Okay, good morning everybody. I know we have some people filtering in but we are at 1030 So I would like to go ahead and get us started. My name is dr. Colin Truitt, and I am co-moderating this session with dr Vinita Sahasranaman It is my pleasure to welcome you to our our next clinical updates Session, so if you're in this room at any point during the conference, that's what you're in for a clinical update So you can always count on us being here it is Couple of announcements before we do get started with introductions in our session today a few reminders are Please turn off and silence all cell phones electronic devices pagers beepers cell phones AI large language learning models. I don't know any other device that may be disrupted during the presentation Also a reminder that videotaping and use of digital photography including cell phone cameras are prohibited in this session However, these slides are available through the app. So you will have access to the resources that are shared with you today All presenters will be either verbally disclosing any relevant financial relationships or show their disclosure slide at the start of a presentation and Please hold all questions until the end of the session as we will have a Q&A The Q&A does include both questions from our online and virtual audience as well as if you are asking a question in the room We ask that you come up to the microphone so that everyone can hear what your question is And the discussion that ensues Okay So it is my pleasure to introduce our session Everything the psychiatrist needs to know about ECGs and providing us with this wealth of knowledge today will be dr. Margo Funk Dr. Margo Funk is a CL psychiatrist and assistant professor of psychiatry at Harvard Medical School Program director of the psychiatry residency and vice chair for the education in the Department of Psychiatry at Brigham and Women's Hospital Dr. Funk directs the cardiovascular psychiatry clinic at Brigham serving patients with complex arrhythmias history of cardiac arrest and advanced heart failure Dr. Funk has served on the APA councils on CL psychiatry and CML She chaired the APA work group on QT prolongation and psychotropic medications and MOUD in the general hospital So just a brief description is we know that psychiatrists frequently prescribe psychotropic medications that are associated with cardiac risk And such risk may include conduction abnormalities and tachyarrhythmias such as Torsades-de-Point and sudden cardiac death so knowing how to Use the 12 lead EKG as a common tool for screening and for functional and structural cardiac abnormalities is vital And so without giving too much of a way we have a bit of an interactive session today And so I'd like to turn things over to Dr. Funk Good morning everyone and good morning to those live streaming so today we are going to try to tackle a it's a very large topic and What what the goal is is to can start with the basics and then work our way up So no matter what level you're coming into this Hopefully this will be a useful session that you can kind of start at the unknown and work up to the known so we will be talking about ECGs and I have no disclosures and Before we begin I just want to recognize two collaborators and Dr. Scott Beach and Chris Solano who are at Mass General Hospital We often get to present on this topic together and they were not able to join me today But several of my slides have been adapted from our joint presentation, so I wanted to recognize Scott and Chris So I first wanted to point out and draw your attention to this APA resource document Which is available on the APA website and you can use this QR code to download it It'll it'll take you right to the site. So this was a document that we put together in 2020 bringing together a group of experts in both clinical kind of cardiac psychiatry cardiac psychiatry research and then in collaboration with the American College of Cardiology And what we wanted to do is to really put together this set of resources For psychiatrists to get a better understanding of how to work with the QTC when prescribing psychotropic medications We've actually just begun work on a five-year revision of this document and so much of what I talk about today Will be in that revision and hopefully that will be out in 2025 We will also be doing some interactive polling today, so Please take a moment to either scan this QR code or you can You know log in through the web through PollEbb.com slash Margo Funk 977 or you can send a text if you text Margo Funk 977 to the number 2 2 3 3 3 that should get you on And we should have enough for 700 responders. So folks online. Feel free to jump on too. We'll see if that works Okay, so I always like to to start this discussion by framing with a clinical case and we're going to use this case to Talk us through much of what what we talked about today So this is a 27 year old woman. She has a history of generalized anxiety disorder and social phobia She's well controlled on citalopram 40 milligrams daily And she's coming to your outpatient clinic to establish care after she's relocated for her first job out of law school She has no past medical history. She takes no other medications She has no family history of an arrhythmia cardiac arrest or sudden death She's got no suicide attempts. She's never been hospitalized psychiatrically and Your clinic just purchased an ECG machine and the medical assistants there were recently trained how to use it So while you believe that this patient's cardiac risk is low Since you have that machine you decide well, let's just get an ECG for the sake of completeness So here is the ECG that you get and The first thing that you may notice is that the computer read at the top of the EKG Has a QTC of 532 Milliseconds and you you may be kind of freaking out internally. Oh gosh. Okay. I was not expecting this This is a healthy woman and now her QTC is 532 What do I do next? So this is a common scenario with with many different you know Variations but something that you may see whether you're you know, an outpatient psychiatrist an inpatient psychiatrist doing CL psychiatry How do we deal with an EKG like this and what really is the risk here? So today what we're going to be talking about one What are the indications to obtain an ECG when we're prescribing psychiatric medications that may have risk for cardiac adverse events? We're then going to Really get into the EKG identify the intervals the waveforms that you need to know and we're going to correlate that with the Electrophysiology of what's actually happening in the heart we're going to practice measuring the QT interval and Calculating the QTC and then we're going to end this session really talking about how to do a risk-benefit assessment Because we know there's no One right answer of when you can or cannot prescribe a medication when the QTC is prolonged It's going to be an individual case-by-case decision for every individual patient. So we'll talk about an approach to that Starting off with the ECG, so this is the computer-derived electrocardiogram and It's a very convenient tool So when you when you notice that you get your EKG in front of you or you pull it up on your EMR There's going to be a reading at the top and that read will show you the various intervals that the computer has measured It may even have some Diagnostic comments on there and the thing to know is that the results of these reads are going to be quite variable between Machine to machine and we often can't rely on them Oftentimes the measurements are derived from these representative or median complexes on the ECG and The thing that I think is most important for us when we are looking at the QTC Is that most machines use the heart rate correction formula the Bizette formula? And so your first take-home for today is Bizette is bad. So remember remember B&B Bizette is bad. So Bizette this formula has been used since the 1920s. It is the formula that most QTC research has used It was the the benchmark used by the FDA for drug monitoring of QTC prolongation up until 2017 They recognized that it is actually a quite inaccurate correction formula What it does and we'll talk more about this It overestimates your QTC at high heart rates and underestimates at low heart rates and so unfortunately, most of our machines are still set for this formula and It's quite inaccurate And so one of the things that I want to instill in you today is that you can get comfortable measuring your own Intervals and doing your own calculations and we'll practice that But remember Bizette is bad and I want you to be thinking about doing your own Measurements when you see an EKG in front of you so this is Two cycle lengths of an EKG These are the the classic waveforms that you would see so starting at the left you have your PR interval And you have your QRS complex Your ST interval which we don't pay as much attention to but the thing that we really pay attention to is this T wave And then this is the QT interval. So the QT interval Starts with the beginning of your QRS complex and it goes until the end of your T wave right here One little point to point out which we'll talk about in a bit is the J point right here so the J point is the end of the QRS complex and many will say that the the JT interval is actually much more reflective of risk of Adverse cardiac repolarization events. We'll talk about this. So just make a note of where the J point is The other thing to note here is for the QRS complex It's important to keep track of the duration of that QRS. So normal QRS complex is 80 to 100 Just keep that in the back of your mind and then and then I'll say more about why we are concerned about that The other interval to know is your RR interval So when you're measuring a QT if you are measuring the RR you always measure the RR That precedes the QT that you're interested in So let's say you don't have a computer read on your EKG and it just spits out The waveforms and you want to know the heart rate Quick and dirty way to do this is you know that your EKG is 10 seconds in length You're gonna count the number of beats and you're gonna multiply the number of beats by 6 That'll give you 60 seconds and that will tell you the heart rate. So this is one little sliver of 12 lead EKG. We're gonna see that it's 10 seconds 12 beats And then we get 72 beats per minute. So quick and dirty easy Let's jump into QTC so Great. And so I many of you have already started. This is perfect. So Get out your phones and I want you to if you haven't already Think about what is your ECG comfort level as related to the QTC? Are you novice you couldn't read the machine measurements, but not quite sure how to interpret Beginner feel like you can interpret them, but you're not doing the measurements yourself intermediate so Comfortable measuring knowing where the T wave ends good can calculate the QTC or advanced Feel comfortable adjusting for pacing know how to interpret a normal T wave Morphology is great Okay, so it's looking like I would say half the half the folks in the room and online are in the beginner category Which is a perfect category to be in and a lot of novice, which is also great So hopefully we will we will at least take you today to the intermediate level. That is our goal and for those intermediates Hopefully we'll take you a little bit advanced So when we are thinking about the QTC What why are we worried about that? What is the thing that that we are worried about? What is the cardiac adverse event that the QTC is a risk factor for is it? Is it a bundle branch block is it Torsade de Pointe Brugada syndrome or third-degree heart block so See a lot of Torsades A little bit of MI a little bit of bundle branch block. So so the answer is Torsades So this is the thing that that we are worried about. This is why this whole conversation exists So let's talk about what that is So this literally in French means twisting of the points And what you can see here this is a rhythm strip on telemetry of Torsades de Pointe happening in a patient and What you can see is that this is a form of polymorphic ventricular tachycardia where you have this variation of amplitude of the waves from small to large to small and It looks like it's twisting around the isoelectric baseline, which we would say is like right here so Literally, it looks like twisting of the points so This is a VT a type of VT and it can present in a number of ways At you know low level of acuity. You might have someone who gets lightheaded. It's a little presyncopal You may have someone who passes out You may have a seizure like activity So so always think about this if you're evaluating like for PNES You don't see anything on the EEG make sure you've done a cardiac workup But the thing that can happen that is hard for us to predict or know when it happens is is actual sudden cardiac death so a cardiac arrest and This oftentimes happens out of the hospital which makes it something that's very difficult to study So there's so when we think about our evidence and the data that we have And how we use that to make our own clinical decisions We also have to remember that the data is based mostly on case reports Not not randomized control trials It's hard to get this data and it's difficult to study. So that's worth keeping in mind So QTC prolongation is our best marker of risk for Torsades And this is is a major drug safety benchmark used by the FDA when new drugs are coming out also used by other international drug regulatory agencies and Torsades will typically happen in one of two settings. So the first is called congenital long QT syndrome. And basically what this means is you have a patient with typically a genetic mutation where that confers high risk of sudden cardiac death. And it may be associated with a cardiomyopathy. Oftentimes there are multiple family members that have the same thing and so you may already be kind of worried about this. It has a typically characteristic QT morphology and a long QTC and high risk of sudden cardiac death. So that's the genetic side. Then there's what's called acquired long QT syndrome. And that's the part where we contribute with, and frankly all physicians can contribute with the medications that we prescribe. So that's the one that we're really worried about. And acquired basically means that the QT is becoming prolonged under a set of certain clinical conditions that will affect repolarization of the heart. And then that can lead to torsades. So we're in the acquired QT realm. So now we're going to jump into the heart and think about, okay, what's happening electrophysiologically. And I find for myself and my own clinical practice, the more comfortable I feel with what's happening electrophysiologically helps me feel confident in the decisions that I'm making and also the recommendations that I may be making to other teams. You know, when I can know, okay, this thing on the EKG is looking like this, that means that this is what's happening electrically in the heart, it will give you another layer of confidence. And so I think as much as you can understand this is worth doing. So let's start at the figure on the left. So you can see you've got a heart at the top and you have the corresponding EKG below it. It's just one cycle length of the EKG. So pink is depolarization, blue is repolarization. And so what happens here in the beginning, yellow is our electrical current. So remember, you've got this rapid fire current starting from your SA node, traveling to your AV node, and this is going to depolarize the atria and that is going to reflect as the P wave on your ECG. And then what happens is you have conduction continue through your bundle of His, so if you go to the second panel, bundle of His, your bundle branches, so you've got your right bundle branch, your left bundle branch, and then out into your Purkinje fibers. And this is also rapid transmission and this is depolarization of your ventricles and that's represented by your QRS complex. Meanwhile the atria are repolarizing but you can't see it, it's obscured by the QRS complex. Now the part that we're really concerned about and where torsades can happen is during repolarization of the ventricles. So that is shown here in blue. And so the repolarization phase starts with the end of the QRS complex, remember that little J point, that's right here, and it goes to the end of your T wave. So that's your JT interval. Now we talk about QT interval, not JT interval typically, and I want you to make note of that. The QT interval includes the QRS and this JT, but what we know about torsades is this arrhythmia happens during repolarization, not depolarization. And so sometimes you may be in a situation, and we'll talk about this more, where your QRS is wide, like if you have a bundle branch block or if you have a ventricular pacemaker, then you may get a reading of a really long QT interval, but in fact, repolarization isn't affected. It's this wide QRS complex. And I'm going to teach you about a way to kind of take that out of the equation so that you aren't in a situation where you think there's higher risk than there actually is and then withhold a psychiatric medication from a patient who really needs it. And I've seen this happen many times on a consult service. You come in after a weekend, it's been, let's say, a new team on the medicine service. They see this long QTC, and it turns out the patient is paced and they have a QRS complex that's 200 milliseconds. And if only they had taken that out of the equation, they would know that the patient didn't need to be stopped of their antipsychotic, let's say, and now they're psychotic. So reasons like this, this is why we want to be aware of that. So now we're going to dive a little deeper. So thinking about what's actually happening ionically in these cardiac myocyte cells. So when we have prolonged repolarization, which is where torsades can happen, this happens because of a blockade of the inward rectifier potassium channel, which is called the HERG channel. And the HERG stands for human etheragoga-related gene. That's what encodes this channel. And so literally, our drugs, or any drug that prolongs the QT, can come in, block this potassium channel. So now we should think about, okay, what's happening in each of these little cardiac myocytes? So this is one action potential, and so if you think about depolarization, so in depolarization you have this rapid influx of sodium coming into the cell. You have a slower influx of calcium. So this is all depolarizing the cardiac myocyte. And then you have an efflux of potassium, and that's coming from this HERG channel. There are other channels, but HERG is the most prominent one. And what happens when that drug blocks the channel is it slows down efflux of potassium from your cell. And so instead of this nice solid line right here representing potassium efflux, it takes longer. It's more slurred out, and ultimately this is what's going to prolong your QT. Let's look at it another way. So this would be normal potassium efflux. This would be your action potential of that cardiac myocyte. Depolarization happening here, refractory period, repolarization. And if you translate this to your EKG, that repolarization looks like this lovely T-wave where it's really easy to tell where it ends. The duration is considered normal. So everything is good. But then when you have this drug coming in and blocking this potassium channel, what happens is repolarization is prolonged. It slows down. So you can see this is longer than in the previous panel. And what happens on your EKG then is that you get this distorted, widened T-wave. You may have a number of different humps to your T-wave. It may slur way out. It may be very difficult to tell where the wave ends. That is when your kind of spidey sense radar needs to be going up and saying, okay, this is not a good T-wave. There's some prolongation of repolarization here. It doesn't look clean. And so I think a take home from today also is it's not just about your QT interval, but look at the morphology. When you see something that looks like this on your EKG, it's a little bit worrisome. So you may want to get some consultation. Okay. So now let's talk about clinically. So we've talked about the electricity. We've talked about the ions. So how do we now apply this to clinical practice? And we know that we have the QT interval, but we also know we have the QTC, the corrected QT interval. So what is that? So we know that the absolute QT interval for any given patient is going to vary depending on their heart rate. So let's say you've got this, we'll say this is the same patient, even though their hair is a little bit different colored. So this patient is laying in the hammock, 70 beats per minute heart rate. And the QT interval for this patient is going to be around 370 milliseconds. The same patient, if they are running a marathon, let's say they're at 110 beats per minute heart rate, their QT is going to be just above 300. And yet their risk of a repolarization abnormality is the same. It's the same person. But that QT interval, if we don't correct it for the heart rate, is going to give us different numbers depending on what that heart rate is. Here's another way to look at that, and this time with a rhythm strip. So here's your hammock guy, and he's got a longer cycle length. This is what your QT would look like, 370. And then here he is running. The beats are closer together because the heart rate is faster. And so just inherent in that, your QT interval is going to be shorter. So what we have to do is correct that so that we have a consistent marker of risk across all heart rates. So this is how we do it. So going back to Bizette I talked about, the formula that is on most standard ECG machines. This is the Bizette formula. I recommend that you never use it. The only time you can use it is when the heart rate is 60. And that is because, so the Bizette formula is the QT interval in milliseconds over your RR interval in seconds. I'm sorry, the square root of your RR interval in seconds. When you have a heart rate of 60, your RR is 1,000. And so in seconds, 1,000 milliseconds, in seconds it's one. So QT equals QTC at a heart rate of 60 for Bizette. Only time you can use it, and then you don't have to correct actually for heart rate. But what I would recommend is you never use Bizette, and you can use any one of these other three. So Fredricia, which is what the FDA now uses, Framingham, or Hodges. The American Heart Association, American College of Cardiology, and Heart Rhythm Society would recommend Framingham or Hodges. These are linear regression formulas. I like Hodges. It's easy to calculate. It's the only one that doesn't require the RR. You can just plug in the heart rate. But take home point here, any of these are fine, but don't use Bizette. The other thing is that you don't have to do this calculation on paper. There are many apps now that you can just plug in in your intervals, and you can actually compare everything together. So definitely use an app. It's much quicker. So in terms of what is a normal QTC, I'll say that we tend to be most concerned clinically when our QTC is above 500. But what you'll see considered prolonged for the purposes of research is in men, about 470 is your upper limit of normal, and women, 480. I've seen it different in different places, sometimes 450, 460, et cetera. But really, 500 is where we generally become concerned. And that's because of the data of torsades that we have, most cases of torsades happen above a QTC of 500. And that's why we use that. We also get concerned if we make a medication change, and we see the QTC increase by 60 or more milliseconds. That would tell us that something major has shifted, and we want to have a higher level of vigilance. All that being said, though, there is no absolute QTC at which an at-risk medication can't be prescribed. It is always an individual risk-benefit analysis. So 500 is a nice frame, but you can certainly give a higher-risk medication to someone at 550 or even 600, depending on the rest of the scenario. So let's go back to our case. So this is our new attorney. She's got this QTC of 532. And so now that we've talked a little bit about this, what do you want to do next? Remember, she's on citalopram 40, no other risk factors. Do you want to lower her dose of citalopram, switch to a different SSRI, order labs to check electrolytes, manually measure her QT interval and use a non-Bazette QTC heart rate correction formula, or stop citalopram and refer to cardiology before you do anything? Okay, yes. Yes, good. If that's all you take home from today, this is great. Okay. So many errors happen because we use Bazette. So fantastic. So you're going to manually measure this. So let's do it. So when you manually measure, we're going to go back to the basics here of ECG reading. First thing to remember is that each small box is 40 milliseconds and each large box is 200 milliseconds. And then you have to pick, okay, which T wave and QT interval do I actually pick? So we usually look in leads B2, B3, or lead 2, and those are the ones that are highlighted here in blue. If you can't find a wave there where it's easy to tell where the T wave ends, then just look throughout the EKG and pick one. That is fine. You want to pick a cycle length where you can tell where that T wave is ending. That's probably the most important thing. So sometimes you may not be able to quite tell where the T wave ends. And so a lovely tool to use is called the tangent method. And when you use the tangent method, what you're going to do is you're going to draw a line that is tangent to the steepest downward slope of your T wave. And then you're going to draw a line that corresponds with the isoelectric baseline. And then that intersection point is going to be the end of your T wave and then the end of your QT interval. Here's another way of looking at this. So here's your beginning of your Q wave right here, or QRS complex. There's not really a Q wave there. Beginning of your QRS complex, tangent to the steepest downward slope of the T wave, isoelectric baseline, intersection point, there's the end of your T wave. And so now we're going to count the number of boxes, remembering that there's 40 milliseconds per box. And so here we're, what do we have? We have about 10 boxes plus a sliver, so about 410 milliseconds, this QT interval. Let's try this for her. So I chose V3. I think it's fairly easy to tell where her T wave ends. So we're going to zoom in. The beginning of our QRS complex right here. Then I'm going to call the end of the T wave right there. And what I'm looking for is where does this hit with the isoelectric baseline? Now you could have used the tangent method here and would have gotten pretty close to right exactly at the same place. So we'll say that's the end of your T wave. We're going to count the number of boxes. So it's nine boxes plus almost another box. So 390 milliseconds is the QT of this woman. So 390. So now you want to go do the calculation. And you're going to use the Hodges formula because it's a good one. If you want to do it by hand, you can use the formula right here. Remember, her heart rate was 92. Or you can plug it in to an app. So her QT interval is 390, heart rate 92. Don't be shy. Okay, I've seen a lot of 446. Matt, that's correct. Look, so you just did it, okay? You measured the QT, you corrected the QT. See, 446 milliseconds. So, that's different than 532, for sure. Here is what one of these apps looks like. This is MDCalc, this is the one I use, but there are many out there. It's kind of a fun exercise to plug in your numbers and then see what the different formulas tell you. And note, just for this patient, her Bizette is 483, but the other three are in the 440 range. I think that's just kind of fun. It always reminds me how bad Bizette is. So, Bizette is bad, that's your take home, okay? So, now you know QTC is 446. So, what are you going to do next? Will you continue citalopram at the same dose? Will you continue it but decrease the dose to 20? Will you cross taper over to sertraline? Will you continue citalopram at the same dose but only after you get a new set of labs? Which one of these are you gonna do? I'm gonna let our number of responses keep going up for a minute. Keep going, you haven't entered yet. Okay, so I'm seeing a lot for continuous citalopram at the same dose. A couple continue but decrease the dose to 20. A few but get a new set of labs. A few consider cross-tapering to sertraline. Great. This is excellent. Okay, so what I would do, I would continue citalopram at the same dose. I think for this patient, we now have a lot of reassurance that after we do this measurement by hand and use a formula to correct heart rate that is more accurate. She's 446. She doesn't have other risk factors. She's young and healthy. I don't think we need to get labs. I'm guessing they're going to be fine. And looking at her T waves, her T waves look fine, so she's probably not hypokalemic. So I'm going to continue with citalopram. I do think, though, it's worth us thinking about these other answers for when we have more complicated patients who do have risk factors, and then these are absolutely going to be part of the discussion. And we can definitely talk about this in the Q&A as well. Okay, so we're going to continue the citalopram at the same dose. So let's talk a little bit now about the medication aspect of things. I know this is an EKG talk, but I think we have to touch on the medications a bit to inform this clinically. So we've talked about how QTC is this major FDA benchmark. We've talked about how it's the best marker of risk for torsades, but it's not the only marker of risk, and it's not an end-all, be-all. There is not a one-to-one causation. So if you have QT prolongation, you're going to have torsades. You have to consider all of these other risk factors, and so the medication is a huge piece of that. And what we know is that when you don't have other risk factors in play, drug-induced QTC prolongation rarely leads to torsades. And that's why in this woman, I'm not worried about it, really, because she doesn't have other risk factors. And even if that citalopram prolonged her a little bit, I still feel very reassured by her EKG. So when we're thinking about risk factors for torsades, I like to group these into two different categories. First, these are the things we can't change. So female sex, being of older age, your metabolizer status. Let's say you're not as good of a metabolizer at a certain medication that happens to be QT prolonging, and you're on that medication as a patient. That would come into play. Certainly congenital long QT. Absolutely can't control that, and that's a huge risk. If the person, the patient, has had QT, drug-induced QT prolongation in the past, that is a risk factor. If they have structural or functional cardiac disease, that is a risk factor. And then a family history of sudden cardiac death is also a risk factor. I always ask about family sudden cardiac death in all of my patients, and I think it would be fair to do that in even a general outpatient psychiatry practice. If you are working with someone who's more medically complex or you're worried about the medication that you're prescribing, I think if you're going to get an ECG, probably worth just making sure you know that family history, because sometimes that's all you know, and then someone drops dead. So it's worth knowing that. That's a really important piece of the history here. So what can you change? Things that are modifiable. So certainly the drugs that we prescribe, and we know that when a patient is on more than one QT-prolonging drug, that that risk is additive or cumulative. So the more they're on, the higher the risk. Certainly drug-drug interactions, drug toxicity, so if you have a patient who overdoses on a medication, you would want to think about QT prolongation there. Severe acute illness. So your patients that are in the ICU, they're going to have a lot of other things going on. They may have renal impairment. They may have hepatic impairment. These are all going to impair clearance of potential QT-prolonging drugs. You may have someone who is bradycardic. Here's a take-home for today, bradycardia. This is a risk factor. When I have a bunch of risk factors and my patient is tachycardic, I am much less worried. So you have this very slow heart rate. It allows a lot of space during that prolonged repolarization for an ectopic beat or a PVC to come right on top, and then that's the thing that's going to trigger torsades. So when I see bradycardia, that also kind of gets my spidey senses up, and I worry more, whereas if you're tacking along at 110, I'm going to be much less worried, even if you have other risk factors. So bradycardia for sure. And then electrolyte disturbance. So hypomagnesemia, hypokalemia, hypocalcemia. These are the things to know. So, you know, we're here because we prescribe a lot of psychotropic medications, but there are many other types of medications that also prolong the QT interval and increase your risk of torsades, and I think of these as the anti-categories of medications. So you have your antiarrhythmics, which is weird that an antiarrhythmic may actually increase your risk for a malignant ventricular tachycardia, but it can. Sotolol, dofetilide, these are ones where you actually have to bring the patient into the hospital to monitor their QTC if you're going to start those. Quinidine was the medication where torsades was first described. Amiodarone is another one that we see commonly used. Your macrolide and your fluoroquinolone antibiotics, your azole antifungals, a few of your antivirals. Chloroquine and hydroxychloroquine are one, and this was interesting during the early phases of COVID when hydroxychloroquine and azithromycin, macrolide, were being given together. People had torsades, and so I'm glad we're past that. And then your antiemetics, most of these are QT prolonging. If you're in a dangerous situation, lorazepam can always be used. Scopolamine, a patch, can be used for nausea, but you do have to consider the antiemetics. Several anti-cancer medications or anti-rejection. Methadone, this is a big one. This is next take-home point for today. Methadone you have to be careful with, but it's complicated because you don't want to withhold a life-saving treatment for someone with opioid use disorder. We'll talk about that. And then some of our psychotropic medications. PCAs, ciprazidone, iloperidone, your low-potency phenothiazines. These are the ones that we would be most worried about. So I think it's important just to remember it's not just psychiatry. It's all of these medications, and so you do have to do a thorough medication reconciliation and make sure you know everything that that patient is on. We talked already about limitations of our data when we're looking at what is the evidence with regard to our medications, and things to think about. Many of the studies that we have are done in a range of populations, from very young to very old, very sick patients. Most of our data is with Bizette, and so imagine you have tachycardic patients getting measured with Bizette, and then that goes into a major study. How do you use that data? Timing of medication doses, concomitant medications. And then I think the million-dollar question is, when you do see QTC prolongation, does that actually mean that that drug is going to confer risk of torsades? It may not. Is that prolongation a clinically meaningful change? Just another way to think about when you have your hierarchy of evidence, this is where the evidence for QTC prolongation and torsades sits. It's not up here. It's down here. It's case studies, case reports, maybe some case control studies. Now, one great resource that we have, there are a few drug registries where they will tell you what the risk of QTC prolongation and torsades is for any medication that's been reported. And Credible Meds is a great resource. It is attached to every medication that they list. They cite the literature, and so you can actually go in and look at the literature yourself. And so I think critical appraisal of the literature is also really essential because you don't want to just rely on a category that a drug registry has said, like, this is high risk. Well, what does that actually mean? What is the data? Because it may be based on a single case report. So go in, look at the data yourself. Okay, so psychotropics. Antidepressants. This is going to be like whirlwind snapshot, but I think we have to cover this to cover the clinical context. So in general, your SSRIs and your SNRIs are safe. Nosotalopram and esotalopram separate out a little bit from the other SSRIs, but the clinical data to suggest that they actually increase your risk of torsades is actually very low. Bupropion, mirtazapine, also considered safe. Your TCAs, I would not be using these in folks that have other risk factors. There's no data on MAOIs, like, none. So don't go there, I think, with anyone where you're concerned cardiac-wise. So also consider cytochrome P450 inhibition. Let's say you're on one of these safe SSRIs, but it happens to interfere with metabolism of methadone. Let's say someone's on that too. You want to be careful there, so always think about interactions. I think we have to just briefly touch on citalopram because it is the one that separates out. We know that over 10 years ago now, the FDA came out with a drug safety communication on citalopram that it should not be prescribed at doses greater than 40 milligrams. They also said it shouldn't be used at doses greater than 20 if you have liver dysfunction or you're over the age of 60. And they also, FDA said, that it's no more efficacious at 60 than 40, so there's no reason to be using 60 anyway. The data to inform this communication was based on a single study, and that showed at 20 milligrams of citalopram, a QT increase of 8.5 milliseconds, and at 60, 18.5. So think about that little tiny box is 40 milliseconds. It's very difficult, actually, to even discern 8.5 milliseconds or even 18.5. And what cardiologists will tell you and our collaborators for the resource document is that below 20, a cardiologist cannot detect that difference doing a manual measurement of an EKG. So yes, there is an increase of QTC. The question is, is that clinically relevant? We're going to look at the data since then, and you can make your own decision about that. S-citalopram also separates out a little bit, but it was not included in the communication. So fast forward a little bit. Many people were upset by this assertion that 60 milligrams is not useful, and so the FDA changed the recommendation. They said it's not recommended at doses greater than 40 and that it should be discontinued in anyone with a QT greater than 500. So what do we know now? So what actually does the data show about cardiac risk of citalopram versus what was the risk of all of these people reflexively reducing the dose when these communications came out? Well, we know that all-cause hospitalization and death actually increased after people reflexively reduced citalopram, and there's no difference in VT, VF, or sudden cardiac death comparing citalopram and other SSRIs. In terms of psychiatric complications, hospitalizations for depression increased significantly. Increased prescriptions for interacting medications occurred, and people were more likely to be prescribed other psychotropics, including sedatives and other anxiolytics, as well as higher healthcare utilization. So, you know, I think we should all be careful, more careful with citalopram. I think, you know, if you have a patient with many risk factors and you're using citalopram, you should be more vigilant. But, you know, this is not a medication to be afraid of by any means at all, and never would I recommend that you take someone off of citalopram or reduce the dose just because you're seeing a change of the EKG, unless there's, you know, a lot of risk factors happening. All right, so antipsychotics, let's look at this just briefly. On your right here, this is a forest plot from a study done looking at about 30,000 patients with schizophrenia, so it is a defined population, looking at adverse effects of antipsychotics. And this one is looking at QTC prolongation. And if you are on the left side of the zero here, this means that you actually didn't have QT prolongation. This is the actual in milliseconds prolongation, the mean. And then if you're on this side, then you have lots of QT prolongation. So lowest risk category for us of most commonly used antipsychotics, lorazodone, aripiprazole, I feel totally safe using. Kind of low to moderate risk categories would be Haldol, cotiopine, olanzapine, risperidone. I also feel fairly safe using these unless I have a lot of risk factors happening. Higher risk, this is gonna be your iloperidone, your zyprazodone, and then your low-potency phenothiazine, so thiazidine, chlorpromazine, and mesiridazine. Sertindol, this is not sertraline at the bottom, this is sertindol, this is not FDA approved in the US, so not included in my high risk. It's very high risk, so don't use it. Clozapine, there's actually very limited data on QTC prolongation in clozapine. And so while we worry about clozapine for other things, QTC prolongation in torsades is not one of them. A point about IV Haldol. So it has been, I think, practice and just what we've learned as residents, trainees, now attendings, for a long time that IV Haldol is a dangerous medication. And it turns out that there's actually a real paucity of data about IV Haloperidol. In 2007, the FDA did put out a warning suggesting increased risk. They recommended ECG monitoring for patients receiving IV Haloperidol. But I wanna recommend this article by Scott Beach and colleagues about IV Haloperidol, where they really go through all of the evidence. And what they found is that most of the studies on IV Haloperidol were really confounded by a lot of things, including study populations that were severely medically ill in the ICU, many, many risk factors, many concurrent QT prolonging medications, people with underlying cardiac illness. And so what they recommend based on their review of all the literature is that if you are using IV Haloperidol, definitely you do wanna get a baseline EKG and at least one follow-up. If there are a lot of risk factors present, get one daily. So if you're in an ICU setting, you have other risk factors, so daily is very reasonable. Make sure you're repleting electrolytes, mitigating other risks. And you can consider alternative agents if your QTC is getting above 500. But again, remember, if you have a really sick patient who's getting IV Haloperidol, the ICU is the safest place to be in the hospital. So just keep that in mind. So it's not quite as dangerous as we all used to think. The data on IV Olanzapine, which I don't have a slide on, but it's also quite safe. And that's something now that I feel like we have enough data to use that in practice too. So I would feel comfortable doing that. Mood stabilizers, pretty safe. So valproic acid may have some protective effects on conduction. With your other anticonvulsants, carbamazepine and the rest here, one important point to remember is that these are sodium channel blockers. So if you think back to your electrophysiology and your ions, sodium, you have that rapid influx of sodium into the cell for depolarization. So if you have someone with a bundle branch block, they already have a conduction disturbance during that QRS depolarization phase, I wouldn't prescribe one of these anticonvulsants or any sodium channel blocker. It's not related to QTC, but it is something to think about if you do see a conduction disturbance in depolarization. Lithium, a little bit uncertain. We have found in most data suggests that there's not significant prolongation in therapeutic ranges, but as serum lithium concentrations go up, the QT does get longer, but the increases are modest and thought to be not clinically significant. So I feel fairly safe with lithium. Okay, so methadone. So take home, methadone, remember this. So this is one that definitely prolongs the QTC and it causes torsades, and it does this a lot. It is a very potent inhibitor of that inward rectifier HERG potassium channel, and it has a black box warning of QT interval prolongation and serious arrhythmia, has been observed during treatment with methadone. So this is one to be vigilant about, but like I mentioned before, this is where risk-benefit really comes into play. It's a perfect example because methadone may be the only treatment that someone has for their opioid use disorder that's working for them. And so you have to balance your risk of overdose, your risk of relapse and death with your risk of torsades with methadone. There is a lovely set of safety guidelines, cardiac safety guidelines for methadone. So for anyone who sees patients on methadone routinely, this is lovely. This is put out by the American Pain Society and the Heart Rhythm Society in 2014. They recommend, in terms of baseline EKGs, if there are risk factors for torsades, get one. If you have a prior EKG above 450 QTC, get one. But if you don't have risk factors, you don't have to get one. So they did not make an absolute, you must get a baseline EKG, and that's because many settings where patients are receiving methadone may not have resources to get EKGs. And we don't want the absence of an EKG to preclude someone from getting life-saving treatment for opioid use disorder. Now, they do recommend to consider alternatives if you're in a 450 to 500 range, to recommend against use when QTC is above 500. And always, always think about ways that you can mitigate any of the risk factors that a patient has. But again, always balancing that with the risk of untreated opioid use disorder. Brenorphine, much safer alternative to methadone. It's actually a HERG channel inhibitor as well, but it's 100 times less potent than methadone. And there's no data to suggest that it prolongs the QT interval. So that one we feel quite safe about. All right, so now we're talking about when do you get the EKG? Let's say you have a patient who's coming into you new and they have an EKG in their file. And you look at that and you wanna know, well, can I use this data? What we would recommend is that if you have a prior EKG, then you don't, you only use it if it's within one month prior to when you're seeing the patient or when you're making the decision about starting a medication. If it's more than a month and you think it's appropriate to get the ECG, then I would get a new EKG. Other times to do it if you have a prior is if they've had a significant medical change in risk factors, then you would wanna get a new one. Again, if you're in a resource poor area, never let the absence of EKG machine or a cardiologist to read that EKG get in the way of starting a medication. And I wanna highlight, and this is why you're all here today to get comfortable doing this, that psychiatrists absolutely can do these calculations. They can interpret risk of using an EKG. So practice, practice, keep doing this. And you can do this. Any medical specialty that prescribes a medication that prolongs the QT should feel comfortable with doing this. Who can interpret? You can, that's the bottom line. Sometimes the question comes up, well, I don't know how to do the full interpretation or what if I miss an MI? Well, you're probably gonna have clinical signs anyway that something really terrible is happening. But we're gonna think of this as a harm reduction scenario, right? Okay, so seriously, you're gonna use the data that you need. If you see something really worrisome, you can absolutely get cardiology involved. But don't feel like, oh, if I miss some other thing, I just shouldn't do it at all. That's not the attitude to have. Get comfortable. You don't have to know everything. You can always consult your cardiology friends. You can always call me. I have a lot of cardiology friends, too. So, and that helps me. Okay, so other ways to kind of just think about when do I get an outpatient EKG. I like to balance what are my risk factors on one axis? What's the risk of my medication on the other axis? The more I have of each or the higher risk, the more likely it is that I'm going to get an outpatient EKG. So you may wanna have this as a snapshot just to have everything together in one place so you can refer to that. So definitely consider EKG as you go up towards the red there. This is kind of similar, similar to the other figure. I think that the main thing here is that there are many cases where you don't need an EKG. There aren't risk factors, it's not a high risk drug. You don't need to get it. Get one if there's a lot of risk factors and it's any drug. Get one if there's no risk factors and it's a high risk drug. If someone has an existing cardiologist and you want to prescribe a high risk drug, then I would have a conversation with that cardiologist. And then how do you interpret? So let's say you've gotten your EKG, it looks fine, you've started a medication and you get a steady state EKG, let's say a month later. Proceed if everything looks fine. If you are not above 100, if your QTC hasn't gone above 60. If you do see those changes though, then proceed with a little more caution. And again, risk benefit analysis is what you're gonna have to be doing here. Consult cardiology if it's high risk drug and you're seeing a major change in your QT interval. So this would be, let's say patient is on methadone, you just started and they're psychotic and you had to start an antipsychotic on an inpatient unit and that QTC went up by more than 60. Then I would consult cardiology. If your patient is having symptoms, then that's immediate cardiology consultation and that's go to the ER. 911 is the best way to do that. Okay, I'm gonna be mindful of our time. So I wanna tell you a few things about pacemakers and defibrillators and how they fit into this. So let's use another case. So this is a 44 year old gentleman. He has a family history of cardiac arrest and his grandfather, his father and his paternal aunt, he tests positively for a genetic cardiomyopathy with a high risk for sudden cardiac death. He's never had any arrhythmias or cardiac symptoms himself but for primary prevention, they implant him a subcutaneous implantable cardioverter defibrillator. His past history is notable for hyperlipidemia, recurrent sinus infections, depression. He takes simvastatin, escitalopram and frequently is prescribed Z-Pak, azithromycin by his PCP. So he develops a viral GI illness. He has a lot of vomiting, diarrhea, can't keep anything down. So comes into the ED, he's dehydrated. They get an EKG and his QTC Hodges is 522 and potassium is 2.7. So the ED resident orders some Zofran on dancetron for nausea, which we know is QT prolonging. And the other ED resident questions this decision and says, well, you know, shouldn't we worry about this? And the first resident says, don't worry about it. He has an ICD. So this is a question that comes up too is do we even need to worry about this at all if someone has an ICD that could shock them out of torsades? So should they worry? No? Yes? Or I'm not sure. I love how fast the responses are coming in. keep them coming. I'm not gonna show you till the end. Keep the suspense going. So should they worry about it? Okay, all right, this is good. So some no's, a lot of yes's, and a few I'm not sure's, which is okay. Okay not to be sure. So what I would say in this case is yes, you should worry. I'm gonna tell you why you should worry. Let's talk about what an ICD does. So an ICD is going to use a high voltage shock to shock you out of a ventricular tachycardia. Sometimes it does that with what's called anti-tachycardia pacing, which is a bunch of slow, not shocks per se, but like high firing pacing to help get someone out of it, which is not as uncomfortable as a shock itself. People will get ICDs for primary prevention, meaning they've never had a cardiac arrest or an event, but they have some sort of cardiac thing that increases their risk, and you can see all of these here. Congenital long QT is one of those, and then you have secondary prevention, and that is if you've already had a cardiac arrest or let's say you've had sustained VT and it was difficult to get you out of it. You had to be cardioverted. Let's say it happened in an ambulance somewhere. You know, they had to shock you in the ambulance. I hear this story a lot. Or you had VT and you just hemodynamically weren't able to tolerate it. So this patient, he has a primary prevention ICD. This is what it looks like. There are two different types. The kind of older version is the model that you see on the right, where it's implanted right under the clavicle. There's a newer model. It's called a subcutaneous ICD, and it's actually placed right under the skin, kind of a little bit lower than the armpit. It's actually a terrible location for women. I hear like women have a lot of trouble with like wearing a bra and just like navigating with that thing right there, but it actually has a much lower risk of delivering shocks that are inappropriate. It's easier to change battery. You don't actually have to like go in and do this major surgery to change a battery out. So these are the two different types of ICDs. If you ever have no idea, but you think there's something in the chest, look at a chest x-ray, and that will tell you what you're dealing with. The clue is that if you see these radio-opaque coils that are really thick, that is the part that delivers the shock. And so that will tell you, okay, this is probably an ICD. And ICDs are bigger than pacemakers. So ICDs can terminate a VT event, but we know that when you get shocked, it's actually not good for your heart, and it actually increases your risk of mortality and morbidity if you get shocked by your ICD. And oftentimes, you'll continue to get shocked. Your VT will recur unless you change the clinical substrate of whatever's going on. So then what can happen is this thing called ICD storm, where you may get multiple ICD shocks in a day. A storm is three shocks or more in a day, and this is what that would look like on telemetry. So this would be the shock. People describe ICD shocks as the classic as being kicked in the chest by a horse. Horses are like a thousand pounds typically. They're huge. So they're very scary, getting shocked by an ICD, and can lead to a lot of psychiatric morbidity. And these are the patients I mostly see in my practice. They've suffered a shock and then have PTSD from that shock. So there is a lot of morbidity that goes along with it. And so, you know, we really can't be cavalier about, you know, what we're doing or not trying to mitigate risk just because someone has an ICD. You actually do want to be really careful and not do something that's going to increase that risk. Now pacemakers, and I should mention too, all ICDs are pacemakers, so they can pace. Pacemakers are different. They will not shock you out of a rhythm. These are implanted to treat bradyarrhythmias. So basically, if your heart rate is getting so low that you can't maintain daily function or daily activity, you may be implanted with a permanent pacemaker. And basically what happens is it will drop below the pacing threshold. If your heart rate drops below the pacing threshold of 30 to 40 beats per minute, typically it'll start pacing. This is what pacing looks like on an EKG. So this EKG actually has both types of pacing. So this is atrial pacing right here. This is ventricular pacing right here. And with ventricular pacing, you have this widened QRS complex. It's a little tough to see here, but these are the two things that you'll typically see. Now often your pacing spike is going to be teeny and not tall, but you'll definitely see this wide QRS complex there. There they are. So let's talk about how this plays into what we're doing with QTC. Because we talked about at the beginning, when you have a wide QRS and you have this widened depolarization, it's going to prolong your QT interval, right? But sometimes there's no effect on repolarization. So what do you do? This is for those of you who answered like intermediate. This is advanced. So if you're feeling like, I don't know about this, it's okay. So this is a diagram of kind of thinking back to electrophysiologically what's happening in the heart when you have a pacemaker. So in this panel on the left, this would be your ventricular pacemaker. This is where it's implanted. And instead of having that rapid firing through that yellow conduction system, now you're going to have cell-to-cell conduction, which is much slower. And that's why your QRS is going to get wider. It just takes longer for that signal to travel from where that lead is implanted, okay? It's similar for a bundle branch block. So literally a bundle branch block is you may have one branch where that rapid fire conduction system isn't happening. So either left or right, same thing. You get this wide QRS complex. We have to do something about that, okay? So here's normal. This is wide. This is a little pacing spike. So this might be what you see if you have someone who's being paced. And we know, like if we look at the QT here versus here, it's much longer here in the paced patient. But that JT interval, it's the same. So remember that when you have someone who's paced and you have that widened QRS, that is not actually going to perturb repolarization. So that widening of the QRS from a pacemaker or bundle branch block is not increasing your risk of torsades. We're going to skip this case. I do want to show you how to approach this. Here's an EKG of someone with prolonged QTC. Okay, so you can see here QTC is 506. Person has AFib, no P waves, irregular, regularly irregular. And they've got a wide QRS complex. Now this patient is not being paced, but they do have a bundle branch block. And that is this where it says intraventricular conduction defect. That's what that is. 144 milliseconds QRS. Remember normal is 80 to 100. So very likely this QT is long because this QRS is long. This QRS represents depolarization. That's not what we're worried about when we're thinking about QTC, which is repolarization. So what do we do? Let's zoom in on this person's EKG. We're going to do some measurements. So we're going to find the beginning of the QRS, end of the T wave. We're also going to measure the QRS complex itself. And if we zoom in, so QT interval, this is what we're measuring. I want you to take a look at that. You're going to get a question. What is the QT interval here? Get it in your mind, out your boxes. 290, 480, 540, 600. Good. Yes, so I see mostly 540, some in the 480s, perfect. So 540 is our answer, so that's your QT. We measure a QRS 130, so that's definitely wide. So wide QRS, no perturbation of repolarization here. So how do we correct for wide QRS? We're gonna talk about this and then we're gonna go to questions. So, first thing you do is you want to look at your measurements. Okay, and if your QRS complex is greater than or equal to 110, then you're gonna go down this yes pathway where you're gonna correct for your wide QRS. You can do that in one of two ways. There are many ways to do this. These are the two that I like, and I'm gonna tell you that the JT interval I think is the best. There's another method called the Bogossian where you adjust your QT interval, but I like JT, it's very simple and you've already seen how to measure that. So we're gonna measure the JT instead of the QT. We're still gonna correct it with a heart rate correction formula, Hodges or Fredricia or Framingham, any of those, just not Bizette, Bizette is bad. And we're gonna remember here that QTC 500 is where our cutoff is. Now this is an important set of numbers to remember. For JTC, in men upper limit of normal is around 355 and women it's 372. And these are on the slides that are available. 355, 372, so that would be the cutoff I would use for the JTC. So here's this EKG we were just looking at. So yes, definitely 130. We're gonna come down here. We're going to do a JT. So what's the JT? It's 540 minus 130, 410 milliseconds. We're gonna correct. You can do that with either of these. 470 QTC corrected or 405 JTC corrected. So that QTC is okay. The JTC is a little, I'm not sure about that. It's still a little bit long. So even when we take that wide QRS out of it, it's a little bit long. Now this patient has AFib. And in AFib, we actually have to get in there and measure a few different sections of the EKG and average them out. You're gonna try to find the shortest, longest cycle and then a medium in between. And you're gonna go in there. Typically you would use the QTC and average those. For this patient that has a wide QRS, you're gonna use the JTC. But you're gonna take an average. And I'm gonna, these are all in the slides and handouts. You can look through this. But I wanted to show you that. And we're gonna skip this part. Okay, so thinking about risk. And then we'll end in mitigating risk and things we've talked about today. So first of all, get comfortable measuring your QTC. Okay, measure your QT interval, get comfortable with the formulas. Don't use Bizette, Bizette is bad. You're all gonna know that now. Practice, practice. Even on EKGs that you're not worried about, just practice and ask questions of cardiologists if you have access to one or to an internist, anyone that may know a little bit more about this. Just get in the habit of looking at them because the more you look at them, the more you will really feel comfortable. Think about what are the other risk factors. Think about what other medications are being prescribed. Get other experts involved when you need to. And especially if there's things that you can mitigate risk-wise, do that if you can. So Bizette is bad. No absolute cutoff. 500 is a nice place to think about, but it's not an absolute. Risk-benefit analysis for everybody. Practice, practice. You can always email me if you have questions and I wanna open it up now for questions for the group. You've been a great audience. Thank you for your participation. Thank you. Oh, yeah, do you wanna field up here? Yeah, perfect. Okay, so we are gonna have some, everybody who has questions line up. I know that we're closer towards the end of the session, but we still have about 10 minutes to get through some questions. So while folks are lining up, I do wanna kind of prioritize because there was a common thread that I think is probably actually fairly common that's coming in in the online questions, and that's folks asking about psychostimulants and considerations for cardiac risk and QTC prolongation and that classification. Yeah. You guys hear me? So the question is about stimulants. So I think in stimulants, the main thing that we are concerned about is one, tachycardia and increased blood pressure. So, how about now? Yes, okay, great. So with stimulants, oh, yeah. So with stimulants, we are worried about blood pressure, we're worried about tachycardia, and I think the biggest thing that we wanna rule out is that there's not an underlying cardiac defect in a patient. So kids with stimulants, an EKG is not a requirement. Kind of similar to methadone, there's a similar argument that you don't want to preclude prescription of a stimulant to a kid if they're in a resource-poor area that doesn't have access to an EKG. And so it is not a must that you do that in a kid. In an adult, however, above 40, it is really best practice to get an EKG. And so what you're looking for would be primarily a conduction abnormality. And what that means is that wide QRS that you would see with pacing or with a bundle branch block, you're looking for things like a bundle branch block. You also want to make sure that no one has ever had an MI or heart failure. You're not gonna wanna prescribe in those situations. But the primary thing is the conduction disturbance and it's that depolarization part of the ECG. So that's what I am looking at when dealing with psychostimulants. Thank you. I'm happy to add more if there are more questions. That's good, that's excellent. So I think we'll start with questions and just a reminder with questions, if they can be fairly concise to one-minute answers or so. That was actually gonna be my question. Asking about stimulants, I guess the black box warning and the risk of sudden cardiac death, like what would that look like? And also for alpha agonist, is that kind of similar? And is it just normal EKG? I don't even know what I'm looking at when I see an EKG. I do work with kids, but what would an abnormal EKG look like? Yeah, so first part of the question with the black box warning, and I guess it sounds like just what are you looking for? Not know, yeah. So I think in, so kids is a whole nother layer here. And I think if you're seeing something come up, frankly in kids, I would use, you're not gonna repeat this, but I would use the top computer read as like my first thing because kids, their EKGs are different than adult EKGs. So if you're seeing a conduction abnormality come up in a kid, or I would say if you're seeing a long QT actually come up in a kid, it's possible that there could be, like there could be a family history of a cardiomyopathy that confers cardiac risk. So I think you can use the same framework you would do for an adult, but I guess have higher vigilance if something abnormal is standing out, and then I would have a lower threshold to send to cardiology. I know that's not the greatest answer for you. Kids are very different and they're tough. If you're seeing symptoms in kids, that may be the thing to get the EKG or to prompt that, and then a referral to cardiology. And symptoms would be things like the lightheadedness or a presyncopal. Anything that is like dropping to the ground in a kid, that's where I would be referring to cardiology. Thank you so much. That was such a fantastic talk and it made me wish I had covered in my residency. So my question was on if the, you have a UTC that you think is legitimately elevated above 500. Can you correlate that with TORSAD's risk? Like if it is over 500, what is the risk of TORSAD's? So I think our data is not good enough to know. Where I think the data is better actually is actually looking at the morphology of your T-wave. I think that's where the money's at, honestly. Let's say you are at 505 QTC, but that T-wave looks okay. It's like one pump, it ends abruptly versus one of these ones that just goes way, way out. And you may have seen these and you can't tell where it ends that maybe even looks like it goes into the P-wave. That's where I am most concerned. So I would actually put my money more on when you see T-waves that look weird, that's where your risk is gonna be, yeah. I'll spare you the clinical vignette. A lot of my patients are on meds that have desmethyl metabolites and the issue of the parent compound on the desmethyl metabolite fluctuates depending on what other agent or what other drugs they're on. Is there a differential risk for QT prolongation from omepramine versus desmethyl, comipramine, clozapine versus desmethyl, clozapine? No data. Yeah, I wish there was. There's just not. I think for situations like that, the closest data we have would actually be HERG channel binding affinity data that would be done in animal models. So you could look at that if that data exists. But in people, clinically, there's no data there. Yeah, you can try it at home, yeah. Morning, thank you so much. The FDA recently put a warning on Lamictal for conduction abnormalities. And I've seen a registry study that challenges that, sort of like citalopram, right? Yeah. Do you have any comments on Lamictal since we use that so frequently? Yeah, yeah. So, I mean, it should be no surprise that Lamictal is associated with conduction abnormalities because it's a sodium channel blocker. And many of those anticonvulsants are sodium channel blockers so that's what they do. Remember, that sodium influx, if you block that, you're gonna have delayed conduction. So I think you should always have vigilance when using any sodium channel blocker in someone that already has a conduction abnormality. But I almost feel like it's like, this is nothing new that, like if you knew how your ion channels worked and what was happening with the drug, you knew this anyway. So I think it's very similar to citalopram situation, yeah. But it seems like the data's challenging. Clinically, is there any real significance to that? Because in this large Danish study, couldn't find any signal of actual cardiac events, but do you have any comments on that? Can you say the- I don't know if you have any comments on that piece. Sort of real world risk versus sort of studies or whatever. Yeah, I mean, I think with, when FDA comes out with these communications, it then takes years for studies to come out, and oftentimes we learn something very different than the original communication. I would say, you know, just use your best clinical judgment, and, you know, this is not a one-size-fits-all. Everybody has a different set of risk factors. This is a one-case situation. I had a patient who had a history of being on clozapine, and she had been sent from one hospital to another because she had some shortness of breath. And at the other hospital, she'd been found to have a QTC of greater than 600, which normalized in the 400s after she was discontinued from the medication. So it's come up in, you know, when I'm working with the internists on my unit, like another case came up, and she said, you know, the clozapine doesn't affect the QT interval. So I know that that's not frequently monitored. Is that true, or as far as clozapine goes? And it was such a pronounced difference, and the other symptoms were less pronounced. The other, like the echo wasn't so bad, and I think the CKs went up, but. Yeah, so the first thing that I think of in this situation is what else, were there other things going on, and was that 600 a real QTC? So I may literally do go back to one, is this from the machine, or did someone actually like measure it and calculate it? Oftentimes there's a huge difference. Two, did that person happen to be hypokalemic at the time, which might give you a U wave that gets pulled into your T wave and your QT interval? The hypokalemia could prolong your QT. So there are a lot of things that could prolong it that are not the medication itself, and so I'm always like going through that list in my mind, too, of like, is this real? That might be like last take home, or another take home, like is this real? And that's where like understanding what's happening in electrophysiology. Okay, that was the only thing that was changed, was the clinical. And I think in someone like that, it probably is worth a cardiology consultation. She went to card service, I think. Yeah, and I would advocate for genetic testing in someone like that, where if you start a medication that isn't really known to be high risk, and then you're seeing this sudden shift of QT prolongation, there could be a congenital factor going on, and there are now like panels that you can get that have many of these different cardiomyopathies that confer risk for sudden cardiac death. They're cheap and easy, and that's kind of becoming a routine part of cardiology practice now. So I think that's something that could be considered, too. Like, is there something underlying in that patient? Yeah, that's helpful, thank you. Yeah, of course. And unfortunately, we are at noon, so I will formally stop us there. But just wanted to thank Dr. Funk one more time for everything. I'm happy to answer any questions. Are we kicked out of the room? We're not kicked out, so you can informally answer questions. Session is dismissed. Do I come up to the table, or do I still use the mic? Keep going. Do I come up to the table? Okay. This is a two-parter, but I'll make it fast. Thinking about our acutely medically ill patients who are admitted to the medical hospital, and maybe are on a bunch of QTZ prolonging stuff, like let's throw in an anti-emetic. Let's say Triazidone and Zoloft, because why not? Let's say two anti-cancer meds. Let's put it all together. And also some opioids. The first part of the question is, we know it seems like that there's some dose-dependent effect on the QTC. Do we also know, is there evidence that there's an additive effect if there's multiple medications? Yes. The second part of that question is, do we know if we get more bang for our buck by decreasing the dose of ones that are maybe higher risk versus trying to eliminate the total amount of QTC prolonging meds? That's a really good question. I think it may depend on the specific medications and what we know about dose relationship with the effect. Some, there's a known effect, and some it's more equivocal. Okay. I think I would say, if you can substitute one of those meds with something else safer, I'd probably go that route. Okay. Before I went with decreasing dose. Makes sense. But I think do what you can. Like the additive effect might be stronger overall as far as like HERG inhibition? Yeah, yeah. Okay, thank you so much. Thank you for the great talk. Hello, I work in a methadone clinic doing psychiatric medications. And we're really, really low resource. And right now what we do is the EKG right before usually, and then we don't test again for one or two years after. We're in the middle of changing all of our policies. Would you recommend basically me fighting to say, should we get an EKG once we get like past like 150 milligrams of methadone or like time before that? Yeah. So the question is a low resource methadone clinic setting often is a baseline EKG, but then oftentimes not until one or two years later. And should you get one more frequently? I think depending on your resources, it may depend on what were the results of the baseline EKG. So if it looked fine and they have no risk factors at all, you're probably okay waiting. If you can get one, then I would certainly get a repeat once you're at the methadone dose that you think you're gonna be at. But if that's not available to you and the risk factors were low, I think it's okay. But if there are risk factors there, or if that first baseline- We have an EKG in the clinic. We just don't like to take the EKGs. Okay. I mean, if you have the machine- Advocate for it. I would get it. Yeah. That's what I'm trying to do. I would, I would. Hi. Hi. So, you know, the QT obviously looks at both depolarization and repolarization. We've focused almost entirely on repolarization. How important is depolarization? Because like tricyclics and overdose, sort of channel blockade, widens the QRS and that's what kills people. So, I mean, how much, you know, the fact that we get that number, and then I look at the QRS, and then, okay, the QRS, that looks normal. So, I think, oh, then I'm not as worried. Should I still be worried? Yeah. So, I think it depends on what you're worrying about. So, if you're thinking about risk of ventricular tachycardia, like torsades, it truly is the repolarization that you're concerned about. But you're totally right that when you have, you know, a sodium channel blocker, and so in a tricyclic, if you have overdose, you're gonna get this very wide QRS. You're gonna have major conduction abnormality. What I would say thinking about that part of a TCA is, let's say there are no risk factors for torsades, but you have this, you know, individual you want to start the TCA on, and you get the EKG, like if that QRS is already widened at baseline, then I wouldn't go a TCA route in that person. So, I guess you're worrying about different things. You're worried about the conduction, basically, like from your atria down into your ventricles, and that ventricular depolarization with your tricyclics versus with your QT prolongers. You're worried about post-refractory period. Everything is repolarizing, getting ready to do it again, and can a PVC come in and go bam, and then set you off into VT. So, just different things to worry about. Is there any kind of ratio that they've looked at with ST versus QRS? I mean, you know, what part, or how much we should be concerned about? So, I would break it down between QRS and JT. So, let's say you're on a tricyclic. Look at both. If your QRS is really wide, then okay, there's a conduction abnormality happening. Your JT may be fine, and so there may not be a repolarization abnormality, or vice versa. So, I think you can split it up that way. Yeah. Hi, thanks for a great talk. So, I'm a geriatric psychiatrist, so a lot of the EKGs that I get on patients, like it's an automatic, like abnormal EKG with a bunch of comments, and I just get very overwhelmed. Can you clarify your method of what we went over, of how to manually calculate the QTC? No, I know that that's kind of in normal EKGs. We also went over that you can do that in people that are paced. You said in AFib we should be doing a few averages. What are some other scenarios in which that method will work and are there scenarios we should be aware of where that method won't work, or it gets more complex? Yeah. I mean, the method will always work. I would look at the JT. I think a starting point, just identify your waves and your intervals, find your QRS complex, find where you think the T wave ends. That's where I would start. If it looks funny, if you can find the J point and just get the JT, that's gonna give you a lot of information. But the method is the same. Okay. So, you know. Even if there's things like, I don't know, it's just like, automates things like, oh, there was like a history of MI because of this, or like inversions of this, but it's still, okay. Yeah, so actually that brings up a great point. So you may see things like T wave inversions in some of your leads. Find a lead that looks like what you're comfortable measuring. Okay. Okay. So, when you see like different types, different looking T waves in different leads, that can also be a marker of risk because it means that repolarization is happening at different times in different parts of the heart, which is just kind of more chaotic substrate. And can you clarify, you said, you know, sometimes a good play, if you can't, you know, calculate the QTC at the JT interval will give you a lot of information. Can you clarify like what you can use that for, the JT interval? So JT, you can use it for anything, actually. I like to use it when I do have a PASTE patient who has that wide QRS complex. I think the thing that you have to think about with the JTC is that many, many physicians will not know what that is. And so they're like, what is this? And so in my documentation or communication, I do put a little note of like what is, what would be considered, you know, upper limit of normal JTC. But can that also be used as a predictor of risk of TDP? Okay. Yes. Okay. Absolutely. It's probably a better one than the QT. Okay. More specific for just repolarization. Yeah. Okay. Thank you. Hello. Thank you so much for this talk as well. My question is in regards to risk benefit, kind of a similar question to that somebody else has, but from a different angle. For somebody who is already on different agents that prolong QTC, you've got on the EKG, it's less than 500 and you still want to add on a psychotropic medication that would have risk of prolonging QTC. What are your overall, I guess, concern levels as far as like risk benefits? They're less than 500, but they're already on other agents, maybe multiple other agents that prolong QTC. Yeah. Yeah. So I think this is where you think, think back to that EKG is a visual map of what is happening in the heart. And so if it looks okay and they're on these multiple agents, you're probably fine and go forward. And if you need to add something else, add it, and then just check it again after you add it. I think as long as your duration of that QTC is okay and your T wave looks okay, yeah, then you're fine. Okay, thank you. I'm gonna take, we're gonna stop here, but I'm happy to take any other questions up front. Thank you all.

ECG

QT interval

torsades de pointes

psychotropic medications

psychiatry

QT prolongation

citalopram

SSRIs

SNRIs

risk assessment

cardiac risks

implanted devices

psychiatric medications