Wide Complex Tachycardia (WCT)

Drs Hagahmed and Traynor are joined by Jeff Reim, a former paramedic and current Physician Assistant in the cardiac electrophysiology department at the University of Pittsburgh Medical Center, to discuss the approach to patients presenting with a wide complex tachycardia. 

Transcript

WCT podcast

[00:00:00] Mohamed Hagahmed: Welcome everyone to EMS Practice Podcast and today we are having a very funfilled discussion with a new guest who is a very dear friend of mine. Obviously I have my co host Dr. Owen Traynor. Owen, how are you? How have you been?

[00:00:26] Owen Traynor: I'm doing well, thanks. I'm looking forward to this today. [00:00:29] Mohamed Hagahmed: Likewise, likewise.

[00:00:30] Mohamed Hagahmed: And if maybe our guest, Jeff, you can introduce yourself to the audience.

[00:00:33] Jeff Reim: Yeah hey, thanks for having me Mo and Owen. I'm glad to be here. My name is Jeff Reim. I am a physician assistant at UPMC Presbyterian, I work in cardiac electrophysiology, so, and I spent 10 years as a city ofPittsburgh paramedic, so I'll be able to hopefully bring a little bit of pre hospital knowledge and pre hospital application into our discussion today, too.

[00:00:55] Jeff Reim: So thanks for having me. Looking forward to it. Now, we're, like, really

[00:00:58] Mohamed Hagahmed: glad to have you here, Jeff. And honestly From back in the days when we weremedics I remember we had lots of interesting cardiology calls. Yeah. So we're gonna start with the case. Is that okay with all of you? Yeah, sounds good.

[00:01:07] Mohamed Hagahmed: Sounds great. Let's do it. Alright, this is a recent case. So this was a 76 year oldfemale that came in from a group home and the reason for the call was nausea. And the staff noticed, obviously during shift change, that she was also having some generalized weakness. So, oh, and if you don't mind just going over some of the things that you consider when you go to the scene and evaluate the patient, and what are you thinking about?

[00:01:31] Owen Traynor: Sure. One of the things with rapid heart rates is that we have an interesting way of categorizing them. We might look at wide versus narrow. Narrow complexes are going to be the ones that are likely supraventricular. The wide ones may be ventricular.

[00:01:48] Owen Traynor: So that's a important initial consideration. Another consideration is regular versus irregular. That's also helpful. But I think one of the earliest things is to ask, is this patient stable or are they unstable?

[00:02:02] Mohamed Hagahmed: So it is interesting you mentioned this because, you know, this patient absolutely had no cardiac symptoms, only nausea and weakness.

[00:02:10] Mohamed Hagahmed: So Jeff, can, can that actually. You know, be correct. Like in that, actually, can some patients just show with non cardiac symptoms?

[00:02:18] Jeff Reim: Yeah. I mean, especially in elderly population, women you know, in terms of arrhythmias MIs, things like that, that population seems to have the more atypical type of symptoms than what we'd you know, normally expect, you know, chest pain, palpitations, things like that.

[00:02:38] Jeff Reim: But the, the elderly females, diabetics those type of people seem to have more of these atypical symptoms like nausea or weakness.

[00:02:46] Mohamed Hagahmed: So what are some differential diagnoses then for somebody who is... 76 year old, a female, and also has nausea and weakness.

[00:02:55] Owen Traynor: Well, the differential is large for those people.

[00:02:58] Owen Traynor: Certainly at the top of it, I think about ischemic heart disease, cause I would hate to miss that. Regarding that, that's the one that's difficult or very bad to miss, but I would think about GI symptoms maybe this is intra abdominal. Some stroke patients will have nausea as a predominant symptom. I think I need more informationabout this patient to understand why they're feeling poorly.

[00:03:23] Owen Traynor: Okay,

[00:03:23] Mohamed Hagahmed: so the patient actually has a history of dementia. So most of the staff provided the history. So, Jeff, you approached the patient. Can you tell me, like, some of the things you want to be considering when... Looking at them or some information that you would like to know.

[00:03:36] Jeff Reim: Yeah, so I mean obviously with a patient with dementia it's going to be difficult to get a history from them.

[00:03:41] Jeff Reim: You may be able to coax out some of things that they're feeling right now in terms of are youhaving pain. Are you having this or that? They might be able to tell you those things, but in terms of historical types of information, medications, everything, you're going to have to get that from the staff and kind of piece together the story.

[00:03:59] Jeff Reim: And it definitely becomes more of a challenge. I think that in those cases relying on yourphysical exam in addition to, you know, whatever history you can piece together. I think your physical exam is something you're going to have to rely heavily on

too.

[00:04:13] Mohamed Hagahmed: Sounds good. So I will share with you what the staff tells you.

[00:04:15] Mohamed Hagahmed: So she has a history of hypertension, hyperlipidemia, hypothyroidism, also CADwith multiple stenting in the past. And now she is on Eliquis for history of AFib. She looks very weak. She looks Just like a disoriented, confused, she's

moving all of her extremities and then she just like moans every time you're trying to like get some more information from her.

[00:04:39] Mohamed Hagahmed: So what do you do, Owen, in terms of like in terms of pre hospital management for her?

[00:04:43] Owen Traynor: Well, I'm still thinking, is this a stable or unstable patient? Historically, we would look athypotension as something that indicates the patient is unstable. And typically, we'd diagnose it or say that it's a systolic pressure less than 90.

[00:04:57] Owen Traynor: However, in an elderly patient, there could be relative hypotension. She is 80 years old. We'd expect a blood pressure 160 to 180, so maybe 110 might even be considered. I would be looking at a change in hermental status. We know that she has dementia so that might be difficult, but if it's decreased I would think that could be unstable.

[00:05:19] Owen Traynor: I would be looking for any report of chest discomfort, because ischemia, causing Ischemicchest pain caused by the arrhythmia might be a problem. I would be looking for evidence of congestive heart failure or difficulty breathing. Perhaps you'd be tachypneic. And I think that would be how I'd get started.

[00:05:38] Owen Traynor: But I know that my early interventions are going to be putting people on the monitor.Getting IV access, giving supplemental oxygen, and perhaps a 12 dkg if they're stable. This is a

[00:05:49] Mohamed Hagahmed: very, I mean, this is like all nice considerations and nice list of differential that you both mentioned. So, I'll give you some vital signs.

[00:05:55] Mohamed Hagahmed: You ready? So, she is afebrile, heart rate is 120. She is hypertensive with blood pressure of 160 over 100. Breathing fine 18 to 20 around that and then oxygen saturation of around 94% of room air.So the next step you put on the monitor and you see this white complex, rhythm That is the monitor is telling you on the machine.

[00:06:18] Mohamed Hagahmed: It says VTAC.

[00:06:20] Jeff Reim: Okay So The first thing I would say is, just based on her vital signs doesn't appear to be overly unstable, meaning she's not hypotensive, she's oxygenating well, she's breathing at a normal rate, doesn't sound like it's too labored. So I think in this case, while, you know, it's definitely concerning that she has a wide complex tachycardia, I think we have a little bit, I don't want to say too much time, but a little bit more time to delve into the diagnostics of what, what is this rhythm, you know, rather than saying, she's, oh my gosh, she's circling the drain. We need to get her out of this rhythm immediately. We have a little bit more time to delve into some of the diagnostic tools that we can useto figure out what this actually

[00:07:06] Mohamed Hagahmed: is.

[00:07:07] Mohamed Hagahmed: And that is a very important point you're bringing up here, Jeff, because I feel likewhenever folks see this white complex rhythm, their immediate tendency to freak out, right. And kind of like. fumbleand do things that sometimes might not be the right things to do. So now we're going to be addressing the differential diagnoses for white complex tachycardia.

[00:07:26] Mohamed Hagahmed: So let's go over some of the potential possibilities. So Owen, maybe can you go over some of the differential diagnoses for white complex tachycardia? Well,

[00:07:34] Owen Traynor: I'm going to start off with, The prototypical one. Monomorphic. Vtac. Mm-hmm. , certainly that's what everybody's thinking about initially. I would also put in there an A S V T with a barren conduction,perhaps, perhaps atrial fibrillation with W P W would be on my list.

[00:07:53] Owen Traynor: Those would be early things to think about. I worry about hyperkalemia in. Renal failurepatients causing Y complex tachycardia. Good point. And then of course there's the polymorphic VTAC or torsades that I'd worry about as well. So I think that would get us started. And if we go down the list a little bit further, we might find toxic things, tricyclics or bucephal overdoses could be an issue for us.

[00:08:19] Owen Traynor: So that's how I'd be thinking in the beginning

[00:08:22] Mohamed Hagahmed: anyway. Well, in this case and we'll show also an example of the rhythm on theshow outline here, but the patient has a regular wide complex tachycardia and, you know, Owen, you mentioned monomorphic ventricular tachycardia.

What is the classic heart rate range for that, Jeff?

[00:08:40] Jeff Reim: For I'm sorry, for monomorphic VT, generally you'd see it A little, hers was 120 if I yeah, generally you see it maybe a little faster than that. You know, these people generally have a heart rate north of 130. Youknow, that's not to say you can't have it at 120. That's like saying you can't have sinus attack at 190.

[00:09:01] Jeff Reim: Well, you both, you and I both know if you go run, sprint up a hill for a half hour, your heart It's gonna be 200, but it'll be sinus tac. You know, so you can't really go hard on rates, but generally speaking, more than130. You know, if I could add something from my field that I'm in now is patients that have had VTAC ablations in the past generally tend to have slower VT once they, if they were to have recurrence because we create lesions that...

[00:09:29] Jeff Reim: You know, at the time may take care of the VTAC, but if they were to develop it now, the re entry circuit has to travel around in a larger area. And it takes more time for that re entrant circuit to complete onecircuit, so your VT is going to be slower. And let's like,

[00:09:46] Mohamed Hagahmed: you know... Clarify this more when you say create lesions.

[00:09:49] Mohamed Hagahmed: What does that mean creating

[00:09:50] Jeff Reim: scar tissue? Yes, so in VTAC ablations normally we use radiofrequency and it actually cauterizes the tissue we want to kill the cells essentially and You know if it basically make it impossible for any type of electricalaction potential to travel through those

[00:10:09] Mohamed Hagahmed: cells So what you're saying is that these patients after ablation?

[00:10:14] Mohamed Hagahmed: They normally present with VTAC with a slower

[00:10:17] Jeff Reim: rate. Correct. If, if, hopefully they don't present with VTAC at all, but if they were to have recurrence and if, and if it was from the same focus or the same general vicinity that we ablated then sometimes yes,their VT will be at a slower rate than what you'd normally think of for traditional VT.

[00:10:36] Mohamed Hagahmed: And we'll talk about the management here shortly, Jeff, because you bring a lot of interesting points, but, you know, Owen mentioned SVT with aberrant conduction and VTAC. Just from your perception, which one is more serious?

[00:10:49] Jeff Reim: Oh, which one is more serious? VT is definitely more serious. It's, you know, while it's possible, especially in a frail elderly type of patient with multiple comorbidities, in general, atrial arrhythmias, don't produce the level of instability that a ventricular arrhythmia would.

[00:11:09] Jeff Reim: So, you know, we're talking about AFib RVR, AFlutter, SVT ATAC, those aren't gonna normallycreate instability, I mean, unless they're left untreated for a long period of time. But VT, quite often we see it that, They deteriorate rather quickly upon, you know, initiation of that rhythm.

[00:11:28] Mohamed Hagahmed: So back to the patients, Owen, this patient is considered stable.

[00:11:34] Mohamed Hagahmed: Right. Yeah. And they're still weak. They're nauseated. Now they had one episode ofnon blood and non bileous emesis. So what will be your next steps and what will be your strategy, whether either to stay and kind of like do some more things or load and go?

[00:11:49] Owen Traynor: Well, since they're relatively stable, I would do a 12 80 kg.

[00:11:53] Owen Traynor: One of the things that can cause this would be an acute MI, and MIs in elderly people sometimes present with nausea. So I'd be interested in that, and that maybe could point us towards what the rhythm might actually be having 12 leads to look at rather than a single monitoring lead. Right. I was wondering, Jeff, too I didn't put on my list of things, but what would happen if somebody has a pacemaker, can they have some rhythm that looks like VTAC or even VTAC from it?

[00:12:22] Owen Traynor: Yeah,

[00:12:23] Jeff Reim: so there's a phenomenon called pacemaker mediated tachycardia. And without getting into too much of the nitty gritty or the academic part of it it's, it's when beats are not sensed appropriately, and it will cause the pacemaker to basically not detect that they're in a fib or a flutter, so it's tracking every P wave, P wave or flutter wave in the atria and pacing thing.

[00:12:54] Jeff Reim: One to one with those rather than switching the mode saying okay the atrial rate's too fast I'm not gonna pace for every a beat. I see that's ridiculous I'm not gonna pay some 180 beats a minute but sometimes it does if it's under sensing and so you can get a wide complex tachycardia and sometimes even when it's paced like that.

[00:13:12] Jeff Reim: When it's that fast, it's hard, it can be hard to see the pacer spikes at times. So it can fool youinto thinking it's a VT, but in reality it's a, it's PMT or pacemaker mediated tachycardia. Thanks. And

[00:13:24] Mohamed Hagahmed: you know what, this is actually a great even segue because... Some medics asked me some basic questions about pacemakers.

[00:13:31] Mohamed Hagahmed: What is the actual point of a pacemaker? Why do we insert it? Yeah,

[00:13:34] Jeff Reim: so, well there's a couple different types of pacemakers. There's, first of all, there's single chamber pacemakers, meaning they have one wire that goes into the right ventricle. We have dual chamber pacemakers, where we have two wires that one is in the atria, one is in the ventricle.

[00:13:52] Jeff Reim: And then we have the more, the most advanced type of pacemakers, which are called CRT devices, or cardiac resynchronization therapy devices, and that you will have three leads. You'll have an atrial lead,you'll have an RV lead, right ventricular lead, and an LV lead. So it really depends on what your problem is.

[00:14:09] Jeff Reim: So patients with, in general, a pacemaker is designed to keep your heart rate above a certain level, and we call that the lower rate limit. However. So we sometimes place pacemakers in patients that don't have bradycardic problems and that's where the CRT devices, the cardiac resynchronization therapy devices come into play.

[00:14:27] Jeff Reim: These people, these people aren't pacemaker dependent in the traditional sense, meaning they don't need it to maintain a rate. However, they have cardiomyopathy, they have a decreased EF and they have an underlying wide complex, meaning they have a bundle branch block where they're... Now their ventricles are beating asynchronously.

[00:14:49] Jeff Reim: You can imagine if you have a left bundle branch block that the RV is going to depolarize before the LV. In turn, that's going to create an RV contraction. before the LV contraction and what happens there is the RV will push the septum into the left

ventricular outflow tract and block the outflow tract when the LV tries to contract and that's going to worsen their heart failure.

[00:15:10] Jeff Reim: So with a CRT we have them pace in the ventricle with both leads a lead in both ventricles and the idea is that you're going to get two ventricles, to contract at exactly the same time to mimic a normal heartbeat as if they didn't have the bundle branch block. That makes a lot of

[00:15:27] Mohamed Hagahmed: sense. And I mean the basics obviously of a pacemaker is to allow the heart to beat at a certain rate.

[00:15:32] Mohamed Hagahmed: Right. Exactly. Without dropping, you know, like as a at a very low rate and causing haemodynamics instability. Sure. So in this patient is haemodynamically stable, Owen. What would be your initial therapeutic management?

[00:15:45] Owen Traynor: Well, if I were suspicious that this was related to hyperkalemia, I would give calcium.

[00:15:52] Owen Traynor: I think if I'm wrong, it's not going to be harmful. I wouldn't do it if I didn't think there was a likelihood of it. But if I did, calcium would be the first intervention because that'll stabilize the membrane potentials and buy me 20 minutes to figure out what I'm going to do next. But in general, it'll be an anti arrhythmic agent.

[00:16:10] Owen Traynor: And for EMS, the two... Most commonly employed are lidocaine

[00:16:15] Mohamed Hagahmed: and amiodarone. So, amio or lidocaine. Do you, is there any again side effects orpreference when it comes to the literature? Is there any medication that works better than the other?

[00:16:29] Jeff Reim: They're pretty, they're pretty efficacious, both of them, on an equal playing field.

[00:16:34] Jeff Reim: You know, generally if we feel that it's truly VTAC we load them with AMO first. And usually, you know, the first thing is 150 over 10 minutes, followed by an infusion for the next 24 hours to get them up to about 5 or 6 grams. And then we would...

Reassess whether they need it or by that point, you know, they're in the hospital.

[00:16:58] Jeff Reim: We would discuss Okay, was this VT provoked by an ischemic event? Is this purely an electrical problem? What are we gonna do about the underlying thing?

Amio, good choice first you can always switch to the lidocaine if they develop hemodynamic instability on the amio, because that's also a possibility.

[00:17:17] Jeff Reim: You have to remember amiodarone has a lot of different properties, right? It's beta blocker, calcium channel blockade, it has a lot of things, so the potential for them to have a blood pressure that drops once youstart the amio infusion is a, you know, that is real. So you just need to monitor that.

[00:17:33] Jeff Reim: That could happen. And in which case you would stop the amiodarone and you could switch to lidocaine. So

[00:17:38] Mohamed Hagahmed: amio, as you were mentioned, has the likelihood of causing hypotension. Right. So let's say the patient was started, was given oh, and you gave 150 milligram of Ebola's amio. Repeat vital signs show ablood pressure now of 90 over 60.

[00:17:54] Mohamed Hagahmed: Heart rate went up to about 140 and the patient is still not looking too good.

[00:17:59] Owen Traynor: So your choice at this point is to Recalculate the stability of the patient. Certainly, they would fall into the unstable category. So you could prepare to do synchronized cardioversion. If you're not quite ready for that, you could try a fluid bolus as well, but I wouldn't give any more amiodarone.

[00:18:20] Owen Traynor: That would be probably

[00:18:21] Mohamed Hagahmed: wise. Yeah. Yeah. That's a wise decision. So you gave, or the medics in this case which I believe they did a great job actually, they gave 500 CC of IV bolus and they were already in a truck by then. They had a little bit of backup crew. So they had an extra person that was a district chief there and the patient was stillhypotensive despite the fluid bolus.

[00:18:42] Mohamed Hagahmed: Now, What would you do, Jeff? Same [00:18:44] Jeff Reim: rhythm. The rhythm hasn't

[00:18:45] Mohamed Hagahmed: changed. Same rhythm. Did not change. Hypotensive.

[00:18:48] Jeff Reim: Yeah. And we did a 12 lead, right? And we've established this is probably monomorphic V tach.There's nothing to suggest that this is a sinus tachycardia or something else. Okay. Correct. Yeah. I mean, at this point, you've, you've really given her every opportunity to not get shocked at this point, I think, right?

[00:19:07] Jeff Reim: I mean, you've... You've given amiodarone, you've given a fluid bolus to bring the pressure back up to hopefully avoid having a cardioverter. I think that in this patient, you know, if their blood pressure seems to beheading the wrong way. And especially in someone with VT, if the blood pressure starts heading the wrong way, it could be a matter of minutes before they go into cardiac arrest.

[00:19:28] Jeff Reim: You know, you can't, you're not going to be able to maintain that rhythm very long. So, I mean, Ithink cardioverting, if that's what happened here was, you know, would be a completely reasonable option.

[00:19:38] Mohamed Hagahmed: So, the medic decided to do exactly that and cardiovert the patient. Owen, myquestion to you now, I know with cardioversion, Some people consider certain things to do certain things before that.

[00:19:49] Mohamed Hagahmed: Do you consider doing something else before cardioverting them? We just jump straight to electricity.

[00:19:55] Owen Traynor: Well I think it would be very painful to receive a cardioversion if you are not sedated. So I think that's a kind thing to do. I understand from many years ago when I was in paramedic school where some people had been cardioverted and had not been adequately sedated.

[00:20:16] Owen Traynor: and told the physician, don't ever do that to me again. So I would love to do some sedation for this patient. I know that the sedation may drop the blood pressure too. So it's always a dicey thing. But I think in this case, I have IV access that I would give sedation and I would cardiovert them quickly and then reassess promptly.

[00:20:44] Mohamed Hagahmed: So, Jeff, I personally like fentanyl. I feel like fentanyl is the mosthemodynamically stable agent. What do you think? I mean, do you have any other choices or agents? In

[00:20:51] Jeff Reim: the field, you're, you know, you're going to have fentanyl, Versed. I think those are fine. Youknow, obviously when we cardiovert people in the hospital, they get some propofol.

[00:20:59] Jeff Reim: But that's not an option, you know, for, for most EMS agencies. But, and going back to Owen's point, was that you know, in this case, you already have the IV, you know, it's not like you showed up and her pressurewas 60 and she was, you know, you needed a cardioverter, right? In that sense, I would say, forget the sedation.

[00:21:16] Jeff Reim: In this case, you know, it's been a gradual progression towards this. Cardioversion. And youhave the IV, give her a little sedation, even if it transiently drops the blood pressure from the fentanyl or the versed, you're going to fix the rhythm. You're going to? Exactly. So, once you fix the rhythm, the hypotension should take care of itself.

[00:21:34] Jeff Reim: Right. You would hope. I mean, that would be the case. And if it doesn't, you have the IV, give more fluids, you could start a presser if you need to, or whatever else needs to be done. So, I think

[00:21:43] Mohamed Hagahmed: that's fine. And in that case, they prepared for it for, for cardioversion, and there were, there were two paramedics there.

[00:21:51] Mohamed Hagahmed: So one was Owen in favor of starting at 100 joules. The other one, his name is Hagamid, in favor of starting at the maximal energy. What are your thoughts on that? Well,

[00:22:04] Owen Traynor: you know, ideally we do it at the lowest effective dose. Unfortunately, you won't know in advance unless you've seen this patient before.

[00:22:11] Owen Traynor: With the AFib patients, often we do know that. They know that 100 worked or 200 worked,and we can take advantage of that. I think if you look at the state protocols, you have to follow that. And ours say start at 100, but I don't think it's wrong to start at a higher dose if you think that's more likely to be effective.

[00:22:31] Owen Traynor: I don't know, Jeff, what do you see in the hospital? [00:22:33] Jeff Reim: Yeah, weshock people. I know Jeff is on my side, right? Yeah, it's,

well, a lot of it is dependent on who you're working with. Some of the EP docs just like to go to the 200 joule shocks. And that's because we have them adequately sedated. So if they're sedated adequately, you could go right to the 200 joules.

[00:22:53] Jeff Reim: I, there's no, there's no problem in doing that. Now if but you know, you're, you're bound bywhat the, you know, if you're by yourself, you're bound by what the protocol says. But in, in just in theory I think a higher joule shock is, is safe and effective, you know, and humane as long as they're sedated.

[00:23:13] Mohamed Hagahmed: I feel like, oh, for me, it's more humane if you shock the patient just once. Just once, yeah, and that's the other argument, right? More than multiple shots, I think that's like my argument

[00:23:20] Jeff Reim: for it. Yeah, would you rather have the band aid ripped right off or pulled off in little sections?

[00:23:25] Mohamed Hagahmed: That's [00:23:25] Owen Traynor: torture.Right.

[00:23:26] Owen Traynor: Well, the other people would say the 100's gonna work. Right. So, unfortunately, you don't know.

[00:23:33] Jeff Reim: You don't know. You don't know. So, I don't think there's any [00:23:35] Owen Traynor: wrong answer. Except not to shock.

[00:23:37] Jeff Reim: Right, exactly. I think if you're shocking someone, you're doing the right thing, regardless of the energy. You know.

[00:23:44] Jeff Reim: After that, it's you know, splitting

[00:23:45] Mohamed Hagahmed: hairs. And you made a great point too, Jeff. With adequate sedation, it's okay. Gohigher. Yes, they're going to become hypotensive if you give midazolam, but you're going to be fixing the underlying rhythm. And in this case, did indeed

fix it. So... You provided maximal joules maximal voltage and went back to a sinus rhythm and then it turned out for the conclusion for this case that the patient had ischemic cardiomyopathy with multi vessel you know, atherosclerosis and disease.

[00:24:14] Mohamed Hagahmed: Then they required, needed a cabbage. So, the patient did well ultimately and wasable to be discharged back to the facility. Some of the thoughts, I feel like, you know, that the crew could have done better when I gave them feedback is to consider sedation because that was not done in this case.

[00:24:30] Mohamed Hagahmed: They just provided the cardioversion, which I also hear their, you know, concerns because they thought the patient was unstable. Sure. So they wanted to move quickly and just cardiovert and stabilize.Sure. Any other, you know, pearls from this case, Owen?

[00:24:45] Owen Traynor: I was just thinking since we have Jeff here.

[00:24:48] Owen Traynor: And he's probably collected more cases of WPW than you or I. If he could talk about... That wide complex tachycardia that's irregular. And you might be thinking, I know WPW is something I read, like one in a million or so, or one in a hundred thousand. So in any place where you live, there is going to be a person or two will have this.

[00:25:12] Owen Traynor: So what do we do under those circumstances? We can certainly harm

[00:25:16] Jeff Reim: that patient. Sure, yeah, especially if they're in AFib with WPW. That's the rhythm that you have to be very careful with. Now there's, there's, there's three rhythms you can have in WPW. Well, two, there's two,but then the one rhythm has two sets.

[00:25:33] Jeff Reim: So there's SVT or AV. RT, AV nodal reciprocating tachycardia, and there's two types of that.There's orthodromic and antidromic. Orthodromic is when you have the impulse or the electrical signal going down through the AV node and follows the normal conduction through the ventricle, but then re enters the atria.

[00:25:54] Jeff Reim: through the bypass tract. So you get a narrow complex with that. The flip side of it is an SVT where it enters the ventricle through the bypass tract. And then you get a myocyte to myocyte kind of conduction through the ventricle and then it reenters the atria retrogradely through the AV node. So that would give you a wide complex.

[00:26:13] Jeff Reim: Those are the two SVTs. And then of course they can have a fib. And that's the dangerous rhythm. The other two you would treat. Just like any other SVT, if you give it adenosine, it's going to break the circuit at the AVnode. If you give it amiodarone, it'll break it at the AV node or the bypass track.

[00:26:29] Jeff Reim: But you know, the AFib is the one you have to be careful with. And if you'd like, I could get into why and what we should do. No, no, please. Because this is

[00:26:37] Mohamed Hagahmed: something that we should also consider. I mean, I'll be honest with youpersonally. I am most fearful about these cases because it's hard for me to tell whether this is actually...

[00:26:47] Mohamed Hagahmed: Some ventricular, like vtac or ABER seed. Right. And I tend to give them sometimes Right. Adenosine Yeah. Or amio. Right. Depending on how wide the rhythm is. Right. But I've run into the problems of causing worse hemodynamic instability. Sure. So tell me more. And the rhythm can speed up. Yeah. Can

[00:27:05] Jeff Reim: go even worse, right?

[00:27:07] Jeff Reim: Yeah. So the hallmark of AFib with pre-excitation or AFib with W P W is. Irregularly irregular,obviously, because we have AFib. And then you'll have, it, you'll have varying amounts of QRS width. So some of the QRSs may be more narrow, some of them will be really wide, and some of them will be in between.

[00:27:28] Jeff Reim: Now, the caveat is, this is not polymorphic VTAC in that the axis doesn't change. Meaning, in a single lead, you won't have some QRSs that are positive and some QRSs that are negative. Like, you have... In TORSAD or polymorphic VT, in AFibWVW the axis stays the same, however the width of the QRS will vary. And that's because some of these impulses from the atria are going through the bypass tract and you get a wide QRS.

[00:27:57] Jeff Reim: Some of them are going through the AV node and you get a narrow QRS. And some of them are going through both at the same time and you get a fusion of the two morphologies and you get, they're in between. Sothat's the hallmark. The other hallmark is that... It's extremely fast in some places, like in some places that, you know, the, the beats are only separated by one big box or 300 beats a minute.

[00:28:18] Jeff Reim: So if you have these varying widths, irregularly irregular, in some parts approaching 300beats a minute, I would say that you should call that AFib with pre excitation or AFib in the setting of WPW. And what, what

[00:28:32] Mohamed Hagahmed: agent are you going to be jumping?

[00:28:33] Jeff Reim: Yeah. So in the field, I think the safest thing to do in the field is to cardiovert them.

[00:28:39] Jeff Reim: That is the safest thing you can do. If you give them amiodarone, you're rolling the dice. Yes. Because amiodarone, as we know, part calcium channel, part beta blocker, it may block the accessory track, the bypasstrack. Or, it might, it'll block the AV node. Which one's it going to do first, though? You don't know.

[00:29:02] Jeff Reim: If it blocks that AV node first, it's, every impulse is going to be conducted through that bypass tract. And as we know, that bypass tract has no refractory period. It's happy to conduct every single atrial fibrillationimpulse you have. So now you're

going to have a ventricular beat, or a ventricular rate that's 300 to 600 times a minute, and by definition, that's v fib.

[00:29:22] Jeff Reim: Right? So, amy is a roll of the dice. And adenosine, if you know it's afib WPW, it's, you're goingto have the same phenomenon, right? You're going to block the AV node, and you're going to conduct through the bypass track. In the ED, you can pull out the percanamide which is nice, because that will block the bypass track only, and has no effect on the AV node, and also has antiarrhythmic effects in the atria.

[00:29:47] Jeff Reim: So you could also hope, you know, if the first effect you'll see is that you'll slow. The rhythm, it'll rate control it a little bit and then after a period of time, you'll see that hopefully they will actually Convert to sinus rhythm from the AFib with

[00:30:01] Mohamed Hagahmed: procainamide. And IV procainamide is an infusion just to be clear.

[00:30:05] Mohamed Hagahmed: Yeah, and Some of the most common side effects of IV procainamide ishypotension. Right. Which to me is like the dilemma, right? Because now if you become hypotensive, they're unstable, right? Right.

[00:30:15] Owen Traynor: Also widens the QRS. It [00:30:17] Jeff Reim: can widen the QRS, right.

[00:30:19] Mohamed Hagahmed: Exactly. I guess the ultimate, the ultimate will be [00:30:22] Owen Traynor: Well, I think that's the easiest thing.

[00:30:24] Owen Traynor: It's what we do all the time. I don't know the last time you used procainamide. When I was a medic in New York City in the 1980s, that was lidocaine and

[00:30:33] Jeff Reim: procainamide. Those were your

[00:30:34] Owen Traynor: anerythmics. But I don't remember how to do it. That would be a

[00:30:37] Jeff Reim: look up thing. Yeah, you know, if it's a younger patient, generally these WPWs tend to be a littlebit younger, at least in our experience, because it's, The onset of the symptoms usually occur adolescence, twenties but rare that you get to your middle ages, elderly, and have this pop up and you've never known about it.

[00:31:03] Jeff Reim: Not saying it doesn't happen, but, you know, generally the people that we treat with WPW or the younger population, you can be a little more... liberal with the percanum and maybe in them in the younger population.However, I think with AFib, WPW, your threshold to cardiovert the patient should be much lower than it would be with Another type of arrhythmia, let's say.

[00:31:25] Jeff Reim: Because it's honestly the safest thing to do. You cardiovert them, you should restore sinus rhythm, you should now see the short PR and the delta wave on your sinus rhythm, EKG, bam, you have your diagnosis. You get into giving some anti arrhythmics, now you're guessing, now you may speed up the rhythm, now you might get hypotensive, you know, you just have the Propensity to make them worse if we start playing with drugs with, with WPW and AFib.

[00:31:55] Jeff Reim: Now, now, now if you've got the, the regular narrow or right neck, regular wide complex tachycardia and you treat them with amiodarone or adenosine, that's fine. You know, that's great. You know, that, that'snot, you know, that's the right treatment if they're stable. But with the AFib, WPW, it gets tricky.

[00:32:12] Mohamed Hagahmed: So Owen, this might be a question for you, but I know some agencies do still carry varapamil.

[00:32:18] Mohamed Hagahmed: Which is another calcium channel blocker. Sure. They see AFib with R V R or they see AFib AFib on a monitor that a patient is having some symptoms, some chest pain, but otherwise hemodynamically stable from a vital signs standpoint. Is there a danger of giving verapamil?

[00:32:34] Owen Traynor: Well, the, since I practiced when verapamil was the only calcium channel blocker we had, I know how to use it, and I would always worry about hypotension as the chief thing.

[00:32:46] Owen Traynor: And when cartosomal diltiazem was new, you had an inexpensive drug and a newexpensive drug, and the expensive drug would be worth it if the pressure were low or soft. It would be worth spending the money. Now these drugs are not that expensive anymore. So the safer one probably is the cortisem or diltiazem.

[00:33:04] Owen Traynor: I would not use verapamil if I were worried about WPW and AFib. I think that's the sure way to death. Right.

[00:33:11] Jeff Reim: Same, same, same principle, right? You're going to block that AV node and they're going toconduct through the bypass track, you know, one to one and you're going to speed their rhythm up instead of help

[00:33:20] Mohamed Hagahmed: them.

[00:33:21] Mohamed Hagahmed: And just to be clear with terminology, when you say bypass track, that's the That's the accessory pathway. That's the accessory. Yeah, we, yeah, yeah, we use them. I don't want people to think bypass,meaning bypass surgery. No, no, no,

[00:33:29] Jeff Reim: no, no. I'm so sorry. Yeah, yeah, no. To clarify, yes. Bypass, meaning an electrical pathway that bypasses the AV node, so it is the accessory pathway.

[00:33:37] Jeff Reim: You could, you know, they're synonymous. You know, I'm just using the other term, but yes yeah, accessory pathway. Awesome. And

[00:33:43] Owen Traynor: what, what about the you mentioned the Delta wave. Can you just, just remind people what that is and where to look for it? Yeah, yeah.

[00:33:49] Jeff Reim: So, normally the Delta wave's gonna be most prominent on your sinus rhythm, e k g, in these people you know, some of the AFib W P w EKGs, you can see some slurring of the Q R Ss in the wider, in on some of the wider complexes.

[00:34:02] Jeff Reim: But in general the Delta wave is a. Slurring of the QRS right after the P wave. So you really have no PR interval. So you have a P wave and instead of that, you know, that flat Period of time before you have a sharp upstroke to the Q R s. You don't have that flat spot. You have a P wave and immediately you get this, just thissloping up into the Q r s.

[00:34:24] Jeff Reim: It's very gradual and it slightly widens the Q R s. You don't see it in every lead necessarily,depending on where the accessory pathway is. You know, not all wpw pathways exist in the same anatomical position, depending on where the. Bypass track or the accessory pathway is, you may see it in certain leads and not in others.

[00:34:45] Jeff Reim: But you're always gonna see a short PR interval. That's, that's actually the most diagnostic part. The most specific, yes. Okay. Yes. Yeah. The short, the PR interval's gonna be short. So what, what do you mean by short? Less than one 20. Less than 120 milliseconds or 0.12 seconds, you know? But, but it's not uncommon for it to be.

[00:35:03] Jeff Reim: Like 90 milliseconds and some of these people like extremely short So if you have a short PR and then you can make out some delta waves and some of the leads Then you have your diagnosis

[00:35:13] Mohamed Hagahmed: Do these patients when we take care of them in the ED and fix them and they go upstairs? Yeah, do they get discharged home with a certain medication?

[00:35:22] Mohamed Hagahmed: Yeah,

[00:35:22] Jeff Reim: generally they get sent home on a beta blocker You know solo presser. Yeah. Yeah, usually Usually we like topral You know, Mitope sucks and a little longer acting. And that's just to bridge them until they're Definitive treatment, which if they elect to, would be a WPW ablation, in which case we talked about VT ablation before, similar principle, we go in, we put catheters all throughout the heart, we use a mapping software and a mapping system to determine exactly where the accessory pathway is, and then we cauterize it.

[00:35:57] Jeff Reim: And that's usually curative, and the success rate of a WPW ablation is north of 95%. That is

[00:36:04] Mohamed Hagahmed: nice. Very cool. Yeah. That's nice. I mean, this is a really nice discussion, by the way. I know, Owen, we're going to make sure that there's some EKG

examples of everything that we just talked about. Yeah. And if you have, Jeff, any EKG cases...

[00:36:15] Mohamed Hagahmed: Actually, I have [00:36:16] Jeff Reim: some niceWPWs. Please, send them

[00:36:18] Mohamed Hagahmed: along. We're going to make sure that it's posted on the show document and outline there on the website as well. Yeah. Anything else, gentlemen, you'd like to add? I mean, this is great discussion. I feellike we hit a lot of pearls, but what are some of the things that you want to emphasize that you want to make sure that the audience can take home with?

[00:36:35] Jeff Reim: I think being able to get a 1280 kg of arrhythmias. It's very valuable. If you can. Now if you get there and the pressure is 50 and they're not breathing, shock them, please. Don't be hooking up with a 12 lead EKG. But, you know, the patients that are relatively stable, please get a 12 lead EKG, even if it's VT.

[00:36:55] Jeff Reim: It helps, it will help us quite a bit in electrophysiology. Because a 12 lead EKG is a great road map to knowing where the VT is originating. We could tell if it's, you know, RV outflow track, LV, apical, all kinds of stuff just by how the ventricular tachycardia is, the morphology of it and how the, you know, the transition of the R waves throughout the precordial leads, all that stuff is important to us, you know.

[00:37:21] Jeff Reim: So if you can document that in the field, that may be our only chance at at seeing this. Otherwise, we're going into an EP study blind. So if you can, as paramedics, if you can get that before that rhythm gets terminated, and that's, that may be the only 12 EDKG of their VT that exists, and you got it for them, and you've madeour life way easier in trying to ablate their VT if they elect to go that route.

[00:37:46] Owen Traynor: Absolutely. I was thinking too of Polymorphic VTAC. We didn't really talk about it today, and we know that's torsades, and if the patient's stable, we use magnesium as the treatment. If they're unstable, we use electricity as the treatment. Yeah. I also think once we've cardioverted someone, and we're grateful that they'veconverted, do the 12 lead EKG and look at that QT interval.

[00:38:09] Owen Traynor: Yep.

[00:38:09] Jeff Reim: Yeah, QT QT interval is the The main culprit in these patients that develop torsad could be hypomagnesia. It could be medications.

[00:38:19] Mohamed Hagahmed: Oh, yes. We have to talk about this because now we have some in our state, in our county, specifically also, we have certain agencies that can carry certain medications, including droperidol droperidol.

[00:38:30] Mohamed Hagahmed: And some, some of our folks even don't even know that sometimes. Yeah. AndDecitron, aka Zofran, has a QTC prolonging property as well, so just to be mindful of that.

[00:38:40] Jeff Reim: Especially in higher doses. You see these people that have had chemotherapy and they get 30mg of it at a pop. You know. Cancer patients. Yeah.

[00:38:50] Jeff Reim: That could be a thing. The other thing is methadone will do it. We actually had an interesting case not too long ago up at Presby where the patient had a torsod arrest. They came in, their QT interval was 600, and she was taking methadone. So it presented a challenge because we knew the treatment was to stop the methadone butwhat do you do with that patient, right?

[00:39:15] Jeff Reim: Because she's obviously recovering. She's doing very well. She had an agent that was working for her for her. So what do you do at that point? So it became a very challenging case. Easy case from an EP perspective, right? Stop the methadone. You know, you won't have Torsad again. But, but how are we gonna deal, how do they deal with the...

[00:39:35] Jeff Reim: The other end of it, right? Drugs that we use to treat patients who have AFib, sodalol, dofetilide.You might, you know, those are newer, especially dofetilide, newer. Newer, not real new, but in the last 10 15 years it's been more prominent. So you may see people that have A fib history that they're on defetilide and all of a sudden now their renal function is declining.

[00:39:58] Jeff Reim: Maybe they haven't been keeping up with their labs. They don't know that they're they don'tknow that they got lost to follow up. Now they're on the now they're on 500 mics of defetilide every day but their creatinine is 2 and they're having worsening renal failure. Now they're getting toxic on defetilide and their QT interval is long and boom, they get torsad.

[00:40:15] Jeff Reim: So lots of things to consider. And even

[00:40:18] Mohamed Hagahmed: some of these medications that are non cardiac related, Owen, that we take careof or that we administer in the hospital antibiotics, right? Can you name one antibiotics that sometimes we give to patients, most of the time with

[00:40:27] Owen Traynor: pneumonia? I would say everybody's favorite, Zithromycin.

[00:40:31] Mohamed Hagahmed: Zithromycin, right? Everybody with a viral illness that goes to an urgent care, and I'm sorry, no offense to all urgent cares out there, don't give a Zithromycin, right? Because... Most of these illnesses are likely viral illnesses. I think

[00:40:42] Owen Traynor: there are also many other choices too. So if it were the only choice, maybe you can take a little risk.

[00:40:48] Owen Traynor: But when there are other choices, you should take them. Yeah,

[00:40:51] Mohamed Hagahmed: absolutely. So just consider that. Consider the underlying culprit, the agent, always,you know. Look at the medication list. Yeah. To further interrogate this and find the cause and of course stop the cause. Sure. Great points. Anything else you want to

[00:41:06] Owen Traynor: add?

[00:41:07] Owen Traynor: Yes, I was thinking about cardioversion. Sometimes the rhythm will be hard for the machine to recognize the QRS and it might Find T waves. Right.

Shocking on the T wave. Yeah. Bad idea. Yeah. Shocking on the QRS. Yeah. During the absolute refractory period. Better idea.

[00:41:28] Jeff Reim: Yes. Yes. Yeah. Shocking on the T wave is a quick recipe for TORSAD or VF, V fib.

[00:41:36] Jeff Reim: So, yeah, it, it can be difficult, especially in some of these patients. Yeah. Where the T wavesare very prominent or the sometimes when the QRS complex is predominantly negative. Yeah. It is. And they get a, they get this huge discordant T wave. Sometimes the machine thinks it's, that can be tough. I mean, depending onthe monitor, it can be difficult to adjust for that.

[00:41:58] Jeff Reim: Unfortunately, sometimes you shock them, and you just got to shock them right again because they went into torsad or v fib. You know, usually all is okay if you, because you get them quick, but still, you know, beprepared for that. You know, if you're out there and you're going to cardiovert somebody, you know, be prepared to...

[00:42:13] Jeff Reim: You know, turn the dial all the way up and unsynchronized too, you know, because that, youknow, cardioversion is generally very safe. But, you know, you have to be ready for, you know, another arrhythmia to pop up when you introduce electricity into the myocardium like that.

[00:42:29] Mohamed Hagahmed: Absolutely, and when you see a tall peak T wave, immediately think hyper K.

[00:42:35] Mohamed Hagahmed: Yeah, [00:42:35] Jeff Reim:hyperkalemia. Then,

[00:42:37] Mohamed Hagahmed: like Owen said earlier, I'd give... You know, yeah. [00:42:40] Jeff Reim: Calcium first and foremost,

[00:42:42] Mohamed Hagahmed: yeah. And a fun pearl to everybody, so there is calcium chloride and calcium gluconate. Owen, the difference between the two for our audience?

[00:42:51] Owen Traynor: Well, I usually prefer the chloride because I'm old. It works very quickly and you get more calcium.

[00:42:59] Mohamed Hagahmed: So three to one is the ratio. So more, more calcium in the calcium chloride than calcium gluconate. However, the safety of calcium gluconate administration in somebody who has a 22 gauge in the right wrist, probably give calcium gluconate. Yeah. You gotta

[00:43:14] Jeff Reim: be a little more careful if it infiltrates.

[00:43:16] Jeff Reim: Exactly. It's corrosive of the muscles. Not a good idea. Not fun at all. But right. Yeah. But yeah. Chloride's all we had. But at least I had, I don't think they have gluconate in

[00:43:26] Mohamed Hagahmed: here at all. I don't think either. No, not anymore. But some people like in, like I say, in a facility, they might give like a calcium gluconate.

[00:43:33] Jeff Reim: Sure. I mean, it's not wrong. It's just you, you might be have to prepare to give more, you know, so yeah. And then obviously your definitive then after that, you know, you've stabilized the membrane. And then you work on your definitive treatment, you know, if it's DKA or whatever, you know, lots of fluids, insulin, and D50, you know, that whole, that whole spectrum, you know, sodium bicarb, you know, whatever else you're going to give to reverse the underlying, but yeah, don't Don't forego the calcium in favor of all that other, you know, fancy stuff.

[00:44:03] Jeff Reim: You got to stabilize

[00:44:04] Mohamed Hagahmed: the Very important. Calcium stabilizes the cardiac myocyte, the cardiac

[00:44:08] Jeff Reim: membrane. And that's what buys you time to fix the underlying problem.

[00:44:13] Mohamed Hagahmed: Nice. Anything

[00:44:14] Owen Traynor: else? One fun thing we didn't talk about, TCS. Overdose. TCA.

[00:44:21] Mohamed Hagahmed: TCA, sorry. Yeah. So that was some of the things that we touched based briefly on.

[00:44:26] Mohamed Hagahmed: Yeah. Agents that can cause dysrhythmias. Right. So a TCA overdose. So TCA stands for?

[00:44:32] Jeff Reim: Tricyclic antidepressants,

[00:44:34] Mohamed Hagahmed: right? I mean, can you name an example, Owen, like an agent? Imipramine. Yeah,imipramine. Okay. So, what do you see Jeff, on the EKG in these patients with

[00:44:46] Jeff Reim: overdose? So, the big thing with these...

[00:44:49] Jeff Reim: Basically, the TCA is a sodium channel blockade toxicity is what it causes, right? So you're you're poisoning the sodium channels, specifically what we're concerned with, you know, in this talk is in in the in the heart. So you get, you know, rather than QT prolongation which you see in those other meds we talked about, in thiscase you see a QRS widening, hence it's part of the wide complex tachycardia case.

[00:45:13] Jeff Reim: So you'll get, you know, the heart rate will increase. QRS width increases a lot of times you get a right word access, you know, if we wanted to get into that. So you get like a deeper S wave in lead one, things likethat, that might, that might point you in that direction. But yeah, it's generally a a wide complex tachycardia that you develop.

[00:45:35] Mohamed Hagahmed: So history is important. History is important. Look at the situation. Look at the house. Empty bottles. Yes, if you find names such as amitriptyline, amoxapine, doxepin, amipropine, nortriptyline, anything with the tylene, then that's likely a TCA agent and think of immediately giving one. First agent. Yes.

[00:45:58] Jeff Reim: Sodium bicarbonate. Sodium bicarbonate. You want to flood those poison to sodium channels with sodium?

[00:46:04] Mohamed Hagahmed: And Paul Quist, our audience, and including Owen Traynor here, do we give thesodium bicarb for the bicarbonate all the time? Is that correct? No! Shaking his head. Why?

[00:46:17] Owen Traynor: We don't need to change the acid base.

[00:46:19] Owen Traynor: Right. We're just looking for those sodium ions. Yep. We're just

[00:46:22] Jeff Reim: looking for that sodium load. Yep. Exactly. We want to flood those channels with as much sodium as possible. A couple other interesting meds you know, that you may see. Cocaine, sodium channel blocker, lidocaine, but in terms of, you know, recreational use, you might have someone that used cocaine and you're thinking that, you know, normally you think they're like, you know, out of control, high blood pressure, tachycardic, but youshould also think about the sodium channel blocking effects of cocaine.

[00:46:50] Jeff Reim: Another one That another med that could be used to treat AFib or SVT in, in the interim or in lieu of an ablation is flecainide which is another sodium channel blocker. Another sodium channel blocker and, and that's, that's the, the, the general overlying theme of all these agents, right? The TCAs, cocaine, flecainide, all those, they're all sodium channel.

[00:47:11] Jeff Reim: blockers, and that's what's causing the QRS widening. And hence the sodium bicarbonate.Correct. And hence the sodium bicarbonate, because you want to reverse the... That's all

[00:47:20] Mohamed Hagahmed: great pearls. I really like this discussion. Now, Owen, I'm going to ask you for the last time, do we have anything else that we missed?

[00:47:26] Owen Traynor: This time, no. I think we covered everything we wanted to, and then some more. I think this is a good review for

[00:47:34] Mohamed Hagahmed: people. I really like this discussion. Again, please either email myself or Dr. Traynor about any questions and I will make sure to include you, Jeff.

[00:47:44] Jeff Reim: Yeah if you wanna, you could put my email up there, I'll give it to you to post too.

[00:47:48] Jeff Reim: If you guys wanna have if you have any questions, you wanna reach out to me or you wannasee some cool EKGs, I can provide you with. many examples of all the topics we talked about today.

[00:47:59] Mohamed Hagahmed: I have a feeling I'm going to bring you back for another discussion, cardiology discussion. You're going to be a cardiology expert.

[00:48:05] Mohamed Hagahmed: And this is really nice. Please let us know how you think about this podcast. Anyquestions, ask us. And I like your point, Jeff, about the EKG, the pre hospital EKG and how important that is. Very important. And make sure at least that. Did you know out there that your EKG in the pre hospital setting matters to us in the inpatient setting?

[00:48:23] Mohamed Hagahmed: Yeah.

[00:48:23] Jeff Reim: I mean, even beyond just STEMI recognition, you know, getting these arrhythmias caught on a 12 lead EKG is, is huge. Because like I said, it may be our only, our only 12 lead EKG that we have of this arrhythmia. A single lead of VT doesn't tell us where that VT is originating, but a 12 lead is extremely useful.

[00:48:42] Jeff Reim: So make sure you get it if, if you

[00:48:43] Mohamed Hagahmed: can. Thank you, Jeff. Thank you, Owen. This has been great and we hope all that we can talk about another interesting topic and some cool cases soon.

[00:48:54] Owen Traynor: Okay, be good, be kind, be safe. [00:48:56] Jeff Reim: Absolutely.Thanks for having me. Be safe.