COMMENTARY

New Pediatric Advanced Life Support Guidelines Raise Questions

Robert D. Glatter, MD; Paul E. Pepe, MD, MPH; Peter M. Antevy, MD

Disclosures

May 06, 2021

This transcript has been edited for clarity.

Robert D. Glatter, MD: Hi. I'm Dr Robert Glatter, medical advisor for Medscape Emergency Medicine. More than 20,000 pediatric cardiac arrests occur annually in the US, but the outcomes for about 7000 annual pediatric out-of-hospital cardiac arrests have remained poor, with no significant improvement for decades in overall survival and neurologically intact survival. To address this ongoing issue, the PALS (pediatric advanced life support) guidelines committee made some recent changes. But the issue with the changes is whether the evidence truly supports the change in practice suggested by these guidelines.

Joining me today to discuss this are two seasoned EMS physicians. The first is Dr Peter Antevy, a pediatric emergency physician at Joe DiMaggio Children's Hospital in South Florida, and medical director for Coral Springs–Parkland Fire Department, Davie Fire Rescue, in Palm Beach County in Florida.

Also joining me today is Dr Paul Pepe, professor at UT Health Science Center in Houston. Welcome, gentlemen. It's really great to have you with us today.

Peter M. Antevy, MD: Thanks, Rob. Great to be here.

Glatter: The impetus for this discussion came from your suggestion that these guidelines need to be discussed , as many people may be unaware of these changes that slipped into the 2020 guidelines. With COVID obviously on everyone's mind, this may have been an issue which may have led to these changes being overlooked. I'll let you dive right in and talk about these changes, since you were the one that really brought this out in the publication Resident Eagle in the EMS world.

Antevy: Thanks, Rob. I appreciate it. The guideline that came out in October of 2020, published in Circulation, was right in the middle of COVID. The concern — not just from me but for many in pediatrics — is that they went from 10 breaths per minute or one breath every 6 seconds for cardiac arrest, and that was for all ages. They then said, "Let's change that for the pediatric population to 20-30 breaths per minute, doubling and tripling the ventilatory rate in cardiac arrest for kids." The level of that recommendation was a 2B. And it was a level C LD (limited data).

When you see that, the first thing you do is look at the actual paper that made that change. It was an observational study that only included 47 children, and it was done from a collection of ICUs (it was a network of ICUs doing this paper). When you look at those 47 young patients in that study — by the way, it took them 3 years to approve those patients — you see that 60% of them had preexisting congenital heart disease. All of them were intubated and had arterial lines. Most concerning was the presenting rhythm.

Now in EMS, and Dr Pepe will tell you this, we mainly see asystole PEA (pulseless electrical activity) in the field. In this particular study of 47 kids in the ICU, 74% of them presented with bradycardia with poor perfusion. When you looked at the children with asystole in that 47-children study, all of those patients died. So, to take an observational paper with small numbers that ended in 2016 and didn't publish until 2019, you start to say to yourself, Is this the same population that we are treating in the field? And I think it's a resounding "no."

When you look at the same guidelines, the actual publication in Circulation in October, ILCOR (International Consensus on Cardiopulmonary Resuscitation) publishes their recommendations and they in fact stayed with 10 breaths per minute. They said it's not enough data, and that this is not good enough to have a single paper that's an observational trial. That's really the issue for me, and I think people should really look at that study before they make a change.

Glatter: Absolutely. So, Paul, what do you think about this — one paper just making a guideline change off that? It seems kind of odd.

Paul E. Pepe, MD, MPH: I think Peter hit it right on the head that the child in cardiac arrest out-of-hospital is a whole different species, so to speak, in the sense of several things. One, they're dehydrated, so therefore they have a very poor preload. Theoretically in the ICU, they're being cared for under that situation, but most of our patients aren't. Two, they're behind the eight ball in a sense that there usually is a respiratory component that does it. They get hypoxemic and then they bradyasystolic into nothing. So by the time we get there, when they have a cardiac arrest, they're far behind, as opposed to our VF (ventricular fibrillation) patients who are still fully oxygenated when they went down. Now we're dealing with a different creature that needs immediate care. Another issue is the ventilatory thing, which is a whole different animal because ventilation has to match perfusion. You have a low perfusion state. Yes, it might have been respiratory before, but it's cardiac arrest now.

And so the concept of just simply giving a lot of breaths is confusing. That's like saying doing really good CPR, but not going deep enough or going too fast. You have to have a lot of components: how fast you deliver the breath, how large a breath you deliver, and how often you deliver it, especially because there are positive-pressure breaths. I'll go into more detail with you later if you'd like to understand the physiology, but in my settings where we've come in and done things, we've improved outcomes dramatically when we control ventilation in a multifaceted way. It doesn't involve going fast.

Glatter: Right. So it's an issue of oxygenation at the expense of flow. If we increase oxygenation, can we also increase flow at the same time? Is that possible? I guess that's what we're trying to balance.

Pepe: Well, the answer is yes. One of the interesting things I think people don't appreciate is that you want to recruit as many lung zones as possible. So you do that. We like to emphasize that there should be a large breath — you can't totally measure it, but if you get a good chest wall rise (eg, on a child, maybe one or two breaths) — but you get that. There's a secondary agenda: Not only are you recruiting every lung zone you can get to oxygen, but you've also got to move blood through there.

If you're doing CPR and compressing the chest, you start getting atelectasis, you're closing off airways, and therefore you can't get blood flow through it if it gets atelectatic. You've got to make sure that all of the lung zone stays open so we can get blood flow. We've shown in the laboratory in smaller animal models, which are closer to kids, that you do get increased pulmonary vascular resistance and less blood flow for the CPR when you don't have a good lung inflation. But by the same token, you give a good lung inflation. That's fine. You have that positive pressure there. But if you don't give it, what we have normally done is not get a breath for every 10 seconds in children, and in that nature we kept the intrathoracic pressure pretty low. And it's been phenomenal what we did when we got right to the kid, gave the drug right away, gave a large breath and only did it very rarely. We improved outcomes dramatically in the places we've gone into recently.

What I'm going to say is that it's multifaceted. It's not just the rate. It's not just the depth. It's how you do it, when you do it, and under what circumstances. Now given that, children have different metabolism; they have different needs. But when you're in a low-flow state and you're dehydrated, positive pressure, ventilation, is going to knock it out. It's a different species, so to speak.

Glatter: Peter, I'll let you weigh in on Paul's comments.

Antevy: Everything Paul is saying is right on the money. What he's pointing to is this flow that you mentioned as well. When you look at the two main organs that we're trying to see — which is the brain and the heart — both of those are interconnected very deeply with the lungs. If you're increasing that intrathoracic pressure to the point where you're squeezing down the heart and not letting the RV (right ventricle) fill, you're essentially killing the cardiac output. Secondarily, you're not allowing the blood from the brain to drain into the heart.

When you look at Keith Lurie and Tom Aufderheide's paper, that actually helped us understand this physiologic issue. They looked at a group of pigs that breathed 12 times a minute — these are pigs that they put into cardiac arrest. Then they had a group of pigs that breathed at 30 times a minute. It was a dramatic change, not only in the cerebral perfusion pressure. The slower you ventilate, the better the profusion of the brain. They only had one pig survive in the 30-breaths-per-minute group, and they had six pigs survive in the 12-breaths-per-minute group. Everything Dr Pepe just said, I think that makes us understand that it's all about flow and using the bags. Thinking you're affecting just an end tidal or SPO2 is really shortsighted. That's where this discussion should be happening; it's all about the flow.

Glatter: So, biasing the committee toward this change? To make a change in the guidelines means that there's evidence that supports a better clinical outcome that would necessitate this change. We don't have data for this, and that's my complaint.

Antevy: I'll tell you just a little bit of history here that's important. In 2015, PALS made a recommendation in terms of fluids for kids in shock. They said it's reasonable to give fluids but be careful. And why did they do that? Because of a study in 2011 by Dr Maitland where she studied kids with malaria in sub-Saharan Africa, where there was no ventilator and no ICU, and found that those children who got fluid boluses happened to do worse.

So, what did the guidelines do? They brought them to the US and scared everybody from giving IV fluids. Now, 5 years later in 2020, they said, "We think it's time to revisit that recommendation." So they have a history of doing it. Here they've done it again. My fear is that people who aren't reading the papers and aren't digging into the guidelines are just going to go and start 20-30 times a minute. Now, they've had to come back and clarify. And they said, "Oh, by the way, the 20 and 30 times a minute only means in an advanced airway," which it says in the guidelines. But then they said, "Oh, we meant intubation."

In EMS, we typically BVM (bag-valve-mask) or we mainly stick a supraglottic airway in. Now there's all this confusion that you start with one rate, you finish with another rate if you're intubated. I personally think out-of-hospital and in-hospital cardiac arrest are really two different animals, and we should probably be thinking of them separately and perhaps have two sets of guidelines that distinguish between the two.

Pepe: The other thing is that ventilation needs to match perfusion, and there are other factors that go in there. So if you're in a low-flow state, you don't need a lot of ventilation because there's no flow going out there, there's no flow going back to the lung, and so on. Once you get pulses back, then it changes. It is all dynamic and there are also other things going on. What I'm saying is that we have thought too much about this or that; it's a binary mechanism, and it's just like CPR quality. You must have it accurate, right in the sweeter spot of the right depth and rate, and good recoil. The same thing for ventilation — you have to have the right depth and rate depending on where you are, whatever device you're using at the same time, and CPR affects ventilation, ventilation affects CPR. All of those things have to be put together in a bundle.

In the resuscitation study in 2019 by Banerjee, he bundled all that stuff together really well, documented what he was doing, and they were able to take 10 years of zero survival neurologically intact — they got 5% resuscitated of the kids — and then jumped it up to like 30% or 40% over 2 years. And even though it's a historical control — I mean, you had no survivors, and all of a sudden it's getting back 40% neurologically intact by doing quality CPR, getting an IO in the right place and in right away, and at the same time simultaneously getting I-Gel or intubation right away, and controlling the rate meticulously with a good large breath, and then giving it less often, like once every 10 seconds. Think about that: It's just the opposite of what we're talking about here. They also made sure that there was hydration. All of those things were bundled together, and they did tremendously better. So, there are data out there to support a different way of approaching it. I hope that helps.

Glatter: It does. My question to you, Dr Pepe, is what is the value of this initial breath, and what role does it play in the outcome of the resuscitation? This large breath that we talk about at the initial onset of resuscitation — if it's not adequate, does that predict outcome?

Pepe: I can't tell you if it's the ventilation that made the difference in the kid's outcome or if it was the CPR. It's really all of those things together because they affect each other. They're interrelated. That's the theme here. With the big breath, all I said as I started early on is that we've shown in the laboratory good models — that if you get a good lung inflation, you diminish the pulmonary vascular resistance that rises as you get atelectatic lungs, that you keep things in an inflated state. But you can't give the breaths that often because you get too much intrathoracic pressure, especially if you're dehydrated and if you get no preload in. Well, then you've got a problem. When we give a breath, we make sure it's a good, long inflation, and they just give it less open. The trade-off on the intrathoracic pressure is well worth it because you get better flow through the lungs. No one really thinks about how the lungs affect the blood flow, and that's part of it, too.

Glatter: Absolutely. Peter, would you want to add to this?

Antevy: I think that the study that Dr Pepe just alluded to, the Banerjee study in Polk County, they actually went the other way. They have six breaths per minute, they have the bundle, they stay on scene, they do all the right things. They have so many more kids who are neurologically intact.

I wrote the op-ed to the American Heart Association and said, "Hey, what about that study?" Then, of course, it wasn't a study for them that really isolated ventilation individually. We all know that there are a lot of papers out there that look at one particular thing. Just like back in the day, they said that the ITD (impedance threshold device) didn't work. Well, it did work when you looked at CPR that was being done at a high-quality level and you were in the sweet spot, if you will. It's hard and it's wrong to take a study, nonetheless a 47-patient observational study, and look at one thing that was done differently. That study where they went up to 20 and 30 times a minute, that wasn't the initial intent of the study. They found that by happenstance, and they're now attributing success because of that increased ventilation rate. There are a lot of things wrong with how we're interpreting the science, and I think everyone should be realizing that when they look at this.

Glatter: Absolutely. I want to move on to the second change that got buried a little bit in the guidelines. I'm talking about cardiac arrest, dose epinephrine for bradycardia with poor perfusion. It's not recommended in ACLS (advanced cardiac life support), as you allude to, but it's still around in the pediatric guidelines. You bring up a point about Dr Holmberg's paper in April 2020 published in Resuscitation about epinephrine in children receiving CPR for bradycardia with poor perfusion. I'll let you get into that because I think we need to discuss that issue as well.

Antevy: Anyone who's an emergency medicine physician or an EMS knows that if I take an 18-gauge and I put it in your right AC and I give you a milligram of epi (a cardiac arrest dose for an adult), we would all end up in the cath lab, every one of us. To think that in children, for some odd reason, giving them a cardiac arrest dose when they still have a pulse is going to be any different or less harmful is shortsighted. This paper by Holmberg had almost 7000 patients in it — not 47 patients, almost 7000. When you look at the risk ratio (and you can see that a majority of these kids would have benefited without getting epinephrine), the conclusion was made very firmly that cardiac arrest epinephrine for symptomatic bradycardia is harmful. The guidelines actually speak about this paper, even though they said, "We saw the paper, we didn't make the change."

What we would recommend is some push pressor epi or an epi drip, just like we would do if it was an ACLS patient. I'm one of these pediatric people who doesn't feel that we should be treating kids differently when it comes to these advanced life support items. I changed my protocol in 2019 based on this paper. I've seen too many kids in my own practice who were, let's say, just vagaling in my emergency department. I see physicians coming and giving them a cardiac arrest dose of epinephrine, and the evidence just doesn't bear it out. Here we are again now having to wait for another guideline for them to want more data. There's inconsistency in how they're picking and choosing which articles they're using to make these changes in the guidelines.

Glatter: Paul, would you agree with Peter's thoughts on it?

Pepe: Yes. If you have a child who's perfusing and been there in a state where they've been okay, you don't have to jump to it there. And again, keep that different from a cardiac arrest because in cardiac arrest, the reason why that's been useful, like with kids who have now been hypoxic while they're having peripheral vascular relaxation, there's no more vascular tone, and the quality of the CPR is not that good because you're got wide-open pipes. That's a whole different circumstance vs a child that's been perfusing fine for prior minutes. I think that's why.

Antevy: I'll say one more thing. When you're trying to resuscitate a child and you're trying to feel for a pulse during a resuscitation to see if you have anything, and let's say you have PEA (pulseless electrical activity) on the monitor, what a lot of people don't do is they don't look at the end tidal. We know that if you have a jump in your end tidal from, let's say, 5 to 35, you still can't feel a pulse. Unfortunately, many people will still go ahead and give that child another cardiac arrest dose of epinephrine, when in reality what we should be doing is using push pressor. So, a lot of those kids who you may have been able to resuscitate are now getting a medication that's putting them back into cardiac arrest. Epinephrine is a dangerous drug when not used correctly, and the only reason it works in cardiac arrest is to push up the diastolic pressure just a little bit so we can perfuse the coronaries a little bit more.

Pepe: But your approach, Peter, is better because what we often see is that when we do give epinephrine, you get this pulse and then you say, "Oh, we got a great pulse back." Then, suddenly it falls off and you have to play catch-up. Whereas your approach, where you steady-state it in, is much better.

Antevy: I'll take it one step further and end with this. In Broward County, we're not using cardiac arrest dose epi for adult and pediatric arrest. We're using an intra-arrest drip that's been done very successfully in other places around the country with great success. I think that this 1 mg in the adult every 3-5 minutes is a lot, just like the .01 per kilo in kids is probably too much.

Glatter: Absolutely. I think this discussion highlights some important points that people need to take away. I want to thank both of you for taking the time to join us. It's been quite informative. Thanks again.

Robert D. Glatter, MD, is an attending physician at Lenox Hill Hospital in New York City and assistant professor of emergency medicine at Zucker School of Medicine at Hofstra/Northwell in Hempstead, New York. He is an editorial advisor and hosts the Hot Topics in EM series on Medscape. He is also a medical contributor for Forbes.

Peter M. Antevy, MD, is an EMS physician and medical director for Coral Springs–Parkland Fire Department in Florida. He is a member of the EMS World editorial advisory board.

Paul E. Pepe, MD, MPH, is a professor of internal medicine, surgery, pediatrics, public health, and emergency medicine at University of Texas Health Science Center in Houston. He's also a global coordinator of the US Metropolitan Municipalities EMS Medical Directors ("Eagles") Coalition.

Follow Medscape on Facebook, Twitter, Instagram, and YouTube

Comments

3090D553-9492-4563-8681-AD288FA52ACE
Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.
Post as:

processing....