So, I'd like to introduce our panel. Immediately to my left, closest to me, is Dr. Alan Walke. He's a professor of medicine at the Boston University School of Medicine, where he's the co-director of the Evans Center of Implementation and Improvement Sciences, and he's the co-PI of the SCCM Discovery Virus COVID-19 Registry. Next to him is Dr. Kayla Lawler. She is an intensive care pharmacist at Emory in Atlanta. She's very active in SCCM. She's the chair of the Women in Critical Care Knowledge Education Group. And finally, we have Kyle Briggs, who is a physician assistant at Emory. He's the director of medical simulation there, and he's the director of the APP Fellowship for Cardiac Critical Care Medicine. We have a very highly interactive session for you today. The format will be the presentation of a case with several follow-up issues as that case moves through care. We're going to ask people to vote with their hands on multiple choice questions, and everybody has to vote. We're looking. We're watching. Okay? And then we'll have some discussion about each of the questions. Without any further ado, let's go ahead and present the case. Thank you so much, Dr. Simons. Thank you so much for the invitation to speak today. Where is the clicker? Oh, the mouse. Last time was a clicker. All right. So, disclosures. I have some funding from NIH to do research on atrial fibrillation and sepsis, but otherwise we don't have any disclosures. So what is this flipped-ish classroom? The goal today is really for us to not have to speak. So we want as much participation as possible from all of you. As a critical care health services researcher, I study practice variation. So if the same patient were to present to any of us or you, how would we all treat them differently in areas where the evidence is vague? That's what we're going to do today. We're going to try to see what's the practice variation amongst all of us when presented with a patient with atrial fibrillation during critical illness. So the goal is to get an interdisciplinary discussion and perspective sharing. We want to know what you would do in these situations, and we want to know why. So we're going to ask some representatives to come up and give a rationale for why they chose an answer that they did. We will also give our rationales for choosing specific answers, and really the goal is to have a discussion. The cases are not designed to have a right answer. You might feel strongly that there's a right answer, which is great. Tell us why. So how this hopefully will work, we'll present the case, we'll present multiple choices, we'll all vote on answers, we'll hear some of the rationale. So I think we're going to flip five and four. We're going to say, why did you choose it? And then we'll talk about some rationale for our answers. And then we'll see if anyone was convinced to change. We'll vote again, and we'll see if any of the evidence presented will change minds or not. So here's the case. Try to remember all of this. It's a 61-year-old man. He's presenting to the emergency room with six weeks of progressive shortness of breath, low-grade fever. His chest X-ray shows bilateral infiltrates. His diarrhea started on antibiotics, but his work of breathing increases. His sinus tachycardia is getting worse, and hypoxemia increase, and he is intubated. He started on a low-dose norepinephrine, and he has a bronchoscopy after intubation that shows copious foamy macrophages. And it is thought that he has amiodarone among toxicity, and his amiodarone is discontinued. Why is he on amiodarone? He has a past history of ischemic cardiomyopathy, ventricular tachycardia, for which he received the amiodarone. He also has a STEMI with a drug-eluting stent. Four weeks ago, he's on lisinopril, amiodarone, aspirin, and clopridogrel daily. So after he gets stabilized with the intubation, things are going well until about 48 hours later he develops new onset atrial fibrillation, heart rate 150 to 160s, with an acute increase in his vasopressor requirements. The question is, what would you do next? How would you manage this patient? Would you switch his vasopressor from norepinephrine to phenylephrine, start a beta blocker, start digoxin, or do something else? And please tell us what that would be. All right. Now's the chance for all of you to shine. So raise your hand if you would select A. Great, all right, thank you. Raise your hand if you would select B. Awesome, thank you. Raise your hand if you would select C. Okay. And raise your hand if you're a D. Something else. All right. So we had, nicely, so just to let everyone know from my perspective here, we had people raise their hand for every answer. So we just demonstrated practice pattern variation. My sense was that C was the most popular, followed by B and A and then D. Okay. Brave souls. Someone who selected A, come up to the microphone and just tell us very briefly why A. Any reason. We won't bite. Yes. Thank you very much. Wonderful rationale. So we will be presenting in a little bit some data to back up what Dr. Hollenberg just said. How about the bee people? Who wants to start a beta blocker? And why can you give us just a very brief rationale? Step right up. Be much more fun if you talk. The more you talk, the less you have to hear me. Anyone? Okay. Well, we'll go through. This is why we have our backup slides. So the bee people, the beta blocker people, I feel like, you know, need, you know, they're like a little anxious. So maybe the propanolol, we take some propanolol and then try to answer. All right. What about the digoxin? Okay. You're so wishy-washy. Thank you. All right. Nice. All right. Thank you for being brave. Digoxin people. Why digoxin? Just has to be quick, brief, to the point. Great, thank you. Excellent rationale. Are there any other rationales for digoxin out there, different reasons that someone might have chosen digoxin? Great. Did Jackson might give you a little bit more squeeze as well. Yes sir. Excellent. So we have lots of experience using digoxin, right? Digoxin is sort of a tried and true medication for us. Excellent. So not only do we have practice variation, we have variation in the rationale for the same practice. So really amazing. Awesome. And then the D people, the something else. Great, so don't just do something, stand there, work them up a little more, find out before pushing drugs, is there other things that we can do that can optimize physiology, pain, sedation, analgesia, oxygenation, all that stuff. Great, yes. Okay. So, combining therapies. Great. All right. All right, re-challenge with Amy Odoron, okay. Great, excellent. I think we'll be coming to that later as well. Well, great, thanks for all these thoughts and opinions and recommendations. I feel bad for the nurses that would have to work with all of us, you know. Right, the same patient, every single person in the, every single clinician in the audience has recommended a different treatment. So this is how all our colleagues. Yes, oh. Yes. Always on the table, yes, thank you, cardioversion. Great, well, we're gonna give a little bit of evidence to back up really any of these choices. So Kayla has chosen A here, so she's gonna tell you why. Good morning. So when I'm thinking about my selection of vasopressors for a patient who's having arrhythmias, I'm obviously gonna shoot for something that is going to be less of an inotrope and more of a vasopressor. I have the selectivities here for you, acknowledging that epinephrine, norepinephrine, and dopamine are kind of our dirtier vasopressors in that they have inotropy and vasopressor activity. And so if we were thinking about, you know, something that's acutely exacerbated, his norepinephrine dose was 0.1 mics per kilo per minute, which I would not consider to be a small dose. And so I think that it's reasonable to see if we can come off of our norepinephrine equivalents and reduce the amount of beta stimulation. And you do so with phenylephrine. There are other vasopressors here on our vasopressor side. I think vasopressin or ANG2 might have also been reasonable discussion points here. There is some data from CHEST 2022 with law and colleagues, including Dr. Walke. And they did a retrospective chart review looking at AFib and sepsis and the initiation of vasopressors. They compared norepinephrine and phenylephrine. And they had about 90, I'm sorry, about 900 patients in each group and found, as you might expect, that there was a more significant improvement in the heart rate with phenylephrine than there was with norepinephrine. I believe it was four beats difference. What the clinical significance of that has yet to be slussed out. And they did also find that initiating in patients with a higher heart rate, those patients had a better response to the phenylephrine. Acknowledging that this is retrospective, that could be patient selection. But again, some food for thought with regards to why our vasopressor choice might be hurting us. So I was a beta blocker person and I'll tell you why. So in another study led by Nick Bosch from Boston University, he looked at about, I think, 600 patients who had new atrial fibrillation in the ICU who were critically ill. And he looked at which treatments were given and what was the change in heart rate after each treatment was given, adjusted for multiple factors, including the starting heart rate, and found that at one hour, beta blockers resulted in the largest change, the largest reduction in heart rate of 15% compared to amiodarone calcium channel blockers and digoxin. But by six hours, they all sort of had resulted in about the same amount of heart rate reduction. So if you wanted to reduce the heart rate fast, this study suggests that beta blockers might provide that. An additional study looking at about 40,000 patients with atrial fibrillation during sepsis, a little hard to read in the purple, but what this shows is beta blockers compared to calcium channel blockers up top, digoxin in the middle, and amiodarone at the bottom, and that beta blockers were actually associated with a small but significant reduction in adjusted mortality for patients who received them during sepsis and atrial fibrillation. So again, observational, but maybe some more rationale to use beta blockers first. Kyle's gonna convince us otherwise. So I noticed that the most popular choice was digoxin, and I like that, because that was mine. So what about digoxin? And as far as rationales, I'm gonna keep things simple. We're talking a lot about the fancy new things, but the FDA says I can use this. It's, you know, tried and true, kind of from the olden days. It's an old classic. And when I look at kind of what I'm gonna treat with this situation here, I know some knowns, but I know several unknowns. What do I know? I know he's hypotensive. We're on norepinephrine, and we're quabbling about which vasopressor to use, but where I can find the right choice there is a question. I know he's hypotensive, and I know, as we've heard, I have something at my disposal that I can get some rate control and not sink his blood pressure anymore, we hope. The other thing, I noticed, as we pointed out here also as well, I've got some good support. We have a history of heart failure, and now I don't know if it's decompensated right now. I don't know if we wanna go down that pathway or I'm thinking through. I don't know if now is the time to really kind of squibble back and forth about some of these tricky details, because I'd really like to just get control of this guy before he gets worse in front of me, before I'm forced with things like an emergent shock. And so for now, I know I've got a history of heart failure. His EF was reduced to 25 to 30%. He had a STEMI four weeks ago. Is there any effects from that? I don't quite yet know why he's in atrial fibrillation, and could it be that he's decompensated from his whole MI? We're talking about amiodarone lung, and again, there's some question to that, and that's by design on purpose, because it's often not clear. And so for now, what I'm gonna stick with is classics. It's tried, it's true. FDA says I can use it. I know he's got some heart failure. I don't wanna make that worse. He's hypotensive. Let's not mess with that. Smidge a didge. And I'll just make a couple of comments from the standpoint of, or the perspective of a cardiologist or, in my case, an electrophysiologist about these medications. The first thing is about the amiodarone. 400 milligrams twice a day of amiodarone is a very high dose. We know that amiodarone lung toxicity is, its incidence is correlated with both actual current dose and also cumulative exposure. So if this person has inadvertently been on 400 twice a day for a year or six months, it makes our suspicion of toxicity a lot higher and the foamy macrophages, of course, in addition. But just about the pharmacology of rate control. From an EP perspective, we think about the autonomics a lot. And it's, of course, when you give beta blockers, you're blocking the adrenergic inputs to the AV node to achieve rate control. I just wanna say a few words about the Joxin, which comes and goes in its favor. As I've gone through my career, it's been preferred, then pillory, then goes back and forth. But the thing is that the way the Joxin works on the AV node, which I think people aren't always acutely aware of, is that it augments vagal tone. So when you think about these two arms of the autonomics on the AV node, there's the sympathetic arm, which makes you go faster, and the parasympathetic arm, which makes you go slower, it's often the case that you wanna treat both. And in fact, the Joxin doesn't work in active people because their sympathetics overcome whatever augment and vagal tone you get at the AV node, but they're synergistic together. And it's an important thing to remember. That would go under other, I suppose. And of course, when you use more than one drug, you can use lower doses of each to get that synergy. So I just wanted to mention the concept of the autonomics. And someone mentioned about maybe get a little kick on the EF from the Dijoxin. Maybe yes, maybe no, but more importantly, it's not a negative inotrope on this person. That's, I think, the most important point because they're probably in heart failure anyway, and giving beta blockers to people in heart failure can be problematic. So those are the comments I had. We can't bring the mouse over there because it's not wireless. Great, so lots of perspectives, lots of experience, evidence. So the question is now, has anyone, so first, I want to give you all a medal for participation here in this first question. So I applaud you. That was great. We saw really a snowballing of participation, so thank you for being willing to do that. Now's the fun part. I know it's been so fun so far, but this is even more fun. You get to re-vote. So who would choose A now, switch norepinephrine to phenylephrine? So we lost some of those, okay. Who would start a beta blocker now? All right, we have, I think, fewer beta blocker choosers, but still some folks. Who are the Dijoxin fans now? Dijoxin has gotten more support, so do something else besides those three things. More support to something else, okay. Can someone who was a norepinephrine to phenylephrine prior person, who switched, be brave to tell us about why they changed their mind? I commend you for changing your mind in the face of new evidence, so that's a good quality. Do you want to tell us about it? Doctor. Yep. Boar Beats didn't do it. Great. How about anyone who was going to start a beta blocker and now isn't? Right, you don't want to give all that peripheral squeeze without any inotropy in someone with a reduced EF. Thank you. Any beta blocker to something else switchers? All right. Well, I chose beta blocker, but I'll be a switcher. So I'll say I switched from the beta blocker choice to digoxin because of the patient's history of heart failure, maybe that heart failure is contributing to the presentation and I don't want to give the negative inotrope, the beta blockade. And so I'll choose digoxin now. Anyone from digoxin go somewhere else? Any digoxin to some other choice? Yes. Great. And anyone who was a D fan, now switch to something else, or do you have... An excellent lesson in general for all the things we do in the ICU. follow back up and stop it if you don't need it anymore. So excellent, excellent point. I think we're going to steer a little clear of the doses and the finer points of all that, because I think we could talk about this for many, many hours. And so I would encourage maybe those finer points for the post session. Thank you for raising them. Yeah, but there's so many times when we can vary our practice. I think it's really fascinating. The other thing I just want to restate is we are not specifically advocating for any of these approaches. Really, the intention of this session is to engender conversation and discussion and people sort of discussing their rationales and discuss a little bit of the evidence for all these rationales. So, and so thank you for all for participating. All right. Anyone have anything else they want to say before we move on to the next? Yes. Great, excellent comment. So again, a lot of calls for caution, also discussion about more practice variation in terms of use of phenylephrine. From our perspective, we don't tend to use phenylephrine very much, but if we do, maybe to try to get a little bit of the reflex bradycardia effect that you saw, again, might not be enough to convince people to use it. Just personally, if I'm using beta blockers for someone sick in the ICU, I will choose Esmolol because if I'm wrong, it will turn off in one minute. So another point is not to use Atenolol or something that if you're wrong, it's just sticking around for days. You want to choose something that will go away quickly. Sure. Does anyone in the audience want to comment on amiodarone or their use? Anyone up here want to comment? I feel like I'm... It's coming. Thanks for the segue. Hold on to that thought. We want to hear more. All right, so question two. Kayla's gonna discuss the developments. We did everything that you guys said, and I don't know why he's worse now. So we did the thing, and now he's compensated. And now he's got his fever irregularly irregular in the 160s, map in the 50s, and worsening organ dysfunction as evidenced by lactate. So what would your next step be? All right, it's voting time. So who's gonna vote for A, the cardiovert? All right, decent hands. Who's gonna vote B, add antibiotics and vasopressin? Okay, a couple, yep. Who's gonna give magnesium? As a bolus, two to four grams. Okay, excellent. I saw someone brave back there. And who wants to do something else? Excellent, okay, there's a few. So it seems like cardioversion is probably the more popular answer. Who would like to tell us why? Sure, thank you. Yeah, I think that's very reasonable. Go ahead. That's a really great point, absolutely, making sure it's true AFib. All right, who would treat the sepsis with antibiotics and vasopressin? Anyone wanna? Yeah, anybody wanna talk about why? Right. Right. Absolutely. Yeah. I think the new fever makes us really suspicious for, you know, a septic component and could definitely be, you know, additive to his decompensation. Anybody want to talk about why they would give magnesium? Well, I tell you that I pick magnesium for this and I'll talk about it more briefly, but one of the things I think when I'm having this conversation with residents is it's magnesium. Our therapeutic or, you know, our toxic limit for magnesium is very high, and so we can give magnesium and feel relatively safe that it will be tolerated and have almost no hemodynamic effects. Who wants to talk about something else? All right, so I'll let Dr. Walke tell you about his side. All right, so my choice was cardioversion here. We have the ACLS guidelines, which, you know, level one, that says synchronized cardioversion is recommended for acute treatment in patients with hemodynamically unstable SVT. So by the book, this patient fits in to that statement. I think, so really not necessarily wrong to cardiovert this patient at this point, because we don't know how much they need their atrial kick, how much the AF is contributing to their hemodynamic decompensation. And so one way to find out is to try to get rid of the AF instantly. As I think someone in the audience just said, you know, often in the ICU, when we cardiovert people from atrial fibrillation, it doesn't stick, and that's borne out by the data. So I think it's about 40% maintained at one hour, and it's down to like less than 20% at 24 hours that have stayed out of the atrial fibrillation. So I just say that in choosing this, you also want to do all the other stuff that we've talked about to try to make sure they stay out of the atrial fibrillation, and we're not just back in the same place in 10 minutes, because we don't wanna be shocking people every 10 minutes. Kayla, what was your choice? Thank you. So I would have given magnesium, and this data is a meta-analysis that was in Heart in 2007. They looked at 10 randomized controlled trials looking at administration of magnesium. You can see here that some of them were in the presence of other antiarrhythmics as well. The three that really showed statistical significance favoring magnesium are the Davey in the presence of digoxin, the Moran in the presence of amiodarone, and the Gouldstadt in the presence of arapamil. Obviously, I don't routinely recommend arapamil as an agent for a decompensated heart failure patient, since our non-DHPs increase mortality in that patient population, but they did show that the addition of MAG to some of these antiarrhythmic regimens did have conversion out of AFib. It's thought to be due to the calcium channel blocker effect at the AV node. That's the theorized mechanism behind it. And they found it worked best in the presence of digoxin. So if you had already given somebody digoxin, and you hadn't yet challenged them with some magnesium, that might be something that you want to do. Six of the 10 trials included people with normal magnesium levels, and so I would feel safe assuming that I didn't have a reason to assume their MAG level would be high. I would feel safe giving a magnesium bolus of two or four grams to this patient. And now Kyle will tell you his thoughts. So I'll put in a stand-in slide for really what is code for there's something else going on. And I'll tell you, we've made this guy a little bit worse, but I mean, his heart rate's up by 10 points, his MAP's in the 50s, but we're also recognizing before, we didn't really clarify or consider why are we in atrial fibrillation? Why did we go to RVR? Because he's on amiodarone, but that's for a history of VT. There's nothing that I know about this guy that suggests he's got a history of atrial fibrillation, I don't know where this has come from, and so that's a question that I've had in my mind ever since I've met him, and now I see a new fever, and he's hypotensive. I mean, has anybody seen a septic patient with a MAP in the 50s, tachycardic? That's the same guy. And so I'm gonna have a really hard time arguing with the crowd that says they want to start to think about cardioversion, because I think that clearly pointed out, we probably would do all things kind of at once, but I think that in this question is really, I mean, I think that I want to avoid in myself just the notion that the shock can fix the rhythm. You know, he's got this atrial fibrillation, it's new onset, let's shock him, let's get him out of it, let's solve that piece, but I fully expect that if I shock this guy, it's gonna do nothing. We've all seen that patient where we shocked him, didn't do diddly, now what do we do? Or, you know, shocks, beep, beep, beep, beep, beep, beep. It gives me a break for about two beats, and all of a sudden I'm back into it, because I still haven't addressed the underlying problem. His catecholamine surges through the roof because of his sepsis, he's got this fever, and I just need to get control of the underlying problem, and so my answer when it comes to vasopressin, trying to avoid some beta agonism and get some pressors, and give him some antibiotics, it's because I want to put foremost in my mind that I need to treat the underlying cause, because if I don't, I can shock him a lot, and I don't have any strong confidence that it's really gonna help. In addition, shocking him is not necessarily free. I mean, this guy's intubated, and so what does that mean as far as his sedation level? But let's say he wasn't intubated. Perhaps in the 50s, he's getting worse. Do I want to, you know, ask for forgiveness later? Do I just hit him? Do I give him some sedation? Do I play that game? What about atrial stunning? I mean, he's already got reasons to be anticoagulated. He's gonna be a bleeding risk thing that we may have a question for coming up for you. But do I shock him? And now I've got to worry about atrial stunning. A shock is just not the answer I'm looking for here, even though I recognize, I think I may be forced into this, but first in my mind is I want to get control of the problem, not the symptom. And I would just make one comment about if he is to be cardioverted. You know, I think most of us would consider cardioverting here, and maybe he'll stick. Maybe he won't, but at least give it a try. But the one thing I would say about that is in terms of maintaining sinus after that, with all these things going against him, you don't have access to another antiarrhythmic drug because he's going to have plenty of amiodarone present, and you really can't safely add another antiarrhythmic to the amiodarone without a significant risk of ventricular proarrhythmia. You know, it's a QT-prolonging drug. But the one thing to think about, and you can get a consultation, is it wasn't really said if this guy has a defibrillator or not. I kind of think he does since he had VT and he's on amiodarone. And most, actually all dual chamber and biventricular defibrillators have algorithms available for atrial pacing to try to suppress AFib. And you know, it's a probabilistic event. It's a few percentage points, but they do some overdrive atrial pacing algorithms. One particular company has an actual very active, aggressive anti-tachycardia pacing in the atrium when they start to have PACs or runs of atrial tach to terminate. So you really want to call your colleagues if there's a defibrillator and you're going to cardiovert to get that thing programmed to try to, you know, really hedge your bets and try to increase the odds that they'll stay in sinus rhythm after the cardioversion. So let me come back. Let me give you another trophy of participation. And as on this note right here, what I'm going to do is I'm going to speed things up intentionally because we've had such a good discussion. And I think really from our hearts to yours, thank you for this, because we weren't quite sure what to expect. And so I think we were ready to be nimble, to carry much of more of the conversation, but thank you for your participation. And this has been very helpful, I hope, for you. And we're going to move on. So this next case, you're doing fantastic. Now we've fixed him. Oh wait, we were going to, do you want to re-vote? I'm going to speed up right here because we're running out of time. So we fixed him. That's what I thought was coming next. You fixed him. You're doing fantastic. You're excellent. Your participation has really helped, and now the patient's better. He's ready to go home. Not because we send him home all the time, but because it was a floorbed disaster. We can't get anybody out to the floor. We're forced to discharge them straight home because this guy's sick and tired of waiting for us to get things together. So he's going home. And I'm here on rounds, and the resident comes to me. He's about ready to present. Comes to me, comes to me and says, hey, we're planning on discharge from the ICU. I don't do that very often. We've got to think about anticoagulation. What should I do, right? I recognize he's got dual antipletic therapy. He's got these things. I know his history. He's got the heart failure. He's got the stent. That was about four weeks ago. What should I do? Should I, A, give him a Doac and keep him on his home aspirin and clopidogrel? Who would go for that? Actually, let me go with it. Who would add a Doac to his clopidogrel but take away the aspirin? I could continue his home medications aside from, as he has listed now, the Doacs, excuse me, the DAPT, the lisinopril, the amiodarone, and just kind of keep it there, and let's hold off any Doac for now. Let's do something else, or stop talking to me about this, call a pharmacist, okay? So now that I've run through them very briefly, how about, A, who would add a Doac to his home aspirin and clopidogrel? Nobody? Okay, we got one. Who would add a Doac to his clopidogrel yet take away the aspirin? Okay, a few more. How about, let's continue the home medications, let's keep the DAPT on, but let's not start any other anticoagulation at this point right now. Okay, still yet some. Anybody have something else strongly in mind, another strategy? Is that strategy, call a pharmacist? Good, good. In that case, how about this? Because of time, the people who had something else in mind, do you mind if I start there? Who's brave enough to tell me the something else? So what I'll do again, we may have to continue this outside, which actually makes me very happy. Good discussions. So let me just run through some of the choices and share some of the things that may have entered our minds. I'll just start out with the first one. Let's just add a DOAC to his DAPT, add a DOAC to his aspirin and his clopidogrel. And the reason why is because, A, that's from 2019, that's what the guidelines say. Technically, although we put it right on the border in the gray area on purpose. But really guidelines say we've had a recent MI with up to four weeks, about a month ago. He's got this recent MI, he's got this new stent. I do know that I've seen an instant thrombosis and they are frightening, V-fib frightening. And so I do know that bleeding is not my favorite, it's not fun, but I would much rather treat a bleeding concern than an instant thrombosis. And so at this point, I look at him, his has-blood score is a two. And so it's not, it's intermediates, but his has-blood is a two. He's not a huge, huge bleeding risk. And so at this point, I'm a little bit more fearful about the clot than the bleeding. That could be a rationale for choice A. So here I am to argue with Kyle, as pharmacists are wont to do. Discussing about the risks that we know with triple therapy, which this trial is from WOST. WOST looked at patients who had an indication for anticoagulation as well as an indication for dual antiplatelet therapy. And they compared these two groups. The primary outcome was all-cause mortality. And they found a significant increase in all-cause mortality, although interestingly, it was driven by non-cardiac death, which is very interesting. They were not powered to assess instant thrombosis. So to Kyle's point, I don't know what this patient's individual risk of instant thrombosis is and this study doesn't really tell me what the likelihood it is of it. But also in WOST, they did have more bleeding. This was also driven by non-major bleeding. And so what is the clinical significance of that? You know, I don't have a strong opinion at this time. But I would argue that the number needed to harm, to have a bleeding event, is four in this study. And so for that reason, I would vote to discontinue the aspirin and keep the patient on a DOAC and clopidogrel. Now Dr. Waukee will give us his thoughts. All right, so we want to ask ourselves, what is the risk of the feared complication of stroke after new AF and critical illness? This is some data from following patients from a Medicare data set who were hospitalized with sepsis and new AF. And we can see on the x-axis that up to five years out, the risk of stroke in those that had no AF during their sepsis in the green line is at about one year, a little less than 2%. Those that had new AF during their sepsis in the red line is slightly higher. And those that have pre-existing AF we know is higher. So patients who have new onset atrial fibrillation during critical illness, about 40% of them will have it recur, at least identified as a recurrence in the year following that critical illness. And so there's just a different risk benefit than patients who have sort of known atrial fibrillation that didn't occur during an acute event or patients with sort of primary AF versus secondary AF. So since we don't know the risk benefit after critical illness, there's lots of competing risks like death after critical illness. And the risk benefit is probably lower than those with pre-existing AF because the risk of stroke is lower. Those were the reasons why I would advocate to have the patient follow up, have the patient have a rhythm monitor of some sort, a long-term rhythm monitor to see if they are one of the 40-something percent that will have recurrence and maybe a longer-term risk of stroke and let them have that follow up. So again, any additional thoughts based on what we said? Anyone changing their mind? This is, by the way, your Rockstar Award for participating today. We really applaud you and thank you for that. So. I'm going to ask Dr. Simons to talk about that. I would just make a few comments first before I answer the question. The first thing is, I think in terms of practice variability, probably the largest variability that I've seen in this area is indeed the pronunciation of WOST. And I'm going to conclude that this is the proper pronunciation as I go forward in the remainder of my career. And the other thing I would say is that in 2023, you know, triple therapy has really – triple therapy being clopidogrel or something like it, plus aspirin, plus an anticoagulant – it's really become a niche thing, and at this point it's really for the one month after stent insertion for patients with AFib and a new stent. And beyond that, as was shown, it's really not appropriate because of this huge risk of bleeding and, frankly, the lack of any demonstrated benefit. In terms of using anticoagulation in patients, that is something that I do with a lot of frequency when I see patients diagnosed with AFib. A lot of them have already come from the cardiologist, but absolutely, they have to be talked to about the risks and benefits. And the one term that hasn't been introduced that I'll introduce as we finish up is it's very important to just state the CHADS-VASc score. And you know, the CHADS-VASc, if you look at the study, actually, it came out of Scandinavia. There weren't more than maybe 1,000 or 1,500 people in the whole thing. It's not – it's our Bible, but if you really look at it critically, it's a little limited. But it's all we have right now in the guidelines. So I think it's very important to quantify the CHADS-VASc score, state the CHADS-VASc score in the medical record, and then tell the patient the CHADS-VASc score and what our guidelines are and the risks and benefits. And the final thing about the CHADS-VASc score that virtually nobody paid attention to is that in the last set of AFib guidelines, they stated that women and men should be treated differently because the CHADS-VASc point for women is more of a risk modifier than an actual risk factor. So the mandatory anticoagulation point in the guidelines is that CHADS-VASc 2 for men and 3 for women. And everybody missed the memo, and it's really important to be aware of that if you are counseling patients and treating them. A CHADS-VASc 2 for women is that gray zone, like a CHADS-VASc 1 for men. And then, of course, CHADS-VASc 0 is don't anticoagulate, and CHADS-VASc 1 for women is similar. So we in cardiology do not anticoagulate women who are CHADS-VASc 1 only because of their gender. So I just wanted to get CHADS-VASc into the conversation before we finished up. Did any of the members of the audience have any other comments they wanted to make before we wrap up? Yes, please. Oh, two. It is a drug that we do use in certain situations, generally as an add-on for patients with life-threatening VT. It's not a drug, as you said, that many people use anymore. It's a class 1A in the Vaughan Williams classification system, QT prolonger. Sort of like quinidine is one way to think about it. But the problem is this patient's got a bunch of amiodarone in them, and the combination of amiodarone and procainamide is really fraught in terms of, again, a risk of ventricular proarrhythmia. And I think that that would be something that would be done with great caution, if at all, unfortunately. Now, again, when we have intractable VT, somebody's got an LVAD, a whole different topic, and they're getting shocked and shocked and shocked. We've done just insane things about mixing amiodarone with procainamide on the intensive care unit many times with the myxilatine and everything else. But in this situation, it would be a tough one to put forward. Did any of the panelists have any final comments before we wrap up? Okay, very good. Just to summarize this all. Making a summary for this was challenging because the whole intent was really to have a discussion and to talk to each other, and we weren't quite sure which points would come out, although we had some suspicions and so the summary we'll have is that atrial fibrillation really is the cockroach of the ICU, right? It's everywhere, it's hard to get rid of, and it's not so much the bug itself that's the problem, so much as it is that it's saying something about the conditions and the environment that our patient's in in the first place about to figure out why do we have these cockroaches in the first place, right? And so with that, it comes a challenging set of questions, a challenging set of problems, and more often than not, there's more than one answer that's reasonable, especially with where we are now with our current research as far as what we have available to us, and we know and hope that that will continue. And with that, we thank you for your time and your participation. Thank you.

panel discussion

atrial fibrillation

critical care

treatment options

practice variation

evidence-based choices

interdisciplinary discussion

perspective sharing

case presentations