Hi there. My name is Sami Zakaria. I'm a cardiologist and a critical care physician at Johns Hopkins. It's an honor to discuss the analysis and therapy of supraventricular arrhythmias and bradyarrhythmias. In this talk, I'll be discussing five major objectives, or I have five major objectives. Number 1 is to learn the epidemiology and significance of supraventricular arrhythmias in the ICU environment. Then we'll spend more time developing a framework for differentiating supraventricular tachycardias. Then providing an overview for acute pharmacologic therapies for supraventricular arrhythmias. Then we'll switch gears and discuss bradyarrhythmias. And we'll discuss how to develop a framework for diagnosing bradyarrhythmias and to learn treatments for symptomatic bradyarrhythmias. Supraventricular arrhythmias are a much more common ICU environment. Setting aside the fact that there's increased detection rates because all these patients are on telemetry, patients in an ICU setting, they all have increased adrenergic drive and their catecholamine levels are all higher. In addition, they're more likely to be hypoxic, especially with those who have respiratory failure. Many of these patients have underlying cardiac disease or have cardiac ischemia or infarction. There are greater chance for having electrolyte abnormalities and there's a higher chance of having adverse medication effects. All of these lead to supraventricular arrhythmias. In fact, they also lead to more ventricular arrhythmias as well. The fact is, if you have one of these supraventricular arrhythmias, that they're associated with higher morbidity and mortality. In one study, there was a higher rate of death with an odds ratio of 1.95. And other studies just suggest that there's a 33% increase in the length of stay. So if you have a supraventricular arrhythmia, it's important to recognize it and treat it. Let's go over my general approach to approaching a patient with a supraventricular arrhythmia. The first and most immediate thing is to determine how fast you need to address the supraventricular arrhythmia. In other words, determining the urgency behind management. If there's evidence of shock, you really wanna be considering urgent or emergent cardioversion. And obviously, if the patient's unstable or unresponsive, then you really wanna be performing immediate cardioversion. Similarly, if there's evidence of hypotension, these patients should also be treated urgently, because the patient can't tolerate having a fast heart rate. And it's important to get that patient out of that arrhythmia. It's also important to figure out the underlying cause, because you wanna prevent the patient from going back into the supraventricular arrhythmia. So the last thing is, is there evidence that this arrhythmia is causing cardiac ischemia? In other words, can the heart rate tolerate the arrhythmia? Because if it can't, it's even more important to treat the arrhythmia urgently. So some examples, like if you have a patient with urosepsis and known coronary heart disease, who all of a sudden develops a new tachycardia, hypotension, acidemia, that needs to be urgently addressed. You would be treating the patient with vasopressors, you'd be getting the patient out of their supraventricular arrhythmia. But you'd also treat the underlying causes with maybe administering vasopressors, giving intravenous fluids, etc. Or if you see a patient with lung cancer, dyspnea, and hypotension, who all of a sudden develops a supraventricular arrhythmia, well, there it could be due to a lot of causes. And so you'd wanna be thinking about things like hypoxia, pericardial inflammation, anemia, etc. So it's important to do that rapidly. Here are the most common reasons for leading to a supraventricular arrhythmia. Includes hypoxia, that's notorious in ICU setting. Changes in volume status, whether it's low volume or a hypervolemic state. Also, it changes in your pH, and acidosis can affect the propensity of the heart to have arrhythmias, as is electrolyte abnormalities. If you see issues with cardiac ischemia or infarction, that could be associated with arrhythmias. Also, direct irritation of the heart, whether it's due to post-op cardiac surgery patients, or those who have a central line irritating the right atria, or other causes can cause an arrhythmia. Patients who have RV strain, whether it's due to lung disease, pulmonary embolism, pulmonary hypertension, etc. These patients are more likely to have supraventricular arrhythmias because of stretch of the right atria. And then toxins and medications can also irritate the heart. Once you go through this checklist, where you've determined how originally you need to treat this arrhythmia, and then try and determine the arrhythmia cause, then after that, then you could determine an arrhythmia type. And while you're doing that, though, you should note that treatment should not be delayed while determining a diagnosis. So let's go through a few of these examples. And here's a case presentation. This is a 60-year-old woman with pneumonia, CFBD, and respiratory failure, who is on mechanical ventilation. And she's noted to have a fast heart rate on the monitor. On the slide, you can see her vital signs. Her heart rate's 120, and she's basically your typical ICU patient. So while you're giving fluids and vasopressors, you also ask the ICU staff to perform an ECG, and this is the ECG that's obtained. And what you see is basically a tachycardic rhythm that's regular. So how do you analyze this rhythm? Well, basically, I use this algorithm to differentiate my tachycardias. If the patient has a wide, complex tachycardia, that's a whole separate algorithm and discussion. And we'll be discussing it in a separate SCCM talk. But if the patient has a narrow rhythm, the next question is, is this rhythm an irregular or regular rhythm? If it's irregular, then there's four possibilities for what this arrhythmia could be. If it's regular, then the next intervention is to perform a vagal maneuver or adenosine. In my practice, I tend to use adenosine because it's much more helpful in the ICU setting. If you try a vagal maneuver, you'll notice that it's much harder to be successful in critically ill patients because they have lower vagal tone. In any case, with either intervention, you wanna see if the arrhythmia terminated. If it did, then it could be due to three possibilities. And if it didn't, then it could be differentiated to three other possibilities. There is another way of differentiating narrow complex tachycardias, which is different from the previous slide, which only requires you to answer three questions. Number one, is it a wide or narrow complex rhythm? Number two, is it regular or irregular? And number three, what is the response to adenosine or vagal maneuvers? Instead, you could do this where you first review the QRS complex. Marriott's practical ECG book says milk the QRS complex. And basically, in other words, what you're trying to do is you're trying to see if there's any differences in the QRS complex from a baseline ECG. If there is, then that may be a sign that there's a retrograde P wave that's inside the QRS complex. The second thing is to look for P waves to see if it's near the QRS complex or somewhere else. Marriott's practical ECG book calls this Cherchez le P. And then the third thing is to determine the relationship between the QRS complexes and the P waves. In other words, who's married to whom? What is the relationship between those QRS complexes and the P waves? And that way, you could differentiate these tachycardias into short RP versus long RP tachycardias. So typically, things that are short RP tachycardias include typical AVNRT, orthodromic AVRT, atrial tachycardia with first degree AV block. And it's also possible that this could be due to junctional tachycardia. For long RP tachycardias, it could be due to sinus tachycardia, atypical AVNRT, atrial tachycardia, and other less common types. In my view, though, this type of way of differentiating narrow complex tachycardias is less useful in the ICU setting. You'd be spending a lot of time looking at the ECG and still may not be able to diagnose the supraventricular arrhythmia. Also, it doesn't help treat the patient. Whereas in the other approach, where if you give a patient adenosine and if you get them out of that rhythm, then the patient may find relief from their tachycardia. So let's go back to our patient. So this patient has a narrow complex tachycardia, and it's regular. So the possibilities for this arrhythmia include the following that are listed on the right. So then the next question is, is what is the response to adenosine and vagal maneuvers? In this patient's case, there was a slight decrease in heart rate with adenosine and vagal maneuvers. Here you could see that the heart rate was faster at the beginning of the strip and then it becomes lower later on. And so because the rhythm doesn't break, you know it's not AVNRT or AVRT. And so the differential is between sinus tachycardia, atrial tachycardia, and atrial flutter. We know it's not atrial flutter because you would have seen F waves running throughout the strips. And it's probably not atrial tachycardia because the P waves in this ECG look identical during the entire time and they should have a different axis than what it is there. In this case, it's actually a sinus tachycardia. So I put these little blue lines here to help show you that when the heart rate slows down, the P wave starts moving away from the T wave. Notice the size of the P waves, how big they are. And that's because this patient has significant by atrial enlargement. So this patient has sinus tachycardia. So for sinus tachycardia, there's basically three types of sinus tachycardia. The first one and the overwhelming causes of sinus tachycardia in the ICU environment is physiologic sinus tachycardia. This is to be expected in the ICU. When a patient is stressed, they're going to have sinus tachycardia. And so the most important thing for these patients is just to treat the underlying cause. There are two other types of sinus tachycardia. One is inappropriate sinus tachycardia, which is extremely uncommon and it's not really an ICU issue. But for those patients, they preferentially get treated with ivabredine. And then there's some patients that have sinus node reentry tachycardia, but that's also rare. And that's something that only an electrophysiologist tends to deal with. So for the vast majority of patients with sinus tachycardia, it's basically physiologic and you just have to focus on treating the underlying cause. Here's another case presentation. This is a 55-year-old man. He has Crohn's disease. He had had a recent X-lap and a colostomy. Comes into the ICU with new intra-abdominal abscesses and septic shock. He developed a sudden onset tachycardia at 160 beats per minute. Here's his vital signs. So his blood pressure is 90 over 60 and his heart rate's 150. In general, he's ill-appearing and diaphoretic and he has a tachycardic rhythm. So you obtain the ECG and this is what it is. So in this case, it's a narrow complex rhythm. It's regular. So the differential for this includes sinus tachycardia, atrial tachycardia, atrial flutter, AVNRT and AVRT, just like all the other narrow complex regular tachycardias. So it's very important to give adenosine here. And this is what happened. This strip really highlights the importance of adenosine vagal maneuvers. Look at the beginning of the strip. Basically what adenosine did was it slowed AV nodal conduction, allowing for clear F waves to show up in the beginning part of the strip. Here you can see it best in the inferior leads where you see a sawtooth pattern. So this is basically atrial flutter. Here's another example of atrial flutter where the AV node was really effectively blocked by adenosine and you could have a long pause. And in this case, it's easy to see the F waves as well. So when you think about atrial flutter, you should really consider it in any patient with a fixed heart rate of 150 beats per minute. And one of the characteristics of typical atrial flutter is a sawtooth pattern in the inferior leads, in leads 2, 3, and AVF. If you block the AV node with either vagal maneuvers or adenosine, it should reveal flutter waves. And that's really the linchpin for diagnosis. Treatment of atrial flutter is hard. You could consider rate control and you could consider calcium channel blockers or beta blockers, but these are less useful in the ICU because of their ability to cause more hypotension. You could also try digoxin, but that's even less effective. You could try amiodarone, which should help with rhythm control and rate control. And if need be, if the patient's unstable, then you should really think about rhythm control with either amiodarone or cardioversion. Once the patient recovers from their ICU stay, you could send them to their AP lab, consider ablation, especially if it's a typical atrial flutter, because you could cure that with greater than 95% of the time. But if you're thinking about ablation or rhythm control therapies, you will also have to be thinking about anticoagulation, especially if the arrhythmia has been present for more than 48 hours, because there's a risk of cardiomolec stroke. Basically, the atria do not contract well, whether you have atrial flutter or atrial fibrillation. And so there's an opportunity for a clot to form in the left atria and then travel to the brain, causing an embolic event. So in any patient who you consider rhythm control or ablation, you also have to be considering anticoagulation. Here's a third case presentation. This is a 50-year-old man who has a repaired atrial septal defect, who presents with septic shock due to pyelonephritis. His heart rate is noted to be 140, and his blood pressure is on the low side. It's 100 over 60. His physical exam is relatively benign, except for having dementia. Like the previous ECGs, this is a narrow, complex tachycardia, and it's regular. So the differential is the same as it was for the other ones. It only could be one of five possibilities. Notice here that there's something a little bit funky in lead 2. You can see almost a retrograde P wave. It's a little bit more complicated than lead 1, but it's a little bit more complicated than lead 2. Lead 2, you can see almost a retrograde P wave. And so you could think, hey, maybe this is a long RP tachycardia, so it could be more consistent with sinus tachycardia, atypical AVNRT, or atrial tachycardia. But you don't know for sure until you ask yourself, what is the response to adenosine or vagal maneuvers? In this patient's case, adenosine broke the rhythm. Notice that the P waves are now upright, and that is especially prominent in lead 2. So this has to be. There's only one possibility in this case. It can't be sinus tach. It can't be AVNRT or orthodromic AVRT. So what it is is basically atrial tachycardia. Here's another example of atrial tachycardia. And in this case, adenosine didn't break the rhythm. Instead, the patient had a slowing of AV nodal conduction. And so when you're thinking about a regular rhythm that slowed down with adenosine, there's still the same possibilities. But in this case, what's interesting about it is that there are P waves marching at a rate of 140 or so. And it's probably atrial tachycardia because the P waves are a different axis. And it's too slow to be atrial flutter or atrial fibrillation or something else. And it's not consistent with any of the reentry arrhythmias since they're not one-to-one conduction. So this is probably atrial tachycardia with three-to-one conduction. There's other abnormalities in the CCG. This patient also has left axis deviation, a right bundle branch block, and an old anterior septal infarct. But the point of this slide is to show you that atrial tachycardia can occur and may not break with adenosine. So let's discuss the atrial tachycardia further. No matter what type of atrial tachycardia, they're characterized by paroxysms of short repetitive tachycardias. And in some cases, the atrial rate will suddenly jump up. But then it will increase slightly in speed over the next first 5 to 10 seconds before stabilizing. There are two mechanisms for atrial tachycardia. There are two mechanisms for atrial tachycardia. So the first one is when it's due to enhanced automaticity. These are patients where you have more of a warm-up and cool-down phenomenon. And when you'll notice that heart rate changing over the first 5 to 10 seconds more dramatically. This is associated with COPD, alcohol intoxication, and rarely with myocardial infarction. In these patients, adenosine cannot terminate this arrhythmia. In 30% of cases, it's due to a re-entry rhythm in the atria. Basically, you have a diseased area of the atria, whether it's due to surgery or whether it's dilated from other kinds of cardiac stresses or myocarditis. And what happens is you have a premature atrial contraction that triggers a re-entry rhythm in the atria. This would be similar to what would happen in a ventricle when a PVC triggers ventricular tachycardia. Except in this case, it occurs in atria. And when that happens, these type of arrhythmias can be terminated by adenosine. And then you would basically break with it. So it can be trickier to figure out atrial tachycardia from other arrhythmias. For either type of atrial tachycardia, a lot of them are exacerbated by underlying illness such as pneumonia, septic shock, et cetera. And so it's important to treat the underlying cause. If you're having incessant bouts of atrial tachycardia, you could consider a control agent with like a beta blockers or calcium channel blockers with the caveat that both these agents can also worsen hypotension. You could also do adenosine. And this is especially important for the 30% of patients who have re-entry atrial tachycardia. But this is not really a long-term solution. Ideally, if these measures don't work, then you could consider a different antiarrhythmic agent or catheter ablation. But if you're doing any of those things, you might want to discuss with your electrophysiology colleagues. So what have we covered so far? We've basically discussed sinus tachycardia, which is probably the most common arrhythmia in the ICU setting. And then we discussed atrial flutter, which in general could be a regular rhythm. And in this case, the adenosine or vagal maneuvers will only slow down the arrhythmia for a while, for about six seconds before it comes back. But it could also manifest as an irregular narrow compass tachycardia, in which case it would be more easily diagnosed. We also discussed atrial tachycardias. And we discussed there's two types of atrial tachycardias. One that terminates with adenosine or vagal maneuvers, and the other one that doesn't. So what's next? Let's discuss this case presentation. This is a 35 year old woman. She has severe asthma, who comes in with acute respiratory failure. In her case, her heart rate is noted to be 180. Her blood pressure is 120 over 60. Our lung exam is characterized by diminished breath sounds and occasional wheezing. And a cardiovascular exam shows a tachycardic regular rhythm. So the first question is whether this is a narrow or wide complex tachycardia. This patient has a QRS complex at around 120 milliseconds. So it's just under the cutoff for narrow complex tachycardia. And the next question is whether this is a regular or irregular rhythm. In this case, it's a regular rhythm. So the differential remains the same as the previous ECGs. And the next question is whether this, what is the response to adenosine or vagal maneuvers? For this patient's case, the rhythm is adenosine responsive, because you notice that there's a tachycardia in the initial part of the strip, but then it's broken in the second to last beat. So therefore it cannot be sinus tachycardia or atrial flutter. The remaining differential diagnosis for this patient is either AVNRT, atrial tachycardia or orthodromic AVRT. I have these arrows that are highlighting where I think they're retrograde P waves. In the beginning part of the strip, there's a short RP tachycardia. And then as the adenosine starts to kick in, the RP interval starts to increase. And then you'll see a retrograde P wave, and then you see a PVC before it goes into sinus rhythm. So that's unlikely to be atrial tachycardia with the first degree AV block, since the rhythm ends on a P wave, or which is the one before the PVC beat. And because the distance between the P wave and the next QRS complex is not very much in general. So the remaining differential diagnosis for this patient is atypical, sorry, is typical AVNRT or orthodromic AVRT. Notice what I'm going through is differential, but it's really hard to tell the difference just on a surface CCG between these various tachycardias. But as a critical care provider, it doesn't matter as much. The whole point is to know that this is an adenosine responsive arrhythmia. For this patient's case, later underwent a EP study, which confirmed typical AVNRT. Just to reiterate, it's hard to tell a difference between AVNRT or orthodromic AVRT on a surface CCG, because both manifest similarly in the ICR environment. Both are re-entry tachycardias, and both are initiated by premature atrial contractions. The medical treatment for both is also the same. You want a slow AV nodal conduction to break the circuit because both types of arrhythmias need the AV node to sustain their arrhythmia. The most effective medication to do so is adenosine, which is 91% effective. Alternatively, you can use a calcium channel blocker like verapamil, which has similar efficacy, and metoprolol or other beta blockers, which are useful as well. For both these medications, though, you have to guard against hypotension, which may be a problem in the ICU environment. If none of these are effective or sustainable, then you consider another antiarrhythmic such as amiodarone or flecainide, but they have less efficacy compared to adenosine or calcium channel blockers. Rarely, if the patient's unstable, then you could consider cardioversion. And once the patient's no longer critically ill, then you could consider ablation, which is 95% to 98% effective. But typically, that's not performed while the patient has other critical care issues to attend to. Let's further discuss AVNRT. So AVNRT is when you see a reentry circuit that's very near the AV node. And notice this black arrow that kind of highlights the reentry circuit here. There's two different types. There's a typical AVNRT, and that goes down a slower part of the reentry circuit first, and then goes fast up, retrograde, up the other part of the reentry circuit. And then there's atypical, which is the opposite, where it goes down the fast circuit and then retrograde up the slow circuit. And that's not really clinically relevant except for electrophysiologists who basically could use it to differentiate between long RP and short RP tachycardia. In either case, the treatment is the same. We wanna use adenosine to block the circuit. Here's an example of a patient with AVNRT. In this case, if you're using the short RP, long RP rubric, I think this is a short RP tachycardia. And that's probably because in lead one, you could see these retrograde P waves in the ones where I have it highlighted by the arrows. However, see how that's relatively difficult to figure this out, whether the patient has location retrograde P waves. And so for that reason, in an ICU setting, I always favor using adenosine as a diagnostic and therapeutic challenge. For the patient with the preceding ECG, adenosine causes patient's arrhythmia to terminate, and in this case now, the patient's in sinus rhythm. AVRT, in contrast to AVNRT, requires a bypass tract. Basically, there's a bundle of cancer somewhere connecting the ventricle and the atria, which allow for electrical activity to pass through it. Orthodromic AVRT, orthodromic means going the correct way down the AV node. The impulses travel normally through the AV node, and then they go retrograde up the bundle of cancer, the bypass tract, into the atria, and then basically cause a re-entry arrhythmia. And here you can see it with the black arrow. And then it goes into the AV node, and then it continues on its pathway. There are patients that have antedromic AVRT. In other words, the arrhythmia goes down the bypass tract, goes through the myocardial tissue, and then goes up the AV node. This cannot be a narrow complex tachycardia because it takes longer to conduct through myocardial tissue, and it will cause a wide QRS complex, and so it would represent differently. Here's an example of orthodromic AVRT. And if you look at this ECG, it's almost impossible to differentiate this from AVNRT. And again, in the ICU and hospital setting, it doesn't really matter. In both situations, you really want to be considering adenosine to break the arrhythmia. Look at this patient's ECG after we administered adenosine. The patient no longer is in supraventricular tachycardia, and now the patient's in sinus rhythm. However, look at the beats that are highlighted in the black arrows. There's almost a short PR interval and a delta wave signifying slurred conduction. So what this patient has is intermittent bypass tract conduction consistent with WPW. This is rarely noted, but it confirms that this patient had AVRT without having to perform an electrophysiology study, since delta waves can only be seen with bypass tracts. For this patient, she ended up undergoing ablation a few months after delivering her baby and did well afterwards. Here's an example of antedromic AVRT. Just to reiterate, this is not a narrow complex tachycardia. This occurred in a 25-year-old man who came in with palpitations and shortness of breath. And notice how it's a very wide arrhythmia. In his case, he was able to get out of it. And this is him in sinus rhythm. And you can clearly see that there's delta waves that are associated at the beginning of each of these QRS complexes. So what have we covered so far? Well, we've covered sinus tachycardia, atrial flutter, atrial tachycardias, AVNRT, and AVRT. So let's discuss the irregular tachycardias. So here's a 70-year-old woman. She has coronary heart disease, hypertension, and lung cancer, who presents with pneumonia and respiratory failure and needing mechanical ventilation. Her heart rate's noted to be 160. Her blood pressure is on the low side. She has diminished breath sounds and occasional wheezing, and she has a tachycardic irregular rhythm. Here's her ECG. It's a narrow rhythm, but in this case, it's irregular. So the differential for this is only four possibilities is atrial fibrillation, atrial flutter with variable block, multifocal atrial tachycardia, or sinus tachycardia with ectopic beats. So she ended up having atrial fibrillation, which is probably the most frequent arrhythmia in the ICU setting outside of sinus tachycardia. Just to reiterate, atrial fibrillation is very frequent in the ICU setting, and it's been noted in various studies to be anywhere between 1.7 to 43% of the time. That's a very wide range, and it's probably due to the fact that in an ICU that basically cares for cardiac patients, this arrhythmia is much more frequent than you'd see in a surgical ICU, for example. The risk factors for atrial fibrillation include increased age, cardiovascular comorbidities, such as having preexisting coronary heart disease or heart failure, patients with multi-organ system failure or sepsis. No matter the cause or the etiology for atrial fibrillation, if you have it, it leads to increased mortality and increased morbidity. And there's a higher rate of strokes as well as an increased ICU and hospital length of stay. So it's a pretty big deal. Tachycardia is induced by atrial fibrillation need rate control so that you could slow AV nodal conduction and allow for a slower ventricular rate. My first line agent tends to be beta blockers, and they're very effective, although there's a risk of worsening hypotension in certain patients. An alternative to beta blockers is to use calcium channel blockers. These are just as effective in reducing ventricular rates in patients with atrial fibrillation, but the downside to them is that they have higher rates of inducing hypotension, which could be a problem in patients who are in shock. The third type of agent is digoxin, which works by enhancing bagel tone and thereby slowing down conduction in the AV node. However, in the ICU setting, this is less effective because patients tend to have lower bagel tone because of their hyperadrenergic tribe. However, the big advantage of digoxin is it's the only AV nodal blocking agent outside of adenosine that does not cause hypotension. So it certainly has a role in the ICU setting. Instead of rate control, you could also consider rhythm control. And the idea behind rhythm control is that you're trying to convert the patient out of atrial fibrillation to sinus rhythm. You could consider either pharmacologic or electrical cardioversion. If you're doing pharmacologic cardioversion, then you could consider amiodarone, which is useful not only for converting the patient to sinus rhythm, but also for maintaining sinus rhythm. And this is especially used often in the post-op cardiac and thoracic surgery patients. An alternative to amiodarone is ibutylide, but to be frank, this is rarely used because the risk of torsades des plantes in this medication is about 4%. If you do decide to use electrical cardioversion instead of pharmacologic conversion, then make sure the patient's sedated beforehand if you're able to. And if that translating works or if it's unsuccessful, you could consider trying it again after you have the patient treated with a different agent like amiodarone, and then you could reattempt the cardioversion hours later. Whenever you're considering rhythm control treatments, whether it's pharmacologic or electrical cardioversion, please note that there's a higher risk of cardiobolic events during the cardioversion time period. And that's because any clot that forms due to having stasis of blood in the atria due to atrial fibrillation is likely to get dislodged and travel outside of the heart to the rest of the body, including the brain. So it's very important to consider transesophageal echocardiography to rule out atrial thrombi, and this especially is important if the atrial arrhythmia has been present for more than 48 hours. Just to reiterate, whenever a patient has atrial fibrillation you always have to consider the risk of cardiobolic stroke. Patients who are at lower risk of this phenomenon is if they have atrial fibrillation for less than 48 hours because there's no time for a clot to form in the left atria, or if they've been therapeutically anticoagulated for greater than three weeks, and this is generally with warfarin or with direct oral anticoagulants. In contrast, patients are at higher risk if their CHADS2 VASc score is greater than two, or if they've had recent rhythm control interventions like cardioversions or amiodarone therapy, which could suddenly jolt them from atrial fibrillation back into sinus rhythm. At all times for higher risk patients, you need to consider anticoagulation, you need to consider therapeutic anticoagulation as long as the bleeding risk is not prohibitive. Some practitioners balance the bleeding risk calculated by the HAS blood score with the thrombosis risk calculated by the CHADS2 VASc score to decide whether they should initiate anticoagulation or not but it's hard to weigh the relative risks and benefits of bleeding and strokes in the various patients, and none of these calculators are specific for ICU patients. Here's the next case. So this is a 78-year-old man. He has a history of coronary heart disease, hypertension, asthma, COPD, and bronchiectasis who comes in with acute respiratory failure. His heart rate is noted to be tachycardic and irregular. Blood pressure's on the low side and his heart rate's 118. On cardiovascular exam, he has a tachycardic irregular rhythm. Here's the patient in ECG. It's a narrow complex tachycardia and it's irregular. Differential diagnosis includes the four that were presented earlier, including atrial fibrillation, atrial flutter with variable block, multifocal atrial tachycardia, or sinus tachycardia with ectopic beats. We know it's not atrial fibrillation because you could see P waves before each QRS complex and similarly, it's not atrial flutter because there's no F waves. So then we're differentiating between sinus tachycardia with ectopic beats versus multifocal atrial tachycardia. In this patient's case, there are three different types of P waves in front of each QRS complex. So that's by definition means that this is multifocal atrial tachycardia. So what is multifocal atrial tachycardia? It's an uncommon arrhythmia and it's almost always associated with severe pulmonary disease such as asthma, COPD, patients who are hypoxemic, those who've had pulmonary embolism. And it's also associated with theophylline use. To diagnose it, you have to have a heart rate greater than 100 and you have to have greater than or equal to three distinct atrial foci. So in other words, three or more different types of P waves. And in general, these patients tend to have a heart rate anywhere between 100 to 180. If you have multifocal atrial tachycardia, the treatment consists of treating the underlying disorder. If you need to rate control this arrhythmia, you could use beta blockers, but these often can't be used in patients with severe lung disease. Or you could use magnesium or calcium channel blockers, but none of these are particularly effective. Similarly, amiodarone has been used, but it's also not effective. Just to reiterate, the most important thing you could do for these patients is to treat the underlying disorder. So we've gone over all the narrow complex tachycardias. We started off talking about sinus tachycardia. Then we focused on atrial flutter. Then we went to atrial tachycardia. Then we discussed AVRT and AVNRT. And then we focused on the irregular tachycardias, including atrial fibrillation, multifocal atrial tachycardia. There's not much really to say about sinus tachycardia with ectopic beats other than it's just a variant of sinus tachycardia. All right, let's switch topics and discuss slow heart rhythms. There are two reasons underlying bradyarrhythmias. The first is decreased automaticity. And this means that the heart wants to beat at a slower rate. This could occur either chronically or acutely and could cause symptomatic bradycardia or even asystole. The other possibility for bradyarrhythmia is impaired conduction. This is due to damage of the conduction system. And this could cause heart block and other problems. There are many reasons for this. In the ICU setting, the most common reasons are listed on the right-hand side. And they could lead to either problems with decreased automaticity or impaired conduction, or both. Before we discuss pathologic bradyarrhythmias, let's briefly discuss the principles of conduction. The fastest rate generally is in the SA node. And that beats, in most patients, between 60 to 100 beats per minute. If that's not working, or if another foci in the atria is not beating, then the AV node takes over and starts beating at a rate of about 45 to 60 beats per minute. If both the SA node and the AV node are not working, then the ventricle will have an intrinsic heart rate of 30 to 40. This is often enough, will maintain normal blood pressure, although the patient will have exertional dyspnea and chest discomfort. And this is often not enough. The only time when you get pathologic arrhythmias is when there's dysfunction in all three of these areas. Let's go over a case presentation. This is an 81-year-old woman with Coynard's disease, aortic valve disease, and a previous stroke, who was presented with a headache. She was transferred to the ICU after a sinkable episode and was noted to have a new intracranial abscess. Her heart rate was also noted to be slow and regular. Her blood pressure was low at 80 over 40, and her heart rate was low at 80 over 40. Her blood pressure was low at 80 over 40, and her heart rate was 43. She was simulant, and on cardiac exam, she had a bradycardic but regular rhythm. Here's her ECG. If you notice, she basically is in a sinus rhythm, but at a slow rate, and she also has prominent U waves. And so this rhythm is considered to be sinus bradycardia. In some patients, sinus bradycardia is typically asymptomatic unless there's absence of conduction distilled to the SA node. In some patients, such as this patient, they are symptomatic, even if they have preserved conduction. And that's because they depend on a heart rate faster than 40 to maintain adequate cardiac output. If that's the case, then you want to use the algorithm on the right to assess and treat bradycardia. The first step is to assess for and treat any reversible causes. Like in this patient's case, she probably has a combination of infection and neurocardiogenic dysfunction that explains her low heart rate. If she has no pulse, then you really want to be treating her based on the ACLS algorithm with CPR medications. Probably the first-line agent is atropine therapy, but you can also consider dopamine and epinephrine. If she maintains a pulse, then the first-line agent remains atropine, but you can also consider using aminofilin in addition to dopamine or epinephrine. If the patient has a pulse, you could also consider pacing the patient, either through transcutaneous or transvenous means. And this is often a useful thing in patients who have bradycardia due to intrinsic cardiac dysfunction. In all cases, though, you want to find out and treat the underlying cause because sometimes even aggressive cardiac treatments won't be successful without treating the underlying cause. Here are a few examples of acute bradycardia. This ECG was obtained in a 65-year-old woman who accidentally overdosed on ephedopine and diltiazem. If you notice, she has no P waves, and she has a very narrow, slow QRS complex, which is consistent with a junctional escape rhythm. She essentially remained in the ICU for about a week before she improved. There are a number of medications that could do this, that could cause acute bradycardia, similar to what happened in this patient, and they're listed on this table below. The most notorious medications include beta blockers and calcium channel blockers, but a number of other stuff could do this as well, such as antiarrhythmic agents. Here's another example of acute bradycardia, but this is due to a different cause. This is from a metabolic reason. In this case, this patient had hyperkalemia and had a potassium that was greater than 7.5. This ECG shows essentially no atrial activity, but narrow QRS complexes, and this is consistent with a junctional escape rhythm. In this third example, this is actually due to neurocardiogenic causes from intracranial hemorrhage. Patients with neurologic injury often have alterations in vagal and sympathetic tone, and this affects the heart because both of these autonomic nervous systems modulate heart rate. In this strip, you can see that the patient has sinus bradycardia and then eventually develops a high-grade AV block. This could just be due to vasovagal syncope, which could also cause increased vagal tone, but this isn't as likely in a patient with an intracranial hemorrhage. In contrast, this ECG shows a patient who has increased vagal tone. If you notice here, the patient starts off in sinus rhythm, and then by the middle of this strip, the P waves go away. Since the patient still has a narrow complex rhythm, this is most likely a junctional rhythm or a high ventricular rhythm. This ECG was obtained in a 42-year-old gentleman with polysubstance abuse, including marijuana, who had altered mental status. During this time, he had intractable nausea, vomiting, and diarrhea, which probably led to an increased vagal tone. Here's an example of acute bradycardia due to intrinsic cardiac injury. This was obtained in an 89-year-old woman who had crushing chest pain and dyspnea and was diagnosed with a large endstemmy. She was then transferred to the cardiac intensive care unit where this ECG was performed. Notice that she has a ventricular rhythm for the first three beats, and then she goes into atrial fibrillation and a narrow complex rhythm toward the end of it. At all points, though, she's not really in a fast heart rhythm, and she was unstable at this point. And then a few minutes later, she then developed progressive bradycardia and asystolic arrest. Here's an example of bradycardia due to hypothermia. What's pathomonic about this ECG is the presence of large Osborne waves, which are the humps that you see after each QRS complex that are most notable in lead II, III, AVF, V3, and through V6. These humps, these Osborne waves, these humps, these Osborne waves tend to go away with rewarming, and that's what happened in this patient's case. So basically, the patient had a resolution of their Osborne waves, and they had an increase in the heart rate. Let's transition again and go over another case. This is a 70-year-old man with coronary disease, severe COPD, aortic valve stenosis, who has three days of positive MSSA blood cultures. His blood pressure is 96 over 40, and his heart rate's at 82. He's essentially ill when you examine him, and he has a two out of six systolic ejection murmur at his right upper sternal border. Let's interpret his ECG. It shows that the patient is in sinus rhythm. Interestingly, he has marked PR segment prolongation, and this is consistent throughout the entire ECG, so it's consistent with a first degree AV block. In addition, he has a left bundle branch block. So what are the common causes of AV block? I mean, there's an exhaustive list of causes here on the right, but in the ICU setting, and for this patient, you want to think of the following six categories. Number one, you always want to figure out if the patient's new AV block is due to toxins. Many patients will have super therapeutic levels of medications like a slow AV nodal conduction, such as beta blockers, calcium channel blockers, or sodium channel blockers. In addition, older patients tend to have degenerating conduction systems, so it's not unusual for them to develop complete heart block within a span of a few months once they're in their upper decades of life. Patients with acute coronary syndrome and other types of cardiac injury can also develop heart block. You can often see complete heart block with either a right coronary artery or LAD occlusions. Another reason for cardiac cause for AV block is TAVR procedures. So transcatheter aortic valve replacements are placed right next to the AV node, and sometimes when you implant the new aortic valve, it could crush the AV node and cause complete heart block. Another reason for heart block is infection. So in the outpatient setting, patients with Lyme disease could develop infiltration of the AV node, which causes heart block. In addition, patients with endocarditis could develop AV block, and this especially can occur if the patient has an AV nodal abscess. Finally, the patients with increased vagal tone or neurocardiogenic injury leading to increased vagal tone could have heart block, and this could be as significant as complete. There are different types of AV block ranging from the relatively benign first degree AV block or delay ranging to complete heart block. First degree AV block is interesting. It's really not a block. It's more of a delay in AV nodal conduction, and it doesn't need a specific treatment. I've actually never implanted a pacemaker for a patient with first degree AV block. In this patient's case, though, his AV nodal block is rather significant, so you have to be suspicious of endocarditis, especially in a patient who has persistently positive blood cultures. Here's his ECG five days later. Notice that he still is in sinus rhythm, but that his PR interval is now wider, and it's about 400 milliseconds. This is very concerning, and what the patient ended up having was an aortic valve abscess. Here's another example of first degree AV block. This was obtained in a 58-year-old man who had syncope and exertional dyspnea after walking for four minutes. If you look at his ECG, it shows that he has sinus bradycardia, first degree AV block, left axis deviation, and early repolarization. In this patient's case, he actually did end up getting a pacemaker, and the reason why is because not only did he have sinus bradycardia and first degree AV block, but he was unable to increase his heart rate with exertion and had chronotropic incompetence, so this patient ended up having progressive conduction system degeneration. Let's go back to the patient with aortic valve abscess. This ECG was obtained a day after the one I just showed you, and it showed that the patient has second degree AV block with a type 1 Wenckebach pattern. What this means is that there's progressive prolongation of the PR interval until you have blocked beats, and notice also in this type of arrhythmia, you have grouped QRS beatings. For this type of arrhythmia, if it's asymptomatic, it requires no specific treatment, and the reason why is because this is usually due to heightened vagal tone, and so the way to reverse this is to either have the patient become more active or stop an AV nodal blockage or something else. If the patient is symptomatic, you want to make sure you treat the underlying cause, and you can occasionally consider using things to increase sympathetic tone or decrease vagal tone. You can use atropine, for example. You could use beta adrenergic agents. You could even pace the patient with transvenous or transcutaneous pacers or give aminophilin. However, this is rarely required, and most patients with type 1 Wenckebach need no specific treatment. This is another example of a second-degree AV block type 1, which has occurred in a 64-year-old man with dyspnea, chest pain, and opioid overdose, and what he had was heightened vagal tone, so he has evidence of sinus bradycardia, and if you notice here, you have progressive PR segment prolongation before you have a dropped beat, and you also notice toward the later portion of the strip, a group of three QRS complexes are in groups. This is characteristic of a second-degree AV block. In the two previous CCGs, I showed you second-degree AV block type 1. This is an example of second-degree AV block type 2. This is different from the previous one because there is no progressive PR segment prolongation. Here, I've highlighted in the blue lines where you see the same PR interval before you see a dropped beat. It's similar to second-degree type 1 block in that there also remains group beating, which is present here. You see groups of two QRS complexes before you see a dropped beat. In contrast to type 1 block, second-degree AV block type 2 is inherently unstable and usually progresses to complete heart block, and the reason is because this type of heart block is associated with structural damage to the infranodal conducting system. So if you're trying to treat it with atropine, it's not going to work, and anything to decrease vagal tone will not work. You could try and use beta-adrenergic agents like isoproteranol, dopamine, dobutamine, epinephrine, because what they'll do is increase the ventricular rate independent of the damage to the AV node. You can also consider aminophilin, but these are all temporary measures, and patients with second-degree AV block will eventually require pacing, and in this patient's case, she ended up getting a pacemaker. All right, going back to the patient with the AV valve abscess, this ECG was obtained three days after the ECG that showed that he was in wanky bach. Notice now that he remains in sinus rhythm. If anything, he's a little bit tachycardic, and his ventricular rate has slowed, and that's because the patient's now in complete heart block. There's no relationship between ventricular activity and atrial activity. For this patient, the reason why we just observed the progressive increase in his AV block is because he had multiple comorbidities, and it was an inoperable candidate, and after this ECG was obtained, about a day later, he actually passed away. This is another example of third-degree heart block, and this was obtained in an 80-year-old woman with exertional dyspnea and chest pain, and she actually, because of her dyspnea, she became more unstable, and then she actually fell and broke her hip. When she went to the ED, this was the ECG that was obtained that showed that she was in sinus rhythm, and you can see here that the P wave is marching throughout the strip, and then that she was also in complete heart block. Notice the ventricular rate that's at a slower rate. For her, she continued to have a pulse, and she was mentating when she was at rest, but every time she walked up, she was unable to augment her ventricular output, and that's why she had her fall. For this patient, and for patients similar to her, you want to treat the underlying cause for third-degree complete heart block. You could consider beta-adrenergic agents, which could increase the ventricular activity, or aminophilin, but in most cases, you need transvenous pacing, and that's what this patient received, and then she had a temporary transvenous pacer placed before we placed a permanent pacemaker a day later. All right, so we've reviewed all the bradyarrhythmias. There's two different reasons for it. You could have acute bradycardia, sinus bradycardia, or arrest. That could be a cause for symptoms, or you could have impaired conduction, and that could manifest as first-degree AV delay, second-degree type 1 or type 2 block, third-degree block, and you could even get high-grade block that doesn't fall under any of the rules that I just showed above. What about a rhythm that alternates between bradycardia and tachycardia? This is called basically tachybrady syndrome, and it alternates between periods of sinus arrest, so that's called sick sinus syndrome, an atrial fibrillation with rapid ventricular response, and this is a result of degeneration of the conduction system. It tends to occur in older patients and idiopathic, but it could also be present in patients with cardiomyopathies, myocarditis, infiltrative heart disease, or due to cardiac ischemia. Treating this can be relatively difficult, and this ECG kind of shows how we treat it. You have periods of atrial fibrillation with rapid ventricular response, and so for that, you need to control it with AV nodal blocking agents. However, that will make the bradycardic episodes worse, and so these patients will need to have a pacemaker implanted to control the sick sinus syndrome. In fact, this is the most common indication for pacemaker, and about a million patients in the United States have a pacemaker for sick sinus syndrome. The ECG on the right kind of shows that. You see periods of AFib with RVR at the beginning of the strip, and then the heart rate slows down, and the pacemaker starts firing. Another reason for arrhythmias is digoxin, so digoxin used to be more commonly used, but it's still a fair number of patients are on this. This is a drug that's fallen out of favor because it has a narrow therapeutic window, and there are many drug-drug interactions with it. It's especially more likely to become toxic when patients have hypokalemia or renal failure. The classic symptoms of toxicity include a change in mental status, nausea, vomiting, and having green-yellow visual halos. The reason why you have symptoms is because digoxin works to heighten vagal tone, and this does it centrally in the brain. The same mechanism leading to altered mental status also increase vagal tone activity going to the SA and the AV node. That causes heart block. However, digoxin also directly works on cardiac tissue to increase cardiac conduction, which increases cardiac automaticity. In the atria, it might convert the patient from sinus rhythm into atrial tachycardia or from atrial flutter into atrial fibrillation. Similarly, in the ventricles, it could irritate the ventricles and cause more PVCs, premature ventricular complexes, or even ventricular tachycardia or ventricular fibrillation. If you see a funny heart rhythm on the ECG in an older patient who has taken digoxin, suspect digoxin toxicity. Oftentimes, you'll see patients with atrial tachycardias, but will have AV nodal block at the same time. In addition, they will have a fast ventricular rate, such as junctional tachycardia or ventricular tachycardia. Here's an example of digoxin toxicity. This is an 80-year-old woman with heart failure, urinary tract infection, who developed altered mental status and fatigue. This is all due to digoxin toxicity. Notice in this ECG, especially in lead V1, where you see small positive deflections, which is due to a fast atrial rate, then she has atrial tachycardia. She also has a fast ventricular rate, and then that's probably either due to enhanced automaticity of the ventricle or the atrial beats are being conducted to the ventricle. For this patient and for others, it's important to stop giving the patient digoxin and to improve kidney function, since digoxin is excreted renally, at least in the preparation used in the United States. There is another preparation, digoxin, used in Europe, which is cleared hepatically, but that's not commonly used in the United States. It's also important to maintain potassium in normal levels and to optimize magnesium levels. For those with life-threatening arrhythmias or patients who have hyperkalemia, you want to consider administering digoxin antibody, because that can block the function of digoxin and rapidly reduce clinical effects of digoxin toxicity. We went over a lot in this talk. We went over tachyarrhythmias, bradyarrhythmias, tachybradyosyndrome, and digoxin toxicity. If you have any questions on any of this, feel free to email me at the email listed on this slide. I'm happy to answer any questions or address any concerns that you might have. In the following two slides, I've also included some references that may be of value to you. The ones that are highest yield have three asterisks in front of them. Thank you very much.

supraventricular arrhythmias

bradyarrhythmias

ICU setting

morbidity

ECG interpretation

treatment options

AV block

pacemakers

digoxin toxicity