topic that you will encounter a lot in clinical practice. Anticoagulation and atrial fibrillation should always be evaluated. We want to make sure we are making good decisions about what drug to choose. We should do that based on assessing their risk. What is the risk benefit ratio for anticoagulation for any given patient? We evaluate the stroke risk, evaluate their bleeding risk, decide on the best choice of anticoagulation and then we set up a monitoring plan. We have the CHA2DS2-VASc score which can help us risk stratify our patients. Points are given to certain risk factors that increase the chance of a patient having a stroke. The more stroke risk factors a patient has, the higher their odds of having a stroke when they have atrial fibrillation. Here is a chart that shows you the CHA2DS2-VASc acronym. We use our clinical judgment when we are deciding who gets anticoagulation. All major studies have concluded that the benefit from anticoagulation significantly exceeds the risk for almost all AFib patients with a CHA2DS2-VASc score of at least two. A patient who has a score of one, it generally depends on the risk factor, but most of the time we are going to recommend anticoagulation for these patients too. You can see there the breakdown of the increasing risk of a stroke as we start compounding these risk factors together. We evaluate the risk of the patient having a stroke, but then we also have to think about what is the risk that we are placing the patient at for bleeding when we add anticoagulation. There is something called a HAS blood score. You cannot directly compare and say the CHA2DS2-VASc score is this and the HAS blood score is this and I can compare them head to head because that is not the way it works. With the HAS blood score, what we are really doing is we are evaluating bleeding risks. This was designed to allow us to identify reversible risk factors for bleeding in a patient where we can say I want to make the risk benefit ratio as favorable as possible when I am starting these medications and I know increase the risk of bleeding. Things like hypertension, abnormal renal or liver function, history of a stroke, bleeding disposition and age, those are all things that increase the risk that a patient will have some bleeding events, but there are certain risk factors there that I can potentially adjust. We cannot change the patient's age, but we can look at the medications they might be on or a history of alcohol abuse, maybe try to achieve better blood pressure control, and we can then lower the chance that that patient is going to have an adverse bleeding event on anticoagulation. A HAS blood score is a nice tool that we have that can complement a CHA2DS2-VASc score. The next question that comes up a lot is how do I choose an anticoagulant because there are so many to pick from. In 2019, the American Heart Association, American College of Cardiology, and Heart Rhythm Society came together and had some updated guidelines for us to look at, and so what we found was that a DOAC or a NOAC, so direct oral anticoagulant or novel oral anticoagulant, that they are great choices. They should be first line over warfarin when there's no major contraindication except moderate to severe mitral stenosis or a prosthetic heart valve. You should look at renal and hepatic function initially before starting one of these medications and then at least annually, and then you can start by considering the patient's scenario when you decide which one of these medications should I use, and the AHA actually offers up a few scenario guidelines that can help you make this decision. For example, very common that we'll see patients that are also on an antiplatelet medication for maybe they had recent coronary stenting, and then we're seeing them for atrial fibrillation. How do we manage that where we can improve our patient's outcomes but also not increase their risk of bleeding any more than we need to? So in this case, you may choose low dose rivaroxaban or dabigatran plus clopidogrel, and that has been shown to have better outcomes. What about patients that have maybe some chronic kidney disease or renal failure? Well, if they qualify for an anticoagulant and they have creatinine clearance less than 15, or who are on dialysis, warfarin or apixaban may be a better choice. So there's lots of data to examine. This is a study that showed a few different scenarios that I thought might be helpful for you to look at as well. So you have to always consider each individual patient's scenario. There's not a strict flowchart you can use in choosing anticoagulants, but certain patient scenarios may point you one way or the other, and I've included a few of those here for you to look at. Aspirin. Lots of patients are on aspirin, and this is a common question that we hear is, well, can't I just take aspirin? Why do I have to take warfarin or dabigatran? 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. That's another common question. Well, can I take aspirin plus clopidogrel? And so when you start combining those, you're not improving your stroke outcomes, but you're almost at the same risk of bleeding as if you took oral anticoagulation. So it's an important patient education point. Aspirin plus clopidogrel is somewhat more effective than aspirin alone in preventing stroke, but there's almost twice the major bleeding rate. A final option for reducing stroke risk is called a left atrial appendage occlusion. One out of 10 patients have a contraindication to anticoagulation, and about 40% are at risk of stroke who are not receiving anticoagulation. So if you look at randomized clinical trials for prevention of stroke, there's about one out of five patients will discontinue these novel oral anticoagulants during follow-up, and those patients are unprotected. So a left atrial appendage occlusion has emerged as an alternative for stroke prevention in patients with an elevated stroke risk based on a CHADS-2-VASc score who have appropriate rationale for avoiding oral anticoagulation. So with this procedure, there's a semi-spherical frame that has a coating on it to block thrombus embolization, and it's got little fixation barbs that anchor the device into the left atrial appendage because this is a place where a lot of clots originate. And so if you occlude that area with this device, then you can reduce the chance of those clots forming and embolizing somewhere else. These patients do have to take warfarin for about 45 days post-operatively, clopidogrel plus aspirin for four and a half months, and then aspirin alone. So it is an alternative option for non-valvular atrial fibrillation patients who are not a candidate for long-term anticoagulation. And these patients have to have a CHADS-2-VASc score of at least two. Cardiac rhythm monitoring, you'll be in charge of a lot of this in the outpatient setting and also maybe if you're in the hospital and discharging patients home for follow-up. There are several options that we have, and it really depends on how often the patients are having symptoms. When patients have symptoms every day, a 24-hour Holter monitor is great. Other benefits of this is it records every beat for 24 hours. So if you want to get a better idea of how often patients are having arrhythmias and a total number of PACs or PVCs out of 24 hours, a Holter monitor is great. However, if patients are only having symptoms a couple times a week or maybe a few times a month, you may not catch that on a 24-hour Holter monitor. And that's where event monitors come into play. So these are more extended wear monitors, and there's different options here as well. But for patients that have symptoms maybe a few times a week, you can give them a monitor that they wear, and then they trigger it whenever they are having symptoms. At that point, it has some retrograde recording that will record the episode that that patient feels. So you can document things in a diary, and then you can look back at their symptoms and compare it to what was going on with their monitor. A final option is an implantable monitor. These are typically reserved for patients that have significant symptoms that you're not able to document, or maybe this is a patient where they've got strokes and you can't figure out a cause for what's going on, or someone with syncope and you're never able to catch it on one of the other monitors. An implantable monitor is about the size of a thumb drive, and we put that just under the skin, and that can be in there for years at a time. And we can have the patient periodically return, and we can interrogate that device just like we would a pacemaker to see if there's any abnormal rhythms. Let's move on to our next topic, which is paroxysmal supraventricular tachycardia. So one of our favorite things that we evaluate in electrophysiology, PSVT. This is defined as a driving circuit of a focus that lies in tissues originating above the ventricle. PSVT is a little bit of an umbrella term for anything other than ventricular arrhythmias, but when we say PSVT, we're typically talking about three things. We're talking about atrial tachycardia, AD node reentrant tachycardia, and atrioventricular reentrant tachycardia. These patients will typically have symptoms that will start very suddenly. They start and stop suddenly, which differentiates it from other things like sinus tachycardia, which tends to be more gradual. Depending on the rate, the heart rate patients have and their physiologic reserve, patients can be highly symptomatic from this. Oftentimes they'll present with tacky palpitations or a sensation that their heart is racing away. If the ventricular rate is very high, they may experience near syncope or even syncope. Your initial evaluation for this should be a 12 lead EKG because sometimes we can see clues on the EKG that can tell us what might be going on. When you catch something like this on telemetry or an EKG, it's going to be a narrow, complex tachycardia. It will be regular. The QRSs will follow a pattern. Anytime you can, you want to try and identify the P wave and look for its relationship to the QRS. This can help us figure out what's going on. here's an example of an EKG of a patient with PSVT, and what you'll notice here is that the QRSs are very fast, they're regular, and when I really look in between, all in between those QRSs, I cannot readily identify a P wave, and so then I can simply call this SVT or PSVT. You can send them over to electrophysiology where we can maybe do some additional testing to try and figure out what's going on, but oftentimes you're left with simply a differential diagnosis of the three things that I mentioned earlier. If you're able to get a 12-lead EKG while the patient's in the arrhythmia and you can see a P wave somewhere in there, that often holds the key to the diagnosis. We can try and do Holter monitoring to capture the patient's symptoms, Holter monitor or an extended event monitor. Sometimes we end up doing an electrophysiology study, and that's ultimately how we treat PSVT that needs to be ablated. So an ablation procedure is essentially curative for most forms of PSVT, and what we do there is we kind of heat up the tip of a catheter and we zap out this abnormal focus that shouldn't be there anyways, and that typically relieves the patient's symptoms. We can also attempt rate control for those patients who don't want an invasive procedure. Things like beta blockers and calcium channel blockers are fine options for that as well. You should always get a baseline 12-lead EKG to evaluate for a delta wave, so I'm spending just a little bit of time talking to you a bit more about a delta wave because we all know what we all hear that and we know what it looks like typically on EKG, but it's important to understand what that actually means and what additional questions you should ask your patient. So patients with Wolf Parkinson-White syndrome is what this is called, where there's an accessory bypass tract called the bundle of Kent. Normally conduction starts in the sinus node and it spreads down through the AV node and goes on to the ventricles, and we see a P wave and a QRS and a T wave and everything repeats itself. Well, if you have a bypass tract, that's an abnormal tract of tissue that's going to be somewhere outside of the AV node between the atria and the ventricles, so somewhere on either side, and what happens is electricity starts in the sinus node and it races down through the atria, so anytime conduction starts in the atria, it's like you drop a pebble into a pond and you drop it into the pond and it ripples out all around, and that's what happens in the atria is the sinus node sends that impulse and it ripples through the atria and it goes wherever there's a gateway, and usually the only gateway is the AV node, but if someone has a bypass tract between the A and the B outside of that, like in Wolf Parkinson-White syndrome, then we can see what's called pre- excitation on an EKG, and so that is a short PR interval and a delta wave, and that's because the electricity is kind of getting to the ventricles a little bit early, so when you see a delta wave, you should start asking the patient more questions, so you ask them, do you have palpitations? Do you have tachycardia? Do you ever feel like you're going to pass out? A lot of patients have evidence of pre-excitation in this accessory pathway and they don't have any symptoms at all, but if patients start having symptoms related to this, that's where we could run into some trouble. What happens is the AV node, it can only conduct so fast. It has what's called principles of refractoriness, which is this really incredible mechanism built in where the ventricles can only go so fast. They have an upper rate limit. However, the bypass tract doesn't have that built in, so if a patient were to go and do, say, atrial fibrillation and the atria are beating 300 beats per minute, well, if that bypass tract works really, really well, those patients can conduct up to 300 beats per minute, and that's when patients can pass out, and they can even die from this sort of arrhythmia. That is not the majority of patients, but it's a reason why we should certainly ask patients a bit more questions when they start coming in with a delta wave, or if they have symptoms of tachypalpitations, that's one of the things that you're going to look for on their baseline EKG. Premature ventricular contractions. We'll switch now to ventricular arrhythmias. This is a premature QRS, comes in early, before the P wave, and it's wider than the dominant QRS complex. It is not preceded by a P wave. There's often a compensatory pause that's associated with this that comes after where there's an electrical resetting. With PVCs, we want to note a few things. One, are they unifocal or multifocal? In this example here, the top strip, you can see these unifocal PVCs. This is a normal beat. I'm going to get a little, show my mouse here. This is a normal beat right here, and then this beat's coming in early, and it's wide. It's a wide QRS, and I don't see a P wave coming before it. There's a little resetting, and then everything starts again. This is ventricular bigeminy, but every one of these PVCs, they look the same. They're monomorphic, and that makes you feel a little bit better because that means they're all coming from the same place in the ventricle. We can compare that to the second example here, where I have three different morphologies of PVCs, and we get a little bit more concern about that. It could still be benign. However, when you see that, that means there's multiple areas of potential irritability there in the ventricles, and we want to make sure that patient's not ischemic. These are PVCs. We want to know if they're unifocal or multifocal. Are they coming in things like bigeminy and trigeminy? Then we want to make sure we quantify those and make sure there's not a lot of them coming all at once. Epidemiology. We think about these occurring more likely in patients that have hypokalemia, so low potassium levels can predispose to this. Men have a slight predilection to PVCs and increasing age. Presentation. Patients may present with palpitations or near syncope. If it's ischemic in nature, they may have angina, and they may even have hypotension. When you're evaluating these patients in the office, you may note that during the time of their ectopy, you may not feel a peripheral pulse intermittently. That's because those PVCs are coming in early when the heart hasn't had time to completely fill with blood before it beats again. That can poorly perfuse peripherally, and that can scare patients a lot because they'll feel their pulse and they'll tell you, my heart rate's 30 beats per minute, and you ask how they feel. I feel okay, I just feel my heart skipping, and that's because if they're in bigeminy, for example, every other PVC is probably not perfusing distally. The evaluation of PVCs should center upon monitoring. We want to know how many PVCs they're having, how often are they occurring, and what is the overall load? The reason we care a little bit more about this is because with a 10 to 20,000 PVC load in the course of a day, or if patients are starting to be 10 to 20 percent of their total beats, there's a risk of cardiomyopathy that can occur from this. Because of the risk of this occurring with structural heart disease, we want to consider getting an echocardiogram as well as a stress test depending on the clinical situation. Oftentimes, PVCs are completely benign, and they don't warrant any further follow-up or management. However, we do need to make sure that we consider the individual patient. PVCs that are occurring in a young, healthy 20-year-old female maybe carry a different prognosis than PVCs that are occurring in a 65-year-old man with heart failure with reduced ejection fraction. We should evaluate those patients differently based on that scenario. So management, we want to consider their symptoms, what is the patient scenario, and what is the total burden of PVCs? If patients don't have very many PVCs, they're not bothered by them, and you're not concerned about any high-risk findings that would be suggestive of underlying pathology, you may choose to do nothing. Some patients will feel better on a beta blocker, and that's typically what we reach for first line. If that does not work, you can consider things like antiarrhythmic medications, and then if it's a focal PVC pattern, a radiofrequency ablation can be attempted as well. There are several different etiologies of why does VT happen. Rarely, it can be adrenergically mediated, so related to increased automaticity. You may see this as what we call triggered activity, which are related to abnormal after depolarizations, and the more common ones, so we have early after depolarizations and delayed after depolarizations, which tell us about abnormal activity relative to that action potential. Patients that have early after depolarizations, that can occur with things like long QT syndrome, so if we increase the relative refractory period, which occurs during that QT interval, a PVC falls there, that can take off as torsades and become a polymorphic VT, where it would normally be blinded by the refractory period is a little bit shorter. If you start prolonging a QT interval, now we increase the risk of patients having ventricular arrhythmias because we create more instability as that ventricle fully repolarizes. Then, maybe the most common one that you'd see is called reentry. Structural heart disease can create scar tissue, either if there's been an ischemic insult or if there's weakened heart muscle, that can create an ischemic insult. That can create a potential nidus for a reentrance circuit around that abnormal tissue. This top example here is monomorphic ventricular tachycardia, and you can almost picture a big old scar there in the ventricle and how this could just circle around and around that as electricity reroutes around that abnormal tissue. On the bottom here, we have polymorphic VT, and as I mentioned, this is something that you're more likely to see when there's a prolonged QT interval. When I see polymorphic VT, I'm going to automatically look for things like hypokalemia or prolonged QT, and then I'm going to evaluate the patient for symptoms specific to ischemia. You always want to document if the VT is sustained. Is it sustained if it's greater than 30 seconds because that can alter your ultimate treatment, if it's monomorphic or polymorphic, and then differentiate from things like aberrantly conducted SVT. Sometimes people that have maybe a bundle branch block at baseline and then they go into SVT, well, their QRS can still appear wide, and that can be a hard thing to really pick out. One thing to always remember, though, is that ventricular tachycardia is much more common than aberrant SVT, so specifically if you have a patient with structural heart disease, you should always assume VT until you prove otherwise. A couple other things we can look at when we're evaluating for VT would be AV dissociation and fusion, so these are really diagnostic characteristics of ventricular tachycardia. A fusion beats, well, actually both of these are more, you're more likely to see these at slower VT rates because as if VT, we've got a wide QRS, and if I speed up the rate, it's going to be harder to see what's going on in between, so it's harder to pick up these little nuances like a P wave buried somewhere like we see with AV dissociation. AV dissociation just means that I've got P waves marching through doing their thing, and I've got ventricular rate marching through doing its thing, and they're not related to one another, so they're occurring independently of one another. A fusion beat is something that is marked here with an F in these strips, and so a fusion beat occurs at slower rates because what happens is the P waves are still, they're still marching on through, and if a P wave slips down to the ventricle and captures the ventricle at a rate similar to where that VT focus is firing away, they can fuse together, and so what you get is a QRS complex that's kind of a mix of the intrinsic QRS and the ventricular beat that's coming in from the VT. VT is highly associated with ischemic heart disease, cardiomyopathies, and it's also associated with things like channelopathies, like a long QT syndrome. It may be idiopathic as well, but generally you're still going to work that patient up for other concerning features before you just say it's idiopathic. Symptoms depend on the ventricular rate, the duration of the tachycardia, and if they've got underlying heart disease. If someone's got an ejection fraction of 15 percent or someone already has maybe a 70 percent coronary lesion, they're probably going to tolerate VT less better than someone who doesn't have those things. Likewise, if someone has VT at a rate of 120 beats per minute, they may tolerate that better than someone with a VT rate of 180 beats per minute. Presentation also depends on if the episodes are non-sustained and if they're hemodynamically stable or unstable, meaning they're hypotensive as a result of that arrhythmia. Evaluation should always look for signs of active ischemia, electrolyte abnormalities, particularly low potassium, a long QTC, and an echocardiogram looking for structural heart disease, specifically a reduced ejection fraction. Management of these patients really depends on their presentation. Are they hemodynamically stable or unstable? Because anytime a patient has hypotension or symptoms that are debilitating like chest pain, pressure, they feel like they're going to pass out, then defibrillation may be pursued in those patients. Acute management, you can use things like IV amiodarone, lidocaine, and procainamide for patients or cardioversion, as I mentioned. So cardioversion, if you're able to sync to a QRS, if they have a pulse with their VT, whereas if it's a pulse-less VT, then you're going to want to just defibrillate that patient. Electrolyte replacement and heart failure management, if there are things that might be reversible, maybe a patient comes in with volume overload, they may do better if you relieve some of that volume from them. And then evaluate for signs of ischemia. Long-term, ablation, if it's monomorphic, may be considered. Beta blockers work really well for suppressing VT, and antiarrhythmic medications may be considered. And then, of course, you want to evaluate if that patient is a candidate for a defibrillator. So I wanted to just go over this a little bit here. This is from American College of Cardiology. So ischemic heart disease remains the most common underlying substrate that's associated with sudden cardiac death. We know that there are high-risk subgroups. Those are our patients that have known structural heart disease, reduced LVEF, patients that have ischemia. And then we've got our moderate-risk to low-risk states. Those are patients that have a risk profile that places them at higher risk for sudden cardiac death. But what's interesting is the patients of the general population that come in with sudden cardiac death, about 50% of them or more, it's their first recognized clinical event. That means that there's a lot of patients out there that aren't being evaluated appropriately, and their risk factors are not being monitored or treated. And these are the patients that come in with sudden cardiac death. So about 50% of all cardiovascular death and at least 25% is their first cardiac event, these patients that have sudden cardiac death. And out-of-hospital survival is about 10%. So even though it's a terrible situation, I love to see those patients in the hospital because we can tell them, you made it. You're one of the 10% that made it. And let's work on those risk factors now. So other risk factors like increased age, men are a little bit higher risk. So we want to make sure we're always evaluating those risk factor profiles in our patients because we want to prevent an event from happening in the first place. Primary versus secondary prevention, implantable defibrillator. So for those with established ventricular arrhythmias and the setting of structural heart disease, you want to risk stratify those individual patients, and that can help guide further treatments. So sudden cardiac death is obviously the most concerning potential outcome for those patients. And ICDs are placed in patients who meet criteria based on them having an increased risk of these life-threatening arrhythmias. So if we look at this chart here, you can see patients with ischemic heart disease with a meaningful survival of greater than one year. Do all of the following apply. They have a low EF. They are at least 40 days post MI and at least 90 days post revascularization. So that's important because let's say a patient comes in, they have an MI, but they get an LAD stent. Well, we want to wait 90 days and place them on good medical therapy and see if their ejection fraction improves before we put a defibrillator in them. If it doesn't, then those patients need a defibrillator. So if their EF remains less than or equal to 35% and their New York Heart Association class two or three heart failure despite guideline directed management and therapy, then those patients qualify for an ICD for primary prevention of sudden cardiac death. If their EF is low, less than or equal to 30%, and they have New York Heart Association class one heart failure, they qualify for an ICD. And then on the other side of things, we look at things like secondary prevention. So these are patients that have sudden cardiac arrest that's due to VT or VF. They have hemodynamically unstable VT, stable VT or unexplained syncope plus inducible VT on an electrophysiology study. And all of these things are not due to a reversible cause, like they've got a potassium of 2.3 or something like that. Then they are recommended for an ICD for secondary prevention. So there are very clear guidelines which help us risk stratify our patients. So VT can progress to ventricular fibrillation. That means there's no meaningful cardiac output. And this occurs most often in association with coronary disease as a terminal event. And one thing to always remember is the longer someone stays in ventricular fibrillation, the less chance you have of bringing them out of that arrhythmia. And then once they get to asystole, we think about that as not a shockable rhythm. So time is very important. Clinical presentation with VF. These patients are not going to be walking and talking to you. Loss of consciousness. They don't have a blood pressure that you can measure. And management should follow ACLS guidelines. Our final topic is pacemakers. So pacemakers can be single chamber, dual chamber, or biventricular. And the indications are to relieve or prevent symptomatic bradycardia that's not due to a reversible cause. So things like second degree type 2 heart block, third degree heart block, types of high grade AV block. Those are patients who qualify for a pacemaker. And then there are additional indications for people who get pacemakers who have significant symptoms related to a rhythm disorder that doesn't fall in one of those categories. So pacemakers can go in the ventricle. You can have a wire in the ventricle, and that's a single chamber device. You can also have a single chamber device with a wire in the atria. Or they can be dual. That allows for atrioventricular synchrony. And we can also thread a wire across into the left ventricle for cardiac resynchronization. And that would be for patients who are going to maybe pace a lot from the ventricle, and we're worried about a pacing induced cardiomyopathy that can occur from that. So there are clear indications for all of these. Single chamber device might be for someone with permanent atrial fibrillation where we don't need an atrial lead. A dual chamber is when we want AV synchrony. So we want to maintain synchrony between the atrium and the ventricle. And then biventricular pacing if the patient has advanced heart failure symptoms, significant interventricular conduction delay, significant LV dysfunction. And so if we think we've got a patient, let's say their EF is 25%, and we think they're going to pace a lot from the right ventricle, and they've also got maybe a big left bundle branch block. So I've already got interventricular conduction delay that's going to lead to decreased synchronization of those two ventricles. If I then pace from the right ventricle, I can actually make that worse, and I can make people do worse in the long run. So by putting a wire in the right ventricle and a wire in the left ventricle, I can force those ventricles to beat together, and that's where we get the term resynchronization therapy. So those patients will actually, a good number of them do better in the long run. So we always want to think about a biventricular device for those patients. Sensing and pacing components. The wires will sense an intrinsic beat. If they do that, they should withhold a pace. If they do not sense an intrinsic beat, they deliver a pace. There's also rate-adaptive pacing, so we can play with the features of these devices a little bit to try and maintain as much physiologic response as possible. So in response to metabolic demands, body motion, respiration, the device can actually increase heart rate. So let's say a patient is riding on a bike, and they've got a pacemaker there. We don't want the pacemaker to continue to pace at 60 beats per minute like it would if they were maybe just watching TV. We want to allow for an increased rate response for activity so that they feel good and they have increased reserve there when they're exercising. We can also program things like AV delays. So we can actually program a PR interval to maintain physiologic responses. So there's lots of things we can do with these devices so that patient feels as normal as possible. We always want to try to avoid RV pacing for reasons that I mentioned. We don't want to worsen LV function, and if we're continually pacing from the right ventricle, sometimes that can happen. So just real briefly, we'll talk about pacemaker modes. We use typically four letters to describe a pacemaker mode. Position one is a chamber that's paced. Position two is a chamber that's sensed. Position three is a pacing response to a sensed beat. And then position four tells us if rate response is turned on or off. For example, DDDR is a common pacing mode, and this mode tells us that the pacemaker can pace and sense in the atrium and the ventricle. It will respond to a sensed beat in either chamber with inhibition of pacing in that chamber, and it will deliver a paced beat in either chamber if it does not sense an intrinsic beat. And then position four will tell us if rate response is turned on. We discussed indications for defibrillators already, primary versus secondary. So the pacemakers that I showed you, all defibrillators will have pacing capabilities, but not all pacemakers have defibrillation capabilities. And there's two different therapies that defibrillators can deliver. One is called anti-tachycardia pacing, and the other is a shock. So I wanted to show you what it looks like when we interrogate a device and we see an atrial channel and a ventricular channel, and I can see what's happening there. So I see the atrial channel up here. So these little pacing beats here. And then I can see the ventricle what's happening here. So the ventricle is much faster than the atria. And so this is an episode of ventricular tachycardia that the device will then sense. So we've got modes programmed that the device will sense that, and it's going to deliver a therapy, but what it's going to try first, this was called an anti-tachycardia pacing. So it's going to pace just slightly faster than that focus that's firing from the ventricle. And a lot of times that'll break that patient right out of that arrhythmia and they don't have to receive a shock, which is a really great feature for your patients. And in this case, you could see that worked really nicely. And now we've got a ventricular beat coming in. Everything looks fine. If that doesn't work though, or if the rate's really fast, we will just want to make sure we deliver a shock, a defibrillation to get that patient out of that, that rhythm. And that's what we can see happening here. I can see the ventricular rate is a lot faster than the atrial rate. And now we deliver a shock and that patient is back in normal rhythm. So those are my topics for electrophysiology for the advanced practice provider. I hope you found this helpful. Here's some readings you can use. These are references that I use to prepare this lecture. And there's some very interesting articles you may choose to read more about, and I hope that you do. So thank you for being with us today for this topic.

electrophysiology

cardiovascular

atrial arrhythmias

ventricular tachycardia

pacemakers

defibrillators

ambulatory Holter monitoring

anticoagulation