Good morning. Happy Monday morning, if your body is oriented. If you're like me and not quite oriented yet, my body's not exactly convinced it's Monday. I think I'm getting to the point where my body thinks it's morning, but it might be afternoon, I don't know. Welcome. You are in the Preventing Complications in ICU Airway Management session. Hopefully, that is the session that you hoped to be at. We're going to walk through some airway management and some data in airway management today. My name is Todd Rice. I am at Vanderbilt in the Pulmonary Critical Care Division. I do very little pulmonary, all my time in the ICU, and I will introduce each speaker as they come up. There's four of us today, and we'll spend an hour doing airway stuff. There's a reminder that the sessions can be evaluated through the app or online after the program, after the session, and that if you want CME, the CME evaluations will open up on Wednesday, and they're open for months, but they start opening on Wednesday, and you can go in and evaluate and get your CME. All right. So I'm going to speak first, and I'm going to speak about just complications during endotracheal intubation in general and whether this is sort of something we should accept as a hazard in our practice or whether there's potentially something that we can do about these. You guys, I just told you who I was. Conflicts of interest, I consult for a couple of companies, none of which do anything with airways, airway devices, anything to do with intubation. Biggest conflicts is that I actually do airway management in my ICU. I also do airway management research as part of the Pragmatic Critical Care Research Group, and I still get very, very nervous and anxious when I go to do an airway, and it just, I think, never goes away, and I think that's probably a good thing because of the risks involved. This is what we're going to do. We'll talk through the common complications that are encountered in airway management, understand the characteristics and variables associated with those complications, and then talk about potential interventions and the ability to modify or reduce these complications, and that's really a big part of this whole session, so that's not a big part of my talk, but the whole session in general. So you guys probably know this, but ICU complications, ICU intubations, sorry, are complicated. Lots of the literature is about intubating in an operating room, and in an operating room, about 1 in 100 patients has a complication. These are patients that are obviously optimized for having surgery, and they don't have a very severe, very high severe complication rate. In the ICU, that rate is, we put on the slide 1 in 3, but you'll see when I show you numbers, it may actually be even on the north side of 1 to 3, maybe even 40% or a little higher than 40% of patients that we intubate in the ICU that are critically ill, or if you're an emergency department physician in the emergency department that are critically ill, have a severe complication. It's obviously a bit of a higher stakes game in the ICU. Here you can see the mortality rate taken from a study called the Intube Study, which is the practice across 29 countries of airway management, and you can see these patients unfortunately die in the near term after we intubate them. Hopefully, they don't die because of our intubation. They die because that's how sick they are, and they're critically ill and at risk for dying. Managing the actual intubation, I think, is probably the easy part. The hard part is trying to manage these complications, and here you can see, this is actually a little bit of an older study from 2006, but I think the data are still pretty relevant today. You can see the rates of complications. In the far left are kind of the more serious complications, severe hypoxemia, severe collapse, cardiovascular collapse, cardiac arrest and death, and then on the right are complications, but maybe a little less severe, things like esophageal inhibition, aspiration, dental injury, et cetera. I guess if it's your tooth that got injured, it's more severe than not. Here's the Intube Study again, and if you look at major adverse events, which is their primary outcome in the Intube Study, they looked at 3,000 inhibitions across 29 countries, and you can see 1,300 plus had a severe complication, and that was 45 percent of the inhibitions in practice had a severe complication. That one in three slide that I showed you is probably me being an optimist, and it's probably a little higher than that. So why do these actually happen in one in three patients? There's a number of things that go into it. One is patient variables. We talked about these patients are sick. They're sick at baseline. They're not optimized for innovation. They're often crashing. They have severe physiologic derangements and an acute compensation. There's also procedural variables, so how good are you at doing this? Does it take multiple attempts? Did you have a good oxygenation strategy, an airway evaluation? How experienced is the operator, et cetera? And then there's potential interventions. We don't really have great interventions on the patient side of this because that's what's dealt to us, and those are the patients we see in the ICU, the ED that are critically ill, but on the procedural variables, there's potential interventions that we might be able to do to improve some of those characteristics to hopefully improve the outcomes of our patients. So quickly, hypoxemia. Hypoxemia is the most common complication of innovation outside of the operating room, and it's the strongest predictor of perianovation, cardiac arrest, and death. Sorry, there's a green arrow on my slide. I was trying to see if it was in your way also. You can see here from the study from 2006, severe hypoxemia occurs in a quarter, maybe a little bit over a quarter of the patients. Here in intube, it's 10% of the patients, but I caution you, their severe hypoxemia definition in intube is an oxygen saturation less than 80%, which I think would make a lot of us really, really nervous when our patient gets below 80%. I get nervous when they get below 95%, but below 80, I think, would make you nervous. So what sort of things are associated with hypoxemia during an intubation? Here you can see risk factors from a study from Andrew McCown and colleagues. It's you're hypoxic and that's the reason we're intubating you. You're more hypoxic when I go to intubate you, you have a higher BMI. Interestingly, a younger age is actually associated with more hypoxemia, inexperienced operator, and then time to successful intubation or first pass success has been shown numerous times to be associated with worse hypoxemia. Can we prevent it? So here's one study that I was actually part of the authorship group for on bagging patients between bagged mass ventilation, between giving them induction meds and actually taking a look. And you can see it actually reduced hypoxemia during the procedure. But even in the blue group, which is the prophylactic ventilation, there was still almost 30% of the patients that had an oxygen saturation less than 90 and 10% of the patients had an oxygen saturation less than 80. And that was an improvement, but probably not the ultimate total answer to all of the hypoxemia problem. Second one, severe collapse or hypotension, cardiovascular collapse, hypotension. This also occurs in about a quarter of the patients in the 2006 study. And I'll show you, it's actually the most common one in the intubes, common complication in the intubes study. It occurs in a third, maybe up to 40% of patients. There's a number of reasons, could be because of the induction agents that we're giving. Also because of the positive pressure, you get decreased venous return to the heart, which decreases cardiac output and can result in some hypotension. Here are the incidences in the intube study. They call it cardiovascular instability, and then they break it down. Most of this 40% was a new need or increased use of vasopressors. But there's other things that are real players here too. Systolic pressure less than 90 was in a quarter of the patients, for example. What predicts it? Not a surprise. If you're already kind of teetering on hypotension when I go to start the procedure, you're more likely to get hypotensive. The shock index, which is actually really easy to do, it's your heart rate divided by your systolic blood pressure. If that's above one, i.e. your heart rate is faster than your systolic blood pressure is high, then you are at risk for hypotension during your intubation. If you're already on vasopressors or you got them in the previous 24 hours, older age instead of younger age for this, and then non-invasive use prior to intubation. Can we prevent this hypotension? There's some early literature, 2010, from Samir Jabir in France that said that if you have a good bundle and a good procedural checklist, that you get less hypoxemia and less cardiovascular collapse. That bundle and that checklist included a fluid bolus. But when we actually studied this, specifically the fluid bolus part, you can see there wasn't actually any difference in cardiovascular collapse with the fluid bolus. So we're still trying to tease out exactly how we can help prevent cardiovascular collapse. Lastly, what about first-pass success? Can we decrease complications of airway management by improving first-pass success? We should be able, at least based off of the association, we should be able to decrease hypoxemia from it. You can see, again, from the intube study, that our first-pass success rate is about 80% in general in practice. So maybe there's room there for growth, improvement, and an opportunity to decrease complications. This is the device trial. The device trial looked at video versus direct laryngoscopy, published in June, and actually showed that you can actually increase first-pass success a fair amount, actually, if you use video laryngoscopy instead of direct laryngoscopy. And 80% you saw in the intube study, this will get you to 85, maybe even using the same definition because the definition here was a little bit more strict. You might even get all the way up to 90% first-pass success rate. A little bit on the somewhat discouraging side of this is that we didn't see in that study, though, a decrease in complications, including severe hypoxemia. Now it wasn't powered to detect these, but hopefully if it had a huge effect on these, we would have seen at least some decrease in complications. So while I think there's an opportunity to improve our first-pass success rate and the outcomes for our patients, it's not going to be the answer, the end-all, the be-all. Quick summary. Hypoxemia and hypertension are the two most common complications encountered in airway management. Interventions to reduce these complications have had some mixed results. So there's bag-mask ventilation, which has had some positive effect on hypoxemia. Fluid bolus, maybe not quite the effect that we thought. And then a question of, you know, first-pass success and making that as high as we can, decreasing some of the complication rates. And as I said, simply improving first-pass success doesn't necessarily mean we're going to have fewer complications. We still have some work to do beyond that to try and decrease these complications. Thank you for your attention. So second speaker in this session is Dr. June Chae. She is an assistant professor of medicine at Mayo Clinic in Rochester, and she's going to talk about periantubation cardiovascular collapse. All right. Good morning, everybody. Thank you for being here today, and thank you for setting us up, Dr. Rice. So my portion is on periantubation cardiovascular collapse. My name is June Chae, and I have nothing to disclose. And I trained in Rochester, but now I practice at Mayo Clinic Health Systems in Wisconsin. Very different temperature to here. So, excuse me, my main objectives today are to review data on how to prevent or treat cardiovascular collapse during endotracheal intubations, specifically in regard to choice of induction agents, fluid bolus, as well as vasopressors. So before we dive in, I think it's important to understand a bit of the physiology. So periantubation hypotension can be caused by various things. One, the types of patients that we are intubating and dealing with, especially in the EDs and ICUs. There's numerous underlying physiologic derangements, including hypovolemia, shock, acidosis, heart failure, and our nemesis, especially the right heart failure. And then, of course, the induction medications that we give have inherent effects for hypotension as well, including direct vasodilatory effects, negative inotropy, sympathetic blunting, RTL dilation with decrease in systemic vascular resistance. And then, what do we use to pre-oxygenate? Positive pressure ventilation. So the things we use for pre-oxygenation, apneic oxygenation, and then also actually initiating invasive mechanical ventilation really increases our intrathoracic pressures. And this decreases our RV preload and increases our RV afterload. And so, mixed together with our underlying physiologic derangements, the induction agents that we choose, this really causes hypotension, and this is something we're all up against. So the DeJong et al. study in 2018 demonstrated that aggressive hemodynamic support and optimization before and during intubation was a very important modifiable risk factor for intubation-related cardiac arrest. I know Dr. Rice extensively just went over in tube, but this study did find that cardiovascular instability was the most frequent adverse event following intubation. And as you can see, 42.6% of the primary adverse events of interest, cardiovascular instability was the most common. And this was defined as systolic blood pressure less than 65, systolic blood pressure less than 90 for greater than 30 minutes, new need or increase of vasopressors, which was, in fact, the most common cause of the cardiovascular instability group, and requiring a fluid bowl that's greater than 15 cc's per kg. In the cardiac arrest group, in fact, the main reason for arrest was hypovolemia and hemodynamic instability. And all this put together results in a really high ICU mortality of 32.8%. So really preventing peri-intubation hemodynamic instability is important. What tools do we have? So the first portion I'd like to talk about, spend a little time on, does choice of induction agent prevent peri-intubation hypotension? So our first induction agent of choice here is propofol. I don't know if there's anesthesiologists in the room, but I'm very comfortable with using propofol. It's rapid onset, short half-life. It has anti-convulsive properties, it reduces intracranial pressure, and it provides great intubating conditions as well. Its main adverse effect is hypotension. And this is caused by venous dilation with decreased venous return. Could cause arterial dilation with decreased SVR and decreased cardiac contractility. And the insights from the in-tube study showed that propofol, older age, tachycardia, lower systolic blood pressure, lower SpO2-FiO2 ratio before induction was associated with cardiovascular instability and collapse. So of course looking at the vital signs is really, really important. But my portion of the talk is what interventions can we do to prevent peri-intubation hypotension? And the only treatment-related variable with a significant impact on cardiovascular instability was the use of propofol. Etomidate, so that's another popular induction agent. It has a rapid onset of action, short half-life. It's deemed to be pretty hemodynamically neutral. Its name is stained because of the adrenal suppression that can occur by blocking 11-beta-hydroxylase. I'm not going to go deeper than that so you don't have to glaze over. But basically the uncertainty about the safety of a single dose of etomidate in critically ill patients, particularly septic patients, has really led to years of controversy and debate. And what about ketamine? So ketamine is another popular induction agent. Its rapid onset of action, pretty hemodynamically neutral. It has bronchodilatory effects, so great for our asthma patients. And it works by actually increasing our heart rate and blood pressure by releasing endogenous catecholamines. It also actually has direct negative inotropic effects. Usually the catecholamine effect takes over and gives us that kind of hemodynamic neutrality and bump. But in someone who's catecholamine deplete, who's been in shock and critically ill, this actually, we don't have those catecholamines to release. And then the negative inotropic effects takes over. And you could actually really have hypotension and cardiovascular demise. Other potential adverse effects with ketamine include hypersalivation and laryngospasm, which obviously are not things we want when we're intubating. And dissociation and emergence, I would say this is more for probably moderate sedation or sedation in the ER, but another potential adverse effect. So should we use ketamine or etomidate? I guess it depends on a lot of our practice, but just to review a couple studies here, in favor of ketamine, there was actually an early survival signal with ketamine at day seven from the EVK trial in 2020, true. But there was no significant difference in survival at day 28. So questions, were there unmeasured conditions? Was this underpowered? In favor of etomidate, the multicenter observational study from the NEAR Registry reported actually a greater incidence of post-induction hypotension with emergency intubation with ketamine, requiring more post-induction vasopressors. But in general, both are considered hemodynamically neutral induction agents, and the randomized KETASED trial did not report notable hemodynamic differences between the two agents. But I would like to point out there was a small group of septic patients here, and it did demonstrate that actually etomidate did have more adrenal insufficiency. But I'd like to just put a plug in for, there is a trial coming out called the RSI trial looking at both etomidate and ketamine. So hopefully we'll have some answers. So the takeaway from induction agents is propofol is associated with hypotension, we know this. Etomidate is hemodynamically neutral, but it can cause adrenal suppression, but the clinical significance after one dose is unclear. Ketamine is also hemodynamically neutral, but it can cause hypotension to the unopposed direct negative inotropic effects in catecholamine deplete patients. But again, like everything we do in critical care, individualize your induction agent choice to match your patient's underlying physiologic derangement. All right, next, what about a fluid bolus? Can we prevent peri-intubation hypotension? How many of you said run the fluids wide open? I've definitely done that, especially in residency. But it depends. I think there's some questions we have to ask ourself. Is there enough time? Do we have time to actually fully give that bolus? And do we give it to everybody? I think it's important to understand their underlying physiology. Are they actual volume responders or not? Are they truly hypovolemic? Of course, if they are truly hypovolemic, they need the volume. And again, Dr. Rice talked about this 10-point intubation bundle. So in the interest of time, I won't go over it extensively, but this did include that 500cc fluid loading. And this 10-point bundle demonstrated that severe life-threatening complications were reduced from 34% to 21% with implementation of this bundle. So what's the evidence behind IV fluid boluses? We, again, talked about the Chabert 10-point intubation bundle. There's actually international airway management guidelines that advise IV fluid bolus to prevent CV compromise. But there have been no RCTs that have examined the effect of fluid boluses on outcomes of tracheal intubation until relatively recently. So the PREPARE trial that Dr. Rice talked about demonstrated that fluid bolus did not affect overall incidence of cardiovascular collapse during intubation. Now, I'd like to, again, highlight a couple things here. So a convenient sample showed that the median fluids given was actually 200cc. Now, I don't think that's enough to have an impact on your hemodynamics. The timing of bolus was not consistent either. Was it pre or during induction? And really, not all patients respond to fluids. And there's different peri-intubation physiologic factors you're up against, such as RV failure. And in fact, the study was stopped early due to futility after enrollment of 337 patients. But interestingly, a post-hoc analysis demonstrated a signal in patients receiving positive pressure ventilation, which makes sense, right? You're increasing intrathoracic pressure. Perhaps volume would help. And so this signal was actually a hypothesis generating for PREPARE-2. And this was a larger trial, enrolling about 1,607 patients. And this also demonstrated that fluid bolus did not decrease incidence of cardiovascular collapse. Here, the median fluid bolus was 500cc. I think most of this was given prior to intubation. And 97% of patients received positive pressure ventilation between induction of anesthesia and laryngoscopy. And about 60% of patients from both groups received either pre-vaccination via NIV or bag mass ventilation. So these two large trials did not demonstrate really any benefit from fluid boluses. And if you have any questions, we have cameos from the trial authors here, so you can ask them. But the takeaway here is it depends. What's the underlying physiology? Are they volume responders? Is there enough time to actually deliver that fluid bolus? And in general, I would say a routine 500cc bolus for everyone does not reduce the incidence of CV collapse for critically ill adults undergoing tracheal intubation. And finally, what about vasopressors? Is this in our armamentarium to reduce peri-intubation hypotension? So historically, fluid boluses were actually given due to fear of peripheral vasopressors. Obviously, the landscape has changed. We do know that peripheral vasopressors are safe, especially in an IV that's working and for a limited amount of time. We know that vasopressors are faster than fluids in increasing blood pressure. Vasopressors are more titratable. And there are real negative downstream consequences with fluid overload. We also know that arterial hypotension is a modifiable risk factor for intubation-related cardiac arrest. Again, the shock index pretty easily measured at bedside, heart rate over systolic blood pressure. And it was shown that a shock index of greater than 0.9 showed higher hospital mortality, greater than 1 predicted post-intubation arrest. Now, what push-dose pressors do we have in our bag? I think a lot of this depends on our shops and where we practice. I feel like we have phenylephrine, ephedrine, epinephrine, ephedrine. I feel like ephedrine is more of an operating theater agent. In our shop, we have premixed syringes of phenylephrine. In general, these are not easy to mix and prepare, and there could be potential adverse effects of missed dosing and mixing. So unless you're really experienced, figuring out a push-dose pressor recipe right during the emergency intubation is not the time. So the takeaways here are push-dose pressors in general are efficacious and overall safe when you're comfortable with dosing. Use premixed syringes when possible, especially when pre-intubation resuscitation is not fully possible due to impending cardiopulmonary compromise and you have to emergently intubate. And the goal is to bridge to a continuous vasopressor. On the downside, it can lead to inadvertent adverse effects due to errors in dosing, dilution, if you're not familiar with that drug. And of note, we use phenylephrine a lot, but in patients who already have, they're in shock and there's depressed myocardial function, this increase in afterload can actually further depress your cardiac output. So of course, tailor your hemodynamic management to, again, your underlying physiology and velocity of decompensation. And start a vasopressor infusion if you have time. All right. Thank you. I was thinking as I was sitting there, we're talking about all the bad things that happen with intubation. Kind of made me nervous. But that's what this session is. So we're going to talk about more bad things. We're going to talk about hypoxemia that happens. And this talk will be by Dr. Stacey Trent. Dr. Trent is actually an associate professor of emergency medicine at the University of Colorado. She's also part of the PCCRG. So we wear a couple of similar hats. And she's going to talk about pre-oxygenation strategies. Thanks, Dr. Rice. We'll just jump right in. I'm Stacey Trent, as Dr. Rice mentioned. Here are my disclosures, which are none other than I do work with this guy over here at the PCCRG. And our objectives here, I won't list them off, but you can see them there. And we'll just kind of jump right in for the purpose of time. So why are we talking about hypoxemia and pre-oxygenation? As was already mentioned, that approximately 10% of patients experience severe hypoxemia during intubation. And we know this both from the Intube study, but also from the NEAR registry which is the National Emergency Airway Registry. And that hypoxemia is associated, sorry, let's see if I can keep it on track here, associated with peri-intubation, cardiac arrest, and 28-day mortality. So anything we can do to prevent severe hypoxemia is important. So what do I mean by pre-oxygenation? I mean administering NEAR 100% FiO2 for at least three minutes. I don't mean a couple liters of oxygen by nasal cannula prior to intubation. We really mean as close as you can to getting 100% FiO2 to your patient for at least three minutes. And the reason that that's important is obviously we're giving them drugs to facilitate intubation. That's going to slow their breathing down and eventually make them apneic. And the amount of oxygen that they have in their body to sort of get them through that apneic period is what's in their functional residual capacity. And if you do nothing, if you give them no supplemental oxygen prior to intubation, you really only have about 500 mLs of stored oxygen in their functional residual capacity. But if you give them NEAR 100% FiO2 for three minutes, you almost quadruple that. They get almost 2,000 milliliters of oxygen in their functional residual capacity. And this gives you an increased amount of safe apnea time. So this is why this is important. We have a few methods to do this. Not all of them get you close to 100%, but they get you somewhere near there. So the easiest one is just a face mask, a non-rebreather. Obviously very available. It should be in every one of our rooms. You know, the benefit of it is that, is that it's super available. The downsides are that you don't get any positive pressure. Obviously you can't ventilate with it. And you're not going to get 100% FiO2. If you do turn up, you know, past 15 liters, you'd really get that flush rate oxygen. You can get maybe closer to 80%. But you're not going to get 100%. But it's super well tolerated, super available, and very easy to use. You can also use a bag valve mask. Again, very easy and available. You can get some positive pressure with this if you put a peat valve on it, which is beneficial. And you can ventilate if the patient's apneic as well. But easier said than done, right, using a bag valve mask. This requires some technique. And generally requires more than one person to get a good seal around that bag to give you close to 100% FiO2. And if your patient's agitated, they may not be tolerate this at all with someone holding this, the mask around their face. You can use high flow nasal cannula. Again, this is maybe easier in the ICU to get than it is in the ED. But you can get 100% FiO2 with high flow nasal cannula, which is certainly the benefit here. It helps minimize your oxygen dilution in your upper airway dead spaces. You can get a little bit of positive pressure with high flow nasal cannula. It's super well tolerated and can be left on during intubation for apneic oxygenation. Again, you can't ventilate with this, which would be one downside. And it may not be as easily available as grabbing a face mask. But if it is, super easy to utilize. The patient's really tolerate it well. And last but not least, would be non-invasive ventilation. So again, easy to get 100% FiO2. You've got positive pressure there. You can ventilate while the patient is apneic. And obviously, it helps recruit your alveoli and increases your lung volumes. But requires a little bit more effort to set up. And again, may not be tolerated in your agitated patient. And there's also the hypothesized risk of gastric insufflation. So with all four of those options, what does the literature tell us about these methods of pre-oxygenation? So the French have been kind of all over this question. And I'll point out four of their studies. This first study was looking at high flow face mask versus high flow nasal cannula. And in six ICUs in France, the patients were included if they were in hypoxemic respiratory failure. And they left on the high flow nasal cannula for apneic oxygenation. And their primary outcome was lowest O2 saturation during intubation. Somewhat of a small study here, just over 100 patients. But as you can see by that plot, just if you look at it, the dots pretty much align. And the median lowest O2 sat was not significantly different in the high flow nasal cannula group was just about 92%. And in the high flow face mask, about 90%. All right, what about bag valve mask versus high flow nasal cannula? Again, sort of a similar group, six ICUs in France. This group was not severely hypoxemic. And again, they left on the high flow nasal cannula for apneic oxygenation. A little bit more patients in this study. But in this group that was not severely hypoxemic, again, the dots pretty much all overlap. And the median lowest O2 sat was essentially the same at about 100%. How about high flow face mask versus non-invasive ventilation? Again, this was a hypoxemic respiratory failure. Patients were excluded if they were encephalopathic or undergoing CPR. And their intervention was three minutes of high flow face mask at 15 liters versus non-invasive ventilation 100% with a PIPA 5. And their outcome was a little bit different here, looking at the SOFA score. But pulling out the relevant outcomes that we're interested here in hypoxemia. Severe hypoxemia, less than 80%. In the non-invasive ventilation group, 18% developed severe hypoxemia. And the high flow face mask group, 28% developed severe hypoxemia. Now that didn't reach statistical significance, but potentially a signal there. Interestingly though, they looked at a subgroup of patients who were on non-invasive ventilation prior to randomization in this study. So the clinical team felt like the patient needed non-invasive ventilation prior to intubation. And the study allowed them to be randomized and then switched to the other group. So they could be put in the high flow face mask group. So taken off non-invasive, put on a high flow face mask. And not surprisingly, those patients did worse. So if you were on non-invasive prior to randomizing this study and you got switched, you were on non-invasive. About 41% of those patients developed severe hypoxemia compared to only 17% of the patients who maintained on non-invasive ventilation. And that was statistically significant. So if they're on non-invasive and they need non-invasive, don't switch them off. Lastly, high flow nasal cannula versus non-invasive. This was a little bit bigger study, 28 ICUs in France. You can see their intervention here was three to five minutes of high flow nasal cannula at 100% versus non-invasive ventilation. And they found that there was no difference in development of severe hypoxemia. So non-invasive ventilation, 23% versus high flow nasal cannula, 27%. But in the subgroup that was moderately to severely hypoxemic prior to randomization, there was a little bit of a signal there. So non-invasive, 24% met that outcome versus 35% for the high flow nasal cannula group. So to summarize, sort of what does the literature tell us about these methods of pre-oxygenation? So face masks versus high flow nasal cannula, we've seen no difference but a pretty small study to compare those two. Bag valve mask versus high flow nasal cannula, again, there was no significant difference in patients who are not severely hypoxemic to begin with. Face mask versus non-invasive ventilation, there may be a signal here towards non-invasive. And importantly, don't take your patients off non-invasive if they are needing it prior to intubation. High flow nasal cannula versus non-invasive, again, no difference in all comers but maybe a signal as well towards non-invasive, particularly in your patients who are moderately to severely hypoxemic respiratory failure. I think the biggest thing we can take away from this is that we need bigger studies in this space. And I'll point to this pre-oxy study, which should be completing enrollment here very soon. 1,300 patients, so a much bigger study than what we've seen previously, looking at non-invasive ventilation versus high flow face mask in ED and ICU patients who are not on non-invasive prior to intubation. And so expect publication here early 2024. Just finishing up, that was pre-oxygenation, so getting to the point of apnea. But what else does the literature tell us about oxygenation techniques after our induction in apnea? So I'll just briefly mention apneic oxygenation. This is administering high flow oxygen during the apneic phase through induction through intubation. And these plots came from a meta-analysis that was published in Annals of Emergency Medicine. And they included observational trials. I've just taken those out because I think there's a little bit more noise than signal. But these are looking at the randomized control trials that were included in this meta-analysis. And looking just at development of hypoxemia or an O2 sat less than 93%. You can see here, the odds ratio favors apneic oxygenation, but the confidence intervals cross 1. So it may not be statistically significant. And then severe hypoxemia, development of an O2 sat less than 80%. Again the odds ratio favors apneic oxygenation, but here the upper bounds of the confidence interval is 1.47. So not statistically significant. And I'll also mention ventilation during apnea, which the study has already been mentioned once or twice before. But this was an unblinded RCT in seven ICUs in the U.S. Intervention was bag mask ventilation between induction and laryngoscopy versus no ventilation. And importantly, the intervention was sort of outlined here. So oral airway is in place. They're using 15 liters per minute. They have a peat valve and only giving 10 breaths per minute with a two-hand seal, chin lift and jaw thrust. And the results here show that if you provide ventilation during that apneic period, you can significantly lower the development of severe hypoxemia. So 11% of patients in the bag valve mask group versus 23% in the no ventilation group develop severe hypoxemia with a number needed to treat of nine. And I think the one complication that we're all worried about is aspiration giving as we're ventilating during this apneic period. And they reported no difference in aspiration events between these two groups. But importantly, this was underpowered to find that safety outcome. So summarizing these two points, apneic oxygenation, I think there's questionable benefit, particularly for preventing severe hypoxemia. But I don't think there's any harm. So if this is what you do, go for it. Bag valve mask ventilating after apnea does help prevent severe hypoxemia with a number needed to treat of nine. I think, though, importantly is the technique. You have to do this well to be successful. But certainly if your patient is moderately to severely hypoxemic to begin with, this can help you make that worse. All right. With that, I'll stop and turn it over to Dr. Jantz. Thank you, Stacey. So the last talk, the fourth talk of the session is going to be by Dr. Dave Jantz. He's an associate professor of medicine in New Orleans at LSU. And he is going to actually teach us how to do all of these innovations without any complications at all. Well, maybe not exactly. But he's going to put it all together and kind of give us kind of an overview of the best way to do these. So Dave. Great. Thank you. Good morning. I was struck during this session that you and I, we've been doing airway research now for almost a decade. And I was thinking back, if this session happened a decade ago, you wouldn't have all this evidence that they just presented to you in such an elegant fashion. You would have had the luminaries of airway experts standing up here, perhaps people as old as Todd standing up here, telling you, you know, do it this way or do it that way because I say so, or because that's the way I was taught. Not because of this wealth of evidence that's now been laid out for you. And so it's, which is a blessing that now we have all that evidence. But now, since we have all that evidence, it's our responsibility to keep up with it. This evidence is being generated quickly. Like Todd and the rest of the speakers have mentioned, there's groups, airway groups now generating this evidence year after year quickly. And so we need some kind of a method to keep up with what's the most evidence-based approach to routine ICU airways, and that, therefore, is my job in the next 10 minutes. I have this disclosure, I have no plans on talking about biomarkers of sepsis. So here's what we're going to try to cover. Again, the very short and quick version of what is the best evidence regarding each of these steps of intubation. There may be more steps of intubation that you don't see in the screen. But I have 10 minutes. I've got to focus on some things. I can't talk about everything in the world. These are routine intubations, routine ICU intubations we're talking about. These are not your war stories of the time you intubated the most difficult patient in the world, or like the time you intubated a giraffe or something that had esophageal varices and it was puke. Giraffe with varices sounds frightening. It's not that. This is, here's an ICU patient. There's nothing unique about them other than being an ICU patient. You need to intubate them. This is what should you routinely do based on the evidence. Inpatients in the ED or the ICU, not focused on kids, only focused on adults. And again, the evidence regarding patient procedural set outcomes. So again, starting at the top of the screen, just the decision to intubate. Who needs to be intubated? There are not comparative trials comparing this threshold of intubation. For example, if you're this hypoxemic, you should intubate versus that. What does exist, it's not perfect in any means. What does exist, though, are lots of studies in regards to who gets intubated. So this is from the Intube observational study that's already been mentioned this morning, describing to you who are the patients that you're commonly intubating in the ICU. Most commonly, as expected, about half of those patients are being intubated for respiratory failure. But a pretty good number of patients, a third of patients, getting intubated because they have some neurologic impairment. So these are the patients who are getting intubated commonly in the ICU. Thresholds for intubation, again, there isn't evidence comparing one threshold for another. What we have is our studies and guidelines that exist of interventions to try to prevent intubation that did include thresholds, which is a slight advance in regards to who may need to be intubated, this decision here on who to intubate. This is the FLORALI trial up on the left side of the screen. This is the threshold they used. This was pre-COVID. The threshold they used of who are we going to intubate, how are we going to make this decision of who needs to be intubated. You can go through some of these. But all of you that have experienced COVID in the ICU quickly probably go through these and say, I'm not intubating half of these patients that's listed up on the screen. Are you intubating every patient in your ICU as one map measure less than 65? Probably not. But still, it's an advance that at least they put their nickel down and said, we're going to intubate patients for this reason. Because maybe over time, with more studies like this, we can figure out whether or not get closer to whether or not these are legitimate criteria to use to decide when to intubate. Same with the gold guidelines. These are guidelines on the study. The guidelines of who is failing non-invasive ventilation and then therefore needs to be intubated. Again, you can read these. At least they put their nickel down and said, here's who we think needs to be intubated. You can say, maybe I'd let some of these patients go a little bit longer. But at the very least, we're making slow advances towards this decision, the decision of who do I need to intubate in the ICU and perhaps who not. What about preparing to intubate? It's been mentioned a little bit so far this morning. This idea of using checklists, preparatory checklists, in your ICU intubations. There's now a meta-analysis. There's been a few studies of using checklists. There's now a meta-analysis, meta-analyzing all the data from those studies. This is the outcome here of first pass success. You can see that there's no significant effect of using checklists to prepare for this procedure of intubation in the ICU. That's a procedure-less centered outcome, first pass success. Then a patient-centered outcome here of hypoxemia, so did patients desaturate more or less? If a checklist was used to intubate the patient, and the answer was, again, in these studies and in this meta-analysis, there does not seem to be an effect of using checklists in preparing to intubate critically ill adults. Already mentioned this morning, but again, to summarize for you, the use of non-invasive ventilation or other oxygen mass techniques. This was talked about in the previous talk. This trial from the British Journal of Anesthesia, again, the primary outcome of this trial was actually highest SOFA score, which they did not hit on the primary outcome. Here, these were secondary outcomes and specifically adverse events that they're measuring here. You can see highlighted in the green boxes, fewer adverse events, specifically fewer desaturations to less than 80% in patients that got pre-oxygenated with non-invasive ventilation compared to a non-rebreather mask. Again, summarizing quickly for you the data on hemodynamic optimization, fluid boluses already mentioned. Fluid boluses, no difference between groups overall in regards to percent of patients cardiovascular collapse. In fact, a numerically higher rate of cardiovascular collapse in the fluid bolus group compared to none, not statistically significant, but numerically higher. That's in a couple of randomized trials now. And in observations of those trials, so again, this was not a trial of using vasopressors or not to prevent cardiovascular collapse. This is just an observational study of when people use vasopressors in this scenario of intubation. Does it prevent cardiovascular collapse? And the rate of peri-intubation hypotension in this observational study was actually higher in the vasopressor group. Again, likely a pretty big selection bias here that may not be able to be accounted for, but at the very least in the existing observational data, it doesn't look like vasopressors are winning by a mile here in preventing cardiovascular collapse. Procedural medications, the age-old question of etomidate versus ketamine, which has already been gone into detail for you, here, again, those two trials, in regards to procedural performance, so difficult airway on the left, failed first-pass success on the right. In regards to procedural performance, doesn't seem like there's a big effect here in regards to comparing etomidate and ketamine, but there's this kind of pesky survival benefit that is statistically significant at some points, not at others, when it pertains to using ketamine. It seems to be somewhat consistent. I don't have it here. There's actually another trial that was just published last week, smaller trial, not significant survival benefit, but still trending in the direction of ketamine having a numerically higher survival rate than etomidate. Again, I think we're going to get a better answer to this question when the RSI trial is finished and published, but at the very least, there's this somewhat consistent signal here with ketamine in regards to patient-centered outcomes, not necessarily procedural-centered outcomes. What about the other procedural medication? So here's succinylcholine versus rocuronium. Again, on the left side of the screen, this is a randomized trial comparing these two things. A procedural outcome, seems that these two different paralytics perform the same in regards to first-pass success, but maybe don't perform the same in regards to severe complication, so a higher severe complication rate in patients randomized, these are critical adults, randomized to succinylcholine compared to rocuronium. Those severe complications were severe arrhythmias, new shock, hypoxemia, or aspiration. That was a significant higher rate of severe complications when succinylcholine was used compared to rocuronium. What about devices to use? Again, already mentioned this morning in this session, the VL versus DL debate likely has now been answered in routine use in critical adults, and that video laryngoscopy is superior to direct laryngoscopy in regards to procedural-centered outcomes such as first-pass success. Positioning, should you use the ramped versus sniffing position? This is the most recent and largest randomized trial of this question in critical adults in the ICU. In regards to preventing desaturation, there didn't seem to be a difference. There was not a significant difference in lowest oxygen saturation in these two positions, but when it comes to these two positions, there maybe was a difference in your ability to get the tube in on the first try, and it seemed to happen at a lower rate if you put the patient in the ramped head-up position rather than leaving them in the sniffing position. The sniffing position here seems superior in regards to first-pass success compared to the ramped position. Already mentioned about should you squeeze the bag or not after you give drugs, after you give a sedative and paralytic drug to prevent desaturation, and in this trial, squeezing the bag, providing bag valve mass ventilation prevented severe hypoxemia. Other devices other than the antitracheal tube and Stilette, so for example, should you not use a Stilette at all? Should you just use the antitracheal tube itself? This was a trial called the Stiletto trial, and in regards to first-pass success shown here, you can see the first-pass success was higher when you used a Stilette compared to not using a Stilette. This was just the tube alone here in light gray, and complications were similar. So it seems that putting a Stilette in the antitracheal tube is beneficial in regards to getting the tube in the airway in the first attempt. What about bougies versus Stilette? This is from the bougie trial, and again, no significant difference in regards to first-attempt success or proportion of patients who are successfully intubated. So let's summarize. This is going to be my opinion. Feel free to disagree. I was hoping there wouldn't be time to disagree, but there's time to disagree, so you'll get the chance to disagree. This part is my opinion. The evidence has been summarized for you. Again, part of my job is to try to make this, summarize all this stuff in the past 10 years into maybe perhaps one slide of in these steps of intubation, what do I think the truth is in regards to what things are routine or is routine use not supported, what things I just don't know if you should do these things or not, and then finally, where do I think routine use is favored? So the decision to intubate, I think we're still lost on this of who needs to be intubated in the ICU and who doesn't. We probably all have opinions in the room of who needs to be intubated and who doesn't, but I think we're making incremental steps towards perhaps groups of people that likely do need to be intubated. It's just going to take a lot more time to get more information on that. How to prepare to be intubated. I don't think checklists are supported by the evidence in regards to if you use a checklist in your intubations of critical adults, I don't think there is evidence that says that's going to improve something related to procedural performance or some patient-centered outcome. Now, some of the attendings I work with say, well, I just want my trainees to know what to get from the equipment room every time they intubate so they don't annoy me and ask me questions. True. None of these studies had the primary outcome of annoyance of attendings when it comes to collecting supplies. So that may still be an important outcome to you. All I'm saying is using a checklist doesn't seem to be the perfect thing ever to prevent complications of endotracheal intubation. What about pre-oxygenation? I think non-invasive ventilation is maybe a tick to the right of this line if I don't know. Maybe there's a little bit of evidence so far that perhaps it may be superior to other methods. But again, I think you're going to get much better evidence hopefully in the next few months of what's the truth of that. But I think it's probably ticking to the side in favor of routine use. It is a big resource. So you probably need more than just a little tick to the right of that line. What about hemodynamic optimization? I don't think fluid boluses should be routinely used. Vase oppressors, I don't know. I think we need a trial. We need randomized trials of vase oppressors because the selection bias is just too huge in observational studies of vase oppressors. Procedural medications, I think ketamine is probably landing slightly on the right-hand side of that line if I don't know. I think rocuronium is somewhere in the same region. But again, I think we probably need bigger randomized trials to become more confident on what are the effects of those drugs. I think video laryngoscopy falls far to the right side of that line that it should be favored, that you should be routinely using video laryngoscopy in your ICU intubations. I think sniffing position, the evidence that suggests sniffing position should be the default. Again, you may have special patient care scenarios that require something different, but at least the default here that you should be using bag mass ventilation after you give drugs for induction. And that bougies likely shouldn't be routinely used, but ET tubes with stylets in them should. And with that, I'm done.

ICU airway management

complications prevention

decision-making

pre-oxygenation

procedural preparations

hemodynamic optimization

procedural medications

device selection

patient positioning