SCCM Resource Library-Atrial Fibrillation in the Critically Ill: What, When, How, and What If?

Video Transcription

Good morning, everyone. Thanks for coming to this session on atrial fibrillation and critical illness. I'm Jake Jenser from Mayo Clinic, and I'll be standing and moderating.  We have three really excellent talks, or at least two excellent talks, and then my talk after that. I would like to introduce our first speaker, Nicole Palm  from Cleveland Clinic, who will be getting us started right now, thank you. All right, thank you. I will jump right in because atrial fibrillation,  as I'm sure you guys are all aware, could be a talk that we have for days and days, and we only have an hour to try to get through everything.  So as a little introduction before getting into the pharmacology, I'll just remind you all that in the critically ill, many causes of atrial fibrillation  that's nuanced in the ICU isn't necessarily related to underlying cardiac dysfunction. We have a lot of other things going on in our patients  that brought them to the ICU that can predispose them to nuanced atrial fibrillation, including inflammation, use of vasopressors, specifically beta-adrenergic  ones, which will directly stimulate our heart, electrolyte derangements, and volume overload causing atrial stretch. In the ICU population, a meta-analysis identified these  as the strongest seven risk factors for nuanced atrial fibrillation in our patients. And as you can see, cardiovascular disease is listed,  but there are other risk factors for our patients that we may or may not be able to control that could predispose them to nuanced at AFib while they're under our care.  So my topic is the first and last line of defense is pharmacology. And so I'll try to do a broad sprinkling of some preventative methods, first line, age old,  rate versus rhythm control debate, as well as talking about some refractory management and anticoagulation strategies in our patients, which, again,  is a lot to cover, so bear with us. As I'm sure many of you are familiar,  our standard rate control agents are our calcium channel blockers and beta blockers. And in the general population, you can see that diltiazem, our calcium channel blockers,  are considered to be the most effective, although beta blockers are also very highly effective in controlling nuanced at AFib.  The problem with diltiazem in our patient population is that it has much more side effect profile, much harder to tolerate in our patients. And in fact, nearly a third  of patients can experience hemodynamic instability and specifically a lowered blood pressure when receiving diltiazem in the ICU. We also know it can cause jitis motility,  heart failure exacerbation. These may be things our patients are already here with or already predisposed to from other things going on.  And so this makes this agent, although it can be effective, not as great of an option for us in the ICU. Beta blockers, on the other hand, are very well tolerated.  We have a couple options, IV or oral. And they really have very little side effect, especially at rate control doses. You really won't see the hypotension, the AV block,  until you're approaching very, very high doses in our patient population. I point to this study not because it was about atrial fibrillation, but because this study gave esmol  to patients in septic shock. And I think a lot of us hesitate to beta block patients who are requiring vasopressor support or presenting with shock  because of that potential for reduced blood pressure. What was interesting about this study was that in using esmol to try to control tachycardia, again,  not tachyarrhythmia, in patients with septic shock, they found not only was the heart rate better controlled compared to placebo, this is not surprising,  but the norepinephrine dose was actually lower in the esmol group, suggesting that not only did the beta blockade not contribute  to worsened shock, but may have helped improve the cardiac output and therefore improve the resolution of the shock state. So I use this study to point out that don't be concerned  about beta blocking your shock patient just because of the fact that they're on vasopressors. This may be an option that is still in our wheelhouse for these patients.  For rhythm control, we know that amiodarone, our Swiss knife agent, is available to us. You can see much of the data about it here. But know that it's very effective  in restoring normal sinus rhythm in the ICU when we do pull it out. Magnesium is a great agent for us. It's very well tolerated. And the number needed to treat  to prevent an arrhythmia is only 13 patients. So this would suggest that optimizing our magnesium levels in our patients can help prevent atrial fibrillation.  But when atrial fibrillation occurs, you can see that only a fifth of patients will actually just respond to magnesium. So it's not a great agent to pull out and use as monotherapy  to treat atrial fibrillation when it happens. So with all that in mind, the rate and rhythm control agents that we traditionally use, are they going to be effective  in preventing atrial fibrillation in our generally critically ill patient population? And the answer is, there's not a lot of data to suggest that that's the case.  In fact, outside of cardiac surgery, there's really not a great role to suggest we should empirically start these agents to prevent atrial fibrillation.  I did allude to that Esmol study, but remember, that was just general tachycardia control. There was no data in the study related to preventing tachyarrhythmias.  So with this in mind, are there any other strategies we could use to prevent atrial fibrillation from occurring in our already critically ill patient population?  Well, there are a couple of novel agents we could consider. Steroids, as you guys are aware, have been studied for many things, particularly septic shock in our patient population.  And also, in fact, for prevention of atrial fibrillation. And in our cardiac surgery data, there's actually significant study that shows perioperative, including single dose,  preinduction, use of any steroid, has corresponded with a reduction in new onset or postoperative atrial fibrillation. And I'm going to caution you guys that a lot of the data  for prevention of atrial fibrillation is in cardiac surgery patients. This is unsurprising, as they're the ones most likely to experience atrial fibrillation.  And we may have to extrapolate some use because we're not going to have a lot of data outside that group. But with that being said, we have a lot of data  for steroids and septic shock. That's a whole other controversy. There's other sessions you guys can attend to learn about that here at this conference. But I will say that many  of those robust randomized clinical trials don't actually talk about new onset atrial fibrillation as an outcome. They're looking at shock duration, mortality,  all these other outcomes. Only one of our large studies that we think of even commented on arrhythmias in general, and they didn't speak to AFib specifically.  There's a small retrospective study of provider-driven hydrocortisone use, which I list here for you, which showed that in septic shock patients who experienced atrial fibrillation,  hydrocortisone compared to no hydrocortisone actually did prevent some new onset atrial fibrillation, even after a propensity-weighted matching.  You can see the risk reduction was lower. Again, this was provider selection of patients who could get hydrocortisone versus not. And so it's hard to extrapolate and suggest  that you should be using hydrocortisone for all your septic shock patients specifically to prevent atrial fibrillation. But I think that this is suggestive.  There may be some benefit there, again, adding to the already controversial use of septic shock hydrocortisone dosing. What's interesting is that the mechanism  of action would be reduction in inflammation, which is driving the atrial fibrillation, and the inflammatory markers that they measured actually did not change in this study.  So I think this needs a little more data to elucidate whether or not steroids can, in fact, prevent new onset atrial fibrillation, but there is some data suggesting this may be a  possibility with their use. Our favorite drug du jour in critical care is, of course, vitamin C. And again, I'm not going to touch on all the other potential uses for it,  but unsurprisingly we've studied it for new onset atrial fibrillation, and specifically in the cardiac surgery patient population again.  What I think was really unique about this meta-analysis was that they included trials from the U.S. and outside the U.S. All the U.S. trials showed no benefit.  All of the trials outside of the U.S. showed significant benefit. And when I look at these studies, I could not find differences in the type of surgery,  in the type of patient, in the dosing of vitamin C, in the choice of when to use it that could explain why some of the data showed a difference and some did not.  And so short of saying depending on what country you're in, maybe it has a benefit, I really could not suggest use across the board of vitamin C to prevent atrial fibrillation.  So another hammer on the nail of the coffin of vitamin C potentially. And finally, dexmedetomidine has been studied in relation to new onset atrial fibrillation, again,  in that cardiac surgery population. Now these are studies where dexmedetomidine was compared to other standard sedative and pain control agents. So it wasn't specifically added  for prevention of atrial fibrillation. But they did find that there was a reduction in postoperative tachyarrhythmias, including AFib and ventricular tachycardia.  And I listed the odds ratio for AFib on this slide. So what this suggests to me is that potentially our choice of agents for other ICU issues, such as sedation,  may impact our risk for atrial fibrillation. And we have that data with our vasopressors. But I think the sedatives is an interesting area to look at in the future.  And certainly the mechanism of action of dexmedetomidine makes sense that it would prevent at least tachycardia. And so the potential for prevention  of tachyarrhythmia is another thing that I think I'd like to look at more outside of cardiac surgery literature to see if it could be beneficial to us in the general ICU population.  So finally, in synopsis, I don't have an agent to fix prevention of AFib across the board in all of our patients. I can tell you optimize your magnesium levels.  I can't tell you to just start a drug and it'll prevent new onset AFib. I think we need a lot more data to suggest the general ICU patients could maybe have a fix.  So what do you do when AFib happens? Well, as with any issue, reverse the underlying causes that can involve treatment with electrolytes, correcting acid base, getting rid  of that beta inotropic vasopressor, switching to other agents, maybe catecholamine sparing agents, whatever it may be. Of course, addressing the underlying state  of why you're treating. And then we look at our drugs. And as always, we have the debate of rate versus rhythm control. And in the ICU, we have some data  to suggest maybe one is better than the other. In this French McHugh study, you can see, and again, I know the numbers are small, but the point  of this study is beta blockers versus amiodarone. At all time points in this study, the esmolol was more effective in both rhythm control,  rate control, and even just heart rate reduction in the patients who didn't meet the rate or rhythm control goals. So this study would suggest to us  that we should beta block our patients first. Let's put it up against a Chinese study that showed rate versus rhythm control, diltiazem versus digoxin versus amiodarone.  In this study, diltiazem was the most effective at both rate control, heart rate reduction, and in fact, may have correlated with a reduction in hospital length of stay.  The problem with this study is that they actually underdosed the patients who received amiodarone and digoxin, and therefore biased the results to favor diltiazem.  So take it with a bit of a grain of salt. In this final study, the general ICU population with just atrial tachyarrhythmia, you can actually see that rate versus rhythm control,  diltiazem versus amiodarone, was no different in efficacy. All this study showed us was that we can't bolus a patient with amiodarone and walk away.  We need to continue that drip to have efficacy. But what's very unique about this study, and I think is kind of my takeaway point from this slide, would be that the bulk  of patients who received diltiazem, or not the bulk, sorry, a third of patients who received diltiazem actually weren't able to tolerate it  and had the infusion discontinued for hypotension. And so this study suggests that there's no efficacy difference, but amiodarone may be better tolerated in our patients.  And I think we all maybe thought that anecdotally, and there is some data to suggest that we are correct in that thinking.  So based on these three studies, you can see there's evidence that beta blockers are better, and there's evidence that amiodarone is better. And so what do we do with this?  Well, survey of current practice shows we all kind of do different things. In the single center study of non-cardiac surgery patients listed to the right,  you can see that beta blockers were the preferred agent in their center, but amiodarone was more effective, both for first and second line control.  In a study of UK providers, which didn't assess efficacy, but just practice, you can see the opposite. People preferred amiodarone.  In these two database studies that I've listed over to the left, MIMIC3 and PREMIER, we have very large patient populations to pull from,  but again, they're retrospective database studies. So take with a grain of salt that these are all provider-driven. It's a survey of current practice.  We can see much more heterogeneity and what providers prefer to use between beta blockers, calcium channel blockers, digoxin, and amiodarone.  These two databases actually suggest, however, that beta blockers are significantly better. You can see that the efficacy favors metoprolol or beta blockers in general,  and amiodarone patients were more likely to fail and, in fact, may have had a higher hospital mortality compared to beta blockers.  In terms of refractory management of your patients, there is one study of a butylide in the CRITIC-LEO, and I bring this up in terms of what is our damage control.  This small patient population that was in refractory AFib and AFlutter received ibutylide. They were hemodynamically stable, no underlying cardiac disease,  and so this is a very niche population. But I think what's interesting is the significant efficacy of this drug, and particularly in the atrial flutter population,  which is more difficult to control, as we know. In this study, patients had to have normal magnesium levels before receiving ibutylide, and that concerns me because 20% almost  of the patients actually had a ventricular arrhythmia when receiving ibutylide, even with normal magnesium levels. All of these arrhythmias were responsive  to magnesium treatment, so the suggestion would be that if you do choose to use this drug, and again, it's a very niche population who's refractory  to many other strategies, I would pretreat the patient with magnesium regardless of their baseline magnesium level before using this drug. And finally, digoxin.  Digoxin keeps popping up. What is its role? When can we use it? What is the population that may benefit? Well, I'm going to be honest. I don't have data to give you that answer.  In general practice, we know digoxin is less efficacious than beta blockers or calcium channel blockers, and in studies of ICU-specific patients, that still rings true.  When compared to amiodarone, amiodarone was superior in an ICU patient population. And so digoxin's role remains in question. I would consider it in the patient population  that's failed many other therapies or potentially cannot tolerate other therapies, for example, drug interactions, side effects, hemodynamic instability.  So I wouldn't pull it out as first line, second line, maybe even third line agent. I'd consider it in that very refractory patient  who's not responding to the other agents we know are very efficacious and potentially more safe. I want to touch briefly on anticoagulation  since I'm the pharmacology talk before turning the screen over to Doug. So anticoagulation, we know patients with a CHADS-VASc score of 2 or greater are recommended in guidelines  to receive anticoagulation with atrial fibrillation. In a survey of current practice of patients that were eligible for anticoagulation based on that as well as a lack  of ongoing bleeding, we can see that's 428 patients eligible, only about a fifth of them actually received anticoagulation, and this is in an ICU population.  So the question would be, where is that gap? Why are we not anticoagulating patients even though it's recommended in guidelines? Well, in a survey of patients  who received parenteral anticoagulation, so heparin infusions, in the ICU, while admitted with both sepsis and atrial fibrillation,  you can see these patients based on their CHADS-VASc score, or sorry, in this study CHADS-2 score specifically, they should have received anticoagulation based  on eligibility, but two-thirds of patients did not. And in that patient population, none of the patients had a stroke while in the hospital. And that, of course, is the benefit  of receiving anticoagulation. You can see the bleeding complications in this group listed here. And when compared to the group that did receive anticoagulation,  there were significantly more bleeding complications in the anticoagulated group. And again, the anticoagulated group had no strokes similar to the unanticoagulated group.  But the majority of those patients also spent less than 50% of their time in the therapeutic range, suggesting that it's very difficult to target that balance  between effectiveness of preventing a clot and the risk of bleeding. And we know, in fact, that these patients had more bleeding and did not have a clot prevented.  And so based on this study, it would suggest that we shouldn't initiate anticoagulation in the critically ill period just for atrial fibrillation  because there doesn't appear to be a benefit in that short-term window. Similarly, in a registry study of patients who presented  to the hospital already on Warfarin for atrial fibrillation with a new diagnosis of sepsis, we can see that these patients not only had a higher rate of bleeding while in the ICU,  but actually had a higher rate of clotting as well. And this, to me, suggests that, again, it's very difficult to maintain a therapeutic range while in the ICU.  We have other risk factors for clotting and bleeding while they're here. And the benefit of maintaining Warfarin for that stroke prevention while admitted may not have been  there, and again, just for atrial fibrillation. Certainly, you would need to anticoagulate other things such as a new-onset PE or other type of clot.  This is specifically just atrial fibrillation. So based on all of this data, I would suggest starting with your beta blocker for rate control  for new-onset atrial fibrillation in the ICU. And again, based on that study of esmolol and shock, I wouldn't hesitate just because the patient is on a vasopressor  to use a beta blocker as my first-line agent. We can defer starting anticoagulation just for atrial fibrillation while in the ICU  if we're just using our rate control because of the low risk for stroke while they're admitted and the potential for additional bleeding while they're with us.  If we do proceed with rhythm control, we've got significantly more data with amiodarone and with optimizing magnesium levels in our patients.  Here, we'll need to do a risk-benefit analysis for anticoagulation because of the risk of throwing a clot with cardioversion. And there may be a niche role for ibutylide  in the refractory patients, particularly those with a flutter who are unable to respond to other agents. But again, remember that almost a fifth  of patients did experience ventricular arrhythmias. So I would caution its use in a general patient group. And at this time, I'll turn it over to Doug. Very nicely done.  Thank you very much, Nicole. I'm Doug Naylor. I'm a surgical intensivist at University Hospitals. I was formerly at the Cleveland Clinic where I had the pleasure  of working with Nicole and actually collaborating with her on several studies. So I was charged prevention is easier than cure. But now, for those of you who are paying attention,  there's been some considerable overlap and we've already talked a little bit about prevention, haven't we, in brief. Now, proving once again that there is no new news  under the sun or, to put it another way, if I have seen further, it's because I've stood on the shoulders of giants such as my colleagues here  on the panel, we're going to look at a couple things. We're going to look at etiologies, all right.  This is exactly the same reference that Nicole used before, no collusion, because I only had an older version of hers. But you will see some of her slides,  which I've shamelessly stolen, and I'll project again for you, but project for a different point, all right.  So we have demographics.  Unfortunately, old guys can get AFib, all right.  If you have concomitant or comorbid diseases, you also can get AFib, all right.  It's based on other additional things that will up the ante or increase your risk of dying.  And then finally, we've had a bunch of investigations which Nicole has nicely covered, all right. And you'll notice this is exactly the same reference that she used, all right.  It depends on how we look into the information. And as I look out over the crowd, I see some people here that, unfortunately, are probably still bearing the scars  that I've trained them and others that have trained me, and I thank you for all your input, all right. So we're going to move along.  We asked a particular question, since I am a surgical intensivist, and I really, it's not that I don't care about cardiac surgery,  but I care more about the general surgery population than I care about cardiac surgery. That's just a slight disclaimer.  So when we were at the Cleveland Clinic, we looked at a particular group of patients.  And if we look here, this is patients from non-cardiothoracic and non-vascular surgery, that is to say the general surgery population, all right, who are recovering from surgery,  and we had some 8,000 patients, all right. They, importantly, they were all on beta blockade, but they had had no documented history  of atrial fibrillation. How do we document this? We look back, with the benefit of our EMR, we look back through and look for tracings or any evidence,  or we did word searches in their history, all right.  We did a propensity matching score system.  And those who resumed beta blockers by the end of their first postoperative day were compared to ones on a later date. Pretty straightforward.  The ones who resumed on the earlier days had a decreased incidence of atrial fibrillation.  This is whether or not they've had atrial fibrillation to begin with. They sat beside somebody on a bus who had atrial fibrillation, or they've read about it on Yahoo News, okay.  So, the conclusions were, resuming beta blockers in chronic users  at the end of the first postoperative day may be associated with lower odds of in-hospital risk of atrial fibrillation. All right.  There seems to be little advantage starting to the day of surgery. Now, why was there little advantage? Unfortunately, our signal was not large enough  because there is still that aspect, and being a surgeon, and I will throw my colleagues as well as myself under the bus, what I know is important. What I don't know, I don't care.  All right. And I'm sorry if that's the way it works. However, with our surgeons, they were always worried about starting the beta blockade too early for a lot of different reasons.  And in just a moment, we're going to be polling the audience, so don't laugh too loud because I'm going to be asking for, or uncovering your own personal biases.  And this was Ashish Khan and the rest, and a very robust group that helped me on this, okay.  You saw this slide before. Didn't you? Shamelessly stole it. Okay. That's fine. That's okay.  So, what do we look? So, in chronic patients, we just said this. We can use it to prevent withdrawal of beta blockade.  All right. Okay. Is this the same as withdrawal from any other substances that are associated with our general population? We're going to get into that in a brief moment too.  All right.  You can start it early in CV surgery. Consider Esmolol. All right. Esmolol is almost a niche drug. It depends on a lot of different things  if it's available or not available in your location.  All right.  And then we talked about calcium channel blockade.  I want you to focus on this dose. We're going to expand on that in a brief moment.  Does anybody, can anybody help me and tell me what an average dose of your octogenarian or your septogenarian who comes in on a calcium channel blocker?  Is it 10 to 15 milligrams per hour if you divide it in 24 hours?  I think not. I think it's a little bit higher, but we're going to look into this in a brief moment.  Okay.  And then we looked at the same pictures, right?  And then we were all over the chart.  All right. Some suggest that we're going to use calcium channel blockers. Others suggest beta blockers. And where this has developed, this has been developed for a historical basis.  How many in the room remember when all we had was verapamil?  Yeah.  Okay. That tightened your sphincter up a little bit when you were given verapamil, didn't it? Right? Because it was such a negative inotrope. All right. Okay. All right.  We'll get there. All right.  So I went to certain things, and with all due respect to my younger colleagues out there, I see a lot of phones are out there and people are furtively looking at their phones.  God bless you.  All right. So what do we do when we don't know what to do? We call Dr. Google, don't we? So I did, and we looked at, from our 2020 knowledge base, this sounds pretty sexy, okay,  they had a list of all these agents.  All right.  There are agents on there that I haven't seen in years. I have, there are agents on that list I haven't seen in the half-life of amiodarone.  It's difficult to evaluate equivalent doses of beta blockers because of this. We all know what we're talking about, but none of us truly know what we're doing.  So what do we base it on? We base it on past experience, local, custom,  and formulary choices. Remember that Premier database?  Premier has locked down their formulary. They're one of the first people to lock it down. So do you believe, or were you willing to submit or accept,  that perhaps that data might be a bit jaundiced? Perhaps. Okay. All right.  Okay. Now, route of administration, oral versus IV. And when you look down from another aspect, being a surgeon, we know that NPO is good, not generally.  Okay, we've learned that in the past because we're feeding people earlier and earlier, aren't we? Okay. But with that particular bias,  with that particular huge set of myopic spectacles,  do we give people oral? Are all doses equal?  All right. Again, great source. No, this is not an advertisement. Please take this as a disclaimer. All right. For Medscape, let's look at these doses.  Starting dose? That's pretty anemic, isn't it? Right. But then we get to a target dose.  How fast do we raise them? All right.  Okay.  All right.  Now, we compare them.  Certain studies, or when we go to our lexicon, but our different pharmacology databases,  they look at metoprolol as the middle ground. And they always choose a dose of metoprolol to base others on. We do the same thing with steroid equivalencies.  We do the same thing with narcotic equivalencies. So, this is not new. All right. Okay.  Now, for intravenous dosing of beta blockers, how many people are really comfortable? Do you have a protocol in your hospital? Anybody?  Okay. All right. So, you give a dose of beta blockade, say, two and a half milligrams, five milligrams. How many two and a half milligram people are out there?  Okay. How many people are still awake? Okay. All right. Good. How many five milligram people are there? Okay. Excellent. Excellent. That's what I thought. What if it doesn't work?  What do you do?  Do it again?  Of course.  Okay. So, and then how quickly do you give it?  All right. All right. So, remember, our targets from the slides that Nicole showed us, and these are eye-greedies, we can use between five and 20 every two to four, six hours.  So, if your patient's an extremist, if they're in trouble, are you going to wait four hours? Are you going to wait six hours?  That's like me telling you I'm going to give you all the oxygen you need in 30 minutes.  No takers for that, I know. I'm not even going to pull up a crowd. All right. For DILT, remember I asked that DILT question?  Well, I gave it to you. The average dose is 180 to 360.  Do the math.  20 milligrams plus, let's say 10 milligrams an hour, because I don't like odd numbers.  10 times 24 is 240.  How long is it going to take you to get there?  That is a glacial pace if your patient is an extremist. All right. What's your end point here?  Is your end point, again, as was previously pointed out, is it rate control, rhythm control, or is it absolute healing? All right. So, we're back to our knowledge-based slide.  Difficult to evaluate? Yep.  Local custom, formulary influence. Metoprolol?  Okay, there we go.  End points, and we're going to check some other things out. So,  how do we think, or why do we think, what do we do what we do?  All right. I know as we get older, unfortunately, you're all going to be like your parents. That's the way it works. All right. But your parents taught you  and brought you to this point. All right. So, are we looking at inductive versus deductive reasoning? Exactly.  All right. Is there one that's superior over the other? Well, unfortunately,  for this little statement, no matter how unrealistic it sounds, I would like to tell you that I'm the most scientific and the most knowledgeable and the most logical person up here.  It's not happening. Not working. All right. However, we go from known to unknown. Sometimes we're helped or assisted because we actually have data.  But what data has been presented so far? We have a mix of cardiac data,  general medical ICU data,  sepsis data, which takes all comers. Remember, bacteria and viruses, they respect no one. All right.  Surgical data. All right. So, what are we talking about? Or are we like the group of people trying, the blind men trying to describe the so-called elephant?  And I'm going to submit to you that's where we are. Now,  where am I going to go with this? We're going to talk about some fluids just for a minute. How many treat oliguria?  Or,  yeah, we do. Any of you? So, what do you do?  What do you do first?  Give a little fluid, right? How much?  Less filling  or better taste? How fast do you give it?  When you give your Lasix, all right, what do you do? Do you say, I'm going to give them a pharmacologically even dose, five milligrams and walk away?  Or does the clever caregiver say, I'm looking back to the history, see if these patients are diuretic dependent and I'm going to adjust my dose accordingly. And if it doesn't work,  what do we do?  Say we start for giggles and grins, 40 milligrams of Lasix.  How many is going to keep that dose, just keep hitting them with 40, 40, 40?  That's what I thought. Who's going to double the dose? Yes, exactly. Exactly. Perfect. All right. Where did this come from? The venerated source, the Washington Manual.  Okay, excellent. So, here's some of our properties. All right. Notice they keep increasing the dose.  Okay. All right. All right. Another way to look at it.  They have maintenance doses. This is for oral.  And then finally,  let's look at some more common drugs.  Insulin.  Do you guys just start them on their dose and say, well,  suck it up, too bad?  Let them, let their,  let their sugars run everywhere?  I don't think so.  Okay.  Don't we, sometimes we're really clever and we start them on a drip.  And what if their drip doesn't work? Do we  goose them a little bit with a little bit of IV insulin to bring that  level up quicker to get them to the target range?  Yeah. Okay.  And we all have difference in sliding scales, right? We have low, medium, and high and this depends on whoever programs your EMR.  Okay. Do we titrate or adjust that dose to effect? I'll let you guys figure that out.  What's this? Hmm. This says, looks like for status. What about controlling a seizure?  Are we going to give somebody a little sprinkling of a benzo or whatever your anti-seizure drug of choice happens to be?  And then say,  well, I'll get back to you later. I don't think so. You will escalate the dose and increase them. All right. So in with status, control, and then long-term suppression. Do we see,  does anybody else not see, do we not see or do we see the parallels between AFib and what we're doing now? So we have observed in the past where we've been going  and we know where we're going to end. All right. So IV therapy. So I'm a big proponent of IV therapy. How fast do you replace those deficits with IV fluid?  The schema for IV fluids, way back in 2005.  All right.  They did a troll, and no, I'm not trolling anybody here, but I thought this was clever. So that's why I used it. All right.  Many guys call for two to three liters of fluid early on. We had gentlemen in the early, in the first part of the row saying, yep, that's what I would do.  Pound them with the fluids. Good.  I like that.  But look at our IV beta blockers.  Okay.  And then finally, armitoprolol, two and a half, a very somewhat anemic dose,  to five, over two minutes, up to three doses. So repeat the same experiment over and over and over and over and over.  You all saw that coming though, right? Okay, good. Okay, very good.  So any given medication is given to achieve a desired effect,  thus filling in a therapeutic bucket. All right, so this is our human here. It's not a bucket. You all remember that. They tortured me in math.  I was a kid who was in the back of the room and said, get a new bucket when they asked about calculus. You got a bucket with a hole in it.  How fast you got to put the fluid in to fill it up?  Remember this? I still bear scars from that. All right, so I'm giving somebody a medication, and this is their ongoing metabolism.  So steady dose, ongoing metabolism, bucket remains relatively full. Okay, the question is  how rapid should my flow be to overcome ongoing metabolism and provide control in the face of ongoing deficiencies? That was our original study. Okay,  so I will tell you to start them as early as possible, treat the symptoms, avoid the fear of the dreaded,  uh-oh, not yet disease. You don't have that yet, but you might get that yet.  So don't withdraw into yourself. Be a little bit bolder. In cases of prolonged fasting or large-volume blood loss, remember, all of your beta blockers or your pre-existing  anti-dysrhythmic drugs have washed out, haven't they? You need to fill that bucket back up again. Consider IV supplementation in addition to your oral doses.  This will put to bed the myth of, well, they're not absorbing from their GI tract. Can you really say that if you haven't given them enough?  Alright, so you can give them five to ten milligrams every four to six for a set period. This is in addition to their regular and customary oral dose,  but put hold parameters for appropriate ranges of blood pressure,  which we'll know from taking care of your patient, looking at that history ahead of time, and check their heart rate. Should a-fib RVR occur, consider doubling the doses.  So maybe if you want to start with two and a half, if you're not that bold,  go to five. Don't go five-five. Don't go two and a half, two and a half, two and a half. Two and a half, five, ten,  twenty. Is there an upper limit? Well, I'm gonna ask you, how sick is your patient?  All right. Now, the naysayers in the crowd, oh, what about hypotension? Dr. Naylor, what are you talking about? You know, you're off the reservation now.  I give them that much motoprolol, boom, their pressure's gonna go down. I don't think so. What's the cause of the hypotension?  Loss of inotropy? Do the ones we use, are they as negative an inotrope as, say, a calcium channel blocker, or are they a little bit safer?  That's why we've chosen that particular modality. That is to say, motoprolol. What about loss of atrial kick?  So if I had a two-stage pump, or if some of you were driving some sort of fancy vehicle with a turbocharger, you know where the turbocharger goes on the fritz?  You lose gas mileage. You don't get the kick. You can't pull out onto the interstate like you could before, right? Same thing works with our heart.  That's the way the Lord designed us, with an atrium and a ventricle, okay? Or is it just altered filling? Am I moving so fast that I've taken the propeller out of the water?  How many of you have seen speedboat race? You know, jumps out of the water. Does the boat, only the James Bond film, does the boat go faster?  I did not put that, I didn't put that little video on there.  However, once the propeller is out of the water, doesn't the boat always slow down and drop back down?  Exactly. So in real life, it works the same way as in medicine, all right? So if you get into trouble,  recall that you can DC cardiovert these people if they're hypotensive, okay?  Symptomatic hypotension, you can volley load them, and then you can get pressers. Thank you very much for your attention.  So that is indeed a hard act to follow. So I'm Jake Jenser from Mayo Clinic, and I'm the token cardiologist here, also a critical care doctor.  And so I'm going to talk to you about what you do when all else fails. As you can imagine, we've had some overlap here already, so I have no relevant disclosures.  So I'm going to talk a lot about cardioversion and atrial fibrillation, and I'm going to talk about rate and rhythm control. Rhythm control implies cardioversion in some form.  We can do electrical or pharmacological, and I'll talk about different strategies for both of those.  And finally, the most serious complication of atrial fibrillation is generally thromboembolism,  and you should never think about cardioverting someone without first thinking about what their thromboembolism risk may be.  So just as a reminder, atrial fibrillation develops in the setting of critical illness because of the interaction between a pre-existing substrate that promotes the arrhythmia  and a trigger that causes the arrhythmia to occur at that time in that patient. And so the substrate may be either acute or chronic.  A lot of patients have chronic atrial remodeling from underlying heart disease, but also they may have acute atrial stretch and inflammation that makes them highly pro-arrhythmic.  And then the most common triggers we think about are excessive adrenergic stimulation,  but other factors in the setting of critical illness can trigger atrial fibrillation in a susceptible patient.  But what's important to understand is that being in atrial fibrillation promotes atrial remodeling, which keeps you in atrial fibrillation.  And this is one of the reasons we think that getting people out of atrial fibrillation may be good, because the more you're in AFib, the more you're in AFib.  So when you are first managing a patient with AFib, you want to ask yourself the question, is this patient sick because of the AFib?  Or more commonly, are they sick and the AFib is a symptom of their critical illness? And there's the simple things that my colleagues have already talked about.  Stop offending drugs like powerful beta agonists, dopamine, epinephrine. These are highly pro-arrhythmic. Drugs like vasopressin have been associated with lower risks of AFib.  Treat all the inciting factors that you can. And in most cases, start with rate control, usually with beta blockers, as my colleagues have discussed. But what if all this fails?  And the answer is, cardioversion. But it's important to understand the timing of cardioversion and understand the indications for immediate cardioversion.  This is do not pass go, do not collect $200, provide cardioversion. If someone has new AFib that causes them to become hemodynamically unstable,  the right answer is electrical cardioversion. Now importantly, the patient may be hypotensive and have AFib.  But that doesn't necessarily mean the AFib is causing them to be hypotensive. So keep that in mind. In addition, patients who have AFib rarely arrest due to the AFib.  There are certainly exceptions. But if someone has cardiac arrest and they have AFib, yes, you may cardiovert them, but don't expect that to be the solution.  There are other forms of acute cardiac compromise that may warrant immediate cardioversion. Someone has acute high-grade myocardial ischemia triggered by the rapid AFib.  That's certainly a reason. And if they decompensate immediately into acute pulmonary edema, that's another one.  Now we think about a lot of potential benefits of atrial fibrillation rhythm control. Getting them back in sinus rhythm should improve their cardiac performance.  We talk a lot about the atrial kick. I know that there are some people who believe the heart is composed entirely of atria.  And if only they were in sinus rhythm, their heart would function perfectly. That's probably not true.  But patients do have better preload and therefore better cardiac output when they're in sinus rhythm. We know that the filling pressures can be lower.  That's the function of the atrium is to allow you to have lower filling pressures and still have good preload. And also the rapid irregular rhythm can impair filling.  And so improving that aspect can help. We know that if you can keep, we believe that if you keep people in sinus rhythm,  you can avoid that electrical remodeling and prevent further AFib in the future. And if the person's in sinus rhythm, theoretically,  their risk of an intracardiac thrombus formation is lower.  Although it's not quite that simple, and I'll talk about that a little bit later. We know that if a patient goes into new onset AFib in the setting of critical illness,  their risk of an adverse outcome goes up. The longer they stay in AFib, the worse they do. And that's this graph here.  We also know that patients who develop AFib that's new and then stay in AFib, they do very poorly.  And so these are all reasons to think that it's rational that getting people back in sinus rhythm would be good for them.  The problem is that there have been many large trials in cardiology looking at chronic AFib rhythm control compared to rate control.  And these trials have, as a general rule, been negative. There's no reduction in mortality, no reduction in stroke.  And in fact, there's an increased rate of serious adverse effects because antiarrhythmic drugs are toxic.  There are some very modest improvements in cardiac function and quality of life  that generally don't justify the added costs of a chronic rhythm control strategy in the average patient. But what about in the acute setting?  Well, if you take patients that present to the ER with AFib, and you randomize them to either immediate cardioversion, just let's get this done, or let's wait.  Let's give them 48 hours of good rate control and see what happens. And then if they're still in AFib, let's cardiovert them then.  And what you see is that at four weeks, there's no difference. Both of these strategies are equally effective.  But if you look at this graph here, what this shows is that more than two-thirds of patients treated with a rate control strategy alone end up back in sinus rhythm within 48 hours.  And in fact, the rates of AFib recurrence are fairly high, but also not different. And in general, the more AFib you have, the more AFib you're going to have.  And so the biggest risk factor for having more AFib is having had more AFib. What about in cardiac surgery?  So when I was a fellow, I cardioverted lots of patients with AFib after cardiac surgery. I thought it was a no P wave left behind scenario. But then this randomized trial came out.  And in fact, if you randomize patients to a rate control strategy versus rhythm control  with amiodarone followed by cardioversion, there's no difference in any outcome that actually matters. And in fact, at seven days, the rates of sinus rhythm were the same.  Now, true, the rhythm control arm was in sinus rhythm earlier and for a greater proportion of that first week. But it didn't really do anything meaningful in this situation.  So this brings up the question. I just told you that rhythm control strategy doesn't really do anything useful.  So why would you cardiovert a patient who's got stable AFib, not an unstable patient, right? That's different.  So the two primary indications for cardioversion in the stable AFib patient are an inability to provide adequate rate control.  For example, if your rate control medicines are causing hypotension, even if the patient's fine on their own, but then they get hypotensive after DILT or metoprolol, et cetera.  Atrial flutter. It's much, much harder to rate control atrial flutter because of the way that the impulses are conducted.  And then one of these bad actors is pre-excited atrial fibrillation. I'm not going to talk about this much.  But in patients with Wolff-Parkinson-White syndrome, they have an accessory pathway. And when they go into AFib, they go into fast AFib. It's very unstable, very, very dangerous.  And if you give standard rate control agents, you can kill them. So in general, we go for a rhythm control strategy in those patients.  Otherwise, if someone just continues to have symptoms that are problematic despite adequate  rate control, and in the acute setting, adequate rate control is actually just arresting heart rate 100, maybe 110 or less at rest.  And if they're still symptomatic, you might cardiovert them. I work in a cardiac ICU.  So I see lots of patients who have decompensated heart failure. And we tend to be a little more aggressive about cardioversion in those people, especially  if they have a new onset cardiomyopathy and AFib. We think maybe the AFib is causing their cardiomyopathy.  Patients with bad valvular heart disease, other bad underlying structural heart disease, RV failure, they tend to tolerate AFib very poorly.  And so we tend to be a little more aggressive about rhythm control in those patients, at least in the acute phase.  And finally, if your patient is bleeding or cannot be anticoagulated, you can make a rational  argument for early cardioversion for the purpose of avoiding the need to anticoagulate them. Because as we know, anticoagulation carries a lot of risks.  And if you can safely avoid it, that's a good thing. So what's the most effective way to cardiovert someone? The answer is synchronized biphasic direct current cardioversion.  But antiarrhythmics play a big role in a lot of our patients. They can be used to treat the patient and cause pharmacologic cardioversion to avoid the need for electricity.  You can make the likelihood of the initial cardioversion attempt more successful by pre-treating with antiarrhythmics.  You can prevent or treat failure of your initial cardioversion attempt. And you can prevent or treat recurrent AFib after cardioversion.  And antiarrhythmics are very effective for all of these strategies. Does it matter where you put the pads?  Well, I was taught you try and do anterior or posterior because then you sandwich the atria between your pads. Turns out that doesn't matter. There's a nice randomized trial.  This came out last month that shows that it really doesn't matter in normal size and normal shape patients.  So we talked a lot about how a lot of these rate control agents we use have some efficacy for converting people or promoting sinus rhythm.  And so the list of efficacy for rate control, diltiazem, it is the most effective.  Beta blockers, almost but not quite as effective. Amiodarone, not quite as effective. And digoxin and MAG are really adjunctive agents that by themselves don't have a lot  of efficacy. For rhythm control, it turns out diltiazem is actually really not very effective for rhythm control. And so you shouldn't think of it as a rhythm control drug.  Amiodarone, on the other hand, is more effective than these other ones. And beta blockers, some come somewhere in between where they certainly can promote sinus  rhythm, although on their own not all that effective. And I really believe in MAG. I give lots of my patients MAG. They actually make fun of me in my ICU.  What, are you going to give this guy 8 grams of MAG? Is that enough? How about 12? So I always add MAG as an adjunctive agent. What about amiodarone?  So amiodarone is our workhorse antiarrhythmic. For most of you, it's probably the only antiarrhythmic you've used in your practice recently or ever.  And the reason is that it does everything. It has all the ion channel blocking properties. It works for both rate control and rhythm control.  But the thing is is that the standard dosing that you see on your chart for amiodarone is not for AFib. Amiodarone is not FDA approved for AFib, so there's no approved AFib dosing.  So what you have to do is give enough amiodarone. That's what I tell my fellows. There's two amounts of amiodarone you can give a patient in AFib, enough and not enough.  So if you're trying to get rate control, I give a 150 bolus, and I keep repeating it until the patient has rate control.  And that may be up to 5 to 7 milligrams per kilogram loading over an hour or two. That's what the European guidelines suggest.  And they also suggest that amiodarone is actually your first line rate control drug if the person is hemodynamically unstable or has severe heart failure, systolic heart failure.  The problem is is that even though amiodarone is a little bit better tolerated than most other beta blockers, it is a beta blocker.  And it does cause hypotension, and especially the bolus dosing. And so people with bad hearts, they will get hypotensive after amiodarone. Expect it, and don't be surprised.  If the patient is rate controlled after my initial bolus doses of amiodarone, but they're still in AFib, then I focus on the infusion to keep them rate controlled and also promote  sinus rhythm. And so I keep them on a milligram a minute until they're in sinus rhythm. I don't put some arbitrary six-hour time limit on it. I just keep it going.  Once they're in sinus rhythm, then I'll decrease it to 0.5 for some time that is arbitrary based on how long they've needed the higher dose.  But oral amiodarone behaves differently than IV amiodarone. It's a much better antiarrhythmic.  And so if I think that amiodarone is my long-term strategy for this patient, or at least I'm  going to keep them on it for a few weeks or a few months, I'll start oral loading of amio immediately. I don't wait. I leave them on the drip. I put them on the oral.  They are complementary drugs. One of the things that I find about AFib is that it really gets people excited. People get afraid of AFib.  Oh my gosh, this patient's heart rate is 160. Well, I worry much more about sinus attack at 160 than AFib at 160.  Because the reason the patient's heart rate is 160 if they're in AFib is that they're in AFib. So I think keep calm and start amiodarone.  So that being said, I talked a lot about amiodarone. We all did. But there are lots of other rhythm control agents. But these drugs all can kill you.  And you should always use these drugs only if you've used them before. You know how they work. You understand their pharmacology. You know their toxicity.  And you know how to use them safely. We talked about ibutylide. I may be the only person in my ICU who's used ibutylide any time recently.  But the important thing about ibutylide is you have to load IV magnesium before, during, and after. It increases the safety. It increases the efficacy.  And makes it a safer drug than it otherwise would be. But ibutylide's very good, especially for flutter. And also, if you give ibutylide to try and cardiovert someone,  if that doesn't work, it increases the success of electrical cardioversion. So if you know how to use it and can use it safely in the right patient, great drug.  In a person with a normal heart, flecainide is safer and is a great drug as well. They talk about this a lot in Europe where they have the IV formulation.  But it can cause atrial flutter. And flecainide-associated atrial flutter tends to run very fast and can be very dangerous.  And so you have to make sure the patient has good AV nodal blockade and a normal heart before you give them flecainide. Procainamide has generally fallen out of favor.  But many people use it. There's a lot of ER literature where they're promoting the use of procainamide. Procainamide is a dirty drug. It's very dangerous when used improperly.  Although, of course, can also be used safely. Patients with bad hearts should not be getting this drug. And it tends to cause quite a bit of hypotension.  And finally, they recently came out with an IV form of sotolol. Now, sotolol is a very powerful beta blocker. So it's not as useful in patients that have marginal hemodynamics  because it has so much beta blockade that it could make them hypotensive if they aren't likely to tolerate that. But that being said, it can be used for AFib.  It is fairly effective. Now, there's a very recent study. This is actually a two-by-two study, the one I just showed you here from last month,  where they randomized patients in the ER with AFib to either procainamide followed by delayed cardioversion  versus immediate cardioversion. And what they found is that the initial cardioversion arm, electrical cardioversion, worked in more than 90% of patients.  The procainamide, and this is a pretty aggressive dosing, by the way, worked in about half of patients. And then the ones that didn't get cardioverted with procainamide,  the majority of them got cardioverted electrically, and the overall success rates were both very high. But what you found, of course,  is more adverse events with procainamide. So in this paradigm, pharmacologic cardioversion followed by electrical cardioversion, you can do it with lots of drugs,  amoei, butylide, procainamide, whatever. But you have to think about the advantages and disadvantages. The advantage is you may avoid having to sedate and shock somebody,  which I think is probably a good thing. But the problem with that is you're doing it at the cost of giving them a potentially toxic antiarrhythmic drug.  So you just have to balance that benefit in that individual patient. So how do I approach acute afib rhythm control? Number one, if they are unstable, electrically cardiovert them.  Do not pass go, do not collect $200. If they're stable, you may still want to electrically cardiovert them because it is the quickest and most effective.  And I gave you a list of reasons why you might do that. But if you think that you don't necessarily have to shock them, you try pharmacologic.  If the patient has a bad heart, reduced EF, left ventricular hypertrophy, use amiodarone. If the person has a lesser degree of heart disease,  underlying coronary disease, a little bit of heart failure, but not bad, low EF heart failure, you can still use amiodarone. But you might be able to use one of these other drugs,  ibutylide or sotalol, in the well-selected patient. If the person has a totally normal heart, then you can use one of these other drugs,  flecainide or propafinone, even procainamide, although it's actually been taken out of the guidelines. The one niche use of procainamide now is pre-excited AFib.  You may see a board question. Pre-excited AFib. I do electrical cardioversion, but for a drug you'd use procainamide.  And again, you can use ibutylide in these structural heart disease-free patients. So how do I approach AFib? Well, you want to identify and treat the precipitating factors.  You have the person on 20 of dopamine. Seriously? This is 2020. Why are you using 20 of dopamine? Of course you're causing their AFib. If they're unstable, cardiovert them.  If they can tolerate initial rate control, I try beta blockers and IV magnesium, because that may facilitate conversion back to sinus rhythm.  If that doesn't work, based on their blood pressure, I'll give them a second drug. If their heart's good and their blood pressure is good, you can add diltiazem.  If their heart's not so good and their blood pressure is not so good, I'll try digoxin or amiodarone. If that fails to achieve rhythm control, or if they still have symptoms,  then I'll cardiovert them. Maybe I'll give them more amiodarone and electrically cardiovert them, whatever is appropriate for their situation.  If they fail that first attempt at cardioversion, I definitely give an antiarrhythmic drug. Amiodarone is the one we usually use, but you could use ibutylide, for instance.  And then try again. If they go back into AFib, you're going to need an antiarrhythmic drug. And then I start loading them with a significant amount of amiodarone.  It takes a while to build up, and then I wait a little while, just to get some amiodarone in their body, and then cardiovert them again. All right, so switching gears.  Although I saved this for last, it's actually the most important. The most feared complication of rhythm control and cardioversion in AFib is stroke.  When the atrium is fibrillating, it's not pumping. It can create stasis of blood, which predisposes to development of blood clots. But there are a number of risk factors,  and not all patients have the same risk of blood clots. The longer you've been in AFib, the more likely you are to have developed a blood clot, but more importantly,  the longer it takes your atrium to start contracting after you've gone back to sinus rhythm. And so you may form a clot after cardioversion if you've been in AFib for a while.  We talk about a 48-hour cut point. And so there's a nice study, 5,000 patients that got cardioverted for short-duration AFib. And you can see that the rate of thromboembolism  was less than 1%, which is not terrible, but you could divide patients at a high risk and low risk. If they had heart failure, their risk was high, especially if they had diabetes.  And on the other hand, if they didn't have heart failure, their risk was low, especially if they were aged less than 60. So when you're thinking about a patient  with short-duration AFib, if your patient has heart failure, then their risk is higher, and you should take that seriously. So what the guidelines say  is that thromboembolism prevention in AFib cardioversion doesn't matter how you do it. Sinus rhythm, induced by drugs and electricity, theoretically is the same risk of stroke.  If you've had AFib for more than 48 hours or an unknown duration, then you should be anticoagulated for at least three weeks before cardioverting.  And if you can't prove that they've been anticoagulated or if they haven't been, then you have to do a transesophageal echocardiogram to rule out clot in the left atrium.  Transthoracic is not adequate. And then after cardioversion, before you shock them, you would start a direct-acting anticoagulant. Could be heparin,  could be one of the novel agents. I like Apixaban for chronic use, specifically. And you do that for four weeks, no matter what. And then, if their risk of stroke  is high with this CHAS2-VASc score, then you keep them on anticoagulation beyond that. However, if you can prove that they have less than 48 hours of AFib  and they don't have one of these other high-risk features like heart failure, then you don't necessarily have to do anticoagulation or a TEE before you cardiovert them.  Although, if you can, you'd prefer to do that. And then after cardioversion, you don't necessarily have to anticoagulate them, but you'd rather if you can.  So, if the person has short-duration AFib and they're bleeding, then, yeah, you cardiovert them and you don't have to put them on anticoagulation at that time.  And just a reminder about this CHAS2-VASc score. Not everyone's familiar with this. This is a cardiology thing. You can Google it. And basically, it's a yearly stroke risk.  And the higher this score is, the higher your stroke risk is per year. So, that means that if you're... A CHAS2-VASc of like 5 or 6 is pretty high. But that's 6%, 8% per year.  That's not... The big one that I worry about, though, is stroke or systemic embolism. So, if someone's had a prior stroke and you're thinking about AFib cardioversion,  no matter what else, I take that extremely seriously because they've already shown themselves to have a bad stroke... a bad embolic risk. And so the chronic anticoagulation  is generally a CHAS2-VASc of 2. Maybe there's a difference between men and women. In the end, rhythm control has not been shown to improve outcomes in patients with AFib.  The only thing you can use antiarrhythmic is amiodarone. And finally, anticoagulation is recommended for patients before, during, and after cardioversion.  You can escape it in certain highly selected patients. Thank you very much. APPLAUSE  So now, I want to thank everyone for holding their questions to the end. There are several microphones here. We're happy to answer your questions at this time.  So, I have a question about the anticoagulation. Yes, sir. If the CHAT score, if we have self-limiting transit AFib in ICU less than 24 hours, we still need to  anticoagulate based on CHAT score? Or if it is one single, one-time episode, less than 24 hours? That's a really difficult question to answer. I think there's controversy.  When I think about this, I think about, is this someone who's likely to go back into AFib? And if so, and their risk of anticoagulation is low, I will consider it.  If I think that they're unlikely to go back into AFib, I probably won't. But a lot of times, I'll hedge my bets and I'll recommend some sort of  prolonged heart rhythm monitor at hospital discharge, either with or without anticoagulation, depending on the patient. For example, if the patient has heart failure,  the risk of future AFib goes way up, and the risk of stroke goes way up, so I'll probably anticoagulate that patient. But if I have some young patient  who's horribly septic and on a bunch of pressors, and his heart's normal, then I probably wouldn't bother burdening him with extra therapies. This is usually when you have the  CHAT score higher, if you have the stroke patient or heart failure patient. But the young patient doesn't have CHAT score high. Yeah, I think, you know,  using the CHAT score to risk stratify these people is very reasonable.  Please. Hi, I have a question about choosing between esmolol and metoprolol. At my institution, I think everybody forgets about esmolol and straight away go to metoprolol.  So in your practice, when do you favor the use of esmolol over metoprolol? Yeah, I think that's a great question. I'm going to be honest that the differences between the two  agents really just comes down to cost. And so your formula is going to drive a lot of your decision making. The drugs act exactly the same. We're looking at  pharmacokinetic differences. So esmolol is that perfect ICU drug, right? Quick on, quick off. If you get into trouble, it's going to be out of your system in a couple minutes.  Metoprolol is going to hang around a little bit longer. But in the end, they have the exact same mechanism of action, same risk of hypotension, which is extremely  minimal at rate control doses. And so I tend to favor metoprolol from a cost perspective. And I think you'll find a lot of institutions will because of the formulary and driving  down our costs. And that is 2020 in healthcare. You're not wrong to use esmolol. There's not going to be data that says it's worse. But there's not anything out there that drives  and says it's absolutely better and has this specific neutral. Again, what's beautiful about it is that pharmacokinetics, but unfortunately, I think the cost outweighs its benefit  at a lot of institutions. So we're very metoprolol heavy because we use a lot of drug. And we really don't have a lot of issue with it. We don't find  ourselves getting into trouble, getting into irreversible AV block and then having to wait it out. Please. Thank you. Regarding the risk of clot formation,  do you have any concerns regarding TXA administration of TXA and atrial fibrillation?  I was going to say, I don't know of any data myself. I'm going to ask my colleague if he knows. As far as I'm aware, there is no data on the use of TXA. The question  using it as a proaccelerant for coagulation, that would be a theoretical concern. We have no information on that right now. The rates of  thromboembolism are higher in the TXA patients though, right? In the studies? Yeah, but it's TXA. Exactly. We haven't pulled out patients who have received TXA with just that  subset of atrial fibrillation. So it's like anything else. We also looked at in the past, we looked at NOVO7 or activated factor 7, or VREF. There were  horrible complications with that with coagulation also, but we didn't have the right data set. For Dr. Jenscher, when you were addressing patients that you consider high risk  based on their CHF for cardioversion and post-cardioversion management of anticoagulation, is that regardless of whether they're preserved ejection fraction  or not preserved ejection? Both are at high risk.  It has to do with I generally think the people who have low EF are worse off, but it turns out that it has a lot to do with left atrial size,  which can be extremely large in patients who have preserved EF. I wouldn't try and split, but I would say I'd be even more cautious in the low EF patients, especially  if they seem like they have low flow. Please. My question is about the use of amiodarone as a rate control agent for AFib of unclear duration. Your septic patient comes in,  AFib with RBR 160, would you never use amiodarone given that you're not sure how long it's going on?  This is an area of controversy. I would say that amiodarone is a double-edged sword, and you should always be sure that you'd be okay with the patient cardioverting  when you're using amiodarone. If you have a patient, for example, who has a known left atrial thrombus, you never would want to use amiodarone for rate control.  In a patient with sort of the usual 75-year-old presents with pneumonia, AFib, you have no idea how long they've been in AFib, it's tricky. I think that in cases like that,  if I've already tried beta blockers and they don't tolerate it, I've already added some DIG and it's not working, then sometimes I will have to bite the bullet,  but in a case like that, I may hedge my bets and try to put them on heparin, just to be on the safe side, with absolutely no data showing that that's a safer, effective  strategy. But in a case like that, if you can obtain a transesophageal echo to convince yourself of the safety, that would be a nice way to sort of  dot your I's and cross your T's and prove that you're being as diligent as possible. Thank you. Hello. I think we have time for one last question. Thank you. Thank you. I actually  have a question regarding the magnesium. At my institution, we use the cardiac wards. We use, we target levels of like 2.4 for like VT.  I was kind of wondering what levels you're targeting or if there's another like treatment effect that we should use to actually like load people  with magnesium, basically. What do you think? Well, I think based on my colleague's statements, I can say they probably practice me, which is that more magnesium is always better.  As long as they have reflexes, it's fine. Yep, exactly. And so we are, and I'm not in the cardiac, I'm in general surgery ICU, we target at least 2.1 in all our patients. And  even if that level is 2.1 and they're in atrial fibrillation, we'll go higher. We'll go closer to 2.5 to 3. Having worked with you, I think that you probably do the same.  Right. So again, magnesium, very well tolerated. As long as they have reflexes, you're not going to hurt them. And a functioning diaphragm and everything.  And so more is always better. But again, once they're in a fib, magnesium alone is probably not going to cut it for most patients. It may, but you probably need something else  too. So to avoid that dreaded yet disease, we'll walk out of the medical wards and go to the obstetrical wards? That's true. Exactly. And so how many pregnant ladies  who we're treating with magnesium have we sent to heaven because we've driven their levels up to 4? Not. So again, you pick your battles. Until your levels get closer  up to maybe 8-ish, you're probably going to still have your reflexes. And the reason that we're saying this is that the cardiac magnesium levels, which is all you actually  care about, and the blood magnesium levels have been shown to correlate very poorly. So just because you have a normal blood magnesium level, it means very little about your actual  cardiac level, which is why we give more even if the level looks okay. Thank you so much. I hope you enjoy the next session, everybody.

Video Summary

The video transcript discusses the management of atrial fibrillation (AFib) in critically ill patients. The speakers discuss the causes of AFib in the ICU, such as inflammation, vasopressor use, electrolyte imbalances, and volume overload. They also mention different pharmacological options for managing AFib in the ICU, including calcium channel blockers, beta blockers, amiodarone, and magnesium. The effectiveness and tolerance of these agents in critically ill patients are debated. The speakers also touch on the potential role of steroids, vitamin C, and dexmedetomidine in preventing AFib in ICU patients, but note that further research is needed. The use of anticoagulation in AFib patients in the ICU is addressed, with a discussion on the challenges of maintaining therapeutic levels without increasing the risk of bleeding. Individualized approaches to managing AFib in critically ill patients are highlighted, taking into account each patient's specific risks and benefits of different pharmacological options.<br /><br />In the second summary, the video transcript covers the management of AFib in general. The speaker emphasizes the importance of identifying and treating the underlying causes of AFib and discusses the use of rate control and antiarrhythmic medications. Beta blockers, such as metoprolol and esmolol, are recommended as first-line treatment for rate control. Amiodarone is highlighted as an effective antiarrhythmic for patients with heart failure or reduced ejection fraction. Other antiarrhythmic drugs, such as ibutilide, flecainide, and sotalol, are mentioned, with the choice depending on the patient's underlying heart disease and risk factors. Cardioversion may be necessary for unstable patients or non-responders to rate control medications. The importance of anticoagulation before, during, and after cardioversion to reduce the risk of thromboembolism is stressed, with the use of the CHA2DS2-VASc score to guide long-term anticoagulation. Individualized treatment based on the patient's clinical characteristics and risk factors is emphasized to achieve rate control and/or rhythm control while minimizing complications.

Asset Subtitle

Cardiovascular, Pharmacology, 2020

Asset Caption

The Society of Critical Care Medicine's Critical Care Congress features internationally renowned faculty and content sessions highlighting the most up-to-date, evidence-based developments in critical care medicine. This is a presentation from the 2020 Critical Care Congress held February 16-19, 2020, in Orlando, Florida, USA.

Learning Objectives

Manage atrial fibrillation with appropriate pharmacotherapy at the appropriate time in selected populations
Determine preventative measures for atrial fibrillation in the critically ill population
Discuss the benefits of interventional cardiology and other measures to treat refractory atrial fibrillation

Pharmacology: The First (and Last) Line of Defense?

Nicole M. Palm

Prevention Is Easier Than Cure!

Douglas F. Naylor Jr

Fibrillation in Critical Illness: Where Do I Go When All Else Fails?

Jacob C. Jentzer

Meta Tag

Content Type Presentation

Knowledge Area Cardiovascular

Knowledge Area Pharmacology

Knowledge Level Foundational

Membership Level Select

Membership Level Professional

Membership Level Associate

Tag Atrial Fibrillation

Tag Cardiothoracic Critical Care

Year 2020

Keywords

AFib

critically ill patients

inflammation

pharmacological options

calcium channel blockers

beta blockers

amiodarone

magnesium

anticoagulation

rhythm control

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