Thank you for being here in Hawaii, and it's great seeing the sessions being full, not everyone's escaped to the beach just yet. In the meantime, though, we're here, we're going to talk about controversies in cardiac resuscitation management and have an interactive discussion, and we have four speakers here today. There will be some audience response questions during this session, so keep your phone handy. You can use the CHESS app to answer audience response questions. Once you find the session that we're in, go to that session, and the questions will come up there. All right, so my name is Kevin Dershug, pulmonary critical care physician at the University of Iowa. I am the first speaker, but I want to start off by giving all credit to Naila Ahmed, whose idea put this into action and coordinated all of the craziness that is me and my other esteemed colleagues. My name is Kirsten Cota. I am a medical and surgical trauma ICU pharmacist at the Mayo Clinic in Rochester, Minnesota. I am Naila Ahmed. I'm one of the pulmonary critical care fellows at Mayo Clinic. I have nothing to disclose. Aloha. I'm Kim Fabian. I'm one of the physicians at Walter Reed Pulmonary Critical Care. I'm really excited to be here with you all. All right, for further information, feel free to scan the QR code. And I did not verbally acknowledge that I have no disclosures. What I'm going to talk about for the next 10 minutes or so is discuss methods to monitor highly effective CPR with capnography during cardiac arrest. And others will be talking about controversies in drug management during cardiac arrest. An important discussion about family engagement during cardiac arrest will follow that. Then finally, evaluate approaches to targeted temperature management. To start off with a case, a 70-year-old male presented to the emergency department with fever, chills, diarrhea, and abdominal pain. It's hypotensive despite adequate IV fluids and started on vasopressors, admitted to the ICU. I think you know this patient. On admission to the ICU, patient evaluated and started on supportive as well of disease directed therapy. Within 30 minutes, you're called to the patient's room due to tachycardia to 180s with persistent hypotension. He subsequently becomes unresponsive and loses pulses, so CPR is initiated. The bedside nurse and ICU physician start CPR and ventilation. Soon after, the respiratory therapist and pharmacist arrive as well as other ICU team members. So during CPR, hopefully the team will be monitoring highly effective chest compressions with capnography. Again, we'll talk about the importance of highly effective chest compressions and recognize that capnography correlates with coronary perfusion pressure, identifies return of spontaneous circulation, probably helps prognosticate and can improve the effectiveness of chest compressions. Question for the audience. How many ideal chest compressions are required to achieve adequate coronary perfusion pressures? People are still voting. 32, 36, 39. All right, well that's a couple people still voting, but in the interest of time, the correct answer is C, about 12 chest compressions to achieve adequate coronary perfusion pressure. So many years ago, Maxwell and his colleagues started looking at animal models of chest compressions and identified that coronary perfusion pressure was specifically related to survival, coronary perfusion pressure during chest compressions, again, suggesting that's what we need to be achieving with our chest compressions. Around that same time, although my reference here is for a review later on, identified that it actually takes quite some time, again, approximately 12 chest compressions to achieve significant perfusion to the coronary artery as well as the rest of the body, that each compression builds upon itself to improve perfusion. And while it takes quite a while to improve coronary perfusion, it takes a very short period of time to lose perfusion. During any pauses in CPR, aortic pressure, right atrial pressure, and coronary perfusion pressure drop very, very quickly. And there's data that shows that the length of pauses in chest compressions is also related to a successful resuscitation, with pauses less than three seconds most likely related to successful resuscitation, pauses longer than 15 seconds, poor prognosis. A lot of that has been in animal models, but we actually have human data as well that shows the chest compression fraction, so what percentage of times during the resuscitation effort are chest compressions actively occurring, that when chest compression fraction in the 60 to 80% range, significantly higher survival compared to when chest compression fraction is lower than that. So these sort of data lead to the American Heart Association recommendations for highly effective CPR, chest compression fraction 80% or higher, compression rate of 100 to 120 per minute, and a compression depth of at least two inches for adults, and no excessive ventilation. Again, these are the 2010 AHA guidelines. But the question, again, for the audience is, what percentage of chest compressions are performed at the correct depth and rate by trained providers? With the options being 10%, 33%, 50%, 67%, 90%. All right, and the answer is, not very often. 33% of chest compressions are performed at the appropriate rate and depth. And that data comes from this publication within the last several years that looked at both compression rate as well as compression depth, and approximately 39% correct depth, 71% correct rate. Many of us can sing the Bee Gees' Stayin' Alive better than we can estimate depth. But 31% correct rate and depth. And again, that correct rate and depth was associated with ROSC. This is another study that looked at compression depth, specifically rates to end-tidal CO2, which gets to the concept of the talk, which is that if you provide adequate chest compression depth, then your end-tidal CO2 will be higher than if you have inadequate depth. And this is data obtained during out-of-hospital cardiac arrest using compression monitor pucks to look at compression depth and rate. And again, that depth is associated with your end-tidal CO2, which again is associated with coronary perfusion pressure. So this is an interesting study here that looked at end-tidal CO2 during chest compressions. And they also looked at echocardiographic images of the heart and showed that actually it's compression of the left ventricle that is most correlated with end-tidal CO2 rather than just correct depth, but really what is the compression of the left ventricle. And I'll talk a little bit more about why that's important. But again, it's the compression of the left ventricle that is the key to chest compressions. What we know is that end-tidal CO2 is probably important for a prognosis that if at 20 minutes into resuscitation efforts you have an end-tidal CO2 of less than 10, the likelihood of survival is very, very low. And at that point, you might consider termination of efforts although, again, that's a complex decision that should go beyond just one data point of end-tidal CO2. Actually, end-tidal CO2 less than 10 at 3 minutes is also bad. So very early on, if you're not able to get adequate end-tidal CO2, the likelihood of getting a good result is low. Next question for the group. The hand position for chest compressions on an adult male is... A, B, C, or D, shown in this picture. Okay, then. Well, the answer is probably C. Uh... Probably C, and I'll explain what I mean. First of all, there was... American Heart Association does recommend chest compressions on the lower half of the sternum and the middle of the chest, again, evidenced by C in that last picture. This study here, they looked at laypersons as well as trained providers to point on a picture where they would place their hands for chest compressions, and you can see that providers in the black, laypeople in the white, there's a tremendous amount of variability in where they would place their hands, which is a little bit concerning. An interesting tweet just out this year of someone that was using a Lucas device and, again, looking at echo images, and I'm sorry it doesn't show, but you should look up this tweet, by Peter Sheeran on May 12. Basically said they saw the heart wasn't getting compressed with the Lucas device. They moved it lower and to the left, and end-tidal CO2 went up 2 kilopascals, like 15 millimeters of mercury, so changing the location from the American Heart Association recommendation to something else to get better left ventricle compressions, which leads to this study, too, that looked at CT images of where is the left ventricle in relation to the external landmarks on the chest, and, again, many, many patients, the heart is actually lower and more leftward than that recommended by the American Heart Association. The guidelines... Well, yeah, so the correct hand position for chest compression on an adult is maybe E, not C. Again, the guidelines are built upon one where many people's left ventricle is and the low likelihood of causing injury, but you have to wonder, then, if you're doing chest compressions at the C location there and you don't have effective end-tidal CO2, should you move to a different location to see if you can get better end-tidal CO2? I'm trying to catch up on time here. So, and again, the reality is we may not perform effective CPR on a regular basis. This is an animal model study where they actually put a monitor so that providers could see their compression depth and rate. They could see what they were doing there, and they were able to measure end-tidal CO2 at that time, and the providers were blinded to the end-tidal CO2. In another randomized group, the providers were allowed to visualize their end-tidal CO2, and when people were able to visualize their end-tidal CO2, that provided a change in compression rate and depth to provide higher end-tidal CO2s beyond just knowing what your depth and rate are. So again, modifying your CPR based upon your end-tidal CO2 is probably an effective way to consider this. And finally, another study that shows that continuous visualization of capnography during CPR actually can improve human dynamics and survival in an animal model of resuscitation. Again, providing further evidence past the guidelines that have been there for 10 years, but actually some evidence-based that it actually really is important to monitor our end-tidal CO2 because we do make changes based upon that feedback from end-tidal CO2, and those changes are important to outcomes. American Heart Association recommends that we use capnography during CPR in intubated patients. They also recommend that we don't intubate our patients. One, here's a shout-out for extraglottic airways rather than intubating our patients. That is a discussion beyond what we have time to talk about. Two, you can place your end-tidal CO2 in a capnograph cuvette between your bag and your mask if you're bagging your patients. But recognize that how you ventilate the patient is going to change your capnograph, that if you ventilate faster, your end-tidal CO2 is going to go down. And so that, again, reminds us that we should be ventilating 6 to 8 breaths per minute, not 12, 20, 36, what happens in my ICU. So keep the ventilation rate slow so you can get an accurate end-tidal CO2 to guide your management. And finally, recognize some newer information out about what your capnograph should look like during CPR. And when you do chest compressions, you are having alternate oscillating changes in intrathoracic pressure. And when you let the chest recoil, it actually creates somewhat relatively negative intrathoracic pressure, which improves blood flow back to the heart, and it's going to increase your end-tidal CO2. But then when the hands are going down for compressions, then the opposite is true, and your end-tidal CO2 is going to go down, and you'll see this oscillatory pattern here. If you see a pattern that looks like this, that suggests that you do not have an adequate airway going on with the patient. But perhaps this one is the interesting pattern here, where you start off with a rising capnograph and then the normal oscillations. And what's happening here is that you have significantly increased intrathoracic pressure probably from overventilation, over-distension of the lungs, that is impeding blood return to the heart. And then as the patient breathes out, then the end-tidal CO2 can return to that oscillatory pattern. So this pattern right here suggests that you need to ventilate less frequently, lower tidal volumes, and get back to the normal oscillatory pattern. So in conclusion, capnography provides information regarding quality of CPR and prognosis, and CPR can actually be improved based upon real-time observation of your capnography. And if you don't have a good end-tidal CO2, maybe you should change your rate, maybe you should change your depth, maybe you should change your position to see if you can get higher end-tidal CO2 values, but recognize that your ventilation also affects your end-tidal CO2. I'm going to hand off now, but we will have questions at the end, and thank you very much. CPR started. If you're lucky, you're in the ICU, and I'm right there with the code cart, and we can get all the medications started as well. If you're not lucky, the patient's out on some abandoned floor of the hospital, and I've got to drag a cart that weighs three times my body weight up and down hallways from the basement. So it might be a little bit delayed before we get some drugs there, which we'll see. That might actually not be a bad thing for some patients. So if you think about my giant cart full of stuff, but then you actually get the ACLS recommendations, the 2021 update, there are three drugs they recommend using in ACLS. So they recommend epinephrine, amiodarone, or lidocaine. And that's it. So I'd like a little bit of a show of hands. How many of you routinely request bicarbonate on a patient during a code? OK, I see some hand raises. What about calcium? How many of you are routinely requesting calcium, even perhaps in the situation before you have an ISTAT back with a level of an ionized calcium to go off of? And I'm seeing some more hands. What about magnesium? And we're going to ignore like torsades, because that's obviously, yes, give some magnesium. But what about that kind of prolonged code situation where we're just empirically sort of adding things into the toolkit? Because it does make us feel better to do things. But the first part of the talk, I'm going to focus really on the fact that epinephrine and amiodarone and lidocaine are the two that we need to emphasize, the three based on what ACLS actually recommends. So the first question, does epinephrine improve outcomes? And the short answer is no. You do have an increased likelihood of achieving ROSC and cardiac arrest. But there's no definitive impact on long-term survival or good neurologic outcomes with epinephrine. And this can really be broken down into two sort of concepts as we think about the way that we approach ACLS as well. If you have a shockable rhythm, it turns out giving epinephrine within the first two minutes after the first defibrillation results in a worse outcome. The study by Anderson and colleagues looked at patients getting epinephrine between the first and second defibrillation in patients with shockable rhythm versus waiting until after the second shock to begin epinephrine and found that if you didn't give epinephrine early, you had an improved ROSC, improved survival, and an increased good functional outcome for the patients. And this makes sense, right? A shockable rhythm is one that is malignant ventricular arrhythmia. And loading a patient who's already in malignant arrhythmia with a bunch of beta adrenergic effect is probably not going to get us where we want to go. On the converse, however, in a non-shockable rhythm, outcomes are actually improved if you're giving epinephrine within the first three minutes. So you have an improved achievement of ROSC in that situation. These are both studies that looked at in-hospital cardiac arrest. Some of the data for out-of-hospital is a little bit different. So if we move forward, all right, we're going to give epinephrine at an appropriate time. But how much? I can validate that this isn't my picture, but yeah, pharmacists are a little type A, and there's a nice little perforation. You just gently open the box. If we give more than five milligrams of epinephrine at a time, it's associated with significantly worse outcomes. If you look at expert opinion, they suggest stopping epinephrine after three doses in patients that have VF and VT. We know that more epinephrine is associated with worsened global myocardial ischemia. It's increased oxygen demand and, again, poor neurologic outcomes. So we don't really know what the right amount of epinephrine is, but I can tell you that we've all been on that code that goes for 25 minutes. And as the pharmacist, I've gone through two code cards worth of epi, because we're giving it every three to five minutes, because it sure feels good to do something every three to five minutes. But we're probably harming our patients when we do that. I've got to say, during the code is probably not the time to have that conversation, because I think people might balk a little bit and say, I'm not giving you any more. But it's something to think about as you've returned back to institutions and continue to go over overall code response. And then best case scenario, we get ROSC. Awesome, but they still need a presser. Is epinephrine the best presser post-arrest? And some of the dogma that I was certainly taught was, well, if it worked during the code, it's going to work after the code. And it turns out that may not actually be the case. The study by Bogan and colleagues looked at starting a continuous infusion of epinephrine versus norepinephrine post-arrest. And they found that in patients that had epinephrine started, they had an 83% incidence of in-hospital death. Whereas if norepinephrine was your presser of choice, you only had a 61% incidence of in-hospital death. So it's something to consider. And obviously, if you've got a really good reason to use epinephrine, go for it. But I think a blanket use of epinephrine and everybody that we get ROSC on is perhaps not the right call. So let's move into our antiarrhythmics. If you look back across the history of ACLS and their various recommendations, you can see that lidocaine and amiodarone have been fighting sometimes with percatamide for about 50 years. I'm going to go up a little bit farther. So in 2005, ACLS decided that amiodarone was effective and lidocaine wasn't. And maybe you could use percatamide. And then in 2010, they said amiodarone's first line, you can use lidocaine only if you don't have amiodarone. And then 2015, they said, all right, amiodarone's first line, but lidocaine, you could use an alternative. And in 2018, they said, all right, use either one if they're unresponsive to shock. And then in 2021, they actually said it's an equivalent recommendation. And if you look across the spectrum of literature, and there's many, many years of literature for using either drug, part of the problem comes that if you have a prolonged delay to medication administration, malignant arrhythmia, you're going to have bad outcomes. And much of the studies of lidocaine that showed not significant outcomes versus placebo was an out-of-hospital cardiac arrest. And so these patients had 15 to 20 minutes delay of a shockable rhythm before they got an antiarrhythmic agent. When you look at more modern literature, like this study that CHESS published earlier this year, this is an in-hospital cardiac arrest comparing amiodarone to lidocaine. And they found that lidocaine was actually associated with improved ROSC, improved 24-hour survival, survival to discharge, and favorable neurologic outcome versus amiodarone. Now, this is one study. There's a lot of longstanding literature that doesn't show a strong, repeatable, confirmed difference between the two. So I would say, honestly, use either one. My pharmacy preference is that lidocaine is in a nice little box that I can open and screw together and just give you, whereas amiodarone, I've got to open two vials, I've got to pull two vials up. It's a really oily compound, so I have to dilute it. It takes a long time, so just go for the lidocaine. Now, let's talk about bicarb. So I've got to say, the people that here work with me at Mayo know that I hate bicarb. So I'm a little biased in this situation, but I'm going to give you some data to back up my dislike of it. We know that prolonged delay of ROSC results in metabolic acidosis, and there's a concern for decreased catecholamine efficacy in acidosis. We also know from various surveys of critical care practitioners that despite the fact that ACLS specifically says do not give people bicarb, we use it in over 50% of our hospital cardiac arrests. So the question I have for you is, is there any data that giving sodium bicarb restores the effect of vasopressors in shock and in a code situation? No, it does not. It doesn't exist. When we look at the overall spectrum of bicarbonate literature resuscitation, again, there are many, many, many studies over many, many, many years. And the end result of the data is that it really doesn't seem like it has any actual improved outcome on either ROSC or survival. And the most recent study is a randomized double-blind controlled trial that was done in the ER published in 2018. And they enrolled patients that didn't get ROSC after 10 minutes of CPR and who were acidotic. Either with a pH of less than 7.1 or a bicarb of less than 10. And they gave these patients an amp of bicarb or 50 mils of normal saline. Their primary outcome, the very clinically relevant helpful outcome, was change in pH at 10 minutes. And they found, as you can see here, for the bicarb group, you went from 6.7 to 6.9. And if you were in the sodium chloride group, you went from 6.93 to 6.90. If you look at the overall bicarb level between 10 and 20 minutes after giving bicarb, not surprisingly, they gave bicarb. The measured bicarb went up. But overall, there really was no difference in outcome. And very small study, 25 patients in each arm. But the placebo group had higher ROSC, higher sustained ROSC, and a higher survival to hospital admission. You may say, all right, well, OK, it might not work. But is it going to hurt? Is there any harm in giving these patients bicarb? And I think yes. So everyone here is very familiar with the oxygen hemoglobin saturation curve. Turns out giving a lot of bicarb shifts us to the left. And so you're actually decreasing the amount of tissue oxygen that's being delivered, which is kind of a problem in somebody who's in shock who's getting CPR. Going back to some medicinal chemistry, because I am a pharmacist. And I'm nothing if not very fun at parties. We have the overall buffering equation for bicarbonate. So you give bicarbonate. In theory, it scavenges hydrogen ions. You get carbonic acid. And then it separates into water and carbon dioxide. Oh, returning metabolic acidosis to respiratory acidosis. Well, that's not great, especially if we're not intubated or we're having a hard time actually ventilating the patient, we end up increasing intracellular CO2, worsening local acidosis, and worsening overall cardiac function. And you may say, but no, but I love bicarb, like maybe just have a little bit, can I have a little bit in my codes? And there are some times that it's appropriate to use, like TCA overdose, you know, the very common in 2023 presenting complaint for cardiac arrest at the hospital. But I will point out that the reason bicarb works in TCA overdose is because the sodium load stabilizes the cardiac membrane. So your HCO3 is not actually doing anything in that instance. And then if we look at hyperkalemia, you're activating the hydrogen potassium exchange pump and causing an intracellular shift. So if you're seeing hyperkalemia and as a temporizing measure, it's a reasonable thing to try. And you may say, well, in the Resuscitation Journal this year just published a study that was a nationwide cross-section that said in out-of-hospital cardiac arrest, they had an improved survival and EMS ROSC with bicarb in patients that had non-shockable rhythms. And I'll tell you that, I mean, large numbers are nice and you get p-values when you look at very large numbers of patients. But the problem here is that this is out-of-hospital arrest. These patients were delayed, you know, 15, 20 minutes to EMS arrival by the time they're actually getting all these medications. So from an in-hospital setting, it just that we don't have the evidence to say that it actually works. And we do have evidence that says it might be harmful. And I've got one other counter to the thing that everybody says about how great bicarb is. So remember how there's no data that bicarb actually improves vasopressor efficacy? Turns out pushing bicarb and epinephrine in the same line runs the risk of deactivating the epinephrine. When you put catecholamines in an alkaline solution, you end up oxidizing the molecule, which means it is no longer biologically active. And again, a lot of med chemistry. That data comes from the Annals of Emergency Medicine in, I wanna say 1985. So we do have some evidence that doing all of this at the same time is probably not helpful. So I am anti-bicarb. And then the last drug I'm gonna talk about is calcium. So we all like calcium, right? It stabilizes cardiac membranes. It's another thing that we can do that feels good to our patients. But this study also published for resuscitation was a sub-analysis of the COCA trial that was a randomized controlled trial originally that took 391 patients. This is out of hospital cardiac arrest. This sub-analysis was patients presenting in PEA and getting calcium either after the first dose of epinephrine and then after the second dose of epinephrine. Planned without any ISTAT, without any measuring. And what the graph is showing here is the relative rhythm transition from PEA after each of these things. So a majority of patients stayed in PEA. Some patients converted to a Chaco rhythm, more in placebo. And actually more patients achieved ROSC that didn't get the calcium. There were, as you would expect, very poor survival to hospital discharge and poor survival to hospital admission. But calcium, just inherently given in the absence of a true indication, may also not be that helpful. So for an overall summary of our medications, epinephrine's still in the algorithm. It has a questionable outcome impact, but timing is everything. If you have a Chaco rhythm, you need to wait to give the epinephrine until after two shocks, which is very hard for us to do because we've got an algorithm and it says give the epi, but you gotta do it at the right time. For a non-Chaco rhythm, remember, epinephrine early is much more beneficial. Bicarb, it's possibly harmful and it doesn't improve outcomes. Calcium, if you're giving it to all comer patients, you can possibly have decreased survival. There was an in-hospital cardiac arrest and pediatric study that did show worse outcomes with inherent calcium administration. I would reserve this for a known low ionized calcium or a situation where you're using massive transfusion protocol. For lidocaine versus amiodarone, they're considered equivalent in the latest guidelines. The most recent study says that lidocaine potentially has improved outcomes relative to amiodarone, but I think with the body of literature that exists, it's hard to really say one over another. Unfortunately for pharmacy, there's no medication that actually improves the long-term outcomes in cardiac arrest. Rapid application of high quality CPR is one of the most effective interventions we possess. And while I've got a box of treats, they're not that helpful. Thank you. Thank you for that, Kristen. I shudder to think about how many times I've asked you for bicarbonate code. All right, so we're gonna continue on with the case. So the gentleman, as you remember, had cardiac arrest after 20 minutes of CPR. ROSC is achieved. Patient stabilized on three pressors, ventilator support, and the team's notified families now in the waiting area. They arrived while the code was going on. So I'm gonna be chatting about controversies and how we approach families during a code situation. We all have our own approaches based on our prior experiences. And we'll chat a little bit about pros and cons of each approach, and then decision making with family during slash after code. So why is engaging the family important? I think we can all agree, right? I think it's not something that comes to mind immediately when you're thinking about how to help stabilize the patient but when the patient can't advocate for themselves, these are the people we need to reach out. Engaged families can advocate for them and reaching out to them can help engage their trust, can help minimize their trauma from this unexpected occurrence, and can help manage their expectations. But a lot of times there are different things that affect how we do that, and so we'll chat a bit about that. So I guess, show of hands, how many people like to have families in the room when they're coding? Fair enough. And how many people don't? Okay, so about a split room, and that makes sense because that's, I think, where we are in how medicine has evolved. As you heard from the prior two speakers, we tend to stick to a lot of what we've learned in the past rather than necessarily changing sometimes, and so no right approach, but it does depend on the situation. It depends on what's going on. How perceptions shape us. So this was a really interesting study that I found by Doyle et al. This was in 1987. This was the pivotal study on family engagement in cardiac resuscitation. It was done in an emergency department in Michigan where they randomly started talking to families and asked them if they'd want to be part of the code situation, and overwhelmingly people said yes, which was surprising. It wouldn't be what we would expect, and so then they made a more formal study, and they divided up into staff members and families and got their perceptions. Most of the staff members, or I shouldn't say most, 30% of staff members reported that they felt uncomfortable about being observed, and they felt concerned that the family might be disruptive or they'd have to manage the family along with the patient. The families, however, overwhelmingly felt it was a positive experience. They felt it would be helpful for them, for their loved one, potentially, if they had any consciousness of what was going on, and 97% said if the situation was to recur again, they would want to be here again, which is fascinating. It's not numbers we would think. So, as a follow-up to that, McLennathan did a survey of all the participants in a CHEST meeting in 2002, so all healthcare workers, physicians, nurses, allied staff, to see what their perceptions were. Only 20% of patients wanted to have families present during relastation, and 39% of the allied staff otherwise would want that, and most of the concern that they had was about psychological safety, performance anxiety, and medical-legal concerns, and it's interesting. These studies are about 10, 12 years apart. We have not much data, but we have some data saying that families don't find it as traumatic as maybe we think it is, so it's interesting. So, I'm gonna talk a little bit about various studies that advocate for or against family presence during CPR and why. So, Fernandez et al. in 2009, they ran a study on simulated codes in mannequins, and they wanted to see what providers reacted as. They noticed that there was a delay in shock administration when they were having family in the room, even during a simulated code, and, surprisingly, that they would also use a smaller voltage of the shock, which is not good for any situation. And then Compton, in 2009, looked at out-of-hospital cardiac arrest. This was a pretty extensive study, but was primarily based out of the hospital. They noticed that presence of the family members during a code situation seemed to increase PTSD, but was it confounded by the fact that there was somebody who you loved who was suddenly having a cardiac arrest at home and having to deal with all of that? Unclear, but that was the result that they found. So, advocates for family presence during CPR. As you can see, a lot of the data was from the early 2000s that showed that maybe having family around may not be super helpful. As of the late 2000s or early 2010s, there was more data that looked at basically how families perceived it. So Compton et al. did another study in 2011. They interviewed 65 family members. The difference was that this time, they did it with the family members having chaperones present who were explaining the process to them, and they noticed that now there was no difference in PTSD outcomes. Jabray et al. did a comprehensive study in 2013, which actually showed that PTSD was higher at 90 days when families did not witness the CPR because then they did not know the outcomes, and they weren't able to be engaged and were more traumatized. They also looked at whether or not it altered care or affected team function and noticed that there was no difference. And this was a study that was done in France, so the medical-legal system may be slightly different, but they didn't notice any medical-legal action from families witnessing the CPR. So it's interesting, the trend that has changed. So where do we stand now? Where is the latest data? So this is a list of some pertinent articles that look through what's going on, and what I've highlighted seems to be an interesting situation. So if you look at the first three or four, they're based out of the USA, and they're in chronological order, and the others are based in Europe. You can see that in the first couple, most of the times, they did not support, and this is in the major findings section, and the staff didn't feel like having family present would be helpful. But as we go on into the 2010s, 2014s, 2015s, they started having more approval and more interest in having family present, partly because we noticed that that helps in the patient's outcomes and the family's outcomes. In Europe, in the studies that were done in Finland, Poland, and Spain, however, even in the late 2010s, there's still less engagement from families as much as we can see, and it seems to be primarily due to the factors that are highlighted in the second text box, which is they don't have support for the family to help with helping them cope with the situation. They don't have clear guidance on how to incorporate this, and they're still worried about the things that we were worried about earlier, and some of us still are. So, to summarize, the American Heart Association in 2010 had said that we should make accommodations to help families be present, including cultural and social accommodations as needed. The European Resuscitation Council joined in 2015 with those recommendations. The European Rehabilitation Council considers family presence to be high value in providing patient-centered care and family-centered care. But some studies still show some concerns about family dynamics and lack of clear guidance, and so there's really no good answer as to how to proceed, and I think a lot of times the final decision should depend on what the family's wishes are, what the situation is, and what the team's comfortable with, as well as what institution allows. So, in our case, the patient's family wasn't present during the code, so this wasn't a discussion that needed to happen at that time, but they were updated by team members about events since the admission, and so they were engaged in that manner. Goals of care were clarified, and they were clear that they wanted the patient to remain full code and pursue additional care, including additional CPR if indicated. So, they discussed next steps, including ongoing ventilation, hemodynamic support, and targeted temperature management, amongst other measures, and so based on discussion, post-ROSC care bundle was initiated. And with that, I'll hand it over to my colleague, Kim. Thank you. Thanks, Naila. So, we're gonna wrap up our session talking about targeted temperature management. And just to kick us off, I'm curious what your current practice is. And so, following either the most recent, or when you think about cardiac arrest in your institution, what best describes your current practice? Do you use targeted temperature management 32 to 34 degrees? 36 degrees? Do you just maintain normothermia and try to treat fevers? Or does it depend on patients? Okay. You can see the number of votes. Perfect. All right. Yeah, so we've got the majority of attendees saying TTM to 36 degrees. But I'm not surprised by the mixed results on this. Am I echoing? Mic's working? Okay, great. I'm not surprised by the mixed results on this because the guidelines are a little conflicting. So, both AHA, updated in 2020, and the ERC, updated in 2021, recommend cooling to 32 to 36 degrees for at least 24 hours. The American Red Cross guidelines on ALS recommends against cooling and says that it's reasonably to actively prevent fever and maintain core temperature of 37.5 degrees or less for at least 72 hours. And so with this conflict, or some confusing recommendations, we're gonna dive into the evidence. So, looking at five landmark studies about TTM after cardiac arrest. And I've got the studies, Bernard and colleagues, the HACA study, hypothermia after cardiac arrest, TTM-1, hyperion, and TTM-2. You'll notice in this slide that the vast majority of patients analyzed are those who experienced out-of-hospital cardiac arrest, as well as those with primarily a shock low rhythm. We're gonna start in 2002. Bernard and colleagues, we had 77 patients that were not randomized, but either in 33 degrees versus treated with standard of care, at that point, normothermia. And in this study, they found that those cooled to 33 degrees were approximately two times as likely to be discharged with good neurologic outcomes compared to those who were not cooled. That same year, we had the hypothermia after cardiac arrest study with 275 patients randomized. In this unblinded but randomized study, found a 14% absolute reduction in mortality in patients who were cooled to 32 to 33 degrees compared to those who were treated with normothermia. It's important to point out that this was not a random, or sorry, not a blinded study, which meant nurses and physicians knew what patients were receiving. Some conflicting biases, potentially that nurses and physicians were in the room more often as they were trying to maintain temperatures, as well as some delay potentially in neuroprognostication for these patients. Also important to point out that those who were in the control arm, your normothermia, actually experienced a good deal of elevated temperatures during this study. But after these two largely positive studies, hypothermia was added to the guidelines, and hospitals across the country started to come up with their hypothermia protocols. Not only hospitals, but also EMS teams that now were protocolized, including giving chilled fluids, IV, as they were taking patients without a hospital arrest to hospitals. And so in 2013, TTM1 is our first larger multicenter RCT that's truly blinded with 939 patients. In this study, they compared to 33 degrees versus 36 degrees, and they found no statistical difference in mortality or neurological outcomes at six months. Around the same time, there were multiple studies looking at hypothermia to treat other conditions. If hypothermia can help with, it can be neuroprotective, should we use it in our TBI patients, patients with stroke, other infections? And study after study came out showing that there was no benefit. In fact, in 2018, we had a meta-analysis of 14 studies in over 2,600 patients, showing not only that there was no benefit, but that there was an increased mortality when hypothermia was used in TBI, stroke, and infection, and concluded that outside of the setting of cardiac arrest, hypothermia should not be used. This brings us then to 2019, where we have the Hyperion trial. This is another RCT with 584 patients, comparing now 33 degrees Celsius versus 36 degrees, with 37 degrees Celsius. This study had a positive finding with increased likelihood of survival with a good neurologic outcome in the population that was cooled. As you see in the chart, similar to the hypothermia after cardiac arrest study, this study also had a significant portion of patients that experienced fever in that first 24 hours in the control group, or the group at 37 degrees. And then this brings us to our most recent and most robust RCT, the TTM-2, published in 2021, had 1,850 patients, and was a multicenter RCT. In this study, they compared 33 degrees Celsius, and the control arm, instead of saying, we're just going to do normothermia, actually had active treatment to prevent hyperthermia. And so what they would do is patients who had a temperature that reached greater than 37.8, they would be put on a cooling system with a goal temperature of less than 37.5. In this study, they found that hypothermia had no effect on mortality or on neurological outcomes, but that there was an increase in serious effects. This actually includes more paralytics, more ventis, and two times as many adverse effects. Most significantly was hemodynamically significant cardiac arrhythmias. And so as we think about and balance the risk of hypothermia, hemodynamic instability, arrhythmia, shivering, requiring more meds, sedation, paralytics, increased ventis, increased ICU time, with this large RCT demonstrating no difference in mortality or neurological outcomes, I question the current guidelines, and think that a more reasonable approach to TTM in 2023 would be that we aggressively treat fevers to maintain normal temperatures. But that includes continuous temperature monitoring, whether it's bladder or esophageal temperature probes. It includes having scheduled antipyretics, lower ambient temperatures in the room, and then if necessary, using cooling equipment to maintain your temperature of less than 37.8. Hypothermia, I'd propose, should only be used in the setting of clinical trials. And so to wrap up our case, like any good ACLS talk, our patient achieved ROSC, they're on post-ROSC care, the family is engaged, and over the next few days, patients' processors are weaned and they are extubated, and it is a very happy ending.

CPR

capnography monitoring

drug management

family engagement

chest compressions

cardiac arrest

evidence

targeted temperature management