Good morning. Welcome to Status Asthmaticus, from the ED to the ICU, a choose-your-own-adventure. This is where we've got you at those tables with those colored cards, so please make sure those are within reach of you. Early in the morning, I see some people with coffee. That's great. We are going to ask you to introduce yourselves to your neighbors, and it'll be a little bit of a team sport in picking the adventure and the pathway of treatment for our patient case today. I'm Megan Conroy. I'm at The Ohio State University with a specialization in severe asthma, and I'll let my colleagues introduce themselves. I'm David Shore. I'm at Penn State University, where I'm med-peds in interventional pulmonology. I'm Erdith Greer. I'm at Emory. I am pulmonary critical care and neuromuscular pulmonary and sleep medicine. And I am Alice Gallo. I'm an intensivist at Mayo Clinic in Rochester, Minnesota. Wonderful. So jumping right in, bright and early in this morning, you are paged by the ED to see a very young 18-year-old with a known history of asthma, who unfortunately has a history of intubation through their teenage years. They come in with a worsening cough and wheezing for one day, which is not improving despite using their asthma emergency plan derived from the clinic. On exam, their heart rate is 85, respiratory rate 24, and they're setting 89% on room air. The patient is sitting upright with conversational dyspnea, but no accessory muscle use on your initial exam. And on pulmonary exam, you find a diffuse wheeze with no rowels and no prolonged exhalation. On a respiratory viral panel, it comes positive for respiratory syncytial virus, negative for COVID and influenza. Further laboratory investigations show a leukocytosis to 16,000 with a peripheral eosinophilia, and an initial blood gas shows a pH of 7.45 with a PCO2 at 30. And a chest radiograph is displayed. So, at your first exam, you sit at your tables. This is where those colored cards come into place. I want to give you guys a few minutes, 30 seconds to a minute, to talk amongst yourselves and let me know what treatment or pathway you would wish to take for this patient next. Would you wish to wrist stratify the severity of this exacerbation? Just start the nebs for this patient, get the steroids on board, or give the patient more oxygen. You'll see those color-coded four-color cards at your table. Wrist stratify for red, yellow for starting the nebs, green for getting the steroids on board, and blue for more oxygen. Somebody at your table, hold up your color as you've got your answer. We got to just start the nebs, okay. I've got one, start the nebs. If you're just coming in, if you can sit at a table that has cards on it, join a team. We've got a non-committal green and yellow. We like that, we like that. Yellow. We've got a red. Yellow. Some people want to do everything at once. Thank you. And for those of you coming in, do you want to just put the case back just so people can read? For those of you coming in? All right. Thank you for joining us this early morning. We are looking at a case of a young 18-year-old who's coming into the ED with an asthma exacerbation. They are found to be hypoxic to 89 on room air with significant conversational dyspnea and diffuse wheezing. They are RSV positive with a peripheral eosinophilia and a blood gas that shows 7.45 and 30. We are asking the teams, those of you please sit at tables with colored cards to join a team to tell us which action you would wish to take first. Among these, I think the yellows have it to just start the NEBS. So, Dr. Shor. So I think we're all very familiar with asthma. Right now we kind of want to be doing a little bit of everything. We're still in an ER situation here, so we have to have an idea of which NEBS we're going to use and which ones potentially have some degree of benefit. Now, albuterol is the mainstay as well as potentially inhaled corticosteroids. One of the interesting questions that we come up is short-acting muscarinic antagonists. So the data behind duo NEBS is actually quite poor. The addition of ipitropium, usually given three times in the first 90 minutes, really has only been shown to reduce the potential need for hospitalization. Once you're actually admitted to the hospital, there's no evidence that does much more than anything except for potentially cause side effects and potentially reduce some of the need for continuous albuterol. But beyond that, the mainstay has always been continuous albuterol or even just short-acting. Now, the question between MDIs and nebulizers varies a little bit by age. MDI via spacer is always ideal in the pediatric population if you can get them to use it. Typically, if you have someone who's more hypoxemic, though, we're favoring a nebulized route. Great. So we're going to use a focus on short-acting beta agonists, muscarinic agonists not necessarily with data after admission. All right. So I saw a couple of red cards and a couple of green cards, but I will ask you one more time, hold up cards, of what is your next action preferred? Get the steroids on board, risk stratify, or give the patient more oxygen? We've got a couple of reds, a couple of greens, a couple of blues. We will go through each of these. So those who wish to risk stratify to start. So really knowing where your patient's going to go can be very useful. When we're talking about risk stratification analysis, there's kind of two main strategies we're talking about. Static assessments, things that you're seeing immediately upon admission in the ER, as well as dynamic assessments, something that you can follow over time. So for static assessments, we discuss things like history, lab findings, as well as potentially spirometric measures. Now, it's important to know, especially in pediatrics, how unreliable spirometric measures like peak flow can be. If you have someone who's not using peak flow at home, especially if you have a six-year-old who's in distress, the likelihood you're going to be able to get them to use it is extraordinarily poor. Now, some of the things that's really useful is peripheral eosinophilia, which has been more correlative with potentially need for advanced hospitalization, intensive care hospitalization later on. While we're talking about things like biologics, knowing that this is correlative with potentially severe disease can be very useful. Now, as we're moving on, some of the really important things we're talking about is being able to predict where your patient needs to go at the outset. Now, risk stratification schema and scores are very useful in pediatrics, where there's potentially 40 to 50 different calculators out there. In the adult medicine, there's just the simplified severity score for acute asthma. Now, what's really useful about these, if you can see this one, this is all basic data you get immediately upon evaluation in the emergency department. There's no lab findings. There's no spirometry. You can calculate this very early on. Now, the way that this was proven and validated was it helps determine whether your patient needs to be hospitalized or potentially can be managed outpatient, but it doesn't yet have validity describing whether or not they need to go straight to the ICU. Now, when we talk about some of the pediatric risk stratification schema, the critical respiratory score, this, for example, has external validity suggesting that higher scores can be sent straight to the ICU, generally patients who have a score greater than eight. So if we were to take a little bit, look at our own patient, we have all the data that we already need to risk stratify potentially with where they need to go. As you're seeing, we have the good things in green and the bad things in red. Being borderline hypoxemic is something that's very bad and can push you up higher on the scale pretty, pretty quickly. Beyond that, we have some wheeze and otherwise no rails, no prolonged exhale, and no accessory muscle use, which are all very reasonable. So right now, if we were to look at the score, it's mild. And again, the best thing about this clinical respiratory score and severe asthma score is that these are simple scales that can be done in the ER with physical exam findings and potentially history, no lab findings, no spirometric data ever required. Now dynamic assessments are things that you're going to be looking at over time, things like how their exam is evolving. If you're getting lab work, which is not necessary as you're seeing of these scores at the outset, but how their respiratory acidosis is changing, if it has at all. Some of the other things you can do is if they are using peak flow, then you can follow it over time and see if they're improving or not. So we've gotten the patient's NEBS. We've considered the risk stratification of how this patient is presenting into the ER. I saw mostly then next green cards. So let's talk a little bit more about steroids, Dr. Shore. So systemic steroids are one of the mainstays that we're talking about for the management of asthma. We know that these are immunologic phenomena. Oh, please. Yes, of course. Thank you. And I can speak very softly, so I appreciate that. So early steroids is really important, but the question is what dose, how long, and potentially via what route? Now when we're talking about pediatric versus adult data, adult data is just a question of do I want to give my steroids by a mouth or do I want to give them via IV? Now the rule of the question that comes down to in this context is can they take anything by mouth? If they can take anything by mouth, feel free to use it. Pediatric data actually is very different. We're talking about both route and dose and formulations. So dexamethasone has been finding much more evidence in pediatrics because you have a half-life that's 36 to 72 hours. So two doses of 0.6 mgs per kg with a max dose dexamethasone of 16 milligrams by mouth, which can be either a pill dissolved in one milliliter of any solution or you can take their IV solution and squirt it right in their mouth. Two doses of that is equivalent to five days of methylpred or prednisone, which is very, very useful for a child who doesn't want to take their pills. One dose in the ER and one dose at home the next day is the entirety of your course. Now the original data for this only supported mild and moderate exacerbation and didn't actually have validity in the ICU, but that has since changed. And so when we're talking about whether to use prednisone, methylpred or dexamethasone, honestly the latest Cochrane review from 2016 says it probably doesn't matter. It doesn't matter if it's high dose. It doesn't matter if it's low dose or the length. It's just a question of getting these drugs on early and then trying to monitor for things like side effects. Dexamethasone is associated with less incidence of gastritis and it's correlated with more compliance with the drug, unlike methylpred, which is sometimes more difficult. Dr. Short, can I ask you a question? I recently heard on Brown someone saying that we should do prednisone guided by CRP. Have you heard anything about that? I have absolutely never heard anything about that. My institution looks at CRP like the boogeyman. It has very little utility in the ICU. Just want to make sure that we made this point because there are a lot of things coming out and on social media as well using CRP to guide steroids and community acquired infections, both viral and bacterial, and the data doesn't support using CRP to guide steroids. Just do what Dr. Short said. Thank you. So we know that steroids early are important here. And I will remind you that our patient was mildly hypoxic on room air to 89%. So Dr. Greer, tell me more about oxygen therapy. It was already on. All right. So oxygen therapy. So obviously you see somebody and they're satting 89% and so you want to fix that number. And something you can put on quickly is nasal cannula and I'm sure it would already be on the patient before you even get the call. So hypoxemia in these patients is usually thought to be due to VQ mismatching because of areas that aren't going to be ventilated. And so we know that VQ mismatch can be improved. The oxygen level can be improved by supplemental oxygen. And so like everything, you know, more is always better, right? I think wrong. We know for many things that you don't want to have too much oxygen on board, not only for oxygen radicals, but in this case because it can actually paradoxically worsen the situation. So some of this can be explained by the Haldane effect of oxygen displacing CO2 from the hemoglobin. And then if you can't exhale, you can't get rid of that CO2. So it's just going to stay in your blood and build up and drop your pH and then further drive your minute ventilation and then further worsen the situation. But the major reason is thought to be worsening of the VQ mismatch. So in areas that aren't going to be well ventilated, they're going to have low oxygen there and the body's going to be smart and it's going to do hypoxemic vasoconstriction. So if you put oxygen everywhere, then that's going to take away the smart thing that your lungs tried to do. And it's just going to send blood to everywhere and it's going to actually worsen that VQ mismatch. And so for all of these patients, the target oxygen for adults should be not more than 92% and for children should be not more than 95%. And we'll talk a little bit more about how you can actually target that more specifically later. Thank you, Dr. Greer. So we've given our patients their steroids. We've started the nebulizers, placed the patient on a little bit of oxygen, and we are called back just an hour later by the ER nurse. The patient is still waiting for an ICU bed, but the nurse is worried because there has been a progressive but acute worsening respiratory effort. Patient is now more anxious and pausing every few words. On exam, heart rate is rising from the 80s to 110s. Respiratory rate is increased from the mid-20s to the 30s. The patient is now at our target SAT of 92%, requiring three liters of oxygen. They are now sitting upright with significant conversational dyspnea and new accessory muscle use. The wheeze is now faint on auscultation and there is new prolonged expiratory wheeze. A blood gas shows a rising PCO2 from 30 towards a more normal number of 38. So here we come back to our team sport and your colored cards at the table. For those of you who have come in a little bit late, we have colored cards at some of the tables. We invite you that you may move or discuss amongst your table which action you would wish to take next. Put the nebs in the vein, give the patient more oxygen, get the BPAP on STAT, or no, not oxygen, but heliox, and hold up your colored cards for your chosen action. Okay, we agree. Oh, non-invasive. Good, okay. You guys agree too? Okay. Dr. Sayad, do you want to tell us why you chose to get them on non-invasive? I'll bring you the microphone. I think the patient is becoming very fatigued, hence the normal ABG, so people could get confused and say, oh, actually it's normalizing, but actually it's just respiratory fatigue and you want to get ahead of that, basically. What would make you choose a BiPAP over a high flow nasal cannula, or have you not thought about high flow and asthma before? Just curious. Probably the use of accessory muscles in that case, you know, is where it can breathe and you want to try to make sure you help with your BiPAP and your PEEP. More support, more support. Okay, all right, great. Anybody else have other thoughts about starting that, non-invasive versus high flow? Dr. Greer, can you repeat what she said, because it was very hard to hear. Oh, yeah, sorry. So I was just asking why two, non-invasive, and she was saying because it looks like they're tiring out, and even though your CO2 is technically like normalizing, that could be a bad sign, because it may mean that they're not able to overblow anymore and that they're actually going in the wrong direction, which I think is a great point, especially for trainees here in the room. And then I asked why not think about high flow, and she said she wants to support them. If they're using their accessory muscles, then she wants to kind of overcome that work of breathing, and so we'll kind of go through that now. Is it okay if I add something? Yeah. I don't know if you noticed, but Dr. Conroy said the wheezes are not faint. That's another very, very important clue at bedside. Again, $0, I understand, is not as sexy as point-of-care ultrasound, but $0. You put your stethoscope on patient's chest, and they were wheezing, and now they are no longer wheezing, or wheezes are getting fainter. That's a sign that they are impending arrest. Right. To make a wheeze, you have to have airflow, and so if you don't have a wheeze, then it's concern that your airflow is getting even worse. So non-invasive positive pressure, NIPPV, so the indications, kind of like we have been alluding to, it's just clinical. So it's just tachypnea, high respiratory rate, and use of accessory muscles. Obviously, if your patient is hypercapnic or hypoxemic, that's concerning, but they don't have to be either of those things for you to be concerned. If they don't look well, then you should feel unwell, right? Their contraindications, I think we all know this, but if they need to be intubated, just don't wait. You know, like if they can't breathe, and they can't even speak at that point, then you're just going to have to take over for them. Facial trauma, that's preventing mask fit, or any sort of congenital or facial abnormality, because you can't have a leak for this to be successful. High secretion burden, so depending on if what is causing their disease, like RSV, can produce a lot of secretions, and then you don't want to just be blowing it back into their airs and cause mucous plugging airways. And then nausea, vomiting, so if they're having to breathe so much, or they're coughing so much that they're actually nauseous, you don't want them to vomit into the mask, and then that pushes back as well. Decreased level of consciousness, I was kind of always taught that's like a contraindication, and I think certainly in overdose and things like that it is, but for patients where it's just the CO2 that you're worried about, it's a little bit less concerning if you think that they don't have these other contraindications. And then severe hypoxemia, hypercapnia, and hemodynamic instability, I think historically we always went straight to intubation, but more and more, and especially since COVID, we know we can tolerate staving that off for a little bit. So those aren't hard and fast rules anymore. You know, we usually use non-invasive in asthma because we know it works in COPD, and so there's actually a lot less data for asthma patients specifically, but they did do a review in 2012 that showed improved spirometry, improved discharge from the ED, and reduced hospitalizations with use of non-invasive. And then in 2020, Blue Journal did a retrospective study, and they showed that there was also a decreased risk of intubation and improved mortality. And then for pediatrics, they did a review also that showed a decreased respiratory rate and improved asthma severity scores, and none of the kids had to get intubated, so there couldn't be a decrease because they were all doing much better than the adults were. One thing that was on that slide that I thought was interesting is that the median time on non-invasive was two days. And so this is actually a slide showing the dark black dots as the rise in use of non-invasive, and that top line is the decrease in intubation in these patients, and the bottom line is the mortality, and it's not different. And you can see 2010 is when this started, that's when I was an MS1, and 2017 is when I was a first-year fellow. And so I watched basically, right, learning to just intubate people right away when I was in medical school to learning how to use non-invasive to avoid that. And so that's just showing how much practice has changed in such a short time, and I thought that was really cool. And this is for the people with full respiratory failure, too. So why does it help? So we've talked a lot about, you know, this breathing, you start to kind of get hyperinflated. If your respiratory rate becomes short because you're tachypneic and you're anxious, then you have no time to exhale, right? If you can't exhale, you can't get rid of CO2, and that's the main problem in these patients. So the gas just keeps accumulating, your FRC keeps getting less and less advantageous, and then it's really, really hard for you to ever get more air in or get air out. You have no ventilation, right? And so, if you want to go to the next slide, how does it help is that we can sort of overcome that auto-peep. So you may have heard about this sort of waterfall effect before, but the idea is that the external peep is just going to come in and like stint open your airway that you were having trouble with, and now you're going to be able to exhale because that barrier is no longer going to be there. It also is going to help recruit any adalectatic lung that may have gotten collapsed from not being able to be ventilated, and that's going to then improve the VQ mismatch, which was the whole problem causing the hypoxemia to begin with. And then, as Dr. Syad alluded to, the support is so important. So it's not just EPAP or CPAP, you really need the IPAP as well because that added pressure support is going to unload the respiratory sort of muscles, those accessory muscles. It's going to remove the fatigue. Once you're not breathing so hard, you're not producing as much CO2, right? All that work of breathing produces CO2, so then your minute ventilation drive is going to decrease, and your respiratory rate is going to be able to decrease, and then you're going to have more E time, and so you're going to be producing less CO2, and you're also going to be able to get rid of more CO2. So what settings do you want? So you just shouted out, what kind of settings do you start, because you know they ask you before you get down there. Ten over five, that's great. What anybody else, anything else people do? Probably not, right? Eight over four. So eight over four, ten over five is completely fine, right? You just have to start somewhere. You just need to get some pressure into this person to relieve that auto-peep that's going on. You're going to increase the EPAP if you think there's really bad auto-peep to try to meet them where they are, but you don't have to. You can keep it low, and then you're going to increase the IPAP to try to get a goal tidal volume, okay? You remember on these machines, the volume that you're seeing is the exhaled tidal volume, okay? And so if they can't exhale, then they're not going to be able to show you any volume, and if you have a good seal on that mask, you'll be able to see that, okay? And so you're going to want to increase your IPAP until you get an adequate volume for them, which can be six to eight cc's per kg, ideal body weight. And then you want the goal also to see that respiratory rate go down, because that's going to indicate to you a decreased work of breathing. You also want to look at some of these settings, like the eye time and the rise time. So the eye time is only going to apply to the breaths that are at the rate you set, okay? It's not going to apply to spontaneous breaths, so don't be confused by that. But you want to make it short. So 0.8 seconds usually is what I put on there, because I want to give them adequate E time, okay? So the default is going to be higher than that, and you're going to have to change that yourself or ask respiratory therapy to do that. The rise time is also something I think people don't consider a lot on non-invasive, but if you were on a ventilator, you would be putting a square wave, right? Like you would want this pressure to get in quickly, again, so they have a longer E time. So you want to actually bump that rise time up, so the breath gets in quickly, and then they have a prolonged expiratory time. Don't over-oxygenate. You can set oxygen on the BiPAP and make sure that too much oxygen is not going to help these people. So this is a way you can really titrate to keep that sat just at 92%. And then you've got to monitor them, right? This is somebody who has to be in the ICU. Status asthmaticus should not be in the step-down, just set it and forget it. You've got to watch them. Watch their minute ventilation. If you have in-tidal CO2, that can be really helpful. Even if you don't believe it, you get your first gas, and then you get your in-tidal, and now you know your delta. And then that way you can know if it's increasing or decreasing. Agitation discomfort, that's going to be like the biggest limiting factor, especially in pediatrics. That can be really tough. And then check the belly. I think this is something people forget about, but if you're using a full face mask, you're not just blowing into the nose, right? You're also blowing into the mouth. And especially in pediatrics or people with smaller frames, scoliosis, things like that, a lot of air can get in their belly, and that puts them at risk for vomiting into the mask. Okay? So those people, you might want to target a lower tidal volume. I think this is my last slide, but if they are agitated, you can give them sedation on non-invasive. I think that's a really important point because it can help you avoid intubation. So Presidex or dexmedetomidine can be used because it doesn't depress the respiratory drive, but it can take like up to 15 minutes to work, okay? And if you have someone who's an extremist, you may need to shut their system down right now, and you can use fentanyl for that. We prefer fentanyl over morphine because morphine actually releases histamine, and then that can worsen some of the symptoms that they're having. And then monitor closely. Again, I usually say I have like a status asthmatic as stool, and so I just sit there, you know, at the bedside, and I kind of do all the rest of my work from the computer that's in that room because that's the person that I need to not leave. That's it. Thank you, Dr. Greer. So for our 18-year-old who's come into the ER with a chest that is becoming more quiet and a PCO2 rising towards a normal of 40, we've given steroids, nebulizers, and put them on BiPAP. The next option that I saw most popular was to put the nebs in the vein. So Dr. Shor, talk to me about this. So the real benefit when we're talking about IV therapy as respiratory adjuncts is if you have significant distal airway collapse, then the bronchodilation and the anti-inflammatory effects you're looking for, you can't get very distal. So this is when we're starting to talk about things like IV albuterol, which is not available in the United States, so we kind of move on from that pretty quickly, and we start talking about things like subcutaneous terbutaline, IV terbutaline, and epinephrine. Now, epinephrine is very available to all of us but can be associated with some downstream effects including worsening lactic acidosis and some degree of reduced SVR and hypotension. Terbutaline is what's most commonly discussed both in pediatrics and the adult side. The only rate-limiting step here is worsening of your tachycardia, which is something important to discuss. Now, one of the things that we're going to be talking about is also systemic beta-agonists, magnesium, as well as methylxanthines, which we'll get to in a second. Let's go into the next slide. So we already discussed terbutaline. Now, the big thing that you want to be stepping away from is any subcutaneous use in this situation. Subcutaneous terbutaline can be given very easily in both adults and pediatrics, but it has more of a variable absorption because it's a subcutaneous route. Typically, you're going to be talking about doing an IV bolus and then starting a drip. Now, let's talk about aminophilin in a moment. Magnesium. So magnesium doesn't have a lot of significant benefits, unfortunately. It doesn't have a lot of data behind it. It does have some degree of bronchodilation, usually given as one to two grams over 20 minutes. Now, the only thing you need to be aware of is things like worsening muscle relaxation, and it's not going to necessarily hurt you. It's not particularly expensive. There's some meaningful data suggesting things like improvement in respiratory rate and peak flow, but it's not associated with any difference in outcomes and potentially progression. And then finally, we talk about things like aminophilin. When I was in the pediatric ICU, the only thing they said aminophilin administration did was guarantee that you're going to check a level of your aminophilin. It certainly causes worsening of tachycardia, and generally, on a whole, in both internal medicine and pediatrics, aminophilin is not recommended anymore. It's just a little bit too harmful. You can have things like tachyarrhythmias, nausea, and vomiting. Thank you, Dr. Shore. As we're moving on through the treatment of our patient, any questions? Absolutely. A commentary on the very, very close monitoring, clinical and laboratory necessary in these patients. By the way, feel free to like shout out and interrupt us during this thing if you want to. We're trying to wake up also. So that'll help us. I think you had a question? So you know, pretty much all of the BiPAPs in the hospital are in ST mode. So it kind of like makes you do a backup rate, at least in our hospital with the Philips V60s. But I'll put it really low. So I would put a backup rate of like eight or something like that, you know? Or even six sometimes, because they're always going to be over-breathing that. Good question. Yes, it worked. That later. All right. So among our last vote, I did see some blue cards, not giving oxygen, but adding Heliox. Talk to us about the data on Heliox. So Heliox, I think, is something that's really great to consider. Now, the big thing you have to keep in mind is Heliox is not well-administered in someone who's already hypoxemic. What you're going to be doing is reducing your oxygen tension, your FiO2, with the administration of helium. This is going to be reducing some of your airflow turbidity and allowing for more laminar airflow, which in theory should show things like improvement in your respiratory rate, improvement in some other respiratory mechanics. Now, the only frustration is there's not good data that actually does anything. Our own Chris Carroll wrote an article in 2010 that says, is Heliox dead in the pediatric population? And it might be. Now, the big thing you need to keep in mind, if this doesn't work within the first 15 minutes of administration, it's not going to work, and you should move on. And what you can see on the next slide is over time, we've been seeing the administration of Heliox in pediatrics and internal medicine significantly decreasing, probably because of just significant inefficiency at the bedside. Thank you. Thank you. Our last option of giving our patient, hypoxic asthma patient, more oxygen. Dr. Greer, talk to us about high-flow nasal cannula. All righty. So, just your RT is unavailable, and they don't have a BiPAP, okay? So, what you want to get is your high-flow nasal cannula. So, why is this different from regular conventional oxygen for these patients? So, you know, if you're putting your patient, they were satting 89% at first, and you're going to put them on some nasal cannula, but that's going to be, most of the time, cold, dry air. And in these patients, that's actually going to reduce their epithelial cell dysfunction. It's going to worsen their mucociliary clearance, increase their airway inflammation. It's actually been shown to induce bronchoconstriction by that cold air hitting their lungs. And so, high-flow nasal cannula is going to be heated and humidified. And so, even if you're not going to be trying to push that oxygen level up super high, just the way that it's delivered is going to be a little bit superior for this type of patient. The flow delivery is greater than the patient's own inspiratory demand flow. That's the definition of high-flow. It's not how many liters. It's that it overcomes your patient, right? And the reason that that's going to be helpful for these patients, in particular, is because you can actually prescribe the FiO2, just like you can on the BiPAP or something with a seal, right? Because they're not going to be entraining room air when you're overcoming their flow. So, you can actually put these people on 21% or on 24% or 28%, and you can just keep it at that 92% O2 target so that you're not over-oxygenating them. The benefit you're going to get from this, in addition to the heated, humidified air, is the flow, okay? We talked about wanting support from the BiPAP. You're going to get support by overcoming their flow. You're going to wash out their dead space for them. So, if you can reduce their respiratory rate by using this, then that's going to reduce their work of breathing, which we already said is going to reduce their carbon dioxide production and give them a longer eat time so that they can exhale, which is the whole point here. When they have compared looking at high-flow to invasive, especially in pediatrics, the benefit is that it's comfortable, right? You can sit. You can talk. You can eat. It's a lot easier for people to tolerate. Anyone with anxiety, PTSD about masks and things like that, it's going to be easier. And it's just going to be quick, and it's simple. So, I think this is something to maybe consider in that moderate group of patients if they're unable to or have a contraindication to BiPAP, and it might do more than you think. Pediatrics in adults. So, the data, when they look at it, they compare it to oxygen, most of the time regular oxygen, and it does improve physiologic parameters, and it can avoid escalation of respiratory support, but didn't show a difference in length of stay. And then, in adults, they've compared it to both oxygen and non-invasive. Compared to oxygen, it did better at improving oxygen, which, like, no one is surprised by that, but it also showed a reduction in respiratory rate and heart rate, although it was, like, a day later. So, depending on the patient, that might be way too long for you. And, again, there was no difference in length of stay. And then, in the high-flow nasal cannula, compared to NIV, unsurprisingly, it was more comfortable, and it still reduced their respiratory rate. The only issue with this is we just talked about continuous nebs, and when you're using a high-flow device, then you can actually, like, lose aerosolized medication. And so, you may need to talk to your respiratory therapist about decreasing the flow or switching to the mask when you're giving the nebs and then putting them back. And there has been some concern that throwing somebody on high-flow actually delayed the starting of the non-invasive, because it makes the patient look a little bit better, but it's not really sort of solving the whole problem of all of the hyperinflation. And so, again, like we've said a million times, it's all clinical. You just have to sit there, watch them. If this is more comfortable for them, great, but if they're continuing to get worse, then you need to just call it pretty quickly. Dr. Greer, can you comment on high-flow nasal cannula being able to give some peep? So, that's controversial, so that's why I didn't put it up there. Because I think there's some data in pediatrics that, like, it's not really increasing or causing peep. And as you saw in the prior slide, the dosage is much lower in pediatrics. But if you can kind of overcome some of the dead space and your flow is so high that there's a thought that you might get, like, three or something of peep. But for that, remember, the patient should have their mouth closed. Yeah. And someone who's breathing 30, 20 times a minute, struggling to breathe, probably that effect is not going to exist. Yeah. I wouldn't count on that. Yeah. And that was the point. I just want to make sure that we talked about it so you don't count on it specifically, especially for patients who have asthma. Agree. Thank you. So, in our 18-year-old patient who presented Vistatus asthmaticus, we've given her nebulizers, we've given her steroids, given supplemental oxygen, employed the use of BiPAP, potentially some Heliox. But you are, despite all of these interventions, next page from the ER, that there is a rapid response being called on your patient for worsening respiratory distress. And this is the part where they get intubated. Despite all of your optimal therapy, they've continued to progress. They're now abtunded with an increasing respiratory rate in the 35, heart rate in the 130s, and they were intolerant of that BiPAP and placed back onto a non-rebreather setting, only 91% with worsening hypoxemia. They're diaphoretic, they're gray, with accessory muscle use, and now a silent chest. A blood gas shows progressive hypercarbia with that hypoxemia. So, Dr. Gallo, talk to us about how do you make the decision of when is the right time to intubate these asthma patients? So, if I personally can leave, if you can leave today with one take-home point from this session, from my standpoint, is deciding to intubate an asthmatic patient is a clinical decision, purely clinical decision. Again, we have been talking about this 18-year-old coming in with no accessory muscles used, getting worse despite initial treatment, using accessory muscles, and now silent chest with acidosis. Again, we could see the first, the second ABG, like we commented before, the pH was still normal, but the CO2 was also normal, and someone who's breathing 20, 30 a minute should not be normal, right? So, again, some clues that this 18-year-old was already getting worse, but the decision to intubate is clinical. So, again, we tried high flow, we tried non-invasive, and they still looked bad. We should think about intubating them. And the normal PCO2 in a patient with tachypnea should always make us pause and think about what's happening, because if they can blow out their CO2, they should not have a normal CO2 breathing 20, 30 times a minute. So, this is what happens, and I'm sorry we don't have a pointer, I think, but this is basically what happens, and it's just piggybacking on what Dr. Greer was saying. This is what happens in hyperinflation. It gets to a point that patients can no longer compensate for their tachypnea and narrower airways. So, you've intubated the patient. I am not breathing. The ventilator keeps calling me. I am not breathing. Do something. Your option. Do something. Again, with your color-coded cards on your table as a group. Yeah, what do you want to do? What do you want to do? Don't hate, sedate. Go to the bedside, or start talking about salad. I saw two yellows already. Thank you. Raise up your cards. Two yellows already. Hurry. The alarm won't stop. Help. Let's go to that bedside. So, Dr. Gallo, talk to us about ventilator settings. So, thank you for going to the bedside. Appreciate you all. So, again, there's no recipe for mechanical ventilation. We should strive to adapt machines to our patients and not the other way around. So, first thing, sedation is never an answer. And recipe is usually not ideal, but I like to give people some things to take home. So, what I mean by this, and I want to make sure I should have boldened the word safe, safe initial settings. The same thing that Dr. Greer was talking about for non-invasive. These are safe initial settings. So, rate 12 to 16, you're going to tell me, oh, but they were breathing 20 a minute. Yes, this is one of the hardest things, is to try to meet what an asthmatic patient wants for minute ventilation. But why do we want to do 12 to 16? Same thing, the same principle that Dr. Greer talked about on non-invasive, to give them the most exhalation time that we can so their flow can go back to their baseline. Tidal volume, 6 to 8 cc per kg of ideal body weight. Again, we're talking about safety. This should be safe. The I to E ratio that we want to aim, again, 1 to 3 to 1 to 4, that should be, again, safe and ideal. And always check for auto-PEEP. If you remember Dr. Greer's graph of the airway with the ovula at the end, you want to make sure that you have, that you check the auto-PEEP, you check how much of the flow is not going back to baseline and adjust your PEEP to match 80% of that to try to stand their airway open. Also decreases a little bit of the work of breathing that still will be happening, decreases the CO2 production as well. And careful with too much flow. Sometimes we want to give flow to make the inhalation faster. Too much flow might induce more bronchoconstriction, just again, because of the speed of the flow might cause bronchoconstriction from release of cytokines. So you put them on the settings and what you want to avoid, what you want to make sure that is not happening is the flow waveform not going back to baseline like it's happening here. So again, safety parameters that we still use. I just want to say, how many of you worry about peak pressures in an asthmatic patient? Oh, I love no hands up. I love it. That's what I was hoping for. So the only time we care about peak pressures, meaning that they are compromising the patient's safety, is if it's rising. So again, you put them on safe parameters. You got that flow waveform going back to baseline. They're doing great. You made the vent sink to them. But you come back and the peak pressure that was 30 is now 50. Something might be going on. You might think about some mucus plugging. You might think about something else going on. And also, we put this image there. Do we have an arrow? There you go. Far left. So the ventilators, most ventilators will have an alarm set up to peak pressure of 40. If you have your patient on a volume control or a volume targeted mode and they reach a peak pressure of 40, the vent will cycle off. And you won't know how much they are receiving for tidal volume, how much they are exhaling, because the vent will cycle off. So those are the two problems with peak pressure, if it's changing or if your alarm is set up to a pressure that will cycle off. Does that make sense? Okay. You can change your own alarm. I just want to be clear. So all these subtle things that we don't typically, especially in fellowship, learn to change on the vent, you've got to fix that yourself. I mean, obviously ask a respiratory therapy. But it's important because you can see on there, you can drive it up to 100, so you might as well. Because you know you're not worried about your peak pressure. And if you keep alarming and dropping back to opening your exhalation port, then you're not going to get any volume in. And that means you're going to get no CO2 out. Yep. And another very important thing, safety parameters, we still want to make sure that plateau pressure is less than 30, driving pressure less than 15, 13, depending on where you're reading. Because those are the pressures that are still giving us surrogate markers for the alveoli over distention. Hypercapnia, permissive hypercapnia is still okay in asthmatic patients. We have newer data from this year that ECOR might be in our future. But for now, we still care about the pH. So permissive hypercapnia is okay. pH above 7.2 is something that you can take it off of your mind to do the rest of the things to and for your patient. So these are our safety parameters. We have the patient on a respiratory rate of 14, 6 cc per kg of ideal body weight, flow is at 60. With that, their I2E is 1 to 1.5. PP is 5. Trigger is minus 2. FiO2 is 70%, and the patient is saturating 98%. Peak is 42, and plateau is 20. But this is still your waveform. This is still the flow waveform and your patient. So what's going on? What do you want to do? Shout it out. Tell us. How would you address this? Things that we need to do. There's no right or wrong answer. Again, we need to adapt the vent to the human being we're taking care of. Yeah, sure. Yeah. Okay. We can increase the PEEP to match the auto PEEP. Okay. That's a good one. Okay. Say that again. Try to decrease the respiratory rate. You're trying to increase the exhalation time, and you're trying to help with auto PEEP. Okay. I like that. What else? Two people. What was the FiO2? She wants to increase the I2E. How can you increase the I2E? Is that something you can dial on a vent? With the flow. Okay. You would go up on the flow. Okay. Sounds great. Somebody else said decrease the FiO2, which means they learned. Yes. Decrease the FiO2. We like that. Sounds great. Say it again. Try pressure control. Okay. Plateau is 20, though. So pressure-wise, it's still safe. Tell us more why you switched to pressure control. Again, that's a great thought. There is no right or wrong. We are adapting the machine to the human. So like doing VC plus so that you can give yourself an eye time. It's not what I time. Yeah, okay So to adjust to be to be able to control the eye time Yeah, this equals uh-huh Okay Only problem with that is you if you're Going above the top limit of the pressure. You won't actually achieve your target volume. Yes, that's the only issue with that Mike yeah, my concern at this point with doing pressure is Well is we're doing pressure is You might not achieve the X Exhaled volume that they will need to also blow off co2 because the pressure will have to be narrow For you to not to reach the the peak that you're concerned about Escape do escape. No, we're getting back in. Sorry me out of the room Bingo Well, that was that was gonna be the next thing So the patient actual respiratory rate is I believe 2426 is that what we had? So that's exactly in this case at least because we were not able to match their Wanted minute ventilation. So again go to bedside, but everything that you all suggested was absolutely perfect again, little tweaks one tweak at a time and Stay there takes about Three five minutes for all of these changes we're making to actually reflect on the patient for the muscles to adapt So one tweak stay there another one. Stay there bedside. I love that. So What I what I started doing I don't know what you all have in your in your institutions in terms of events, but mao we have Hamilton g5 and ASV if you put them on ASV The Hamilton g5 will tell you what pressure support they want For the minute ventilation that you would like them to have so I usually do exactly what you're saying I put them on ASV. So the machine will calculate the pressure that they want. That's a great thought That's a great tool to to use to adapt the machine to the patient Yeah, so there you go, so they were breathing 24 and Again, because we needed to go to bedside to make sure that we addressed all these things But again everything you said great things to do and great stepwise approach. I think somebody also had wanted to Sedate the patient and I feel like it might be time for that So if you want to go to salvage therapy, or if you want to do sedation hold up your cards This will be our last choice, right Red is to date your alarms still going off despite all of the amazing things you did on the ventilator Go to bedside you gotta go you gotta go So can sure talk to us about sedation So we've already established that the patient's over breathing the vent to the best of our ability to do anything else mechanically to interrupt So it's time that we took control of the situation. We need to establish two things with our sedative choice We want some bronchodilation if we can get it, but we also need to curb the respiratory drive It's time that we prevent them from hurting themselves. So propofol is an excellent choice. It's a sedative It also has bronchodilatory properties to it The only downside that you need to be aware of is a theoretical increase in your carbon dioxide But you also have potential hypotension, especially in patients who have a lot of increased respiratory insensible losses And you don't want induction or post induction to be associated with any degree of hypotension This is where we start talking about ketamine So ketamine in the context of asthma is a wonderful discussion You have both dissociative and nondissociative dosing someone who's for example having trouble establishing themselves on BiPAP Using ketamine at nondissociative dosing is a wonderful choice Once they're intubated or even using it as an induction agent The only things that you need to be aware of is ketamine can worsen respiratory secretions And the last thing you want for the vicious cycle of status asthmaticus is respiratory secretions and mucus plugging But otherwise ketamine is an amazing choice You do need to be worried about a little bit of tachycardia Which our patients are already having a heart rate of 150 at this point. So it is worthwhile to keep an eye on I Think one of their ketamine point just because somebody had brought it up earlier is like we are very supportive of you using that when you intubate the patient and also before you intubate the patient when they're on non-invasive and a lot of your Emergency medicine colleagues will be doing that before you even get there And so if they can show that it did worsen the bronchorrhea or the secretions while they were giving it before they got intubated Then that's helpful for you to know that the patient's probably going to tolerate it once they do get intubated if that happens Now your patient's appropriately sedated and they're still having trouble This is when we're starting to talk about paralysis now using induction dosing with your RSI for your rocuronium Just buys you time for a little while even 60 minutes is potentially going to be helpful in the crashing status asthmaticus patient now when we're talking about using something like this This is acuracuronium drip What you need to be aware of long term is you're giving these patients a lot of steroids and then you're paralyzing them and so They are at risk for myopathy upon recovery But again, we have to get to recovery first. And so that is what we're trying to do with our paralytics here So we've gone to the bedside we've troubleshot our ventilator as much as we can maybe sedating our patient But despite that they continue to have rising hypercarbia Potentially hemodynamic consequences of this leaving us to our final component of salvage therapies Before you start I want to ask people in the audience Can you shout out what type of salvage therapies you guys have used before or what you have at your institution? Just so we know and we're talking about like the stuff up here Dr. Shore if you want to give some examples So I think for example, everyone's always talking potentially about ECMO and Ecore and those are wonderful options in this situation We're going to discuss what data there exists as it is. But for example, is anyone having any use of inhaled anesthetics? How has that gone for you? Is that been easy? No, which one did you end up using? Okay, what about biologic therapy Which therapy Dr. Shore? Biologic. Oh Biologics meaning like meppo and stuff like that. Dr. Shore, it's hard for us to hear you on this side of the room Okay. Thank you. Is this better? Yeah, perfect So what we're gonna be talking about right now is a little bit of Rarefied air in terms of what our options are. This is a place without significantly good data But you know, you don't always have to measure whether parachutes work when you're falling out of an airplane So for example when we're talking about biologic therapies, these are in the realm of case reports in case series Now Fisenra is potentially useful because you can be using this IV This is a various case reports using omelizumab and nepolizumab as well and some of these are in patients who couldn't tolerate steroids because of Ophthalmologic consequence that were predicated that they couldn't get steroids ever and these are other patients who are on ECMO for two weeks before improving These are non FDA approved uses But what they're showing here is improvement in respiratory rate and biologic metrics for example in their IgE versus their eosinophil counts When you're talking about for example ECMO, which is the next slide We're often talking about removal of oxygenation Now these are much reduced flow rates and Ecore can potentially be very useful if it ever makes main stage This is a 2020 case series retrospective showing about 23 different patients and everyone survived to discharge which is amazing It gives you time for you to break the status asthmaticus The one thing you need to be aware of is ECMO and Ecore is not without consequence Nearly 50% of the patients had some degree of deep vein thrombosis many of which were catheter associated other Complications of their treatment like iatrogenic pneumothorax The last thing we wanted to discuss was inhaled anesthetics, which you don't have a slide for these are logistically challenging to use you need to have Potentially a respirator brought up from the OR and potentially depending on your hospital and anesthesiologist bedside 24-7 to manage the inhaled vial tile gas now there are studies describing these used via a mask that's held against the patient But if you can imagine a child or an adult who's gasping to breathe if you're gonna shove a mask on them How well that's gonna go and the answer is not well at all You have options of halothane, zevoflurane, and desflurane, but keep in mind most of these inhaled anesthetics are Irritant and cause vomiting and they can be very challenging logistically to use Thank you So in our intubated patient with all of our prowess on the mechanical ventilator Using all of our best sedation options Thankfully our patient improves Does not need salvage therapies and is extubated to room air on day three They are discharged home and in follow-up in asthma clinic ultimately are doing well So we hope that after this discussion of our patient case that you can remember that your clinical assessment tools for use in early Evaluation of asthma exacerbations can both guide disposition and management Steroids take a while to get effect. So get them on board quickly. They're very important in hoping to break that bronchospasm Don't be afraid to use non-invasive ventilation and any patient whose respiratory mechanics are worsening and it's a clinical Clinical monitoring very closely at the bedside to make sure that you are improving those mechanics High flow nasal cannula can be considered in the right patient if there are no contraindications to non-invasive ventilation With the benefits of humidification and reduction of bronchoconstriction The decision to intubate is not a great science. It's clinical and patients really may decompensate quickly but long expiratory time on that ventilator to the best of your ability is very key to improving that ventilation and Don't be afraid once you do pull the trigger and intubate that patient for sedation and paralysis

severe asthma exacerbation

emergency department

nebulizers

ventilator settings

sedation

close monitoring

salvage therapies

biologic therapy

individualized management