Tanner Smida: Prehospital Transcutaneous Pacing in the US (10/4/24)

So today we're going to be talking about the practice of pre hospital transcutaneous pacing in the United States. And so all the data presented in this presentation was both presented as an oral abstract at NEMSP last year, and since then it's been published in the journal Pre Hospital Emergency Care.

So what do we know about transcutaneous pacing? We know it's a first line treatment for bradycardia that's causing hemodynamic instability. We know that it's a rare procedure and it's been studied repeatedly in the context of brady asystolic out of hospital cardiac arrest and found to be largely ineffective for this patient population. So there's multiple randomized controlled trials out there that tell us that, but we really don't have a lot of data on kind of the population this therapy is applied to today. Right. Like the outcomes of patients that receive transcutaneous pacing for bradycardia that's causing hemodynamic instability outside the context of cardiac arrest.

And so our group wanted to address this question using the nationwide ESO datasets. And so we really had three questions that we wanted answered. So we wanted to know who's getting transcutaneous pacing in the pre hospital setting. So what does this patient population look like? We also wanted to understand what are the outcomes of these patients. And then finally we wanted to understand factors associated with pacing failure. At least in our experience, a large proportion of these patients, after pacing is attempted, they continue to deteriorate and experience cardiac arrest. And so we wanted to identify some factors associated with treatment failure.

So again, we started with the, with the ESO Data Collaborative. Right. So for any, any newcomers that aren't familiar with eso, it's basically a software company that provides electronic health records to EMS agencies all across the United States. And providers put all sorts of data into this EHR. Right. Demographics, clinical characteristics, and then about 1 in transported patients included in this data set, they have hospital disposition data. And so we started off with basically every encounter in this data set, so, which was over 30 million patient records. And then we trimmed those down to patients who received transcutaneous pacing following a 911 call. We also excluded patients who didn't have a transcutaneous pacing time documented and patients who had a cardiac arrest without a CPR start time. And we did that because we wanted to sort our cohort into three different groups. And so these groups are patients who basically were rescued by transcutaneous pacing. So they had the therapy applied and then did not receive a CPR in the pre Hospital setting. The other group was that kind of failure group I mentioned. Right? So the patients who have pacing applied and then deteriorate into cardiac arrest prior to hospital arrival. And then finally, and this is a pretty sizable chunk of patients who receive transcutaneous pacing is those post Ross patients, right? So you resuscitate them and then they experience bradycardia that requires pacing. Now, the reason we wanted to kind of stratify our cohort into these three groups, I think it's pretty obvious, right? Especially for the patients who experience cardiac arrest, these three groups are going to experience very different outcomes, right? So we wanted to report them in a stratified manner.

And so in terms of the outcomes we were interested in, we were interested in survival to hospital discharge. So for that subset of patients that had hospital disposition data, that was an outcome we were interested in. And then we're also interested in failure. Right? And so as I said before, we define that as patients who had not experienced a cardiac arrest at the time of therapy initiation, who subsequently had a cardiac arrest that required cpr. We explored the association between a number of clinical variables and these outcomes using multivariable logistic regression. All of our models were adjusted for age and sex. And then we performed a set of sequential models where we added in weight, provider impression, and then a series of vital signs.

So in terms of our results, and who actually received transcutaneous pacing. So what we found was it looked like a pretty standard population in terms of, you know, elderly patients who experience cardiovascular emergencies. So the mean age was close to 70. Slightly more males than females, particularly in the groups where cardiac arrest occurred in the pre hospital setting. And then in addition.

An interesting finding, whenever we looked at the primary impression that EMS providers documented, you know, we saw all the things that we would kind of have expected, right? Cardiac arrhythmia, altered mental status, cardiac arrest, and the groups where that occurred. But interestingly, in the top three primary impressions, respiratory distress made an appearance. And so, you know, that's important and we'll talk about that in a little bit.

Okay. So for the second part of our results, we were interested in, you know, what are the outcomes of these patient groups. So for the group of patients that did not require pre hospital CPR, still about 1 in 3 of these patients died prior to hospital discharge. As for those patients who experienced pre hospital treatment failure and had a cardiac arrest following attempted pacing, about 87% died. And then for that post ROSC pacing cohort, 91% of those patients died prior to discharge.

Now, when we pooled so we looked at all of the patients who had a pulse and had not yet experienced the cardiac arrest when transcutaneous pacing was attempted. We found that one in five of those patients required CPR prior to hospital arrival. Right. So when you get to a patient, they're bradycardic, they still have a pulse, you're going to be doing CPR on one in five of those patients prior to hospital arrival, which is a pretty startling failure rate. Right.

And so then we went on and we explored, you know, what are the factors that are associated with failure. Right. With the hope that we could kind of get some clues onto maybe how to better deliver this therapy. And so we had a couple interesting findings. So we found that body weight was associated with pacing failure. So if you weighed more than 100 kilos versus 60 to 100 kilos, you were at higher risk of pacing failure. We also found a dose dependent relationship between peripheral oxygen saturation and failure. So in comparison to the reference group of patients who had a lowest SpO2 greater than 90%, if you had a lowest SpO2 between 80 and 90, you were 2.8 times as like, your odds of failure were 2.8 times as high. And then if you had the lowest SpO2 less than 80%, your odds of failure were six times as high. Kind of similar like, you know, looking at the respiratory failure picture. So for patients who had a primary impression of respiratory distress versus all those other primary impressions that we discussed, right. Altered mental status, arrhythmia, etc, you were six times or almost seven times as likely to experience failure, looking, you know, at another vital sign. We also found that a lowest pre pacing heart rate of greater than 50 vs less than 40 beats per minute was associated with failure. So so basically a non bracing heart rate was associated with failure. Right. And so the question is, you know, what does this tell us about the practice of transcutaneous pacing? And so we'll start with body weight. Right. And so this isn't really a modifiable factor in the pre hospital setting. Right. We can't modify our patient's body weight, but it suggests that pacing failure might be related to transthoracic impedance. Right. People who weigh more typically have more adipose tissue, thicker chest walls, and that might lead to impaired current delivery and decreased capture and increased pacing failure. Right. And so what do we do about this? The literature tells us that maybe pad position plays a role. So there was an excellent randomized controlled trial that suggests that if you switch from Al positioning, the AP positioning right kind of Decreasing that transthoracic impedance, you go from 40% capture to 80% capture, right? And so maybe pad positioning is a measure we can take not only in our obese patients, but patients who have increased transthoracic impedance because of things like, you know, respiratory diseases, copd, et cetera.

And then, and then, you know, we have all these vital signs that are associated with outcome, right? So low SpO2, respiratory, respiratory distress will kind of lump that together as respiratory failure and then that non bradycardic pre pacing heart rate, right? And so, you know, I think the best way to illustrate this would be with, with a case study, right? So let's say, you know, you're an EMS provider. You respond to a call for respiratory distress. You know, you get there, the guy with a history of COPD, he's clearly experiencing an exacerbation, right? He has a SpO2 of 60%, heart rate 112. He's normal, intensive. And then as you're treating him, right, you're treating him with, you know, oxygen and you're giving him some bronchodilators. Minutes later, you look back at the monitor, he still has an SpO2 of 60%, but now his heart rate's 42. And your blood pressure cuff just, just threw out some question marks, right? And so in this case, I think it's pretty clear that this patient's probably experiencing bradycardia because of hypoxia, right? The bradycardia is secondary to hypoxia. And so in this case, jumping to transcutaneous pacing and flogging this patient's heart with electricity probably isn't the solution. Right? And so maybe what we're seeing here, right, the signal of respiratory failure being associated with pacing failure is just pacing being applied inappropriately to patient populations that, you know, this therapy really isn't designed to treat, right? This guy needs aggressive airway management. He doesn't need electricity delivered to his heart, right? Same with a non bradycardic pre pacing heart rate, right? Bradycardia is kind of the end stage of many pathways to death, right? If you're hemorrhaging, right, Once you hemorrhage enough, eventually you're going to brady down to a systole and die, right? If you're in septic shock, eventually you're going to brady down to a systole and die once your shock has progressed far enough, right? So for those patients that start out tachycardic and then their heart rate declines to bradycardia prior to pacing initiation, you know, Again, maybe we shouldn't be applying pacing to those patient populations. We should be prioritizing the management of their shock or the management of their respiratory failure. Right. Which is something that we can address in training our paramedics to perform this procedure.

Another facet of this that's kind of recently been highlighted in the literature is the role of false electrical capture. Right. So kind of ECG changes that are induced by transcutaneous pacing in the absence of mechanical capture. This was recently actually addressed on this webinar by Josh Kimbrell and Judah Krein book and others who published a case series recently in pre hospital emergency care. The role of this in pacing is being further explored. So actually our group at WVU is coordinating a multi center study with a number of other sites to study this phenomenon, establish its incidence, look at outcomes associated with false electrical capture. And that study is currently ongoing.

So in conclusion, transcutaneous pacing is an uncommon procedure associated with a high mortality rate failure and subsequent cardiac arrest is extremely common in the pre hospital setting. And we were able to identify some factors including increased body weight, hypoxemia and a non bradycardic pre pacing heart rate that are associated with progression to cardiac arrest and failure. So yeah, thank you all very much for listening and I'm happy for any questions or commentary that you have to provide.

Oh, okay, got it. It's unmuted. Thanks very much. Good job. Tanner. I'm sorry, I was supposed to introduce you and I don't know if we got the CME number out there today. 1940. Okay.

I didn't put it in the chat.

For some reason I was blocked from. I was muted when I was trying to do the introduction for you. But thank you for doing that for us today. So I just wanted to make sure you got that message. She didn't know. I didn't mean to let you down. So. Okay, let's see if you have any questions. Let's look at what's in the chat. Is there any questions for you there?

Not so far. I don't see any hands raised or anything so far. Feel free to put a question in the chat. Shout it out.

Now, were there different, Let me ask you this, were there different pacemaker types or is there just one out there? I know there's not, but I mean, just saying we're able to break it down according to the different.

You know, let's say brands or whatever it may you want to call it, you know, people who make them manufacturers. And did you, did you notice any differences there?

Yes. So that's definitely a very important area of future investigation. Right. Because you know, similar to defibrillation, it's possible that, you know, the way that these different devices deliver current is important in this data set. Right. So we used, we used ESO for this. So we didn't have any waveform data. We weren't able to determine if it was a LifePak or a Zol monitor that was used. But so our future, you know, the multi center trial that we're multi center observational study that we're currently enrolling patients in, we'll be able to look at variables like what monitor was used and we'll have continuous waveform data to get some, some more granularity.

Yeah, I mean, I suspect that you'll see some differences there and it'll be really cool to take the delineate those. You know, unlike AEDs that for the most part are now pretty standardized, et cetera, in terms of how they operate. These are a little different. And so that'll be. So I hope you do break it down and stratify accordingly. So.

Yeah, absolutely. Larry McCarter says it sounds like AP placement of pads should be considered for all. I think that's definitely. Again, you know, there's, there's randomized data out there. The, the highest level of evidence suggests that that's probably the, the best move. So I would, I would agree with that.

And then in terms of a link to the study, I'll see if I can, I'll, I'll put that in the chat as well.

And I just like the fact that you're emphasizing that, you know, when you have people that you think, oh, we gotta pay stuff, you know, a large part of that is, you know, is exactly right. It's the underlying problem that you gotta fix like the hypoxemia or the lack of perfusion if it's a trauma patient bleeding out, etc. So that's really important aspect to get on top of. Now having said that, also, it may be too late in some of these cases too. So that's the other issue you might want to look at is to see, you know, the timing to this, et cetera, especially with regard to other products. A lot of multi factory things happening all at once under these circumstances.

So yeah, especially for that, that post dross cohort, I mean that made up a significant chunk of our, of our sample. And so, you know, for future studies, I mean, you know, these patients rearrest for all sorts of reasons. Right. And there's a number of disease processes at play for this. It's a heterogeneous population, I'll put it that way.

Yeah.

Right.

Okay. Well, if we have. Oh, there's Sam. Go ahead. What's he have to say in the chat?

Yeah, so he talks about assessment of perfusion using end tidal CO2. Yeah. And so I think that just in general, multimodal confirmation of mechanical capture is important. Right. We should be, you know, trying to get a pleth wave with our pulse oximeter. We should be trending end tidal CO2 values. You know, if you have ultrasound. Right. That's probably the gold standard way that you can actually confirm that you have mechanical capture. You know, at this point in time, there isn't a paper I can point to that says that those are reliable markers of mechanical capture. Right. Like entitle CO2 and, and you know, kind of synchronization of the PL wave. Right there. There's no data out there now, but those are kind of pre specified aims of that, that multicenter study that I discussed before. So I suspect that entitled CO2 might not be as useful just because of how noisy that data can sometimes be. Especially because many of these patients, particularly the patients not in cardiac arrest, do not have advanced airway management. And so they're just using kind of the, the nasal prongs, which, you know, there can be a lot of variability there based on if you're, if you're running oxygen through them at what rate, if it's positioned correctly in the nose, kind of reservoirs positioned over the mouth. But again, it's a tool in our pool. I think it should be deployed on these patients. Right. We should be super aggressive about throwing every monitoring modality to make sure that we're actually pacing these people. Right. Yeah. Excellent comment. Yeah. And I put the, the link to the article in the chat, so. Yeah. So Mr. Zalkin said the basics. You need to be able to palpate a pulse. You know, I think sometimes that might be easier said than done in a lot of these patients.

Right.

I think that the literature shows that we're sort of unreliable at being able to accurately palpate pain pulses, especially, you know, when it comes to the kind of the contraction of thoracic muscles. Right. Definitely don't go for the carotid. Even the radial, I think, is suspect. There's been some suggestion, at least in a case series that.

The, the transcutaneous pacing can actually induce kind of a pseudo pulsatile flow that can even change the pleth waveform that we're getting. Right. So, you know, if you're going to palpate a pulse. Definitely go for the. For the femoral site. But again, I've. I've. I've seen during some calls. Right. It takes a while sometimes for people to agree if they have a pulse and if it's at the appropriate rate. So definitely a limitation. Tim Ryan is asking, is there any use in increasing milliamps with. With larger patients? You know, again, I don't have any data to suggest that higher milliamps is better. I would assume that in the setting of increased kind of transthoracic impedance, that increasing milliamps would lead to more effective capture. Again, you know, there's not a lot of data in this space. We need a lot more research on the practice transcutaneous pacing, which I think, you know, a lot of these questions illustrate.

Luke, you have your hand raised. Go ahead. Yeah.

Hi, Tanner. Three things. One, did you have any way to check what the confirmation method was that these patients were actually paced or with a pseudo paste and maybe that contributed to the downfall?

No, that's. We had no way to confirm, you know, what method was used. Right. We didn't have access to any free text fields. Right. So we weren't able to see if people, you know, what site they palpated the pulse at, if they even documented mechanical capture. Right. So. So for some of these people. Right. You know, providers could have known that pacing was unsuccessful. Right. They could have been dialing up the milliamps to the maximum that their device allowed them and just. And just still not getting capture. So, again, you know, kind of using this registry data from ESO does have its limitations, and that's definitely one of them. Right. We definitely miss out on some granularity in terms of kind of the practice patterns for confirming mechanical capture, but I promise it's going to be addressed in our upcoming observational study.

Okay. I don't remember most of them, but my last patient I paced who was in an idiopentricular rhythm, unconscious, hypotensive. I knew I had capture because I got 60 opms hours per minute until I sedated her. So that was a pretty reliable that we had captured. The other one is for you and Dr. Patty. We've talked about epi, either drip or push dose post cardiac arrest, you know, as a kind of prophylactic means. Do you think, and this is a surmise, it's not part of your study, that that might make a better difference than, if that's a word, than pacing afterwards?

Yeah. So. And just to make sure that I'm understanding your question. Right, so, so in terms of either adding on or, or starting with pharmacologic therapy. Right. So so like an EP drip, like you're saying, are you asking, do you think that's a strategy that should be pursued?

Right. Well we've talked about in some of the webinars that routinely the possibility instead of pacing post arrest, we get Ross, we've given fe, it's going to wear off. You know, should we start a drip, a push dose and would that help alleviate what's been happening afterwards with your cardiac arrest postpacing?

Right, right. Yeah. So I think again, again, I will, I will disclaimer. I don't, I don't think there's any necessarily good evidence that to say that that would impact outcomes, but I think it definitely has the possibility, you know, even in that post rest patient to eliminate the need to even go to pacing. Right. If you get ahead of it and start supporting their hemodynamics with you know, some of the, some of the beta effects of epinephrine as well. So yeah, I think it's a reasonable, a reasonable strategy to pursue. Right. And you know, we know that, that 40% of post duress patients are going to require, they're going to be hyp, become hypertensive in the pre hospital setting and require hemodyn. So yeah, I think it's an excellent strategy to have that vasopressor chip running and then just titrate it down or up as needed. Could, could get around some of these.

The high incidence you're getting alpha and beta, which can both be helpful in that post arrest situation. If I can bypass your bit. Dr. Pepe, can you weigh in on that please?

I just had to find the mute button here. Right. So first of all it's, it's, it's not a binary answer like yes or no. It depends on the situation a little bit. Etc. And I'm sorry I'm getting all these text at the last minute here, sorry about that anyways, but here's, let me just think, what's the utility of it? One of the things that people do when, if they have an IT event trigger the rhythm or they got a SIS layer or whatever it might be, it probably represents they were down for a while in most cases, not always, but generally will.

And so what happens and during cardiac arrest, what people don't really appreciate too much is that because you have such a low profusion state, you're not getting a lot of blood flow out to the tissues, etc, what's happening is you're getting progressive vascular relaxation. So right now you have a blood pressure because you have vascular tone. And so if you suddenly don't have oxygen going out there, you're going to start losing a lot of that vascular tone. And so as a result, even if your heart was beating really well, it's beating out against, you know, loose pipes as opposed to tighter pipes that would give you the cordial perfusion that you want, you know, at the end of the day, so to speak. So part of the rationale for doing that epinephrine is to actually tighten up the pipes a little bit, hopefully, if it's not too far along. That's what I'm saying. It could be too far along and attempt to do it. And I like the idea of the drip, largely because in the old days, we give a push, you get a boost, you get a part, you get pulses back, you go, wow, that's cool. And then what happens? It wears off, and then it just kind of crashes that it's harder to get them back on that end. But. So there is some rationale, but you can't. You know, you got to be careful. There's this. The issue that are you irritating the myocardium even further with beta effects if it's a v fib case? But if we're talking about a lot of these cases that are, you know, idio, ventricular or whatever, I think it's worth a try. The secondary rationale for doing that is that you could get that set up hopefully a lot sooner than you can get some of the pacing stuff set up. That's. That's the other thought there as well. Right.

Thank you.

Oh, yeah. And one last part is that maybe if you do get some reperfusion, if you get to them in time where you can get some better coronary perfusion, you may be more responsive as a result, to the pacing, if it's a hypoxic heart or whatever, or underperfused heart. Okay.

Makes sense.

And I agree with you on the drift. The steady state is probably going to be better than the intermittent pushing.

Well, and everybody got to see me for today, then. What was it? 1 94, 35. And then I got to switch over to the other meeting here pretty soon. Any other questions or anything else that you want to talk about?

Okay. Well, if not, thank you very much. I'm going to head over to the other. The other show. Thank you all for being here today. I hope that was helpful to you. So thank you, Tanner. All right. So we'll see you on the other end.

The link to Dr. Pepe's webinar is in the chat.

We're going to talk about more boring stuff today, so you'll see. All right, See you. Take care. Bye. Bye.