Welcome to the session. This is 1044, ICU Management of Patients with Obstructive Lung Disease. I'm Margaret Disselkamp. I'm the chair, and we have Dr. Ruben Restrepo as well as Dr. Eduardo Morales that will be speaking this morning. Dr. Stockdale could not make it, so I'm going to, what we're going to do is have a case presentation, and then we're going to follow through the ICU management along, using this sort of case reference. So, admittedly, this case is not mine, but I will present this case for Dr. Stockdale who couldn't make it. And I do have a couple of audience response questions, so if you guys want to go ahead and point your camera at this QR code. All right, our session objectives, so we're going to describe the magnitude of acute respiratory failure in patients with obstructive lung disease. We're going to explain the role of non-invasive ventilation, and we'll then describe mechanical ventilation strategies, and then outline rescue strategies when all else fails. So, our case, we have a 55-year-old woman who presented with shortness of breath, chest tightness, and wheezing for the past 24 hours. She does have a past medical history of some features of asthma and COPD overlap, and she's an active smoker. She reports that she'd had a productive cough with clear sputum for the past three days. She's been using her rescue inhaler four times a day without really any relief, and she denies any recent travel, other sick contacts, or nausea, vomiting. Other past medical history, again, she's an active smoker with about half a pack a day, uses alcohol socially. She's prescribed a long-acting beta agonist and inhaled steroids as well as a PRN short-acting beta agonist. In her review of systems, really only positive for pulmonary symptoms. So, she has some chest tightness, some shortness of breath, and wheezing. The other review systems were pretty unremarkable. On physical exam, she is requiring some supplemental oxygen, but she's setting 99% on four liters. She's obese. She's diaphoretic, using accessory muscles with some nasal flaring and diffuse expiratory wheezes. And in the ER, she was given a continuous albuterol and nebulizer, IV steroids, and antibiotics. Following this course, her symptoms actually improved, and she was admitted to the regular floor. And you can see, this is her blood gas in the ER on admission. However, her first day in the hospital, she started to decompensate and was then transferred to the ICU and was placed on BiPAP. And this was her gas even after BiPAP. So, you can see, she's still not compensated. And from here, she did go on to become mechanically ventilated. Initially had some, a little bit of improvement in her blood gases on the ventilator, but this was not sustained. And you can see her best blood gas, 72870. And she ended up becoming worse even on mechanical ventilator. So, again, things that we will answer during this session, what's the utility and what's the evidence for noninvasive and critically ill patients with obstructive lung diseases? What are the ventilator strategies that we can use? And then, what do we do when all else fails? All right. So, now I'm going to move into, again, that was our, that's kind of like the case outline for this talk. I'm Margaret Disselkamp. I work at the Lexington VA Healthcare System. I have no disclosures. So, specifically for my talk, I'm going to describe the magnitude of acute respiratory failure in our patients in the ICU, explain the role and the evidence with noninvasive use in the context of this case. So, to review, we had our 55-year-old patient who has both some features of asthma and COPD, who was transferred to the ICU after initially being admitted to the floor. So, first is how extensive is our problem with obstructive lung diseases in the ICU? The asthma prevalence, you'll remember, is about 8%. We end up with about 1.6 million ER visits every year, with somewhere between 10 and 30% of those patients being admitted to the hospital. And somewhere between 2 and 5%, depending on the studies that you read of those patients, will end up on mechanical ventilation. And 20 to 30% of patients who are initially placed on noninvasive will fail. The mortality in ICU patients with asthma, again, ranges somewhere between 4 and 11%. For COPD, the prevalence varies. So, it's low. It's about 4% here in Hawaii, to about 11% where I practiced in Kentucky. So, it's a good place for a pulmonologist. And there are about 2 million ER visits for COPD. This was about 2016 data. Again, similar to asthma, about a third of those patients will be hospitalized. About a quarter of those patients will end up in our ICU. And somewhat similar mortality for COPD patients as asthma patients. And looking at the sort of physiology behind acute exacerbations and obstructive lung diseases, we have hypercapnia, which in our patients leads to worsening dyspnea, which leads to anxiety, tachypnea as they try to compensate. This leads to inadequate expiratory time, which is going to cause lung hyperinflation and auto-PEEP. That's going to lead to our flat, ineffective diaphragm and our increased work of breathing, which when we have increased work of breathing, we have more COPD production, CO2 production. We have more hypercapnia. And eventually, we have this spiral of death. And in the beginning with hypercapnia, we get dyspnea and anxiety. But as we all know, with increasing levels of CO2, it becomes, it has amnestic properties. And so we get some CO2 narcosis. With the use of noninvasive, we're really targeting the work of breathing. We're targeting that dyspnea sensation. We're targeting the auto-PEEP and the tachypnea. And you could even argue with some of this, you're going to also improve patient's anxiety as well. We know potential indicators of success for noninvasive. And some of this our patient had. So younger age, only moderate hypercapnia and moderate acidemia. And that we should see some improvement in the first couple hours when our patients are on noninvasive. Contraindications, again, we're all going to be familiar with this, cardiac arrest, inability to tolerate or handle their own secretions. And when we look at the history of noninvasive use, so this was attempted in the early 60s, in the 80s. In the early 1990s, we had several studies that really started to be performed. But the outcomes weren't entirely clear. And then as we got more and more studies, we started to actually see some real tangible improvements in terms of length of stay and then mortality. So looking at those studies that were published from 1991 to 2000, this led to the very first guidelines from the ATS. So again, back in 2001, they said, if you have COPD exacerbation and rapid clinical deterioration, it's probably okay to try noninvasive ventilation. So things that seem like second nature were brand new back in 2001. We were certain that it could improve gas exchange in patients with emphysema. We weren't exactly sure at that time where those patients belong. But we wanted to do lots more studies. And again, that was back in 2001. So first question, which of these following best describes the use of noninvasive? So it's been associated with lower rates of nosocomial pneumonia and COPD. It's been shown to have a reduction in asthma mortality in prospective randomized trials. Bi-level but not CPAP can reduce left ventricular afterload in patients due to cardiogenic pulmonary edema. Or NIPV is recommended for treatment of patients who develop post-extubation respiratory failure. So again, there's the QR code. All right, let's see. Okay. And the actual correct answer is the first one. So non-invasive has actually been associated with lower rates of nosocomial pneumonia in COPD patients. And we'll look at that. So fast-forwarding from those 2001 guidelines to 2017 when they were updated after more data. So now we are clear that non-invasive should be used in acute respiratory failure due to COPD. And these are the reasons. It decreases the need for intubation. It decreases mortality. And it decreases that nosocomial pneumonia. So that was why that one was the correct answer. Either one, non-invasive or CPAP, has been shown to reduce left ventricular afterload. So both of them can be used for patients who have cardiogenic pulmonary edema. We should not use it in the treatment of patients that develop post-extubation respiratory failure. But you can use it to prevent post-extubation respiratory failure. So remember, if you plan to do it, that's when you want to use it for your extubated patients. But if you develop it and it was unplanned, so those patients actually have increased mortality, you shouldn't use it for that. And in 2017, ATS actually will make no recommendation on the use of non-invasive for asthma because there was really no evidence. And what was the evidence? Well, the Cochrane Review that came out in 2012 had a total of five studies. So not a lot of evidence. Those five studies, there were no prospective trials. There was no clear mortality benefit, no clear reduction in intubation rates, and no clear improvement even in blood gas results. Well, that was the ATS. The British Thoracic Society actually went further and said we recommend that you don't actually use it. So don't use non-invasive for asthma exacerbations, although this was a grade C recommendation. However, the very next recommendation said, well, patients who have COPD might have some features of asthma, so maybe it's okay in those patients. Although, again, this is a grade D recommendation. So those are our current guidelines. But what do we actually do in the ICU? So this was a prospective observational study. So at four time periods, this was observational data, in 98, 2004, 2010, and 2016. And what we see is that the rates of COPD, or rates of patients with COPD on mechanical ventilation have gone down. The rates of asthma patients remain about the same. And again, this is pre-COVID data, because you'll see the ARDS patients are very low population. But look at our use of non-invasive. So our use of non-invasive is increased rapidly, right along with the guidelines. So back in 1998, when we were first bringing these around, non-invasive was not as common as it is in 2016. So we're using non-invasive very, very often. And now it's 2003, or 2023, so surely we have some asthma evidence now. And the answer is we don't have great evidence still for asthma. This is about as good as it gets. So this is a retrospective cohort study. It is very large, although, again, retrospective. So over 50,000 patients that were studied for this. So of those 50,000 admitted for just asthma, everybody else was excluded, they looked and did propensity matching on about 13,000 patients. So again, here is the outline. So initially, there were almost 112,000 patients, but they excluded COPD patients, patients admitted for other causes. So you either had to have asthma as your number one diagnosis, or respiratory failure, followed by asthma exacerbation. And then eventually, you get down to about 13,000 for the prospective propensity match group. The overall trends for the entire population. So an increased use in non-invasive, which matches some of the other evidence that we've already seen. And a decrease in patients receiving invasive mechanical ventilation without first a trial of non-invasive, which I think is pretty common with what we all practice. So not really anything earth shattering there. About 27% of the patients received mechanical ventilation for asthma exacerbation. So again, consistent with some of our older studies. 25% total were on non-invasive. Of the patients who got non-invasive, about 22% of those failed and required mechanical ventilation. Those patients tended to have some other diagnosis as well. So pneumonia, sepsis, acute renal failure, and any history of active smoking or drug use. When you looked at the entire cohort, so all 50,000 patients, the overall mortality was pretty low, 2.4%. So that's pretty good. And you see the patients who were on non-invasive and the non-invasive work, their mortality was also very, very low, 0.8%. Patients who were on non-invasive who then failed and required mechanical ventilation, so this is the gray bar. So their mortality was higher, 4.5%, higher than just non-invasive, but not as high as the patients who had to go straight to invasive mechanical ventilation. So 7.6% for those patients. And again, this is retrospective data, so you could say, well, the ones who were the sickest were on mechanical ventilation first, and that's fair. Versus the ones who at least had a trial of non-invasive, but even those patients that had a trial failed, did have a higher mortality, but not as high as those patients who went straight to mechanical ventilation. Looking at just those propensity match cohort groups, non-invasive was associated with lower odds of needing invasive mechanical ventilation, and it was associated with lower mortality. Again, retrospective data. But that might be as good as it gets. What about which mode of non-invasive should you use for these patients? Well, just as for mechanical ventilation, few studies have actually looked at the differences in head to head trials of which mode for non-invasive is going to be best. All of the modes have been shown to have either some physiologic or clinical benefit. We know in acute exacerbations of COPD, assist control, pressure support, and even proportional assist have all shown improvements in minute ventilation, respiratory rate, and blood gases while unloading the respiratory muscles and helping respiratory distress. A study from 2019 compared pressure support with adaptive ventilation and showed similar outcomes. And again, as I mentioned, adding PEEP counteracts the effects of intrinsic PEEP and reduces the diaphragmatic effort. It reduces oxygen consumption, so you're going to have a reduction in CO2 production. Volume and pressure controlled modes, and this makes sense, they reduce the inspiratory workload better than a pressure support mode, right? So it makes sense you're taking more of the work from the patient, you're going to have an improvement in terms of the workload at the expense, of course, of patient comfort and mask leak. So there's no clear evidence to support a specific mode. You should pick the one that either you're the most familiar with, your institution is the most familiar with, and you're going to have some, depending on your ventilator that you have at your institution, you're going to have some proprietary mode, right? So controlled modes may be better for patients with severe respiratory distress or severe hypoventilation, but otherwise, assisted modes may be best in those patients. All right, next question. All right, excellent. So this is slam dunk, right? So the best evidence is going to be for our COPD patients in terms of good data supporting patients, even with this pH and this CO2. So moving back to our patient case. So again, patient continued to decompensate despite the use of BiPAP. So this was her blood gas after BiPAP, and she was intubated and placed on mechanical ventilation where I will pass this talk off to the next speaker. But to summarize, using noninvasive for COPD exacerbation, it decreases the mortality risk by 46%, it decreases the need for intubation by 65%, as well as reducing the hospital length of stay and reducing those complications, especially nosocomial pneumonia. In asthma patients, it's less clearly defined. So I would say based on that retrospective data, I think that those less severe patients do deserve a trial of noninvasive. I would not do that outside of the ICU. So that's one caveat that I would say compared to your COPD patients, which might be in your progressive care unit. Those would not be patients with asthma. If I was trying noninvasive, I wouldn't do it in a step-down unit. And then there's no clear evidence for one mode versus the other. But your controlled modes are going to give you more reduction in that work of breathing. All right, and I'll pass it off to Dr. Strickland. Thank you. Okay, so what I was charged for the next two hours was to, no, 20 minutes, just to awake, was to speak of the invasive mechanical ventilation during chronic obstructive lung disease. So I'm Ruben Restrepo, I'm a professor and the coordinator of research for the Division of Respiratory Care at UT Health, San Antonio. I don't have any response, audience response questions. Here are my disclosures. Anything that deals with this presentation doesn't endorse any mode or ventilator. And what I chose for the objectives will be to review some of the principles that you know about pathophysiology behind COPD, asthma, hyperdynamic hyperinflation, but mostly to review some of the ventilator strategies that deal with the management of these patients to hopefully improve outcomes. So we inherited a patient who was already acidotic, hypercapnic, sometimes hypoxemic, sometimes they are not severely hypoxemic. And we choose to ventilate these patients when we have certain indications. Particularly in this patient we have, of course, acidosis and hypercapnia, but it would be sometimes at the expense of cyanosis, encephalopathy, or sometimes when they are hemodynamically unstable. I think there's no question that sometimes we have some precursors to workload of the respiratory system on these patients at the expense of airway obstruction. And it is when they have bronchospasm, mucosal edema, when they have mucus, when they have dynamic airway collapse, that this has a tendency to overload the system, and of course they have a chance to sometimes develop respiratory failure. When we have exacerbations of an obstructed lung disease, we will have the increased alveolar ventilation at the expense of a massive effort for the patients to keep this ventilation enough to clear CO2. The only problem is that they have a tendency to now, of course, increase the tidal volume and you have seen this on PFTs to the expense of just getting to TLC, or even over that, or just beyond FRC. Also at the expense of respiratory rates, and of course that will promote what we have as, which is the common denominator would be air trapping. That's when the end-expiratory lung volume will exceed, the predicted FRC causes hyperinflation, the overall compliance of the respiratory system decreases, but also they have a risk of exhaustion. That's exactly the main issue that we encounter on these patients. Fortunately enough, again, as Margaret said, it's 2-3%, 2-3%, but then those who get admitted to the hospital, sometimes a quarter of those will be admitted to the ICU for assistance or undergo mechanical ventilation. So you see that they have a very high increased workability, but the main thing is once they buy the tube, once they are intubated, that's when we start just reviewing all of these equations that we learned like probably about 25 years ago, or 40, which is the radius. So now we have an endotracheal tube that is going to severely compromise the airflow, is going to increase resistance. So this is when we are intubated. So now it comes to the point where we have to review what happens in normal subjects, because I think what we have to realize is that many times we ignore the waveforms. We have a very solid foundation in regards to the pathophysiology, but everything is just right there. So remember the days when we had the Puritan-Bennett, the 780, I'm sorry, the 7200, and everyone was looking at the numbers because nobody wanted to look at the waveforms? Well not anymore. That is not exactly the case anymore. So as you see, regardless of the flow waveform that you choose to select for your patients, what you're going to see is that there is a return of the expiratory tracing back to baseline before the next breath. That's exactly what is supposed to happen. So there should be no interruption of flow just prior to the next breath, which again brings us to the point of what is the effect of this dynamic hyperinflation. I'm going to show you this graph. Let me see if I have the mouse working here somewhere. Maybe not, okay. So I'm going to be explaining this, which is actually a very nice graph indicating how progressively the expiratory tracing doesn't come back to baseline. But it doesn't matter if you're using the AVEA, if you're using the Draeger, this interruption of flow, the expiratory flow, is what actually is the landmark of gas trapping. So remember that even though we have a tendency to say that this is auto-PEEP, this is reality, gas trapping. Auto-PEEP is never measured on the flow versus time tracing. So as a consequence, what we will have is that all of these variables, and I think this is the key, and I just decided to just bold and just put this in red, is because those are the ventilator strategies. These are the ventilator parameters that you're going to modify to make sure that we are able to control some of this hyperinflation and intrinsic PEEP. So this is not a new term. It's funny because I wish I could tell, you know, we found a new way to do things, but you're going to see references that date back to 50 years ago, and some of those things haven't changed. So from the first time it was described in the 70s to the point where now the clinical value was explained by Pepe and Marini, not too many things actually have really significantly changed. So consequences of the, so the other last name, let's say the bad companion of the hyperinflation will be airway collapse. So you have the critical closure of the small airways, and that will be only doing one thing, which is to promote gas trapping. And of course, in the presence of gas trapping, as I'm going to show you, something that you have seen before, the patient will demonstrate increased effort. That's going to be an issue because not only have gas trapped with CO2, so CO2 clearance is going to be heavily compromised. So what are some of the consequences that you expect to see in regards to this trapped air? So you see this is the airway collapse. And I want to thank Eduardo just for sharing this with me because those are just very critical to understand. This is exactly what happens in this airway. So once you have airway collapse, there is no other way than probably just increasing the pressure, applied pressure, to have a mechanical stent for these airways. So what about the hemodynamics, which is actually the most fearful thing that you can have when you are so desperate to sometimes disconnect the patient? And there is a reason for that. I'm going to show you also this, the last item here, Pepe and Marini. And I think clearly demonstrate that at some point when you have patients severely compromised, there will be no choice that disconnected the patient because in this particular study, they showed about at least 50% of gas trapping, or the measure ROP, was reduced when mechanical ventilation was discontinued. So there's no question that it's better to have a patient with COPD and asthma in the ICU extubated, very well monitored, because all of these things will happen. And the hemodynamic compromise will be at the expense of what we know happens every single time we apply positive pressure to the chest. So we will increase PBR, we will decrease preload, we will just actually just affect afterload. So everything will be just very severely compromised on both ends, cardiopulmonary. So this brings us to the point that, yes, we probably know this, but I think the key is to be able to identify these things. And I think based on scalers and loops, believe it or not, just Neil McIntyre just called me the loop guy because nobody looks at loops, but they are just essential to the waveforms. So scalers will give you some information. As you can see, I promise you, you're going to see this four more times, it's just the flow versus time referring to the inability of the expiratory tracing coming back to baseline. Remember, this is not auto-PEEP. This could result in auto-PEEP, but this is really gas trapping. So when we want to assess the impact, and I'm going to emphasize on this, is that just the degree of gas trapping doesn't mean that every single patient with this degree of air trapping is going to have exactly the same degree of auto-PEEP. So even if you have this example as the one, let's say 100 liters per minute or so, it's not going to be just the same auto-PEEP. So let's review. So it seems like every single time we are trying to ignore the peak pressures on these patients, there is a good reason for that, because we are always just paying attention to the plateau pressure. After all, we're trying to define if this is a resistance issue or compliance issue, and it doesn't matter how high the peak pressure is, of course, we are going to be looking at protecting lung no matter what. So in every single equation or every single protocol that you have for mechanical ventilation, the plateau pressure seems to be a very key aspect of applying extra PEEP to counteract this airway occlusion. And it's very simple, because sometimes you don't have to use a very long inspiratory pause to determine exactly the gradient between the peak and plateau. That's all it takes. So these are taken from the Bella Vista, one of the ventilators that I use for a chapter. So that's exactly what I'm going to be showing. But I want to emphasize, well, it didn't seem to be updated from what I saw. So the question was, remember, doctor, when I was not intubated? So that's exactly how I titled this. Because it seems to me that if you are using albuterol quite often, you should be able to anticipate exactly the response these patients have to a return of this beautiful baseline, expiratory to baseline. But if you do not have that, why are we giving more albuterol or beta 2 agents to these patients? So that means that there's something beyond the bronchospasm that could be explaining why these patients have gas trapping. So again, we just want to just go back and determine, are we using waveforms to determine just the response to bronchodilators? And of course, the scalars. Scalars are going to be useful for, again, trying to determine if there's a significant gradient between peak and plateau, if there's a return to baseline, or basically barely, barely getting to baseline prior to the next breath, even though you don't have interruption of the expiratory tracing, this would be a good sign that this is getting awfully close. And it could be just at the expense of respiratory rate. And again, you have to analyze, is this a matter of reducing the respiratory rate or analyzing exactly what's going on? The patient could be on pain, or it could be just, again, the simple stuff, febrile, or it could be just having some CNS issues. And it's just trying to determine maybe you can measure exactly the degree of the percent of air trapping. Well, if we are using this now for APRV, because we determine if we are not gas trapping at least 50%, how we call this TCAV or APRV, well, this would be actually just a very nice way to determine if whatever we are using on the vent reduces the degree of air trapping. But what about the loops? Because PFTs 101 showed us that the concavity of the waveform on the expiratory tracing is consistent with airway obstruction. But then we add the degree of air trapping that is below baseline. But what about the PV loop that shows sometimes increased workability, but this is actually the flattening or the widening of this hysteresis. And sometimes we have a tendency to ignore how valuable this information in the loops is. So this is why, because now when you think about it, this is actually the description. Of course, on exhalation, pressure is going to come down. But do you see a significant drop in volume? So that's your air trapping. So you're coming from what we call the fat football to skinny one. We used to have a tendency to use this analogy more on, let's say, ARDS, but I think it is just a good time to start using this on also air trapping. And it comes to, let's say, the research area where you have to analyze, okay, do we have a way to monitor tracheal pressure to determine which one is the dynamic, the dynamic auto PEEP or the static auto PEEP? For the most part, the most clinical, the practical one is going to be the static. But it's also going to be a good reflection of so many time constants, because this is going to be filled up by the first unit that has a short time constant. So as a good example, by the time we get to this point where we have this severe gas trapping, you have units that are going to be all over the place in regards to the amount of auto PEEP. And it will be just probably the average that we get on the static measurement, which is, again, it's a good tool because it's a trend. It's not perfect, but it gives you a lot of information. And just as a reminder, this is actually very useful because if you have a set PEEP, of course, all you have to do is apply an expiratory hold, and this is going to be the amount of inadvertent PEEP. You add the two of them, and you have the total PEEP. But something that we have to think about is just not only the recognition, but the impact that these particular patterns will have. And one of them is the missed trigger, which is actually very serious in the ICU, because we see more and more patients just doing exactly this. They're working, and the vent is just simply ignoring. So this is, again, the trigger asynchrony. I promised I was going to bring this back. So let me just show you an example of, let's say, apply PEEP. This is the circuit PEEP. But then you have esophageal pressure that is very high, showing that the true airway pressure is about 20. So imagine that if the patient has to trigger this breath, it would have to come down all the way to almost baseline. It doesn't matter what the trigger sensitivity is. The patient will have to do a lot of work. If you're trying to set up your respiratory pressure or your trigger pressure to be maybe 1 centimeter water, think about it. The patient will have to come down from 20 to 4 to trigger that. So no wonder you have on this diagram showing so many missed efforts. The patient is working, and the vent is simply ignoring that. And I'm going to show you, since now this is not my set anymore, but I'm going to show you this, that now the application of external PEEP, about 80% to match what you have on the external PEEP, will be able to allow the patient to have a significantly less effort to be able to trigger the vent. So now you go from six missed breaths to only about a couple, or maybe three of them. So how do you titrate the external PEEP? This may be a good way if you try to measure the level of asynchrony. And sometimes we have a tendency to minimize the impact of expiratory time. And this is a good example of the cycling asynchrony. At this particular point, you haven't noticed that there's a beak. I learned from somebody in Marietta, Yucatan, just by giving a presentation, well, you know, if Batman is looking to the right side or the left side of the screen, there's something wrong with the cycling asynchrony. Because at this point, the patient really wants to excel, but you are, as the operator is saying, just hold on one more second, just 0.1 second. And all of this is indicating now intra-abdominal pressure is very high. And of course, you don't want to see exophthalmos or anything like that. But at this point, the patient is about to say, I got enough. So recognition, even something like this, could be making a difference on this patient. So ventilator strategy is really, the foundation is to avoid as much auto PEEP as you can. Scanning is the key. And of course, if you're applying plus repressor ventilation, it's to decrease the amount of the mean airway pressure the best way you can. You could probably sedate those patients, but ultimately, sometimes, you may have much more severe compromise of the cardiovascular status. And at some point, I don't know how many of you, I have both actually, believe it or not, on chronic lung disease, and pediatric and adult patients just do this a few times to prove the point that PEP and Merini were not wrong when those patients are hemodynamically stable. And you're doing everything you can with the eye ratio. You're doing this with flow cycle percent. Whatever mechanism you have created to decrease air trapping, just to realize that none of them actually work. So you may have, this is not, don't pay attention, you don't have to answer this. But I think it comes to the point where, of course, you're breathing faster. That's going to be a significant point. And of course, the less time you have to exhale, it's, of course, important. So thank you for the answers, you were right. So this is actually showing, thank you, Dr. Lee. So this is actually a good slide showing that at low rates, even a change in one breath per minute could have a significant impact on your expiratory time compared to, let's say, a decrease in 0.1 seconds. At high rates, it may not be exactly the same impact. So no wonder why we recommend, of course, lower respiratory rates to start with, because even one breath at that low rate will have a significant impact on expiratory time. So of course, the greatest impact is going to be on respiratory rate. Just be aware, of course, that the same thing that we learned, believe it or not, over 23 years ago, with how we just deliver tidal volume at the protective strategy by the expense of doing what? Increasing respiratory rate. Well, this is going to be something that patients are going to be able to notice. They have a very high tidal volume. Sometimes you have to just ignore that, except when it deals with plateau pressures. And of course, increased expiratory flow. So if you were to just do a summary of how differently you will manage patients, you will be surprised how similar sometimes you deal, except with, again, non-invasive ventilation. That you're trying to protect the lung no matter what. That you're trying to slow down the rate so patients have as long as they can to exhale. That you're trying to, in a sense, ignore peak pressures, but at the same time, you're trying to promote some degree of hypercapnia. And this is, again, from Eduardo. He should be giving this lecture, by the way. But this is actually just a very good overall review of what you need to do. Aim low, but tolerate high tidal volumes per ideal body weight. Lower respiratory rate. And I think I learned this a long time ago by becoming a therapist. Do not aim to normalize ABGs. Neil McIntrye said sometime in one of the presentations, normal ABGs are for normal people. And we don't deal with normal people in the ICU. So finally, let me just review some of this, is the role of applied PEEP. And I think, just versus reading all of this, I think the key is that PVA. So if you have patient ventilator asynchrony, you should be looking at titrating PEEP to decrease the amount of asynchrony. And I refer back to you, looking at those flow tracings and loops. But I think it's very key. You are simply stenting the airway open. So you stent the airway open, and with that, you decrease the overall alveolar pressure. And that's pretty much what it is. I wanted to just finish with just a couple of resources that you can find. This is actually a very excellent paper by Louis Blanche and his group in respiratory care back in 2005. Just ignore my name, but I think this is actually a good textbook that you can get. All the waveforms that you see, so those are actually in my chapter. But also, I found this paper just by doing this review. This is a very practical review from Mousser and the Emergency Medicine Clinics of North America back in 2019. And I think it's a very practical approach to how you manage patients with chronic lung disease. And it will show you also a protocol, what if, the what if, what if, which is actually very key sometimes to understand how to simplify the management of these patients. So I think in summary, I think it's important to realize that you have dynamic hyperinflation, that you have auto-PEEP. But I think it's very critical to me is that every single clinician knows about the physiology, but most of all, ventilator graphics. Ventilator graphics, let me just finish with this stupid analogy. What I thank you for just coming here is that how would you feel going to the cardiologist and asking, so what do you think about my EKG? And the cardiologist will say, you know, I'm not that good about EKGs anymore. So if we are working in the ICU, there is no excuse not to be able to master the patient-ventilator interaction to promote better outcomes in patients with chronic lung disease. Thank you. There's some chairs here on the front for anybody that it's getting tired, please. There's no problem with walking all the way to the front. All righty. It's loading, and there we go. So I'm gonna talk about rescue therapies for status asthmaticus. So, and in general, this would apply also for somebody with very severe COPD. But in general, the people that require the rescue therapy is gonna be usually a status asthmaticus patient that you're gonna see. I'm Eduardo Mirales-Cabodevilla. I do have some disclosures to say about in here, and none of them are related to this chapter, to this talk. But I do want to, before we move ahead, to ask who has treated here a patient with ARDS? Just show of hands, everybody. Do you have a protocol for management patients with ARDS in your institution? Around 50%. Who has treated a patient with severe asthma or status asthmaticus? Same amount. Who has a protocol for asthma or obstructive lung disease? Yeah, we don't, right? So the first part, one of the lesson objectives is that I'm gonna talk a little bit about our protocol and how I see these things. Then we're gonna review the definition of our rescue intervention. And you will argue at the end with me that maybe a lot of the things that we do in asthma are rescued based on the amount of evidence that we have for that. We're gonna talk about some medications, interventions, and extracorporeal life support. And then we're gonna talk about how to prioritize these interventions. And so I would say this is our protocol that we use at the Cleveland Clinic. And I would say that this took us a while to develop because there's not much evidence. And many people come to me and say, Eduardo, can we have the protocol? Absolutely. But I would say that you actually have to design it for your own unit. Because the amount of resources that we have are not the same elsewhere. So many of the things that you're gonna hear today, you may say, Eduardo, that doesn't apply to me, that's not something that we would do. Or we do this differently, and that is potentially fair. So what is a rescue intervention? The first thing is that an intervention that is known to achieve a physiological outcome. However, there is limited evidence for benefit on patient-centered outcomes. This is a classic inhaled nitric oxide for patients with ARDS. It improves oxygen, but it doesn't improve outcomes, right? There is a risk that would outweigh the benefit in most circumstances. So you saw that the mortality for asthma and for COPD on mechanical ventilation is relatively low. Around, depending on where you are, 7%, 4%, it's a low number of mortality. So if you put a patient in certain interventions that can have a higher mortality, like for example, extracorporeal life support, you may be saying, well, should we or not doing that? And the implementation is costly, challenging, or unregulated. So I'm gonna talk about some of those that we do. So when should you use a rescue strategy? And we all have been against the wall. You have the patient, you cannot ventilate it, and everybody starts bringing out ideas, right? What I would say is that this is when you cannot deliver, with conventional care, safe ventilation or safe hemodynamics. And this is the patient in which you have a pH below 720 persistently, even after you have optimized the care for these patients. If you're in a situation like this and you will see these patients are usually and probably they should be paralyzed during this period, because you don't want any problem with interaction with the ventilator. And so you have achieved maximal settings, meaning that your plateau is high, you're getting a lot of out of keep, it's affecting the hemodynamics of this patient, and you cannot achieve your goal. Majority of the patients that we get referred, for patients that we're gonna put on a rescue therapy, come in with settings that could have been optimized. And that when we optimize, the patient avoids the placement on extracorporeal life support. So you have to really sit back and say, where are we? How do we optimize this? This is especially relevant because every bronchospasm will eventually break. It will go away. The problem is the time that you have to get there and if the patient can tolerate there. In terms of hemodynamics, the biggest question is, Eduardo, how much out of keep is bad? And as Ruben said, the number depends on the more dynamic effects that you're seeing with the patient. The patient can have an out of keep of ten, but if the blood pressure is stable, the patient is urinating, the capillary fill is appropriate, she lacks. The ten is okay. It will go away eventually. Now if you have a patient that is in shock that you unplug from the ventilator and you see the pressure rise and the color come back to earth, that patient is in trouble. You need to do something to improve it. Make sense? A question is often, well, this patient has viral trauma. This is one of the patients that came in with obstructive lung disease, and you can see the amount of subcutaneous emphysema. And when you see this, you may be pushed to think that this patient needs extracorporeal life support or a rescue therapy. I would poise that if you have improved the settings and it's not causing a more dynamic compromise, let it be. It will go away. Now it's not pretty to see, but if it's causing obviously a more dynamic compromise, it's causing pneumothorax or other problems, then obviously you will have to go there. So what are the rescue strategies that we have in severe asthma? And I put just a few, because they are commonly done right now. I put ketamine, inhaled anesthetics, because they are always mentioned. Heliox is commonly mentioned. Some alternative modes, and then I put the extracorporeal life support on the two common modalities that we use. I'm gonna start with ketamine, because right now we're in the ketamine love phase. Everybody loves ketamine. Who loves ketamine? Yes, lots of hands, yes. Now the problem is that we all think that it causes bronchodilation. However, the evidence for that is very, very, very tiny. Five randomized controlled trials, three of them are in pediatrics. All of them use different dosing strategies, different clinical endpoints, different time frames with mixed results. It's in guidelines and it's recommended throughout. But the problem with it, and we saw this through COVID that we started using more ketamine, is that we are not used to know how to wake up these patients. How do they come out? What the emergence phenomena for these patients? What's the delirium? And you have to remember that it also causes emergence reactions, and those are tough to manage. And you can increase the number of respiratory secretions on these patients. So I would say that although you may consider this in some of these patients that are going through the exacerbation, just think for a second that the amount of evidence that we have is low. And that we should be capturing and trying to do some physiologic studies to see how are we managing ketamine for this group of patients. The second one that comes is, Eduardo, let's put them on inhaled anesthetics. And it's isoflurane or cevoflurane. Anybody has put a patient in the ICU on this, on an inhaled? Was it easy? It's a pain, right? Because you have a series of items. And the thought is that this will cause bronchodilations by decreasing the neural input. But there's no randomized controlled trials, and I don't think that there will ever be one. Because the number of patients that you see with status asthmaticus is very low. I mean, we see very low. We're a center of reference. We probably see one once a month, twice. Sometimes when Canada is burning, we see more. But otherwise, you don't see that many. So it's very hard to recruit for a randomized controlled trial. Sorry. The problem is that the ICU ventilators are not designed to do that. And if you try to bring a ventilator from the anesthesia suite, as some of us did during COVID, it is not the same as a ventilator designed for ventilation in an ICU. You also have to think about gas scavenging. And that's probably one of the bigger issues, why we would stop of doing that in a regular ICU. Now there's a new device, new here in the United States that is being trialed. It's called the Zetaconda device that you can give inhaled anesthetics in the ICU with a little device. This has been available in Europe. There's been tested right now over here. And that may be an alternative that will come our way if it gets approved, obviously, within the states. Because it makes it certainly much easier to give these medications. However, they do cause hypotension, myocardial depression. And we don't know what happens when you give it for prolonged periods of time for some of these patients. There's evidence being generated, but there's some concerns there. The next one that is usually talked about is Heliox. And so, remember, we're talking about patients that are intubated. And there's a good amount of information, especially in the pediatric population, regarding how to use Heliox for improving delivery of bronchodilators. And it does generate more laminar flow, it decreases the work of breathing. There's no question about that in the pediatric literature. However, on mechanical ventilation, it's an issue. Because our ventilators, with some exceptions, do not have what we call a Heliox package. And the Heliox package is that it has to adjust the flow sensor. If not, it's gonna give you erroneous tidal volumes that are being delivered to the patient. And so, you may be thinking that you're giving a small tidal volume and you're giving a large tidal volume to that individual. And then there's the problem that for the Heliox to work best, it has to be high dose. So the more oxygen that the patient needs, the less Heliox you do, the less effective it's gonna be. So it's usually one of those that they mentioned that you cannot give on the ventilator, unless you have that package. Now, modes of ventilation, and I put these two there, knowing that I was putting myself at risk of a shoe flying over here. The HFOV and high frequency percussive ventilation, there's several articles out there in the literature. Again, these are case reports. And the usual teaching is that you don't want to increase the mean airway pressure on these patients, because it will cause more hemodynamic compromise. But there's a series of cases in pediatrics, in obstructive bronchiolitis, in status asthmaticus, when they did not have access to extracorporeal lab support to use these type of modes. In the cases, obviously, these are biased by report. They were positive outcomes. They don't report the ones that didn't work. But I put it there for you to be aware that you may find these there. And if you are in one of those situations in which you cannot wait and the patient is gonna die, that that may be an alternative if you have expertise on that. The key in the block that every algorithm ends with is extracorporeal lab support. Who has access to extracorporeal lab support now? Here. So a large amount of you. And if not, you refer to centers within close to you. So the ECOR, or Extracorporeal CO2 Removal, uses lower flow, depending on which machine you use, and essentially just removes the CO2. It's very efficient at doing that. And that's the one that all of us are very excited about, that you could put a cannula, extubate the patient, remove the CO2, and let them chill. It sounds great. The problem is that it has not panned out completely. There's some evidence coming out. Hopefully, it will do what it does. But the problem, the main problem that we have with extracorporeal lab support is the amount of complications. The best review there is by Losanos-Pinoza in respiratory medicine this year, that they saw all the studies that have been done. And what you can see there is that for ECMO or ECOR, the survival was between 83 to 95%. So you may be wondering, do I want to put my patient at the risk of mortality? But you're pushed against the wall. And that's why we wait until we cannot have safe ventilation or EMO dynamics are affected, because the mortality can be higher. And the time of support is around the same that they will require when they're on mechanical ventilation, about six to seven days. The complication rate is high. These patients that we put on extracorporeal lab support will require blood transfusions. They generate clots, infections, ischemia of their limbs. So it's not as pretty, and for all of you that have done it, you have seen what it can do. We save them, we feel happy about it, but it comes to a cost. So we do it when the safe ventilation cannot achieve it. I do want to say something in terms of how do you ventilate them when you put them in extracorporeal lab support. One of the common behaviors is to say, let's put them on rest settings as we would put somebody with ARDS. And the risk in this population is because of the bronchospasm that you have. If you put them on pressure control with a low delta, those patients will develop reabsorption at the lactasis. So the lungs will collapse because they will reabsorb the gas that it's inside the alveoli. So if that happens when you put a patient on, you change them to pressure control, just think, this patient, if it has obstructive lung disease, it needs volume. So we put them back on volume control, reinflate them at very low rate so that they don't generate that. So finally, here's the algorithm, and this would be my closing slide. The way that we do it is, do you start saying, is it meeting the ventilation goals? And I always think, is the medical therapy optimized? Remember about the phenomenon of tachyphylaxis, although controversial. Some of these patients have come albuterol, albuterol, albuterol after albuterol. Now you're giving them continuous, they are not responding at all. It's time to back off and let them clear out for a second. Use your ipratropium and let them come back. We use neuromuscular blockers on all these patients when they are at that level, in which we are thinking about a rescue strategy. Our ventilation targets are to have a pH above 715, that they are saturating, and that they have a delta P less than 15, or a plateau less than 30. And evidently, the hemodynamic goals is to allow the auto-PEEP that allows perfusion, that the patient is urinating, that they're having a good capillary refill, and that the lactate is not elevating. And so if you cannot optimize that for us, the rescue therapy is to put them on extra-corporeal life support. That's our next, we don't use heliox, we just don't use inhaled anesthetics. And we do use ketamine, because right now we're on the ketamine train, but we're studying it to see what's going on. So with that, I want to thank you for your attention, and thank you very much. Thank you.

obstructive lung disease

ICU

acute respiratory failure

non-invasive ventilation

mechanical ventilation

rescue strategies

severe asthma

COPD exacerbations

extracorporeal life support