SCCM Resource Library-Mechanical Ventilator and Pharmacologic Strategies in the Treatment of Status Asthmaticus

Video Transcription

I'm Sophia Rogers, and I'd like to welcome you to the Mechanical Ventilator and Pharmacologic Strategies and Treatment of Status Asthmaticus. Just a couple of housekeeping notes.  Please make sure you have your phone silent. And we are going to take questions at the end of the sessions. The speakers will disclose any kind of financial conflicts.  And if you are tweeting, please use hashtag CCC49. So it's my pleasure to present the first speaker, Dr. Mitchell Buckley.  He is a pharmacist at the Banner University Medical Center. And he's going to start off our presentation with medications for the treatment of status asthmaticus.  So help me welcome Dr. Buckley. Thank you. It is a pleasure to be here. It's a little chilly for my guy from Phoenix, so if my teeth start chattering, please bear with me.  So as the title suggests, I'm going to be talking about drug therapy that we use for the treatment of severe acute asthma.  In regards to disclosures, I have done some consulting work. However, with that being said, none of the products or agents I'm going to be talking about today  have I've had any direct or indirect involvement with. Our learning objectives are going to be threefold. First and foremost, I think it's really  important to just lay the cards out there. What options do we have that are available to us in the management of severe acute asthma,  more specifically, when the patient has not adequately respond to the standard of care therapies? And then what I would like to do  is spend a little bit more time focusing on ketamine. Seems that this drug has had a lot of buzz in other areas, and I think some of us have used it in severe acute asthma.  And so really, I want to dig in and do a deeper dive into the clinical data supporting or refuting its use. And then finally, hopefully, that we can kind of summarize  very quickly, what do the guidelines say and what kind of recommendations do they suggest as far as, again, these adjunctive therapies that we can use, also including ketamine?  So drug therapy options, there's probably going to be little to zero debate as far as what we would use right out of the gate.  So clearly, beta-2 agonists and cholinergics and steroids kind of seem to be the backbone of management. But then what happens, again, when the patient does not adequately respond?  What kind of options do we reach for in those kind of scenarios? So clearly, there are several options out there. Ketamine, again, being one of them.  And again, this is not a complete laundry list of options. So for example, I'm not going to go down the rabbit hole of looking at nebulized furosemide.  I'm going to be kind of touching upon, again, what the guidelines have suggested. And so we will be revisiting these agents at the latter part of my session.  So ketamine made its big entrance, actually, in 1963. It was structurally derived from PCP. However, with that being said, it wasn't introduced into clinical practice until 1970.  Now, as you can see here, this is the first published case report of ketamine's use in an asthmatic child. And this was in 1971.  So really, what happened was that this child was experiencing wheezing symptoms during the procedure. The treating physicians administered ketamine.  And lo and behold, magically, the wheezing subsided. And so this really kind of opened the door to say, OK, we may be wrong to something here as far as ketamine's role  for inducing bronchodilatation. So with ketamine, as far as inducing bronchodilatation, what is the exact mechanism? And so clearly, we've had many theories and thoughts  that kind of adequately explain how this may go about happening. The one point I want to really get across to the audience is that we don't clearly know whether it's  multifactorial or there's one major pathway. But again, there are many different mechanisms that may explain of how ketamine can actually induce bronchodilation.  So kind of segwaying into the clinical data, so just kind of give you a heads up. We're going to be talking about two trials.  One is going to be more focused in the adult population. The other one is going to be more in the pediatric patient population. And so we're going to be looking at just  the randomized controlled trials.  So if you recall, 1971 was the first report. Since then, there's been many case reports, case series, as well as observational data. It wasn't until 1996 that the first RCT  was actually published. So up to this point, there has been some signals, again, suggesting that ketamine may have a role in it,  but it hasn't been studied in a robust fashion up until 1996. So to briefly go over kind of the study design so you can get an appreciation for what the investigators were  looking for. So ultimately, they were investigating the impact that ketamine had in 44 adult patients. And again, these patients arrived at the emergency department.  And with the administration of albuterol, as well as systemic steroids, their PEF still was not at quite a level that was comfortable.  And again, this was after the failure of three treatments with albuterol in addition to corticosteroids. Those patients were then randomized into the trial.  And so when they were included, all comers, whether they were in the control group or the study group, were then transitioned over to continuous albuterol at 10 an hour.  23 of those patients were randomized to the ketamine group. There's two points I want to make about this. One, ketamine was given in a bolus followed by continuous infusion.  And it was only over for three hours. So again, understand that this was a very short-term evaluation. The other thing that I want you to really appreciate  is that the ketamine strategy here that was adopted in the RCT, again, was kind of adopted from a previous case report, case series, and observational data.  So again, big question mark as far as like if it was truly studying the optimal dosing strategy. Nonetheless, this was still a sub-dissociative dose that was evaluated.  And of course, 21 patients randomized to matching placebo group.  So looking at the pulmonary function impact. And again, this was over a three-hour period. I'll walk you through the slide. On the left-hand side is the peak flow,  and the FEV on the right-hand side. If you look here from baseline up until the final evaluation, so again, three hours later, the ketamine in blue  and the placebo in gray, you can see the trajectories that both groups essentially got better from a pulmonary function standpoint.  Similar trends were observed on the right-hand side as well. So essentially, there's two points to take away from this. The first being that both groups showed improvement  from baseline and the final. And again, this was statistically significant both in the ketamine as well as the placebo group. The other point to take home is that there  were no significant differences between treatment groups in regards to the magnitude of change from baseline. So in other words, they all seemed  to get better using these tests to the same degree.  As far as outcomes, even though it wasn't the primary focus of the evaluation, they still described them. And there was no significant differences,  whether it be hospital admission rate or adverse events. There's a couple of things also to take away from this slide. The hospital administration was determined  by the treating emergency medicine physician. The study site did not have a pre-specified protocol or criteria that constituted admission. So again, this was at their discretion.  Nonetheless, we still did not observe any differences. The adverse events you can see here numerically seems to be a little bit higher, suggesting some concern.  Statistically speaking, it didn't meet that. However, there is one caveat to this. At the start of this trial, they actually changed the bolus dose from 0.2 to 0.1  after six patients were randomized. And the reason why is because half of those patients that receive ketamine actually experienced adverse drug events.  And so then they lowered the dose and then started with the 44 patients that were included. So again, kind of a little bit of a guessing game in regards to the optimal drug regimen.  There was actually also a second phase that these investigators were looking at. And they wanted to gain the perception from both the physician as well as the patient  if they thought that the study drug, whether it be placebo or ketamine, if their symptoms got better. In other words, after they received the steroids  and the albuterol, once they were randomized to the group, did they feel like their symptoms got better, equivocal, or actually worse? And so this was a 1 through 5 scale.  And as you can see here, 5 being that they thought that this study regimen that they were randomized to, that their perception was that there was some improvement,  and then 1 being basically it was worse. As you can see here from the patient survey, statistically speaking, it favored more of the ketamine groups.  So more of those patients actually felt like they were getting better. Whereas from the provider's perspective, they both suggested that overall it was slightly a little bit better,  but there's no differences between those groups.  So again, this was the adult patient population. Now transitioning over to the pediatric patient population. Similar study design. Again, very small sample size, 68.  And this was actually at the study site a protocolized regimen that patients with severe acute asthma really much got out of the gate as albuterol, epitropium by 3,  and then followed by corticosteroids, either oral or IV. Now again, if there was no improvement with symptoms, these pediatric patients were then entered into the study.  And then again, very similar to the previous study, received continuous nebulization of albuterol. And again, 33 randomized to ketamine, 35 in placebo. Similar dosing strategy.  The bolus dose was at 0.2 here. Same continuous infusion as the previous slide, but again, short term. This one was only evaluating up to two hours.  So the investigators looked at the pulmonary index score. And then so one thing I want to do is they'll give you a point of reference. A PI score of 8 or greater suggested  that moderate to moderately severe asthma symptoms. And so as we walk through from time 0 up to 2 hours, you can see here the ketamine in blue and the placebo in red.  From where they started at and each increment after that, at the evaluation period, there was no differences between the ketamine or the placebo.  Furthermore, there was no differences from where they started at to where they ended at between ketamine and placebo. So again, this was a little bit eye opening as far as not  suggesting that ketamine provided additional benefit, again, beyond what was received initially out of the gate. Or could it be that continuous nebulization?  Because again, remember, all of the patients received that. Maybe that was the 900-pound gorilla that actually did the legwork to make improvement.  The investigators also looked at patient disposition. So once they were entered in the study, where did they end up? If they would happen to be hospitalized or went home.  As you can see here, the bulk went to either a general ward or a step-down unit, with even smaller amounts went to the ICU.  None of these had any impact on the patient's overall health. These had any significant differences between the study group as far as where they landed within the hospital.  So again, not suggesting that ketamine avoided, say, like an ICU stay. That was not found in this particular trial.  So up to now, like I said, we have two studies. And so these investigators actually wanted to find a pooled analysis, really evaluating the use of ketamine  in a pediatric patient population. Now, I have to give you a heads up. The next slide will change your life and will change your practice. And I'm completely kidding, because it's  going to be the most anticlimactic slide you see here at this Congress, I promise you. So I know everybody's in anticipation. So without further ado, these investigators,  bless their hearts, after they were looking and doing their literature search, they only found five records. And of course, going through the process of meeting inclusion  criteria, they get a whopping N of 1. That N of 1 is the study that we just talked about from the Allen group. And so unfortunately, they weren't  able to do, obviously, meta-analysis techniques. So maybe it's not completely anticlimactic. Maybe it kind of solidifies the fact  that we do not have really good, robust data on ketamine. So we can debate whether it works or not. But again, the information that we have has not provided a signal that ketamine,  in addition to standard care therapy, actually provides additional benefit.  So those are the individual trials. What's kind of curious is, what do the clinical practice guidelines say from an international standpoint, as well as here in the United States?  So here we have a busy slide. And we're going to walk you through it. So I have staying true to objective number three. I don't want to talk just about the star of the show  being the ketamine. I also want to kind of cover some other therapies as well. So here we have the different various therapies.  And I'll give you some insight as far as how a man works, his brain works, when he's given color-coding options within a PowerPoint slide.  So each individual guideline is represented by a column. And so I have the references down here for you reviewed, if you would happen to look it up later.  So what's also interesting is, one guideline was published over a decade ago. But we also have more recent compilations as far as evidence-based recommendations.  And so here in the red kind of represents for that particular therapy, what each guideline suggests. They actually come out and they make a statement to say, this is not supported.  So they either recommend or suggest it not actually be used. Now, the green, you could probably guess as far as why they am actually coming out, making a statement in support,  whether low or medium or high level of evidence. Everything else is kind of gray, which I think is good to kind of emphasize the fact that even if you see that they have a question  mark and a positive, they don't necessarily make a recommendation. But rather, they kind of make a consideration statement  that, well, we can't come out and say that we should or may be using it, but you could consider it. So they didn't completely take it off the table.  But nonetheless, they didn't actually get behind it and support it from that perspective. So I think this slide says a lot. So for the IV beta agonist, it's just  very questionable if it is available for you to practice that. The anesthetic gases, so this might present a logistical nightmare to actually administer  it in the emergency department and or even ICU. It's not even mentioned in the majority of the guidelines. One is questionable, and then the one  that was published in the analysis of intensive care, they actually come out and said, don't use it. IV aminophilin, again, for the most part, probably not one to readily recommend.  IV magnesium, you can see where the pendulum's swinging for. Clearly, we have more data with that. And so this is where we feel like there's a signal to,  again, that might be something to consider a little bit more heavily compared to the other options right out the gate. And again, going to ketamine, so what's questionable here  is one of them actually came out and said, don't use it. Now, again, I showed you the data. And the other ones either don't mention it  or they just say, again, a blanket statement of, well, we can't really be for it or against it. It may be a consideration based on this clinical situation,  the severity, or if you think it's a part of the kitchen sink that needs to be thrown at the patient. So in conclusion, the cornerstone of therapy  in severe acute asthmas include beta agonists, anticholinergics, as well as corticosteroids. The inhaled anesthetic, again, is the inhaled anesthetics, like I said,  it's just really the lack of data and, again, the logistical concerns as far as like pragmatically administering that therapy. Magnesium appears to be a signal to, again,  this may be the more preferred agent to kind of gravitate towards over the other additional therapies. Now, with ketamine, the positive data really begs some questions.  One, if it truly is beneficial, we just haven't found it just because of the sheer lack of limited data. However, with that being said, a lot of the guidelines,  even though they don't come out and suggest we use it, this means it's completely off the table. Now, clearly, what happens as a clinician,  if you're going to be intubating the patient and rather than grabbing maybe, say, for the propofol, you wanna grab for the ketamine, some of these guidelines actually suggest  like there may be a role, but again, keep in mind that they're not actually coming out and recommending that type of strategy. So again, it remains an intriguing agent,  but the lack of data, it's really hard to get behind and suggest that we start using it again as standard of care after they filled traditional therapies.  Nonetheless, if we have the patient who's intubated, you wanna use it as more of induction or a continuous infusion, there's nothing out there to stop you from doing that.  However, with that being said, again, the limited data, it's hard to use it as an agent to help with mitigate after they filled therapies, so.  Thank you.  Our next speaker is Richard Branson. He is from the University of Cincinnati Medical Center, and he's going to review accepted treatment approaches, including the role of Heliox,  pressure versus volume ventilations, and pitfalls. Help me welcome Richard Branson. Good morning. So I want to touch on a few issues about ventilating the patient with severe asthma  and maybe do a little bit of basic background. This next speaker is going to talk primarily about how to set PEEP and deal with auto PEEP and air trapping,  so I'm going to avoid that in this talk. These are my disclosures. The companies either sponsor research for me or I have relationships with.  Disclosures are all about disclosing, but none of these have anything to do with my talk. So when it comes to a patient who needs mechanical ventilation  or has status asthmaticus or acute severe asthma, estimates are that it's somewhere between 6 and 10,000 patients a year in the U.S.,  and there are generally two types of presentations. The most common presentation is one that smolders over a few days and the patient comes to the emergency room.  It's usually triggered by a viral illness. Sometimes we don't know what it's caused by. The mechanism of airway obstruction is usually mucus  plugging and severe airway edema that actually is worse than the bronchospasm. The airway inflammation is usually from eosinophilic, and these patients don't respond very quickly  to bronchodilators and the ED, and if they require mechanical ventilation, which is a serious undertaking in severe asthma, they're usually on the ventilator for a couple of days.  The more rapid onset, which isn't as common, comes on very quickly, is usually due to an allergen, some airway irritant, or, you know, we all know some patients just from stress,  and the major mechanism there is bronchospasm, and there's less mucus production, and some people call this dry lung, the dry lungs of asthma,  and the airway inflammation is mostly white cells. These patients respond very rapidly to bronchodilators, and generally, if they're going to be on the ventilator,  are on the ventilator for less than 24 hours. So here's kind of a classic chest X-ray of a patient with severe asthma with the flattened diaphragms and the hyperlucent lung areas,  and you can see the overdistension. And the pathophysiology of severe asthma is the markedly increased airway resistance, pulmonary hyperinflation, an increased dead space  to tidal volume ratio, hypercapnia, respiratory acidosis, and if things get bad, respiratory arrest. So when you think about how we're going  to ventilate the patient, these are the challenges that we're facing. So managing, my topic was managing ventilation. Well, the best way to manage the asthma patient who needs  to be ventilated is not to ventilate them, not to intubate them. So this is from a paper that Dean Hess published in Respiratory Care, and this talks  about the things you can do before you intubate. So continuous bronchodilator therapy, which was kind of discussed in the previous talk, the use of Heliox.  I'll tell you, I don't think Heliox is very helpful once the patient's intubated and on the ventilator, because at that point the ventilator's doing all the work.  It's not a matter of having to make the gas easier to breathe. And then also use noninvasive ventilation. So let's discuss these couple of things here.  You know that Heliox, compared to air and oxygen, has a lower density, a similar viscosity, and a much different thermal conductivity. And you think, well, why do I care about that?  You do know that helium is biologically inert and insoluble in blood, why we use it in the pulmonary function lab. But the important things I want to tell you here  about the thermal conductivity is this thermal conductivity, if your ventilator uses a hot flow anemometer to measure the volume, this change in the gas will completely confound it,  and some of the ventilators will shut down. But the idea with Heliox is to do two things, to change turbulent flow in the airways, because of the relationship with density  and the radius of the airway. But it also impacts the way nebulizers works in the face of an orifice. So nebulizers actually can be more efficient,  you have to turn up the flow, with the use of Heliox. So what does this look like? So here's a diagram of giving Heliox, you're giving continuous albuterol probably  through this nebulizer that's connected to helium oxygen flow meter. And generally speaking, you need 80% helium, 20% oxygen, once you get down below 70,  30 you kind of lose all the advantages. Here's a picture of that same device to let you know. And Cresson and his colleagues, it's been quite a while now,  looked at delivering Heliox and continuous albuterol in the emergency department for patients with status asthmaticus. And what you're looking at here is, this is the control,  so just air and oxygen running the nebulizer, and then Heliox running the nebulizer, and this is the percent change in FEV1. So here the difference is about 15%,  and here's the control nebulizer 2, and this is periods over time, and here's Heliox here again. So there were significant differences as the time went on that Heliox improved FEV1.  Heliox is kind of one of those drugs a little bit like nitric oxide though, it doesn't actually treat the patient, it makes it easier for the patient to breathe,  it reduces the work of breathing, it increases the FEV1, it decreases air trapping. But the second you take it away, there's no residual effects.  So it's a temporizing measurement, a temporizing measure and an attempt to prevent intubation.  So what about non-invasive ventilation? Like the last speaker, I could show you the most recent Cochran review about using non-invasive ventilation for acute asthma,  and it would say there's not enough data and it's inconclusive, frequently what Cochran tells us. And there probably is a lot of, or a big need  for a study probably have to be multi-center if you think about 6 to 10,000 patients a year trying to enroll enough subjects in a study to look at the use  of non-invasive ventilation. But again, quite a long time ago, Maduri and his colleagues, this is PaCO2 in the dark line, pH in the red line,  and this is a patient on a pressure support of 14 over 4 of PEEP. Start off with a pH of 7 to 5 and a PCO2 of 16. And 15 of 17 patients with acute asthma that they took care  of were able to not be intubated. And you can see that the effect improves with time. Less than two hours, you have a significant drop in PCO2 and an improvement in pH.  And then over 24 hours, PCO2s that are just on the high level of normal. This is kind of the sum total of work that's been done on non-invasive ventilation and asthma.  Again, the paper by Maduri. And this is from a paper by Sororsky that's published in the European Respiratory Journal. And as you look, I mean, 17, 33, 30, 44 patients.  Just less than 150 patients. Some of them using CPAP with pressure support. You know, BiPAP is pressure support by any other name. And you see improved gas exchange,  improved gas exchange in both groups. And preventing endotracheal intubation in some groups. And decreasing hospitalization rate. And improved FEV1 with increasing pressure support.  So both Heliox and non-invasive ventilation do not have a really good evidence base for use in status asthmaticus. But I think from a clinical standpoint,  with such a small number of patients that you come across in a year, in select patients it's worthwhile. So I'll kind of give you this idea. In the patient who you might want  to use non-invasive ventilation. This is the kind of patient presenting with acute severe asthma. So, you know, accessory muscle use. A pulsus paradoxus.  More than 25 millimeters of mercury. They're tachycardic. Breathing as fast as they can given the air trapping they have. Have difficulty speaking.  And the peak flow or FEV1 of less than 50% of predicted. And, you know, low normoxia. So who should you not try non-invasive ventilation in?  Obviously anybody who needs to be immediately intubated. Anybody with a decreased level of consciousness. Excessive respiratory secretions.  With so much of this mechanical ventilation stuff. And I say this, right, because I'm the respiratory therapist. The devil's in the details. You have to provide sufficient heat  and humidity to these patients. You can't put them on non-invasive ventilation. And blow cool, dry gas into their face at 100 liters a minute.  Especially if they have a secretion problem. You're going to dry out the secretion and worsen mucus plugging. And, of course, this typical contraindication  that the mask won't fit for any reason. And then relative contraindications are hemodynamic instability. Really hypoxia. When an asthmatic patient gets hypoxic,  you're really on the downward slide. Patients who won't cooperate. Patients who are severely agitated. And then lack of trained staff around  who can manage the ventilator and take care of these things. So from that standpoint, the ideal patient for a trial of non-invasive ventilation with asthma is patient  who's tachycardic, using accessory muscles. Has a PF ratio more than 200. Has a PCO2 less than 60. And that FEV1 or less is pretty good.  So the really severe patients you're going to, you know, like usually, you're going to intubate just on site. You don't need to make any measurements.  You can tell they need to be intubated. So let's say those things fail and you move to ventilatory strategies. This is just going to be, again, there's not a lot  of evidence for this. I would say assist control. Tidal volumes of 6. Some people will say 8 mLs per kilo. A respiratory rate of 10 or 14 breaths per minute.  A minimum inspiratory flow of 60 liters a minute. So 1 liter per second. And either use a square flow pattern or decelerating flow pattern in volume control.  A minimum level of PEEP. Probably 5 or maybe a little bit less than 5. But again, the next speaker is going to really talk about the idea of matching PEEP to intrinsic PEEP.  And what that means in asthma and COPD. Then whatever the minimum FiO2 is to maintain the SpO2 greater than 90%. And of course, keeping plateau pressures less than 30.  And if the plateau goes above 30, this is one of the unique aspects about ventilating the asthma patient is when the plateau starts to rise, sometimes the best thing  to do is decrease the respiratory rate. And I'm going to show you why that's true. So this is from a paper by Leatherman that, or Tuckson, that was in when the Blue Journal used  to be called the American Review of Respiratory Disease. And kind of shows you this idea of what happens. So these are, is a normal patient breathing near total  lung capacity or normal FRC and a normal TLC. And your asthma patient is literally breathing all the way up here, reaching total lung capacity because of the amount of trap volume.  And when you put them on a mechanical ventilator, now you even are putting them up above total lung capacity and really stretching the lung and worsening air trapping.  And one of the best ways to look at that is do a trial of apnea where you allow the exhalation to go all the way down before you start ventilating again.  And you can kind of look at this dynamic hyperinflation and lung volume. Again, your patient has to be able to tolerate this,  tolerate the, this is only about 15 or 20 seconds at the most. But this just gives you the idea of what the problem is of trying to ventilate these patients to get the gas out.  Getting the gas in isn't all that difficult. Okay, same paper. Comparing just normal lungs. Here's your FRC. You give a breath. Inhibitory time. Exhibitory time.  The patient with obstructive lung disease and asthma continues to climb, continues to climb. And this is then is that dynamic hyperinflation,  the end expiratory lung volume in excess of normal end expiratory lung volume. And again, with this idea of measuring this trap volume  by doing this prolonged exhalation gives you an idea of how much gas is trapped and what you can try to do to eliminate it. So I think this is a representative diagram showing  you what happens at different levels of minute ventilation, different inspiratory flow rates, and different expiratory times. So this is a minute ventilation of 10 liters a minute.  A minute ventilation of 16 liters a minute. And a minute ventilation of 26 liters a minute. The pink area on top is the tidal volume that's delivered.  And the purple area on the bottom is that end expiratory lung volume that's trapped. Inspiratory flows from 100 to 70 to 40 liters per minute,  which with the, you increase inspiratory flow, you shorten inspiratory time. So here you have a five and a half second expiratory time. Five, four and a half at the faster rate  at a minute ventilation of 16. Three, two, and just more than two. And then here between one and two seconds. And it goes to show you that there are times  in the asthmatic patient where doing something to decrease the minute ventilation requirement, treat the fever, treat the pain, treat the agitation,  treat the dyspnea, I didn't want to talk about neuromuscular blockade. But the acute asthma patient, sometimes neuromuscular blockade can be helpful. But there are times in asthma  when you're making the ventilation, or your PCO2 is rising, where the answer is actually to decrease the rate and increase the inspiratory time. Same thing here.  So here's end expiratory flow. So when you're looking at the flow pattern on the ventilator, patient gets a breath and they start to exhale.  This is the end expiratory flow in an asthmatic patient. And this is from Jim Leatherman from 2004. A respiratory rate of 18, a respiratory rate of 12, and a respiratory rate of 6.  At these faster rates, you still have 60 liters a minute of flow because there's so much air trapping. So there are times when being able to reduce the rate is really important.  If you do happen to ventilate the patient, I want to make sure I stay on time, you're going to see missed triggers. And hopefully you've all seen diagrams like this before.  So this is inspiratory flow. And you can kind of tell this is a patient with obstructive disease. This slow filling up, this is a pressure support breath.  Then exhale, this high peak flow is due to the, basically the circuit exhaling. And then you'll see these little notches that I've highlighted here in the flow.  But you don't see it in the airway pressure setting. And this is a patient with esophageal manometry. And each arrow is a patient effort where the patient is trying to breathe.  So we have a respiratory rate. The patient's rate is 1, 2, 3, 4, 5, 6, 7, 8, 9, 10. But the actual rate during that 20-second period is only 4.  It's because the ventilator doesn't detect these breaths because of air trapping. So what can you do about that? Well, and this is from a paper from Arno Thiel that look,  again, these are patients with COPD. But you can decrease the pressure. And that's one good way. That's probably the best way. Decrease the pressure or the tidal volume  to reduce the asynchrony index. And these are all missed triggers. Changing the inspiratory time can be helpful to an extent. But it's not nearly as helpful  as simply decreasing the tidal volume that's delivered. And, again, it just shows you, here's a patient who, again, you see these breaths trying to be triggered here  in esophageal pressure, the little things that you see on the flow diagram, and as you decrease the level of support, all of a sudden, the patient seems  to become more tachypneic when, in fact, their rate's the same. It's just now the ventilator can detect every breath. So there's not a lot of information  about using pressure control instead of volume control in acute asthma, and I'm going to caution you that that, you know, the pressure breaths are a problem  because since you set the pressure, when that air trapping goes up, the pressure stays the same, and the tidal volume just continuously falls.  At least if you have the volume control, you get that same breath, that same tidal volume to maintain the minute ventilation that you need.  So on the whole, I think most people would discourage you from using pressure control instead of volume control during severe asthma. So I'm going to kind of end up there and say,  in acute severe asthma, you want to try to avoid intubation if you can. When you ventilate the patient, you want to avoid hyperinflation, and the way you do  that is reduce the minute ventilation, both the setting and the requirement through pharmacologic treatment, reduce the respiratory rate, respiratory frequency,  increase the inspiratory flow, shorten the inspiratory time. You have to accept relative hypercapnia, and I'm not going to talk about PEEP because that's mostly what you're going  to hear about next. There's no reason to make these patients hyperoxic, and they generally don't tend to be very hypoxic. And if you see a plateau pressure that's getting  too high, it's the respiratory rate that's the control that you need to look at because of those slides that I showed you before that's completely different  than the patient with ARDS. So these are kind of the ideas. So I'm going to end there and appreciate your attention. Thank you. Okay, our last speaker is Eric Magana.  Dr. Magana is a pulmonary critical care physician at Presbyterian Hospital in Albuquerque, New Mexico, and he's going to talk about ventilator strategies  for status asthmaticus based on the Starling resistor. I have nothing to disclose. So I'm just going to present a case where I'm going to illustrate an alternative approach  to ventilating our status asthmatis patients. This is not a new approach. This has been going on for years. It's just underutilized, and that's one  of the reasons we're presenting that today. I'm going to talk about the clinical effects of applied PEEPs in these clinical situations. So we have a 36-year-old male.  He has a history of poorly controlled asthma, and he comes to the ER in status asthmaticus. He's been having more dyspnea since for the last week or two. He'd been torching weeds,  which is where you take a propane tank on your back, and then you burn the weeds instead of pulling them, and it's less work, but it's not good for asthmatics.  He typically has one to two asthma attacks a year. He's never been intubated. His attacks, they get better with a MedDRAL dose pack. He doesn't use any control or medications.  He just uses PRN albuterol, and over the last couple of weeks, his PRN albuterol just is ineffective, and that's why he presented to the emergency room.  So in the ED, he's tachy at 135. He's tachypneic. He's afebrile, but he's diaphoretic because he's working so hard. His blood pressure's fine. This is his X-ray.  This is a real patient, nothing modified in it. He received standard treatment. He received the albuterol neb. He received 2.5 to start with. He had a duo with some isoproteropium.  Then he got a 5-milligram neb. Then he gets continuous nebs. It doesn't work. He'd already gotten solumedrol on board. He was given magnesium. None of these worked.  So he was escalated to noninvasive. So he was placed on 15 of IPAP and 8 of EPAP, and that really didn't make much difference in his symptoms either.  And then he had an episode of an arrest. ACLS protocol was followed, and he had restoration of spontaneous circulation after he'd gotten some CPR and ampivepi and ampibicarb,  and he was intubated associated with this.  So asthma patients ventilating these, I find them to be the most difficult patients to deal with, or many people find them the most difficult to deal with.  During his hospitalization, he had profound dyssynchrony on the ventilator. He was ventilated using volume AC, and in volume AC, it has a set flow.  The patient was outstripping the flow because he had higher flow demands than the machine was giving it to him. He was demonstrating paradoxical abdominal activity.  The machine was throwing all kinds of alarms at you. It's throwing high respiratory rate alarms, volume not delivered alarms, high peak pressure alarms, and when patients look bad  and they throw us all those alarms, we sedate the patients, and when sedation doesn't work, then we paralyze the patients, and the alarms get better and we feel better,  but the patient's not really that much better.  He was ventilated with respiratory rates in the teens. He had inspiratory times on the short side of about 0.6, 0.7. Minute ventilations were kept around normal  to try to prevent further hyperinflation, and permissive hypercapnia was allowed. He was running PCO2s in 50s and 60s. The patients tolerate the elevated PCO2s  a lot better than the providers do. Even though the providers know they're supposed to let the PCO2 go up, they get wiggy, and in this particular patient,  the provider was contemplating ECMO because the PCO2 wasn't getting better.  Peak pressures were running in the 50s.  So the problem that we have in asthma is auto-peep. The patients just aren't able to get all the air out, and you can see on the top curve on the right, that's a flow time curve,  and so the flow doesn't return to baseline before the next breath is delivered, and that's just as indicative that the alveoli aren't emptying all the air out  that they got in before the next breath is delivered, and they end up having a positive pressure within the chest that we call auto-peep.  Auto-peep has kind of two different origins. It has an origin from a high minute ventilation and a short expiratory time. We see this in a lot of our ARDS patients.  This isn't the hard auto-peep. If we shorten the inspiratory time, as we've done here in these first two breaths, the flow didn't return to zero before the next breath.  Here, we increased the flow, which shortened inspiration, and that gave the patient more time to exhale before the next breath was delivered, and the auto-peep was resolved.  It can also be resolved by dropping your minute ventilation, because if you have a lower minute ventilation, you have more time to exhale, and it just results in a,  it's a great way to decrease the auto-peep that's accumulated in these patients, but in asthma, the auto-peep has another mechanism  that is generated by, and it's called the Stirling resistor.  This is not a new concept. This was described by the same Frank Stirling that developed the Stirling law of the heart. This was developed back in the 1920s and 30s,  so it's almost 100 years old, or it is 100 years old. A Stirling resistor is, in his instance, he had a fluid-filled tube, and the fluid flowed from this end to the other,  and it was inside a box, and in this box, he could increase the pressure, and he could increase the pressure so much that it would completely collapse down the tube,  and there'd be no more flow through it. This is essentially what happens in the airways, with our thoracic cavity being the box and our airways being the tubes,  and so if patients get enough auto-peep going on, they can compress the airway, the alveoli, the pressure in the alveoli can pinch the airway closed  so that the patient's never going to exhale no matter how much time we give them.  If the patient has increased expiratory effort, so when we all exercise, or if you're compensating for a metabolic acidosis, we'll increase our menopinylation dramatically,  but we're able to do this without auto-peep because we're using our accessory muscles to increase expiratory flow. When these patients increase their expiratory flow,  they're actually increasing intrapleural pressure, and they're increasing the pressure that's compressing the airways, worsening the auto-peep.  So using the expiratory muscles to prevent auto-peep works up until you have the lumen of your airways narrowed to a point that it's not going to work anymore. What's that point?  I don't know, but it happened in this patient.  So when these airways are closed off, that results in more volume within the lung, different than the patients who had auto-peep  from elevated minute ventilations. With those patients, we could just give them more time to exhale. You give them another 20, 30 seconds, they're gonna get that air out.  In these patients, since they have swelling in the airway, this airway's closed. If you give them 20 minutes, that air's not coming out. We have to wait for all the swelling  that's developed in the patient's airways over the past few weeks for that to go away, and it's not gonna go away in the first day.  And so this is a problem that we're gonna have to deal with for a long time on the patients. To understand it, let's look at normal breathing. If we have normal breathing,  the pleural pressure, let's say it's negative five. In order to get a breath, you have to create a gradient from the mouth into the pleura of about negative one  to two centimeters of water. So if the diaphragm displaces downward, that creates a further negative pressure within the chest. We get flow going from the mouth of the ventilator  into the normal lung, and the lung inflates. Our patients with asthma exacerbations or severe auto-PEEP, they may have 15 centimeters of water auto-PEEP within their chest.  They've gotta overcome all of that before they can get a breath to come in. So the patient's gonna have to go from positive 15 back down to his negative seven  that we're all doing right now. But instead of doing two centimeters of water work, this patient's doing 22 centimeters of water work. And that's what's causing him  to be in severe respiratory distress. Another way of looking at this is looking at a pressure-volume curve. And these patients are hyperinflated.  They're at the top portion of the pressure-volume curve where the lung's very stiff. It takes a lot more pleural pressure in these patients to generate the exact same tidal volume,  which is why they're so short of, one of the reasons they're so short of breath. The hyperinflation also affects the diaphragm. The diaphragm is displaced downward,  putting it at a mechanical disadvantage. This shortens the diaphragm.  You lose the optimal length for generating force, and the diaphragm just can't create as much force as everybody in this room can now.  So you have a diaphragm that's at a mechanical disadvantage, and you're asking it to do 10 times as much work by overcoming the auto-peep. It's no wonder these patients  look like they're being waterboarded. It's a good attention-getter.  What you'll see in these patients also, it takes a while for them to generate those negative pressures. You will see some patients where they have missed efforts,  where they clearly did an abdominal effort, but the machine didn't pick it up. But what you'll see in a lot of the patients is a delay in inspiration.  So I call it a two-piece breath, because you'll see the abdomen will move out, and then there's a delay before the ventilator triggers.  And when the ventilator triggers, the chest inflates. So it's abdomen, chest, abdomen, chest.  And it's almost that dis-synchronous of, it's hard, you can look at the vent, but it's hard to have one eye on the vent, one eye on the patient.  You can put one hand on the patient's abdomen and then look at the vent. What I tend to do is I pull the patient's sheets down to their waist, and then I pull their gown up  so I can look at their abdomen, and then I listen for the ventilator to cycle to see how much of a delay there is, because there really shouldn't be any delay  if the patient's synchronous with the vent. So can you back up, can you back up this slide?  So the way to treat this is by using applied PEEP.  If this patient has 15 centimeters of auto PEEP, we magically know that, and so we use 15 centimeters of PEEP, or 15 centimeters of CPAP to the patient.  When we do that, we can compensate for the auto PEEP that's present and decrease the amount of work that's necessary to trigger the breath.  So since we've matched his exact amount of PEEP that's present, he only needs to have that gradient  of one to two centimeters of water in order to get the lungs to inflate, and they're able to inflate with dramatically decreased work of breathing.  This has been demonstrated in numerous studies. The first citation is from 1982. It was a letter to the New England Journal of Medicine  where they're talking about using this strategy. There have been two formal studies where they've shown that if you match the patient's auto PEEP  with applied PEEP, you can decrease the patient's work of breathing or increase the work that it takes to trigger the breath. But this is an underutilized method.  Why is it so underutilized? Well, people have been taught for years, and they're afraid that if auto PEEP is the problem, that if we add any applied PEEP,  we're gonna make the hyperinflation worse, and that doesn't happen most of the time. It can. A lot of this is analogous to when you're fluid  resuscitating somebody who comes in volume depleted. How much fluid do you give them without fluid overloading them? I wish I had that one test that would tell me,  and it's the same thing when we're talking about auto PEEP here. This is the waterfall analogy that was described in 1989 by Tobin and Lodato, so it's not new either.  I've made a little modification to it, and I've put a little house here. So pretend you have a house on a stream. It's nice and dry because the stream doesn't flood into your house.  The stream flows this way, and then there's a little waterfall, and the waterfall drops down 10 feet, and that's just the place where you live.  On the left is what we're gonna call auto PEEP, and this is applied PEEP. So your house isn't flooded in this baseline situation. How about you increase the downstream level  of the stream to five feet, or five centimeters of water with applied PEEP? Have we done anything to alter the level of the stream at my house? We haven't.  How about if we increase the level of the stream to 10, the exact same level that the upstream portion's at?  My house is nice and dry. But once I increase the level of the stream, or the level of the PEEP applied to higher than the amount of auto PEEP,  now I have resulted in hyperinflation. I've added to the patient. But we're not adding to the patient until we exceed the amount of auto PEEP that was already present.  So it's okay to give it to the patients. It's not just okay, it's beneficial to give it to the patients, because that's how we can decrease their work of breathing.  So how do we measure auto PEEP to find this exact number that they have in their chest?  We do it with an end expiratory occlusion. You just hit a button, doesn't let any air out, doesn't let any air in, and we're able to determine what the optimal,  what the amount of auto PEEP is.  Problem with this, and the Stirling resistor is, when we do end expiratory occlusions, we're only measuring the PEEP in airways that are communicating with the Y of the ventilator,  where our sensors are. So in this instance, we're gonna be measuring five, because this airway where it's got downstream pressure of 13, or this one's at 15, or this one's at 20,  the ventilator can't sense them, because those airways are completely occluded by the Stirling effect. So the auto PEEP that's present in the lungs is very heterogeneous,  but that which we measure is only the lowest value. The studies have shown that we can underestimate the amount of auto PEEP with a seclusion method by as much as 90%.  You can use an esophageal balloon, but that's not used very commonly outside research settings. I work in a clinical hospital, and it's just not something we use.  Auto PEEP also can be overestimated by this method. If you have a patient who's spontaneously breathing,  the fact that they're using their expiratory muscles can make the auto PEEP readings be falsely high as well. You can put a balloon into the stomach  and try to eliminate that, but once again, it's not used in everyday hospitals.  So what's another reason people are afraid of PEEP? It's over-inflating the lung. Tuckston had described years ago where he added PEEP to patients,  and it resulted in hyperinflation. This is where this concern generated from. All these patients were paralyzed. Maybe if they were unparalyzed, they would have had more auto PEEP  because of the Starling effect. It's unclear. But there was a recent study by Karamez where he found that yes, applying PEEP does increase hyperinflation in some patients,  but in others, it actually deflated the lung. So which is gonna happen to your particular patient? I don't know. It comes back to the fluid volume analogy as well.  How much fluid do you need to give the patient? I don't know. Let's give them a bolus and see what happens. This is the approach that we need to have  when we're titrating PEEP on our patients, just like everything else. So I look at the patients clinically.  I can generally tell, or I look for auto PEEP in every patient I deal with. Certainly in these asthma patients, I'm gonna say, okay, this patient may be having auto PEEP.  I'm gonna look at their abdomen. I'm gonna see if they're having a delay between their inspiratory effort and the ventilator trigger.  If I see that, then I start applying PEEP on the patient until I can abolish that delay and inspiratory trigger, until I can get rid of that two-piece breath.  And it's pretty effective. This has been shown in, I've seen at least four studies where they've shown that applying PEEP to patients decreases their work of breathing.  This is effective, but this is not the word that's being spread out there most of the time. So in this patient, I switched him to pressure control.  And you do have to be careful with pressure control that you don't have set volumes in those patients. I changed the patient to pressure control  only when I was standing at the bedside 100% of the time. The reason I changed the patient to pressure is I wanted to give him a flow variable form of ventilation  so that would eliminate any aspect of flow starvation that was contributing to his dyssynchrony. Incidentally, the auto PEEP was measured by the ventilator and found to be 10.  What's that number mean? It's at least 10.  It didn't, I just put it up there because everybody's interested in it, but it doesn't matter. We lightened the patient's sedation. And as soon as he got lightened up,  he started becoming dyssynchronous again. And I was there to sit there and gradually increase his PEEP. I had to increase his PEEP to 19  in order to get rid of the inspiratory delay. When we decreased him to 19, we were able to eliminate completely his pressure support. And he was extubated that day to CPAP.  When he was extubated, he was still in distress, but we applied CPAP of 16 centimeters of water and that abolished his dyssynchrony or the distress that he was under.  Extubating him aggressively in this manner allowed us to decrease sedation, decrease paralytics, decrease loss of muscle mass. He was able to participate in physical therapy.  He was able to eat. There was less chance of a hospital-acquired or ventilator-associated pneumonia  if his upper airway refluxes are present as well. You can have decreased resource utilization as well because he didn't have to be in the ICU at this time either.  So the auto-PEEP that's generated in ARDS is different than the auto-PEEP that's generated in asthma. And it's because of the Starling effect. It makes it independent of the...  There is some hyperinflation that's contributing to auto-PEEP in asthma, but that which is caused by the Starling effect is independent of your expiratory time.  It's gonna take time for the airway swelling to get better because the airway swelling's what's causing the auto-PEEP in general. We can't do anything about that.  We have to be patient. They've been given all the appropriate drugs, but we can compensate for it. And the way we compensate for it is by initiating applied PEEP,  which dramatically decreases the work of breathing. How much PEEP do you give? I'm not gonna say give them 85% of what's measured because what's measured is inaccurate  unless you're using an esophageal balloon. Titrate it clinically, just like we do all of the other medications that we use in the hospital. Thank you.  If I could invite all the speakers back up for questions.  If you do have a question, I ask you to please go to the microphone and speak there.  Thank you. Thank you.  No questions.  It's perfectly understandable, that's why. You guys did such a great job. I was told if there's no questions, you either did a really great job or a really bad job. Yeah.  Sorry, I let you guys down.  Go ahead.  Yeah, this is Wheeler-Jervis. Can you comment on setting PEEP in the patient that you actually did have to intubate? I mean, did have to paralyze, excuse me?  Because I have PEEP in a patient you do have to paralyze. Yeah, as far as paralyzing the patients, I try to get them off the paralytics as soon as possible.  I'll go into the room, turn it off. The reason we paralyze is just because they look so bad when they're on the vent and they start throwing all the alarms at them.  Once I see the patient unparalyzed, if I'm physically there, I titrate the PEEP until I get that inspiratory delay eliminated. And then I find it's not necessary  to keep them paralyzed anymore. All the nurses, all the staff are completely comfortable because the patient doesn't look like  they're in distress anymore, if you can optimize that PEEP.  I think, if I can follow up, I think in a patient who's paralyzed, adding PEEP to auto PEEP really doesn't help because, yeah, you're doing it  so that the patient can trigger the ventilator more easily. So in that, if you're gonna take the patient out of the equation, then adding the PEEP won't help and might hurt.  Right, that was my concern. Right, and the other, the issue that he raised about auto PEEP is, in order to measure auto PEEP  with the ventilator, there has to be an open communication from the airway where the pressure is and the manometer. So if the airway is completely collapsed  in front of the alveoli and the pressure behind there is 19, you can't see it. So that's why you always will underestimate auto PEEP in those patients.  I think we had a question over here real quick. Yeah, hi, Dave Chase from Phoenix Children's. Do you guys have any experience using decelerating flow volume modes of ventilation  like pressure regulated volume control and other such, rather than going to a pressure control, gives you the best of both worlds,  pressure regulated volume and a decelerating flow pattern?  I've seen that mode and used that mode often in ARDS.  Pressure regulated volume control is a pressure breath that the pressure changes on one breath. One, what happened on the last breath  between the difference between the total volume you asked for and the total volume you got?  I think that you gotta be careful in these cases because you can always set the high pressure setting, but I think you're gonna be butting up against it fairly frequently.  A decelerating flow waveform in volume control you can do, you just have to realize,  if I have two different ventilators, one of them I switch from square to decelerating and the flow increases by 50% and the instatory time stays the same.  Somebody else's ventilator, I go from square flow to decelerating and the flow stays the same, but now the instatory time increases by 25%, which would be bad in asthma.  So it's really understanding it.  Understood, and you would monitor your plateau pressure. I mean, the inspiratory hold would tell you if you were really getting into trouble, I would imagine.  So again, in a pressure mode, the only way to get a plateau is to assure there's zero flow during inspiration, which doesn't always happen.  Just because you're using pressure control or PRVC, the pressure that you set is not necessarily the plateau pressure.  Unless you have zero flow at end inspiration.  And usually there's a pretty big difference. That delta P is kind of for us- Oh yeah, huge. We call it a surrogate for resistance. That'll narrow as the resistance improves. Right.  Thank you. Yes, ma'am. Dr. Magana, I'm Julie Williamson from Emory Children's Hospital. Understanding that you're staying at the bedside and looking at the mechanics,  have you ever used Bi-Vent or APRV to match the auto-peep? You can use any mode that you want to accomplish any of these things. I'm a big advocate.  I can get any mode to do anything I want.  The point is that these people need to have their peep matched. And I can have them in volume AC, I can have them in pressure AC, pressure support, APRV, PRVC. It doesn't matter.  It has to be the mode that you're most comfortable with. One thing I see people do in general that I want to caution is if you have a favorite tool  and you use that favorite tool for everything, and you can use, if you have a hammer, you may use the side of the hammer, the top of the hammer,  because it's just your favorite tool. If you get into a really difficult situation, you don't want to grab your tool that you're least familiar with. You want to grab your favorite.  But I see people do the opposite of this in the hospital a lot of times with their difficult vent patients. And if you use PRVC or APRV or BiVent,  if that's your favorite mode and you can smoke that, use it in those patients. But if you're not comfortable with it, you're going to do way better managing those patients  if you use your favorite, most comfortable mode on them and making sure that you give them enough peep.  I think definitions are important. Most of us would consider APRV something with a prolonged time at a high pressure and then a really short expiratory time.  Again, exceedingly bad idea for asthma or obstructive lung disease. And then BiVent just becomes, and again, I don't make up these terms. The ventilator manufacturers do.  It's a pressure breath with a normal IE ratio, but the patient can breathe during the inspiratory time or the expiratory time spontaneously.  And I agree, if you're good at managing that, probably use that. It'd be fine.  Yes, sir. Are you just standing in the back? No. Oh yeah, you're in the blue shirt.  You were just standing there. I thought maybe you had a question.  You're just stretching your legs.  Yes, sir. Hi, my name is David Silberstein from LA. Any difference, because you talked about, you know, the difficulties of a pressure trigger.  Any difference in using a flow trigger?  You know, once upon a time, You can deal with it, but, you know. Once upon a time, maybe, but today, It's all the same. It's all the same.  The patient has to create a change in pressure in the lung to create a flow or a pressure. And we, you know, there are a dozen case reports  in the literature now where patients who are brain dead are not declared brain dead because the beating of their heart triggers the ventilator.  So, you know, I don't, the triggering aspect of the ventilators are not the ventilators anymore. It's the presence of air trapping and things like that.  So it probably doesn't make any difference. There's a slight, you know, 20 milliseconds faster maybe, but.  I'm a fellow in Montreal at the pediatric ICU. I was just wondering if you use NAVA, I was just wondering if you use NAVA, what, if this can help to,  to more, to have a better effect on the trigger problem, because you detect the effort of the diaphragm directly.  So the question's about NAVA. So NAVA triggers the ventilator from a NG tube that has an array of electrodes by looking at the diaphragmatic contraction.  I know of no research at all about NAVA in asthma.  Again, NAVA improves synchrony. There is, in my mind, there's no doubt. There's no arguing about it. The problem is all the studies that show it improves synchrony  still fail to show that it improves outcome. So if you're, again, if you're comfortable with that technique, again, my big concern would be, you know,  depending on the patient, putting the NG tube in. Now, again, if you're gonna sedate and paralyze, no big deal, but if you're gonna try to let them breathe spontaneously,  that's, to me, that's the problem with NAVA for COPD exacerbation. The patient comes in, they're incredibly short of breath and anxious, and there's a science behind getting them  to tolerate the mask in the ED. You know, first you just let them hold it and just let them feel the flow, and then you hold it tighter  and then you increase the pressure a little bit. You know, if you go to the patient and say, I'm gonna help you breathe better. Here, let me stick this down your nose.  I mean, that sometimes can be the difference between it failing and passing. But again, if you can get the patient to tolerate the catheter with COPD,  you eliminate the air trapping as an aspect of causing the inability to trigger. It's a good idea. But we are used in pediatrics as the impact of a distension of the stomach  is already important impact on the respiratory compliance. We put in a nasogastric tube very easily. And it's like, sometimes it's true that we need some sedation at that time,  but afterwards we are winning a lot on the next part of the event of the ventilation because we already put it in. So if we choose directly to put in a NAVA tube, it helps us.  Yeah, and all the problems with NIV leaks, you know, synchrony mis-triggers because of air trapping go away with NAVA. But it's really about using PEEP to overcome auto-PEEP.  Each mode, you can use any mode. Each place you go in the nation, they're gonna have regional variation where they're gonna say, oh, this is the best thing.  Each has its own characteristics and its own problems. But the principle is they have increased work of breathing because of auto-PEEP.  And it doesn't matter which mode you're gonna have, you're gonna, we need to overcome that.  And maybe I'm a critical care fellow. Our institution, we don't use Heliox very much. So I'm trying to understand where in your structured escalation does Heliox fit into  if a patient is already intubated? Once the patient's intubated, I don't think there's any advantage of Heliox. Not at all. Okay.  Again, the Heliox reduces the patient's work of breathing, helps get air through narrow passages, helps carry aerosol more distally. But once, you know, the ventilator can create  too much pressure. So the work of breathing is no longer an issue. That's, I think once the patient comes in, you give them the albuterol or whatever you wanna use,  you give them the other pharmacologic agents, steroids or whatever you're gonna do. And then if that doesn't work, you can try Heliox. And then once you intubate them,  then the Heliox and the other stuff, especially if you're gonna paralyze them, no advantage at all. Got it. Thank you.  How often do you encounter pneumotorics with the increase in peep to overcome auto-peep?  I haven't encountered it yet if, because I'm not adding to their auto-peep. If I look at their inspiratory delay or I look at the two-piece breathing, as I call it,  once you make it go away, I back it off as low as I can. I'm not over-inflating the patient, so I'm not making them any worse. I find a lot of times after about 15, 20 minutes  of having overcome their auto-peep, if you have them on non-invasive, for example, their anxiety decreases, so their minute ventilation decreases.  So you can further decrease the amount of peep that you're applying because they don't have as much auto-peep. But just make sure you don't over-inflate them  and I've never encountered it. You generally see that after they were rested and they're getting bagged during the code. Thank you. Same experience.  One more question. Sorry, one other thing. Last question. Can Helios be used through a BiPAP circuit? So when you say BiPAP, you mean a non-invasive ventilator.  So the answer is if you use your ICU ventilator to do face mask ventilation, yes. Okay. The answer is if you use the device, and I hate to, you know, again,  the BiPAP devices from Respironics, the V60 or those devices, the problem is the flows are so high, especially in the presence of a leak,  that it's hard to get enough Heliox to make a difference. And there's really, there are a lot of technical challenges in delivering Heliox through a device  that's intended to do non-invasive ventilation in the presence of a fixed leak. Got it. Thank you. Well, thank you so much for coming. Help me thank the excellent panel  and have a good rest of the conference.

Video Summary

The video discusses the treatment of severe acute asthma, focusing on medication strategies and mechanical ventilation. One speaker discusses the use of ketamine and other adjunctive therapies when standard therapies are not effective. The other speaker discusses mechanical ventilation strategies, emphasizing the importance of non-invasive treatments before intubation and outlining guidelines for ventilating intubated patients. Both speakers highlight the need for further research to establish evidence-based recommendations for severe acute asthma treatment. Additionally, the video mentions the use of volume control ventilation over pressure control ventilation, the importance of avoiding intubation if possible, strategies to reduce hyperinflation, and the use of applied PEEP to compensate for auto-PEEP. The video also briefly mentions different modes of ventilation and the benefits of aggressive extubation.

Asset Subtitle

Pulmonary, Pharmacology, 2020

Asset Caption

The Society of Critical Care Medicine's Critical Care Congress features internationally renowned faculty and content sessions highlighting the most up-to-date, evidence-based developments in critical care medicine. This is a presentation from the 2020 Critical Care Congress held February 16-19, 2020, in Orlando, Florida, USA.

Learning Objectives

Discuss how intrinsic positive end-expiratory pressure (auto-PEEP) affects ventilator triggering, peak airway pressure and effective driving pressure
Explain how increasing applied PEEP decreases the work of breathing and improves synchrony
Review accepted treatment approaches, including the role of heliox, pressure versus volume ventilation, and pitfalls
Describe the pharmacologic treatment of acute asthma using inhaled and systemic bronchodilators, steroids, magnesium, and leukotriene inhibitors

Medications for the Treatment of Status Asthmaticus

Mitchell S. Buckley

Mechanical Ventilation Strategies for Severe Asthma

Richard D. Branson

Ventilator Strategies for Status Asthmaticus Based on the Starling Resistor

Eric Magana

Meta Tag

Content Type Presentation

Knowledge Area Pulmonary

Knowledge Area Pharmacology

Knowledge Level Intermediate

Membership Level Select

Membership Level Professional

Membership Level Associate

Tag Asthma

Tag Ventilation

Year 2020

Keywords

severe acute asthma

medication strategies

mechanical ventilation

ketamine

adjunctive therapies

non-invasive treatments

intubation guidelines

evidence-based recommendations

volume control ventilation

hyperinflation reduction

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