Hi there. My name is Sammy Zacharia. I'm here to discuss case studies, specifically focusing on cardiac arrhythmias. In this session, we'll be recognizing Bregada and non-QT syndromes and discussing their acute therapies. Then we'll review the indications for implantable cardioverter defibrillator devices, so ICDs, and then finally discuss the interpretation of paced rhythms. Here's case presentation 1. This is a 40-year-old man with no significant past medical history who presents with dyspnea and palpitations. His blood pressure is 110 over 70, and his heart rate is 100. In general, he's in a wake and alert, but he's fatigued. A pulmonary exam, he has diminished breath sound in his left lower back. He's tachycardic and he's in regular rhythm. Then we obtained an ECG. Take a look at this ECG. Your eyes are probably drawn to leads V1, V2, and V3. Notice the abnormalities here. There's a pseudo right bundle branch block pattern here, where you see a RSR pattern or the rabbit ears. Then the SC segments are also abnormal. It's especially notable in leads V2 and V3, where you see a down-sloping, coved ST-type pattern, or a saddleback, which is probably the most notable in lead V3. That patient's ECG findings are characteristic of Brugada pattern ECG. There are three different types. Type 1, or the pattern that's most like the patient in the previous slide, probably had a type 1 ECG pattern. This is the coved type, which is a rare finding. It's not very commonly encountered. But if the patient has that and has the right clinical scenario, then that's enough to diagnose Brugada syndrome, which we'll be discussing later. Most patients with Brugada pattern ECGs have the type 2 or type 3 patterns, which is less specific for Brugada pattern. It's much less specific for Brugada syndrome. If you suspect that a patient has clinically significant Brugada syndrome, then you might want to try to convert their type 2 or type 3 ECG pattern into a type 1 pattern by using provocative maneuvers, such as giving procainamide, which can often shift the ECG findings into the type 1 pattern. This isn't typically done in the ICU. It's usually done in the EP lab, and it's done only in equivocal cases of Brugada syndrome. So what exactly is Brugada syndrome? It's basically when a patient has a Brugada ECG pattern and symptoms resulting from this. Unfortunately, the most common symptom that occurs from having a Brugada ECG pattern is ventricular arrhythmias. Clinical manifestations of that could be ventricular tachycardia, ventricular fibrillation, or just sudden death. The alternative way to diagnose Brugada syndrome is when you have a Brugada ECG pattern and there's a family history of sudden death. That just makes it more likely that the patient has a genetic form of this. Note that in isolation, if you just have a patient who has a Brugada ECG pattern, it's of unquestionable significance. So it's hard to determine if the patient will develop ventricular arrhythmias or not. Oftentimes, the patients who develop ventricular arrhythmias, their symptoms are maybe a little bit different from the other average patient. Some patients will have near-sinkable or sinkable episodes, but they may not feel any palpitations. Others tend to have more episodes of ventricular arrhythmias at nighttime, and so bystanders may notice nocturnal agonal respirations, or the patient may just have sudden death episodes. The risk of these episodes is dependent on a few characteristics. There's some specific ECG criteria and some clinical criteria which are listed on the table on the right. But again, this is not really an ICU issue, it's more something for the electrophysiologist to use to determine if the patient needs an ICD. For our practice in the critical care world, we just have to recognize that anyone who's had a history of ventricular arrhythmias or symptoms that could be caused by ventricular arrhythmias, and this ECG patterns is a higher risk of having Bregada syndrome. Just as a reminder, ventricular tachycardia or ventricular fibrillation in patients with Bregada syndrome, typically, these episodes occur when there's increased vagal tone. For some reason, in patients who have nausea, vomiting, or have had large meals, or when they're sleeping, tend to have more of these episodes. Other things that could provoke ventricular tachycardia or ventricular fibrillation include fever. There's a bunch of provoking medications that could do this, including some antirhythmics, psychotropics, propofol, alcohol, and cocaine. If you want to see the full list, you can see that at www.Bregadadrugs.org. How do you manage Bregada pattern and Bregada syndrome in the ICU setting? Well, if the patient has a Bregada type 2 or type 3 ECG pattern, you really don't need to do anything. There's no specific recommendations on how to manage these patients. For those with a history of Bregada syndrome, in other words, you've had symptoms, consists of ventricular fibrillation or ventricular tachycardia, and the characteristic ECG, or if they have the type 1 ECG pattern alone, these patients, you want to advise them to avoid large meals, avoid cocaine, alcohol, or other triggering medications or substances. These patients need to be aggressively treated for fever. The reason why is because these patients are much more likely to develop symptomatic arrhythmias. In this patient's case, he ended up having community-acquired pneumonia. He was actually admitted to cardiac ICU because of that type 1 Bregada ECG pattern. Unfortunately, a few hours later, he developed a fever, and then all of a sudden developed this arrhythmia. At this point, he had ventricular fibrillation and needed cardioversion and rapidly gained spontaneous circulation. But now that we've already known that he's had ventricular tachycardia and ventricular fibrillation, the question is how to further treat it in the ICU setting. Well, the pharmacologic treatment of choice is to use quinidine. Interestingly enough, other sodium channel blockers do not help prevent ventricular tachycardia and ventricular fibrillation, so quinidine is the drug of choice in patients with Bregada syndrome. You could also use something like isopreterinol, and the reason why this is a helpful medication is to increase the heart rate and prevent premature ventricular contractions, which could set off the ventricular fibrillation. Later on, you could also consider implanting an ICD, because all patients who have had prior cardiac arrest or sustained ventricular tachycardia due to Bregada syndrome really need this therapy because they're much more likely to have recurrent symptoms. In rare cases, you could consider catheter ablation to ablate the foci of ventricular tachycardia, but this is uncommonly done. Let's move on to the second case. This is a 56-year-old man who comes in with delirium tremens. In the emergency department, he was noted to have significant ectopy on the telemetry monitor. His blood pressure is 144 over 86, and his heart rate is 115. In general, he's awake, he's alert. He's noted to be tachycardic with a regular rhythm, but he has frequent ectopic beats, and his extremities are warm. His first ECG was hard to obtain. This is the first one. Notice that he's in sinus rhythm, but he has frequent PVCs and he had short runs of non-sustained ventricular tachycardia, approximately seven beats. This is most prominent toward the middle part of the strip. A few minutes later, another ECG was obtained, and this one also had ectopy, and notice the ventricular tachycardia is at the beginning part of the strip. Here's the third attempt. This time, there is no ventricular ectopy, but something that your eye may be drawn to is the markedly prolonged QT interval. This patient basically was in sinus rhythm, had some ST and T wave abnormalities, especially noted in the lateral leads, and had a QT interval of 525 milliseconds. If it's corrected, it's about 507, so it's definitely long. There are many, many causes for QT prolongation, and all of these need to be ruled out before you can say that the patient has idiopathic QT prolongation. Certainly, if you have structural heart disease, whether it's due to coronary heart disease, acute infarction, dilated cardiomyopathies, congenital cardiomyopathies, or myocarditis, all of those could cause abnormalities and repolarization, and all of them cause increased QT intervals. There are electrophysiologic causes for QT prolongation if there's conduction block with left, either right or left on the retinobonds, and they could cause increased QT intervals. Certainly, electrolyte disorders and metabolic abnormalities can cause QT prolongation, including all the hypos, so hypokalemia, hypomagnesemia, hypocalcemia, hypothermia, and hypothyroidism. A number of medications could cause prolongation of QT. There's whole websites that are devoted to listing the medications that could prolong the QT interval. Probably the most notorious ones are fluoroquinolones, antifungal agents, some antidepressants, and antipsychotics, but other commonly used drugs such as methadone and antiarrhythmics can also prolong the QT interval. Street drugs can prolong the QT interval, such as cocaine, amphetamines, and ecstasy. And then also, patients with neurologic injury could have prolongation of QT interval, and this is due to abnormalities in sympathetic and parasympathetic tone. This is especially notorious in patients with subarachnoid hemorrhages. If a patient doesn't have any of those causes of QT prolongation, then maybe the patient has a long QT syndrome. And how to diagnose this is you first need to have a long QT interval. So a QT interval that's corrected has to be greater than 500 milliseconds. Or you have to have a long QT syndrome risk score that's greater than 3.5. So how do you figure that out? Well, you could use this table on the right-hand side of this slide. And if you add up the points, and if they're greater than 3.5, then the patient most likely has long QT syndrome. The other way of figuring it out is if you do a genetic screen and you see that the patient has a pathogenic long QT variant. Just to reiterate, you cannot diagnose long QT syndrome if there are reversible causes for QT prolongation or if there's other causes for QT prolongation, such as myocardial injury. For patients that have long QT syndrome, it's very, very important to avoid electrolyte abnormalities because these could exacerbate and worsen the QT interval and predispose the patient to tursades de poids. It's also very important to avoid QT prolonging medications, provoking medications, and to manage the underlying provoking stressors. For patients who have long QT syndrome and who are otherwise asymptomatic, it's probably reasonable to treat the patient with beta blockers, most specifically a Natalol or another non-selective beta blocker. You could also use a class 1B antiarrhythmic like maxillotine and that's especially important if there's recurrent ventricular tachycardia or ventricular fibrillation. Any patient who's had polymorphic VT or ventricular fibrillation will eventually need an ICD. So if the patient recovers in the ICU setting, but before they get discharged, they need to have an ICD implanted because those patients are much more likely to have recurrent episodes in the future. Since there's a correlation with episodes of ventricular arrhythmias in patients with long QT syndrome with sympathetic tone, in rare cases, you could also consider sympathetic denervation, but that's almost more of a last ditch effort. Here's a slide obtained from the guidelines on ventricular arrhythmias, basically describing how to manage patients with long QT syndrome, which is more of a reference slide. But basically the bottom line is if a patient has had episodes of ventricular tachycardia or ventricular fibrillation in the past, and they need an ICT therapy, they need beta blockers and they might need other additional medications or sympathetic denervation in the future. For those that are asymptomatic, if their QTC is greater than 500 milliseconds, you could consider a beta blocker or even implanting an ICD, but you don't need to be as aggressive in managing those patients compared to those who've had asymptomatic ventricular arrhythmias. Let's move on to case presentation three. This is a 65-year-old man who has hypertension and hyperlipidemia who presents with a type one endstemmy. So basically acute coronary syndrome. While he's in the cardiac ICU, he develops worsening chest pain. His blood pressure is 148 over 95. His heart rate is 94. He has an obvious discomfort. Cardiovascular exam is notable for regular rate and rhythm and he has a positive S4. You might recognize this ECG. This is the same ECG that I used in the ventricular arrhythmias talk. Basically this patient developed ventricular fibrillation. He ended up being successfully treated for it with cardioversion and he was doing fine afterwards. So now a big question is whether he needs a implantable cardiac defibrillator. On the right hand side of this slide, you can see this figure, which kind of discusses how to decide whether a patient needs an ICD or not. Essentially, if a patient has had ventricular fibrillation or sustained ventricular tachycardia, the first question you have to ask yourself is, does this patient have ischemia-warranting revascularization? In other words, is this ventricular fibrillation or ventricular tachycardia associated with acute MI? If a patient has acute MI and has VT or VFib, the treatment of choice for these patients is to send them to the cardiac cath lab and relieve their ischemia. If you do that, then there's no indication for an ICD in the future. And they're less likely to have symptoms in the future. And those patients should be just treated with beta blockers and other medications for secondary prevention. For patients who have VT or VFib and it's not due to acute coronary syndrome, then those patients should really be considered for a different blader and they need that before they were discharged from the hospital. Let's say this patient never had ventricular tachycardia or ventricular fibrillation. Let's say he just came in with acute coronary syndrome. He was managed successfully for that. And now because he had a large heart attack, that his ejection fraction is below 40%. So for these patients that are treated differently, and these are considered differently for different fibrillator therapy. Look at this algorithm here. If a patient came in with acute coronary syndrome or myocardial infarction, you really need to wait 40 days and reassess and determine if their ejection fraction remains low. The reason for that is because early implantation of ICDs does not help patients who've had an MI. You really have to wait, make sure that they tolerate goal-directed medical therapy well, and then see if their ejection fraction improves. If it does, and if it's above 40%, then those patients are not candidates for different bladers. If it doesn't, and let's say that the ejection fraction remains below 30 or 35%, then those patients should really be given a different blader. There's a little bit of a gray area between 35 to 40%, and those patients should be referred to electrophysiology team and be considered for an electrophysiology study to determine if they're at a higher risk. For patients who have non ischemic myopathy, in other words, let's say that their ejection fraction is low due to a previous myocarditis or some other cause, those patients should be considered for different bladers if they've had episodes of ventricular tachycardia or ventricular fibrillation, and it would be a class one indication basically to put implant different blader in those patients before they leave the hospital. Similarly, those who you suspect have had ventricular arrhythmia such as let's say the patient has recurrent syncope or something of that nature, then those patients should also have a different blader implanted. In the absence of those, the only time you really wanna be placing in a different blader is if the ejection fraction is below 35%. If it is below 35%, then you try to optimize your medical therapies for at least three months, and if their ejection fraction does not improve, then they should be considered and referred for a different blader. All right, let's go to the fourth case presentation. This is an 83-year-old man. He has Coyne-Hart disease. He has an EF of 25%. He has tachybrady syndrome, and now he comes in with respiratory failure and acute decompensated heart failure. His vital signs include a blood pressure of 90 over 60. His heart rate's 60. He's intubated, sedated. He has coarse breath sounds, and his heart sounds are relatively regular, but they're soft. Here's his ECG. So the whole point of this is just to go over how to interpret ECGs in patients who have pacemakers. The first thing is you want to look for pacemaker artifacts. Are the artifacts in front of the P waves? Are they in front of QRS complexes, et cetera? Because if it's in front of a P wave, like in this case, it's probably facing the atria. On the other hand, if you see the artifacts in front of the QRS complexes, it's probably facing the ventricle. Notice this ECG where each pacemaker spike has a slightly different amplitude, which is probably most notable in the areas that I've noted on the right-hand side in lead two. This is of no clinical significance. This is completely a result of digital sampling because sometimes the digital ECG machine will sample slightly before or after the pacemaker spike, and in that case, the pacemaker spike will be a little bit lower. Of note, usually pacemakers are set to pace on demand. In other words, you're not going to see pacemaker spikes if the patient's heart rate is faster than the set rate of the pacemaker. Take a look at this ECG. Here at the beginning of the strip, you'll see that the patient is being paced at a rate of 60 beats, but then at the fourth beat, which is indicated by the first arrow, the patient has an intrinsic beat there, and that's because it's at a rate faster than the set rate of 60. The following few beats, the patient has pacer spikes, and then there are intrinsic beats that follow that before the pacemaker takes over again toward the latter part of the strip, and that's because the patient's heart rate will drop below 60. Notice also in this ECG that the patient is only being paced in the ventricular area, and that's because the patient's in atrial fibrillation here so there's no point in pacing the atria. Here's another example of demand mode, so basically similar to what we discussed in the previous slide. The patient here is in sinus rhythm and has normal PR intervals and conduction into the ventricle, so there's also normal QRS complexes. But then what happens is toward the latter portion of the strip, the patient's sinus rhythm starts slowing and so the atria starts being paced by an atrial pacer. This is an example of demand mode. Just to summarize, this patient's ECG shows that the patient is in sinus rhythm, but then has atrial pacing and probably ventricular sensing, but you can't tell that because there's no ventricular beats anywhere in the strip and it's otherwise normal. What if during most of the time that you're seeing a patient that you notice that there's no pacemaker spikes anywhere and the patient's heart rates relatively fast? The quickest way to find out if the pacemaker is able to pace is just applying a magnet on it. If you put a magnet on a pacemaker, it converts the pacer to fixed-rate pacing. If there's one lead in the ventricle, it'll convert it to VOO mode and it'll just pace at a set rate, usually a rate of 60 or 80. If it's a dual-chamber pacer, in other words, there's a lead in the atria and the ventricle, it probably will convert it to fixed, basically DOO mode where it'll pace the atria and the ventricle at a set rate. This is important for a few reasons. Number 1, it's basically a safety mechanism. Let's say the patient needs to go to the emergent surgery and there's no time to reprogram the pacemaker or anything else. You could easily apply a magnet to the pacemaker and it basically tells the pacemaker to ignore all electrical activity and just pace at a certain rate. That's important because in the OR, you might have electrical activity that comes from a BOVI or some other type of electrical corduroy device, which could confuse the pacemaker. The second example is if a patient, for example, appears in a electromagnetic field or something else, you don't want the patient, especially if the pacemaker is dependent, to all of a sudden lose pacing ability because it's confused by the electromagnetic field. It's a safety mechanism basically to convert them to fixed rate pacing. I should note that putting a magnet on a pacemaker will convert it to fixed rate pacing at a certain rate, but that's different for a defibrillator. If you put a magnet on a defibrillator, then it just turns off its ability to defibrillate. Basically, it turns off the machine. Just a key point, if you put a magnet on a pacemaker, it'll start pacing at a fixed rate. If you put a magnet on a defibrillator, it'll turn off its ability to defibrillate. Just to recap, when you're looking at an ECG with the patient who has a pacer, you want to interpret the ECG as if there's no pacer spikes, and then afterwards, assess what the pacemaker is doing. There's two major questions you want to ask. The first thing is you want to assess the ability of the pacemaker to pace. What chambers are being paced? Then another important question is, is there a failure to capture? In other words, is the pacemaker able to successfully pace? The second question is you want to assess how well the pacemaker is sensing. You want to assess what chambers are sensed, and is the pacemaker under or over sensing? Let's take a look at this first ECG. Notice here that we see pacemaker spikes in front of every P-wave. This is 100 percent atrial pacing, and because you see a P-wave after each pacer spike, you know that it's capturing appropriately. You can't really assess sensing in this patient because they're 100 percent paced, but there's really no obvious abnormality here on the CCG. Also, you can't really comment on ventricular pacing or sensing because there's no pacer spikes anywhere into the ventricle. I just want to point out, just don't forget to interpret the native complexes. You can't just say, oh, this patient is atrially paced beyond your very way. The QRS complexes here are not normal. This patient has evidence of left axis deviation, left ventricular hypertrophy, and poor R-wave progression. This ECG is a little bit different from the preceding one because there's fewer pacer spikes. In fact, there's only two of them which are located in the beginning part of the strip. This is an example of atrial pacing here because there are P-waves that are appearing after each of the pacer spikes. Since these are present, that means that the pacemaker is appropriately pacing the atria. Then we are also assessing for sensing here. It's probably the case that the pacemaker is sensing appropriately because whenever it sees an intrinsic P-wave, which appears in the latter portion of the strip, the pacemaker is not firing. So that means it's sensing appropriately. So just to summarize, this is an atrial pacer. It's pacing well and it's sensing well as well. Just commenting on the rest of the strip, there's also a QRS complex is abnormal. This patient has a native left mental branch block. Let's take a look at this ECG. Here, when we're assessing for pacing, it's unclear if you could see any pacer spikes in front of P-waves, but I don't see it. There is evidence of ventricular pacing spikes. After each pacer spike, you see a wide QRS complex. So that means that this patient is being paced appropriately. So the next question is sensing. So it's obvious that this patient doesn't have any atrial sensing. In fact, there's no relationship between the ventricular pacing and the atrial pacing here. In the dotted arrows there, you can see the P-waves that are just marching on through. The fact that there's no relationship between the pacer spikes in the ventricle and the P-waves indicates that there's no atrial lead there. This is probably a single lead pacemaker. Then we could go to the ventricle and then we could say, is the ventricular lead sensing appropriately? This is a little bit harder to tell because this patient is 100 percent ventricularly paced, and so there's no intrinsic ventricular activity, and you can't really evaluate that. So just to summarize, this patient is in sinus rhythm, and you can see that because of the P-waves marching on throughout the strip. Most likely, the patient is in complete heart block because otherwise the P-waves would have conducted to native QRS complexes. Then the patient has a ventricular pacemaker that's pacing appropriately. Let's take a look at the CCG. So this is a little bit different. The pacemaker spikes are a little bit bigger than the previous examples. Here you see both atrial pacer spikes and ventricular pacer spikes. If you look at the atrial pacemaker spikes, they're in front of every P-wave, which although they're small, they're present. So it's 100 percent atrial pacing. You also see a ventricular beat, basically a QRS complex that follows every pacer spike that's in the ventricle. This is 100 percent atrial pace and ventricular pacing. It's hard to assess sensing here because this is 100 percent pacing, but it seems like there's no obvious abnormality here. So just to recap, this is an atrial and a ventricular pacemaker, and it's pacing 100 percent of the time. So this CCG is markedly different from the prior example. This comes from an 80-year-old woman who has sick sinus syndrome and a dual-chamber pacemaker. She's really coming in with severe dyspnea and bradycardic episodes. Notice here that it's really hard to interpret the CCG. You do see some atrial spikes, and after that you see some deflections consistent with P-wave. That's in some parts of the strip. However, the areas that I've circled there, it shows where you should have seen atrial spikes. The reason why we suspected that should have been the case is because right after that you see a QRS complex. So before it should have an atrial paced beat there, and that's not present. So that means that there's abnormalities in atrial sensing. However, the atrial pacing is probably okay. Then if you go and you could turn to the ventricular beats, notice that there's some major abnormalities here. The dashed lines show ventricular pacing, which sometimes are in the right location. Occasionally, they're pacing after a native QRS complex, and occasionally it captures the ventricle and causes a pacemaker QRS complex. So this ventricular lead is not sensing appropriately, and you know that because it shouldn't fire inside a QRS complex, and it's not pacing right either. Because sometimes it doesn't capture the ventricle. So in summary, this patient has inappropriate atrial sensing because there's missed P waves before QRS complexes, and there's inappropriate ventricular sensing and pacing, which is obvious when you take a look at where the ventricular spikes are occurring. So she was taken to the EP lab to adjust her pacemaker. She ended up having a fractured atrial lead and abnormally functioning ventricular lead and basically needed a new pacemaker and two new leads. Here's another example of a dysfunctional pacemaker. Notice the arrows which show the pacemaker spikes. Sometimes they're firing inside native QRS complexes, so it's not sensing appropriately, and other times it's firing and it's not capturing the ventricle, so it's not pacing appropriately. There is a little asterisk where it shows one pacemaker spike followed by a QRS afterwards, so it intermittently is capturing. So just in summary, this is a patient who has inappropriate ventricular sensing and intermittent capture, so it's basically an abnormal ventricular pacemaker. I should also note that there's no atrial activity here. This patient's in atrial fibrillation. The only reason I bring that up is because you don't want to overlook atrial fibrillation if you have a paced rhythm, because these patients still need anticoagulation to prevent a cardiombolic event. Here's another example. This one's a little bit different. Here, the long arrows are showing atrial pacemaking, where intermittently you see a P-wave after the atrial pacemaker spike, but at other times you don't see that. So what this means is that the atrial lead is not capturing well. Notice also that there's spikes in front of each QRS complex or at least in most of them, and so it means the ventricular lead is capturing appropriately. Here's one final example of this. Basically, you see that there's a pacemaker spike that's firing in odd locations. That shouldn't happen. So if it's firing inside a T-wave or right after a QRS complex, it means the pacemaker is not appropriately sensing. Notice here that the pacemaker is capturing appropriately because there's a QRS complex that follows every pacemaker spike. Here's another ECG. Feel free to pause the recording to interpret this ECG before you move on. Notice this patient has a number of abnormalities. There is evidence of sinus rhythm, and here I'm marching out the P-waves. Then this patient also has a ventricular escape rhythm, which are shown with the dashed lines. There's also some pacemaker spikes, but they're at odd locations. Notice here that there's pacemaker spikes that are occurring consistently after each P-wave. However, they're very rarely capturing. When you see that, then you know that the ventricular lead is not capturing appropriately. The pacemaker is also not sensing appropriately because you see pacemaker spikes inside the QRS complex. That same ventricular lead is also not sensing appropriately because it shouldn't be firing. When you see that, you know that the pacemaker is not sensing or capturing appropriately. Basically, what this patient has is an abnormally functioning ventricular lead. The whole point of this ECG though is to show you that you must interpret the ECG as if the pacemaker is not there. You should be able to recognize that this patient is in sinus rhythm, has a ventricular escape rhythm, and has third-degree heart block. Only after that can you consider saying, hey, what's going on with the pacemaker? This is where you determine the patient has a dual-chamber pacemaker. You know that because the only way to have a ventricular spike after a P-wave is when you have an atrial lead as well. In the previous slides, we discussed abnormalities in ventricular pacing and ventricular sensing. The most common reason for this is when you have an abnormality or a complication with the lead itself. There is a 2-3 percent lead dislodgement rate, which could lead to difficulties in sensing intrinsic cardiac activity. But you could also have loose conductor pins, you could have fractures in the conductor coil, you could have insulation breaks, and other problems. All in all, this could cause difficulties in pacing or sensing, and oftentimes requires for another lead to be placed in the heart or a new lead so that the patient could have appropriate sensing capture. Patients could have abnormalities in a pacemaker when they're around sources of electromagnetic interference. This could be very deleterious to pacemaker function. This is not such a huge issue in the ICU setting because there's no real industrial strength welding equipment nearby, degaussing equipment, or induction ovens. But if the patient had that before they showed up in the ICU, the pacemaker may not work well because it could have been reprogrammed or they could have led to battery depletion. In the hospital setting, there are two big causes of pacemaker interference. The first one is electrocautery. Again, just to reiterate, if a patient needs emergency surgery and electrocautery is needed, place a magnet on the pacemaker because it will refer the pacemaker to VOO or DOO mode. In other words, the pacemaker will pace at a fixed rate in the ventricle or in the atria and the ventricle together, usually at a rate of 60 or 80 beats per minute, and it will ignore all intrinsic activity. Just want to reiterate again, if you put a magnet on a defibrillator, it will also turn off defibrillator function. This is actually also important in the OR and operating room because electrocautery could be confused with ventricular fibrillation and you don't want the defibrillator going off during that time period. The other common reason for electromagnetic interference for pacemakers when a patient needs an MRI, there are some institutions that are able to perform MRI successfully. Basically, what happens in those situations is they have an MRI specific protocol where they interrogate the pacemaker before the MRI, then they interrogate it afterwards as well to make sure that no settings have changed. However, that's not available in many institutions. Thankfully, most of the newer pacemakers can handle being in a MRI machine. We see a patient with a dysfunctional pacemaker. The general algorithm is to first perform a thorough device interrogation because sometimes problems could be fixed by doing that. Then the second thing is to really determine the etiology for this function. For example, the patient has a lead fracture, then you really need to consult the electrophysiology team to figure out what to do for it. In the acute setting, if a pacemaker is not working appropriately, you may need to place a temporary pacemaker, so a transgenus pacemaker that you place yourself, or if there's issues with sensing, then you could put a magnet on the pacemaker to convert it to fixed rate pacing. Dealing with the other device-related complications that are implant-related can be trickier. Some patients can have discomfort or hemothorax or other problems around the pacemaker site. You can also have other issues that are listed on this list here, but these tend to be not ICU-related issues. This is also not really an ICU issue, but this could happen. For patients with fresh pacemakers, you can sometimes see patients with hematomas. These are generally managed supportively. You don't want to consider surgical evacuation unless there's continued bleeding or compromised incision site. The reason why you don't want to surgically evacuate these things is because then that sterile space will be compromised. Probably the worst thing that can happen to a pacemaker is if it becomes infected. Fortunately, infection rates are low and occur in less than 2% of patients, but if this happens, it's really a life-threatening problem. The only successful treatment for this is to remove all parts of the apparatus, including the leads. This is associated with high complication rate, including cardiac damage, sometimes cardiac perforation. You have to go to a specific procedure room or operating room and basically slowly yank these leads out or extract them in other ways. If you do that, then the patient needs to be going to an ICU afterwards because they may need a transvenous pacer or a different type of temporary wire until a new permanent pacemaker is eventually placed in some other location. Thank you very much for listening to this presentation and these case presentations. We went over a lot here. We first talked about Brugada syndrome, then went over Long QT, both etiologies of that, and just discussed how to manage Long QT syndrome. Then we discussed the management of patients who have had previous ventricular tachycardias, including the use of defibrillators. And then finally, we spent a lot of time discussing pacemakers, discussing how to interpret an ECG in a patient who has a pacemaker and discussing the causes of pacemaker dysfunction. If you have any questions about any of this, please feel free to email me at the address listed above. On this slide and next, I listed some references that may be useful for you. I've also asterisked the ones that I feel like are the highest-yielded references.

cardiac arrhythmias

Brugada syndrome

ventricular arrhythmias

ICDs

prolonged QT interval

long QT syndrome

beta blockers

pacemaker placement