All right. Good morning. So, my name is Dr. Salim. I am from Mayo Clinic, Director of Respiratory Care Unit. I have been asked to talk about mechanics, modes, and algorithms. I would like to thank the chair for inviting me today, and I will be talking a little bit about practical tips. So, this is going to be the foundation for the talk that will be coming, disease-oriented. So, I will say that, first of all, I just wanted to say I have no relevant financial relationship. I'm going to be talking about brands. You can't talk about non-invasive ventilation if you wanted to make differences in algorithms without talking about brands. But, again, I have no financial interest in any of them. So, I'm going to give you a very, very practical approach to non-invasive ventilation basics. First of all, before you choose your non-invasive ventilation mode or setting, so you can fancy, you need to know the timing in which you can apply the non-invasive ventilation to your patient. So, it's not the same to apply your non-invasive ventilation to someone who is in the ICU, to the wards, when the patient is going to be discharged. So, it may be the same mode, it may be the same settings, but it's going to vary depending on what type of patient in that continuum do you have. So, tip number one, you need to know the timing in which you're going to be applying this non-invasive ventilation. The second thing that you need to know is about the physiology that you need to treat or you want to treat with non-invasive ventilation. If you want to treat problems with oxygenation, you're going to be paying attention to your mean airway pressures, how you can reach that mean airway pressure through CPAP or bi-levels. If you're talking about problems with ventilation, augmentation, then you're going to be talking about pressure support. And with the pressure support, not only you're going to be augmenting that ventilation to arrive to a minute ventilation that you want, but also you're going to decrease the muscle effort to put that muscles to rest. So, think about the continuum of your patient, think about what is the physiopathology that you want to apply for these devices. And therefore, it's going to make sense to you that we have two big groups of devices, the CPAPs that stands alone, and this is the ones that they're going to be splinting your upper airways and you're going to be keeping your lungs inflated. And the second one is that there are all the NIVs, all the bi-levels, and these are your BiPAP-S, ST, your VAPs, your ASPs. So the third tip is about the box. How are you going to deliver that non-invasive ventilation? And these are the two boxes that you're going to be having. You're going to have boxes that they are relatively simple. This is what we call, and I'm going to make a pause here and tell you that this doesn't exist, this word. This is all commercial, sorry, this is all DME and qualification use of this word called RADS. You're going to find out that my colleagues will talk to you about RADS. RADS are Respiratory Assist Devices. They have this code, so 0470, 0471, the 70 is without backup rate, the 71 with backup rate. The RADS are all these devices that you see in that photos, and I'm sure I can put many other brands that also can be there. They're all modes that they will deliver, sorry, they will deliver pressure. The difference is that from the ventilators, I repeat, the difference from the ventilators is that they have no batteries, no alarms, they are not designed for track ventilation. These are simple devices. These are the devices that you use, for example, for your ASA patients, and they have a single lumen and it's going to be with a vented mask. On the contrary, you have the home mechanical ventilators. My colleagues will talk to you, this is oriented, these devices. These devices are the ones that you probably may have seen in your practice in that pictures that you see there. In the middle column, you see the modes. It can deliver pressure, but also can deliver volume. These are the devices that you can use for mouthpiece ventilation when you need to extend the ventilation from nighttime to daytime. And these can be used for double-limbed circuits and also for invasive ventilation through a track. These are the ventilators that you think that if the patient gets disconnected, will die or have a very bad outcome. These are the devices that you're going to use. Otherwise, you should be thinking about just using a RAD device, a device that is not a home ventilator. Tip number four, when you're looking into NIVs, you need to know the building blocks of these devices. They are bi-levels, so they have to have a lower pressure called EPAP. You're going to have a higher pressure called IPAP. So if you start with the EPAP, one of the elements that you're going to have, the machine needs to understand is when to change from EPAP to IPAP. And that is going to be the trigger. Then it's going to be a rise of the pressure. This is pressurization time, and this is called rise time. Then the machine will keep that IPAP certain time. This is the inspiratory time. And at some point comes the most critical point in which the machine needs to understand when the patient is ready to exhale, when the patient does not need more IPAP. And this is the cycling. And that cycling, that it will turn the IPAP to the EPAP, will be either by time or by flow. And we're going to see that in a few seconds. Remember that the area in which either the pressure support or the time in inhalation will determine, based on the mechanics of the respiratory of your patient, the total volume that you're going to be generating. So if I have a 10 over 5, if you have very good lungs, you're going to be moving normal total volumes. But if I give it to a COPD, or I give it to an ILD, it's going to be decreasing independently of the numbers. So always remember the mechanics to give you the results about that total volume that you're going to move. For example, if you have diseases that they're going to go in more details, like COPD or obesity hypoventilation, regarding the rise time, you want that pressurization time to be shorter for the COPD because you want a longer time in exhalation. And in patients who have obesity hypoventilation for neuromuscular disease, you want that rise time pressurization to be longer because you want to be spending this patient more longer time in inhalation. What about the respiratory time? Applies exactly the same. If you have COPD, you want your respiratory time to be shorter. You want to extend your respiratory time, and in the contrary for neuromuscular disease. Now here comes the difference in between algorithms and devices. And this is the part that I need to go through certain brands oriented comments. There are certain devices in which or algorithms in certain devices that the inspiratory time is not applied equally to all breaths. As you can see here, you have a breath that they are mechanically generated or spontaneously generated. The inspiratory time in certain algorithms only apply in mechanical breath. Breath that has been generated by the backup rate. In spontaneous breath, that inspiratory time will not be applied. If you do ICUs, you may have a B60, for example, respironics, and you spend a lot of time thinking very seriously about the inspiratory time that you're going to put in your settings. Guess what? If the patient is spontaneously breathing, that particular algorithm is not going to apply in spontaneous breathing, only in the mechanical breath. You need to turn your device into pressure control to apply that inspiratory time in all breaths. And this is why I'm telling you that devices like these, you may need to be thinking about turning into pressure control to apply that inspiratory time to all breath. The patient will cycle by time, is not going to be happy with you if it's too awake and alert and interactive, but definitely it will be very effective, given some degree of predictability in the tidal volume and mini ventilation. You have ventilators in which that algorithms not necessarily have that handicap. And these algorithms in these devices, even in the same brands, with more advanced generations of these devices, the inspiratory time will be applied to the mechanical breath and to the spontaneous breath. I promise you that I'm going to talk to you about cycling. Cycling is synchrony. If you cycle, if you trigger on your cycle accordingly to your patient, you have synchrony. If not, you have asynchrony, increase your work of breathing, and your patient is not going to be able to tolerate the device. So synchrony is everything. So pay attention to the advanced mode of ventilation. The inspiratory time, as I mentioned to you, is the conversion from IPAP to EPAP. And that could be either by time or by flow. What is by flow? Remember, when you breathe out, right now, you're breathing, what you're doing is this. When you're turning into that, you can tell the machine at what stage to cut off that inhalation. And that is going to be based on a peak flow. And that peak flow is going to be a percentage, a number of liters, depending on which brand you're going to be managing. The higher the peak flow that you're going to cut off, the earlier your inhalation will be stopped. Think about COPDs. The longer you allow the inhalation to go in by flow, the larger is going to be the total volume. Think about neuromuscular disease or obesity hyperventilation syndrome. Tip number five, each breath is part of a cycle. Never forget, never get too obsessed with your inspiratory time without paying attention to what your exhalation time is. And that is why you have the restricted diseases and obstructed diseases with IE ratios that your devices will tell you every time that you change your inspiratory time, your machine will remind you about what is the IE ratio depending on your restricted versus your obstructed physiology. Again, the hand of God, the hand of the machine, time to touch the patient and try to see if we can reach synchronization. And that synchronization, as I mentioned, you do have a patient that have a brain and have a lung. It has, and you have a machine that it has a PCU, a central computer system in which we coordinate as a brain. And you will have the mechanical component into going into that. So the trigger sensitivity and the cycle sensitivity are your advanced mode of ventilation that you need to pay attention for synchronization. So not only is just how much IPAP I had, that is for people that didn't come to the session. For people that comes to the session says, what else should I be thinking about? Disease-oriented will be in each of the sessions just mentioned that. So in these cases, the question is, should I be toying around trigger? Should I be toying around cycling? And as you can see, I put in that slide the changes that I do. It's rarely that I will manage much of our changes in the trigger, but I do a lot on the cycle sensitivity of these patients. So the take-home messages is you need to know your physiology. You need to know what are you treating, oxygenation problem, ventilatory problem. You need to know what is the algorithm and the device. Each of you know which device do you use in your hospital and as an outpatient. You need to know that because each one will have an algorithm that may work slightly different. And when you ventilator offer volume modes, remember that the ventilators are the ones that they are the big guns. When you bring them is because you have a very sick patient that you will have complication if you get disconnected. Otherwise, think about if you can qualify this patient even though sometimes it's difficult for the rats. And so adjust your advanced settings for synchronization. I leave you with that ideas because my colleagues will take it to the next level and it will give you a patient disease oriented. Thank you. There's a few more people coming in. I think we're going to sit by the side. So if we can open some space for the newcomers, that would be awesome. I want to thank you for being here and I'm going to take a picture of you guys. So if you can say hi for the Twitter, awesome. You guys are awesome. We're going to talk high intensity NIV and COPD. And these are the learning objectives for this session. And I just want to start with mortality. Quality of life is a big one too. We did a session on high flow because it impacts quality of life. But so far we don't know that it impacts mortality for stable COPD and their current clinical trials ongoing for that. But one of the few therapeutic tools that actually improves mortality in COPD is NIV. No bronchodilators, maybe the trilogy, which was a bad choice for wording with NIV and the trilogy. But the clinical trials are important to kind of keep in mind. These are the European trials, landmark trials. The initial ones were very few patients. It's the European studies by the Germans. They actually didn't titrate by tidal volumes. But they admitted the patients to the hospital, increased the pressures, and saw their work of breathing. This is high intensity ventilation. So you see that they used IPAPs as high as 42. So we're not talking the 10 over 5 that we tend to see in our hospitals. And they actually saw that with the high intensity pressure ventilation compared to low intensity, which is usually around 14 over 5. It's still higher than our 10 over 5 we see. The patients had lower CO2s, tolerated better, and had better outcomes. They also did a crossover trial where they randomized the patients to first high, then low or low high. And they saw greater improvements in CO2 levels, which also translated into better tolerance and better outcomes. So we have then this trial by Strzok that didn't show any mortality benefit. And the thought is that they enrolled patients that were not so hypercapnic. So they took them from hospital admission, acute exacerbation of COPD, and they sent them home with non-invasive ventilation, kind of like what we would do now. And these patients didn't show mortality benefit. Now their CO2s were on the lower side, like just slightly higher than 45. And the patients were recruited directly from the hospital. The landmark study, the HOT-HMB trial, which we all should be familiar with, then showed this important mortality benefit compared to oxygen alone. And what the difference is, they recruited patients that were more hypercapnic. So they used a cutoff of 52, which is one of the reasons why this is included in the current approvals for insurance. And they also waited for that patient to go home. And they recruited them like six weeks after the index admission. And they were still hypercapnic. The thought is that you have some patients that, like 60%, their hypercapnia will improve after a COPD exacerbation. So that patient may not benefit from NIV. But the patient that is still hypercapnic at six weeks, then that patient benefited. Now the one thought for us is, if you have a patient that is coming and is in admission and their CO2 is 100, I wouldn't wait for that patient to go home and wait six weeks and then repeat the CO2, make sure it's 52, and then get them started. The majority of those, we know they're chronically hypercapnic at rest. And for insurance approval in the US, you don't really need to show that it's six weeks after discharge, blah, blah, blah. So take it into the clinical context these days. Now finally, we have US data. It's not a randomized controlled trial. These were all trials done in Europe. And in the US, there is this Medicare data that showed reductions in death, hospitalizations, and ER visits. And so right now, all these trials were also done with our classic COPD patient, which is the skinny patient that has very severe airflow obstruction, gas trapped, and is hypercapnic. We've all had those patients. But the truth in my clinic is that I'm seeing less and less on those classic patients. The majority of my patients have either a triple overlap of morbid obesity, is like BMI is 40, 45, 46. They're hypercapnic. And they actually truly have severe airflow obstruction, where they're not mislabeled obesity hyperventilation syndromes, which we also see the occasional 32-year-old being labeled COPD. But I'm non-smoker to lifelong. But the majority, I'm seeing more and more of this. And they're getting complicated. And then we're seeing even the heart failure, pulmonary hypertension, AICD, that is obese and has COPD. So these are the patients that are coming to our clinics and to our labs. So for treatment options, we know non-invasive ventilation. And we're talking positive, not negative. And the volumetric pressure support modes we're discussing are bilevel SD. So just keep it like that. It's a BiPAP with a backup rate. You got this. The central drive drops in REM, right? So that's one of the beauties. The beauty is the machine that BiPAP with a backup rate can adjust for sleep hyperventilation in REM and can deal with the upper airway resistance with your EPAP. And so the patients that are very obese that tend to have more of these drops in REM and more upper airway resistance obstructive sleep apnea may benefit from an auto-EPAP. Those patients, I'm not going to bring to the lab to see if they have sleep apnea and then titrate the CPAP, EPAP. We're not talking COPD overlap, which is COPD-OSA only. We're talking hypercapnic respiratory failure. Then that patient may benefit from a ventilator, not the 10 over 5. And so we did a little study. And we tried to recruit COPD patients for a non-invasive ventilation for home. And the majority of the patients that we recruited were actually obese with severe sleep apnea and hypercapnia. So these are patients that I could try the CPAP data, but they are very sick. They've been readmitted multiple times. So instead of trying to do a sleep study and an outpatient titration, I send them home on a vent with auto-EPAP. So that's the advantage. COPD principles, we want to keep the expiratory time long. And so for that, you want to shorten your eye time. So you have an IPAP and EPAP. You want that to be at least 8 to 10. Just keep that as a principle in COPD. And then you want the minimum expiratory time to be short. And also titrate it at bedside. I've done this at bedside with my patient's pressure control. And then they look really uncomfortable. So then maybe I'll do 0.4 or 0.5 to make sure that it's also adjusting to what they want to get, how fast they want their breath. And then I want to make sure they're cycling quickly to EPAP so that even when their flow is really fast, they're cycling to EPAP. And I want to give them time to exhale. And so the other thing is, when you're inpatient and you're sending them into outpatient, you can use that information, right? So I'll go to bedside, and I make sure they're moving 8 ml per kg ideal body weight on the settings that I'm putting at the bedside. And the respiratory rate has decreased, and the work of breathing looks better. So it's not only about 8 to 10, the tidal volume, it's the rise time and the cycle. It's also how the patient looks and doing that quick bedside adjustment so that it works for that patient. We talked about the difference between the RADs and the VANS. And for COPDs, mainly, they order EPAP. And also, if you're going to choose a device, and talking about brands, I don't get any money. We have to. And actually, Luisa and the VIVO45 have high-flow nasal cannula options, so I'm going for those for COPD, because there is some preliminary data that it helps with quality of life. So they could switch to high-flow nasal cannula during the day for the flow, not so much for the oxygen. And so the other particular to COPD is auto-EPAP, and the EPAP levels, because you want to make sure you're helping them trigger the breath, right? We know that they have gas-trapping hyperinflation, so their alveolar space is positive. They want to get it to zero, and then negative to pull the breath. So if you give them a higher EPAP, they are easier to trigger the machine. So that I do at bedside, too. If I see that they're really struggling to move that air, then I'll increase slowly the EPAP from a 4, 5, 6, up until 10. And I make sure that they are now actually easier for them to move the air in and out. So if you're doing an auto-EPAP, I may go 8 to 15, or 8 if they're on the obese range. So keep that in mind. Your EPAP is also for auto-PEEP and COPD. When do I choose a BiPAP versus a VENT? If they need it a long time during the day, if they're very hypercapnic, already on a BiPAP at home, if I need the auto-EPAP feature, if they have dyspnea that I think they're going to benefit from high flow, or even mask use during the day, or if I think that they're really going to need some more RIT support, right now is the only way to get it. Because the DMEs can send RITs at home. Then I see them as an outpatient. You'll see them in your clinics. They'll come with their VENTs. Do they still need the VENT? Then at that point, I may switch them to either a BiPAP device, or I can do CO2 monitoring oximetry and de-escalate to Burley. I've never done two CPAP all the way. Have you guys? No. It's usually either VENT to BiPAP S or ST. And then you have to follow them, right? These downloads are spectacular. You have IPAPs and EPAPs. This is an STA that can do volume and short pressure support. But then in this case, you see that the sleep apnea is controlled. Everyone focuses on sleep apnea on devices. But for this patient population, we also want to focus on ventilation parameters, right? So CO2 and oximetry. And I blended, for this patient, an oximetry to the RADS device. And I got download data, and you see that they were hypoxic at times, so an ODI of 16. So AHI of 0, but ODI of 16, the oxygen desaturation index. So in this case, the question is, why are they still desaturating? And is it tying in with leak? And for this particular patient, it turns out that that was because of leak. That was happening in REM sleep, and the patient was still hypoventilating in REM. In this case, I'm like, oh, what happened here? You see that there is a spike of respiratory rate and minute ventilation and a drop in tidal volume. And this patient actually had a COPD exacerbation at that time. So maybe AI can help us monitor these patients closely, and then detect COPD exacerbations earlier, treat them earlier, and prevent admissions to the hospital. We talked about also, obviously, for the patients with the auto EPUB, you want to keep an eye on the AHI. The disadvantage of the respironics devices is they're not giving you an AHI number. It's another reason why in some patients, I may choose VIVO or Luisa or astral devices. And so then I see them. When I come to my clinic, I'm like, you're going to bring that machine here, whether you have to bring your cousin or you're like, bring the machine. And then I'm like, and don't tell me no one told you. So then I have my screens here. This is the Luisa. It has three programs. I had her on mouthpiece ventilation and high flow. I adjusted the high flow for comfort. The VIVO, they can have a range. So if they need more, the patient can increase it. So that gives them more advantage for when they're not feeling well. And you see that the machine, she was on 10 over 5 and intolerant. So that's why they didn't increase the pressure. But she was intolerant in the hospital to the low BIPAP pressures. So when I increased the pressure, she's like, oh, yes, now I can breathe. You're almost asphyxiating them. If you're putting them on low pressure modes and they need more. So it's not always high pressure intolerance. And now she's progressed where hopefully she's gained weight and for transplant evaluation. And so she's needed even higher pressures. You can get the downloads. You have to get used to the different downloads. And to be honest, I don't know all of this. So sometimes I'll just sit, study them, contact the manufacturer, be like, what does this mean? So it's a combined team effort. I'll talk to my RTs and the patient, how they feel. And I make sure that I'm monitoring blood gases. I don't know at your institutions, but mine is like, I'm at UChicago. I'm a director of the Advanced Respiratory Care Program there now. And it's really hard to get ABGs. Is it hard for you to get ABGs? Can you raise your hand? OK, that makes me feel better. I'm actually drawing them myself. And you can't run VBGs, but my problem is I cannot qualify anyone for VBG with a VBG. So please, that's my MO. So take on home points. It reduces mortality. There is still questioning about this. I don't know why. And the pulmonary world is like, but does it really? I'm like, yes, yes, it does. And then make sure you're targeting volumes, pressure support, and that the EPAP can be adjusted. There's going to be resources, and that sure drives us still to the end. And I'm going to give it up to Meredith. All right. So my name is Meredith. I'm from Emory. I do pulmonary critical care, sleep, and neuromuscular, kind of like all of us here. And today, I'm going to talk to you guys about obesity hypoventilation syndrome. I do not have any conflicts of interest. So we're going to have four points to get through. The first thing is just to define OHS and describe its pathophysiology. Then we're going to talk a little bit about the data for pap therapy in OHS. We'll then touch briefly on the strategies for patients with OHS. And finally, just a short point on the acute exacerbation management of those with OHS. So let's talk about the definition. So we all know that you have to have a BMI greater than or equal to 30. You also have to have an awake resting PaCO2 greater than or equal to 45. So it has to be awake. It has to be resting. It has to be arterial. And so that can be difficult for us to get sometimes in the clinic. And they can't have an alternative cause of hypoventilation. So you just heard about a lot of overlap syndromes. And that can make things really confusing if they have severe pulmonary, neuromuscular disease, chest wall disorders, et cetera. Most of the patients who have obesity hypoventilation syndrome will have sleep disordered breathing, either OSA or hypoventilation. 90% of the patients with OHS will have OSA. And 70% of those patients will have severe OSA. The remainder 10% is going to have sleep dependent hypoventilation without OSA. And so I want you to kind of think of these two groups separately as we go forward discussing treatment. It's really, really important in the patients who do have OSA to look for OHS. So to check their BMI, to look at their bicarbonate, to get an ABG if you think that they may have elevated CO2 levels, because even when you treat those patients obstructive sleep apnea appropriately, they still have a two times mortality risk compared to those who only have sleep apnea without OHS. And why is that? So there is a lot of pathophysiologic changes that occur in patients with OHS that don't happen when you only have OSA. So respiratory mechanics are affected just because the actual adipose tissue and the weight that is reducing the chest wall compliance. So they're going to have lower lung volumes. When you have lower lung volumes, you actually have less airways open that are sort of pulling a tug all the way back to your trachea, and that reduces the tractional tug of your airway that actually keeps it open. And so that changes your PCRIT. And so that's what's going to make you more likely to have sleep apnea and lead to airways resistance. They're also going to have a lot of times concomitant heart issues like right heart failure or diastolic dysfunction. So that's going to lead to edema. And there's something called the rostral shift. So you know all your patients probably say, yeah, I have swelling in the day, but it goes away when I put my feet up. Well, where does it go? It goes to their airway. All that water goes to their lungs and their airway, and it makes them have worse sleep apnea and airways resistance. They also have a decreased respiratory drive, and that's a big difference between OHS and OSA without it. And this is because of an increase in leptin resistance. So if you remember, ghrelin makes your tummy growl, and the leptin makes you feel full. So it also affects your response to CO2 and O2. And so if you have a leptin resistance, you're going to have a reduced response to a rise in CO2 and a drop in O2. This is going to lead to nighttime hypercapnia. And when you continue to build up, you kind of reset your CO2 thermostat, that's going to lead to further blunting of those chemoreceptors response. And now it's going to start to bleed into the daytime, which is how we get our daytime ABG elevated CO2. And the kidneys, you know, the lungs and the kidneys, I always say are frenemies. So they're like trying to help each other, but they often screw each other over, and that's exactly what happens. So you retain your bicarb, and they think they're doing a great job keeping your pH normalized, but then unfortunately your lungs stop breathing to try to keep that homeostasis. And so that's all of the differences that lead to the worst outcomes in those with OHS. So what's the data for how we can help them? So the current guidelines say that you should just start CPAP in patients who have OHS and severe OSA. And remember that's the AHI 30 or more, because CPAP does a lot. It stabilizes that upper airway. So it eliminates the obstruction. It is PEEP, right? So it's going to increase those lung volumes. That's going to reduce that air flow resistance, flow limitation, and kind of help with work of breathing. It's going to break some of the cycle of the CO2 accumulation, because if you have really bad sleep apnea, you're just not breathing. And that's part of what's building up that CO2. And so that's going to reduce your bicarb as well, hopefully. And then last, it can reduce intrathoracic pressure swings and lead to improvement in your fluid balance. I'm sure y'all have seen that in your patients with OSA and heart issues. The one thing though that it doesn't do is it doesn't overcome the literal work of breathing that's from the reduction in compliance. Remember from high school physics, work is force times distance. So to move your chest wall a distance, you have to overcome a force. Force is equals MA. Do y'all remember that? Mass. If you have a lot of mass, you have a lot more force. The literal work of breathing is increased, and that's what you need IPAP for. So for the patients who have mild, moderate, or no OSA at all, we recommend that you titrate non-invasive ventilation. And we've talked about all the different modes for that. So again, we break them up in our minds for insurance purposes to RADs and home mechanical ventilators. And the RAD devices support BiPAP-S all the way up through STA, which includes VAPs. And then the home ventilators are the ones that we've mentioned before. And as Dr. Saleem already stated, the difference is that those home ventilators have the higher IPAP max. So like for those European trials and COPD, you can only get that IPAP max on a home ventilator up to 45. They have a backup battery for daytime use and for emergencies. And then also if they progress, you'll hear about this with neuromuscular disease, to trach, then you can just keep them on the same machine and settings. So the data says that some type of PAP, whether it be CPAP or non-invasive, reduces hospitalization and improves survival. And I think we're all probably trying to really convey that to you today with each of our diseases. These things improve mortality. Non-invasive compared to CPAP, if you also have severe OSA, does improve some of your pulmonary and cardiac function. And non-invasive compared to lifestyle modification, those without severe OSA, improved your CO2 sleepiness and quality of life. There has not been any studies that are done to show superiority of VAPs compared to like a fixed BPAP mode. But I think it just depends on, are you sending somebody home from the hospital? Were you able to titrate them? Do they have another concomitant issue at the same time? And that takes a little bit of clinical gestalt. So let's talk about the strategies. So what are the signs that CPAP are not enough? So basically, if they come back to your clinic and they're still having excessive daytime sleepiness with a high EPOR score, you should be worried that they are retaining CO2 overnight. The bicarb on the BMP or the CO2 is not gonna be getting better. It's gonna be similar to what Dr. Lasher talked about, how like your AHI looks better, but the patient doesn't feel better. The overnight oximetry, and you can do it on CPAP, is showing persistent hypoxemia. And if you have it available to you, you can get overnight capnography as well. And then finally, if they still have a residual AHI, then you know it's definitely not working. And if you brought them into the lab to titrate them and they got all the way up to CPAP 15 or above, then you know you should switch to BiPAP at that point. So what modes can we use? So this is kind of the three main modes I think about with obesity hypoventilation. You have BPAP-S, which is just spontaneous no backup rate. I think about that one mostly for patients who have the concomitant severe OSA that's just not adequately treated by CPAP alone and need higher pressures. Once you start getting into the patients who don't really have sleep apnea and who have true, true hypoventilation, you need a backup rate. And so at that point, I would move to looking at BiPAP-ST or an ST-VAPS mode. And remember, you can get all of these on a rad. You don't need a ventilator. What you might need the ventilator for is if you want them to use it during the day and you want them to be mobile with it and they would have a battery for it. Again, I reemphasize some of the nuanced settings like trigger, rise time, and cycle. And we'll talk about that a little bit more in the next slide. I think Dr. Sleem already talked. There's some brand dependency here. So if you don't already know the nuances of the settings, it can help to review with Restoray Therapy or even read the manual and find out which ventilators allow you to set a minimum eye time and a maximum eye time and which ones don't. And typically it's the ResMed devices that will and now the Trilogy EVO from Philips will as well. Oh, the other thing I did also want to mention is the auto-EPAP. So I totally agree with you. For patients that may have some sleep apnea, you're bringing them home from the hospital, you're not gonna titrate them yet, just put them on auto-EPAP. A lot of times I'll give a good auto-EPAP range for these patients and then I will get a data download in like two weeks after they've been on it and I'll take the 95th percentile, what the EPAP is, and then I'll fix it and that'll be their EPAP. All right, so customized settings. So this table over here is from a three-part table from Dr. Saleem and Dr. Wolf's article on these settings. And so this one is specifically for obesity hypoventilation. So let's go step-by-step. So EPAP's the first thing you're gonna set. You're gonna have to set a high EPAP. Think about all of that resistance and weight and mass and everything you're gonna have to overcome to open up their airway. Next, you're gonna set their IPAP, same thing, high IPAP. They're gonna need a lot of force to be able to generate a volume because they're gonna have reduced compliance. If you're on BiPAP ST, then you're gonna adjust up to a tidal volume goal of like eight, up to even 10 sometimes people will say, mLs per kg ideal body weight. And then if you're doing a VAPS mode, which is a volume-targeted mode, remember you can just set a huge range. I think it's really important to understand how sensitive these patients are to being in different sleep stages, being in REM, being on their back, being on their side. So the benefit of VAPS is that you can have less pressure when you're on your side and in two, for example, and they can really go up to their high end of their pressure when they're on their back in REM. And so I usually set a very wide range as long as it's tolerated. The trigger sensitivity, these patients don't really have a weakness. So typically you can set it at the medium rate, which would be three. Sometimes I'll put it at two, which is just a little bit more sensitive to make sure that they can get a breath. The rise time, something we don't often think about, but as you can see here, the area under the curve depends not only on the delta pressure, but also on the time. So if you can't get too much higher pressure from, sorry, more volume from higher pressure in these patients, then you just extend the time, and that's where you're gonna get your volume. And the more volume you can get them, the more CO2 they're gonna exhale. So I usually will bump up their rise time a little bit to give them a longer breath. And then same thing about the instructory time. So you may have a little bit longer eye time, definitely longer than you would in COPD, maybe like one or 1.2 seconds. But you have to work with these patients to make sure they can tolerate it. And then cycle sensitivity. So for these patients, they don't have a weakness problem. So you can generally do the default cycle sensitivity, which is around 25%. But sometimes you might wanna bump it down just a little bit to like 15 or 20%, again, because that's gonna prolong their instructory time. That's gonna get them a better volume. And this is all for the chronic compensated obesity hypoventilation syndrome. But what about for the acute people? So in the hospital, if they have a pH below 7.35 and they're somnolent and you think it's from hypercapnia, you have to put them on noninvasive. You're gonna start it just like you would titrating in the sleep lab. So at least an EPAP of six. Honestly, you're gonna get up to 10 like very quickly, okay? And you're gonna be increasing that to eliminate snoring if they're asleep, obstructive events, desaturations, okay? Once you feel like you've got their airway open, now you're gonna start increasing the IPAP. And you're gonna increase the IPAP till you can start now seeing the chest wall sort of expand. You're gonna see their respiratory distress get better. You're gonna look at their volumes, their exhaled tidal volumes are gonna get better. And then they're gonna wake up and their gas is gonna get better. So this is something where you have to go to the bedside, kind of start them high and wide, and then push them up pretty quick until you just start actually seeing their chest wall kind of relax and see those exhaled tidal volumes. You might need pressures up to 30 of IPAP and 10 to 15 of EPAP. So you really have to not be afraid to push them up. It's very similar to the COPD people. They'll feel smothered until you push them all the way up. And if the volumes still aren't being achieved, then you may wanna switch to VAPS. And the Philips V60s that many of us have in our hospitals have an ST VAPS mode. They also have pressure control, which Dr. Saleem alluded to. And that is a mode where you can fix your eye time even for the spontaneous breath. So that's good to be aware of. I think as long as you have a good seal and a good mental status, you should be able to avoid these patients getting intubated in most scenarios, as long as it's just an exacerbation and there's not a concomitant pneumonia or something else going on. And hopefully avoid tracheostomy. To monitor them, if their pH gets worse, if they're not getting better at one to four hours, then you're just gonna have to call it and you're probably gonna have to say that they need to get intubated. I usually will always have them in the ICU and I will always call anesthesia to help me with this because I don't wanna have any complications. This is not the person that you wanna be trying to crike. Monitoring is recommended. Even if you just have them on BiPAP, you have a step-down, I would still bring them into the ICU. Worst thing that can happen is they do fine and then they can go to step-down tomorrow. They should wake up and they should have reduced work of breathing. And when you reduce their work of breathing, they'll stop producing as much CO2 and then their CO2 will also improve. And then finally, once they do improve, you can take them off 24 hours, go to just nightly with naps, and then you can discharge them with the noninvasive that they were doing well on, on that last few days in the hospital. Then what we wanna do is see them back in clinic and this is the guidelines within like three months and just like with the patients with COPD, you wanna titrate them and see if you can downgrade them. And it's not only because downgrading them to less pressures may be more comfortable for them, but also it's so much more affordable if you can downgrade from a home mechanical ventilator to a RAD device. So in summary, remember definition of OHS includes a daytime resting CO2 and 90% of the people will have sleep apnea, 70% is gonna be severe. PAP is greater than lifestyle changes with regard to improvement in like hospital stay and outcomes, PCO2, quality of life. High BMI, high pressures. If you take nothing else away, just remember that, okay? High BMI, high pressures. Do not be afraid to push it all the way up and do sweat the small stuff. Pay attention to those little differences, that'll make them more comfortable. Adequate EPAP's key, you're never gonna get air into those lungs if you can't get it past a resistive airway. So you have to open it up first. Once you do, just push it up as high as you can go until you get their work of breathing reduced. All right, thanks for having me, guys. Thank you to the chair for allowing me to participate in this awesome session with these great speakers. And thank you for coming and spending your time with us as I'm pulling up my presentation here. I'm Jeanette Brown from the University of Utah and I focus on a lot of chronic neuromuscular respiratory failure patients. I know that not everybody has the luxury of structuring their clinic to support these patients, but I'm hoping today to take the time to give you some advice on how to adjust some of these patients' settings to make them more comfortable and be able to think about how you can adapt your practice environment for these patients to get a little bit better outcomes. And I have no financial relationships with any device companies. I think this is a big thing to point out. And if I hear supply chain issues one more time during COVID, one of the takeaways is that you can't be married to any one device. I have a seven-state catchment area that I take care of and I work with all the DMEs. And so the reality is like you kind of have to learn to play with all the different devices, but I can't be married to one device because that's just not realistic. So today our goals are gonna be for thinking about using NIV for neuromuscular patients, we really wanna resolve this breathlessness and improve their work of breathing. We talked about this earlier in the session, but this is really what patients will complain about and can really diminish their quality of life. They can also have really poor sleep quality as a consequence of this. And many of them, once we finally get them situated on their device, we'll say, gosh, I don't wake up to go urinate in the middle of the night or I'm sleeping all through the night and I'm so much more refreshed and makes a big difference in the morning. And then overall their quality of life improves. And when conditions with ALS and other muscular dystrophies it's been shown to actually extend life. And for example, in ALS with some of the medications that are out there, they will extend life by a couple of months. If you're an ALS patient, non-invasive ventilation can give you up to 15 to 19 months of extra survival. And I would argue with that actually quality of life. So if that puts that into perspective, how much of an impact we can have on these patients' lives. And the thing is like, frankly, they'll come in and be like, it just doesn't feel comfortable, doc. You know, thinking today, I hope to give you more of a systematic approach to going through this. The first thing I think about is the interface. You know, one of the downsides of being in the acute side sometimes is in the hospital, we have the cheapo masks and you see these poor patients and they've got this thing strapped to their face and then got the bridge of their nose, has like a nepallex or deuterium hiding under it. And they're just like, this sucks. And so like, if the mask does not fit, they're not gonna use it. They're gonna feel terrible. So there are tons of different kinds of masks that are on the market. I don't have time to show you all of them, but they can do everything from a true full face mask to the smaller hybrid mask, to a nasal mask. And then my patients have taught me about cute and very useful things like gecko pads or using the physical therapy KT tape. Actually a little section over the nose can be really helpful for preventing that nasal bridge breakdown and it's really inexpensive. But really thinking about like, what's the best mask for this patient and thinking about their face shape. A little bit of effort that way will go a long way for actually getting patients to use this. And then again, claustrophobia. You know, the mask designs that tend to have the typical triangle that we're all used to that goes like this, that blocking of your field of view can actually induce a lot of claustrophobia with patients. And that again, can be a huge barrier for getting them to use it. One of the ways I desensitize my patients will use cognitive behavioral therapy, have them work with a psychologist. But one of my favorite things is actually Netflix because most of us in the evening sit down and watch TV, watch Netflix or whatever. And I'm like, put on your favorite show and then put your device on and just kind of get used to having something on your face and breathing with it as opposed to just go to bed, put this thing on your face and don't stare at the ceiling for four more hours. So again, you know, trying to really also get them to understand why we're doing these things and get them on board with sort of your shared goals. And it's a dance, right? The device, Dr. Saleem talked about it. You know, like you really have this device between, device dance between the patient and the device. And you really wanna get it as comfortable as possible because the people will start using it more and then they get really used to it and then they like it and then, you know, better outcomes for you and them. So again, I have to deal with a lot of different DMEs because I have a wide catchment area. It would not be the first time nor the last time that I have a patient show up in clinic with a device setting that is not what I ordered. And so check to see if it's what you ordered. A lot of the times I will put pressure control, AVAPS for example, and it'll come back AVAPS AE. And that is actually one of the bigger mistakes because then the device, if it's not set correctly, will auto trigger all the time and drive the patient bananas. So again, is it the right actual thing I prescribed? And again, like we were talking about here, CPAP is not sufficient for our neuromuscular patients. And this is another thing I will have heard. Oh, well, they tried me on CPAP before and I hated it. And so they're not even willing to talk about BiPAP and I'm like, no, no, no, no, wrong thing. So having to also get them to understand like that was just the wrong therapy and somebody missed that they had a neuromuscular diagnosis. The other thing is the target tidal volume ballpark about eight cc's per kilo for ideal body weight. We talked about that. And then again, reviewing those data, downloading the leak, the pressure, the AHI, the respiratory rate, and then the percent trigger breaths. If I have a patient that's really weak, I may see like 2% triggered breath. You know, they're really relying on the device at night because they're very, very weak and depending on your stages of sleep as well. The other thing I'll do though is for a lot of my patients, because I work with a lot of spinal cord injury patients, for example, and a lot of neuromuscular folks is I will use transcutaneous CO2. Again, I have no brand affiliation, but this one happened to be someone that I'd worked at with at the University of Michigan. And we use transcutaneous CO2. So instead of having to poke somebody for a blood gas, you know, dealing with hematoma, getting the lab itself, getting, you know, dealing with anticoagulation, this allows me to look at the CO2 through the skin. The confidence interval is plus or minus six millimeters of mercury. So it's nice to be able to see that. The other aspect of this allows me to see this over time. And it has a pretty close to real time adjustment rate. So you see how this kid is always smiling with his little sticker on his forehead with the probe. I can then put his non-invasive ventilation on him and then sit and adjust his settings. And it's kind of like the eye doctor. They're like, do you like one or two better? I will sit there and be like, do you like this rise time? Do you like this TI? You know, whatever I'm playing with. But I also can give feedback to the patient and myself by saying, oh, look, your CO2 is now not 55, it's 43, you know, and show to them it's working. And then they get that sort of feedback as well as I do. And then again, please don't be scared by the alphabet soup that is our field. It is a pain. And a lot of it is because I remind people that like the thing over there that we all say Band-Aid for, that is a brand name. And BiPAP is also a brand name. And AVAPs and AE and all these things. So don't be afraid. Some of them do have little quirks, but talking to the manufacturers, there's a number of us that are willing to chat with folks as well. Kind of getting through this soup that is a little bit painful is important because these comfort settings are really key for getting patients to use their devices. And Dr. Saleem talked about this as well, but I wanna highlight the things that for neuromuscular patients are really gonna be comfort driven. And I'm gonna give you a series of questions on the next slide that is how I kind of go through this a little bit systematically, because it can be hard because the patient's like, I just don't like it. And you're like, is it too big? It is too small. It's like Goldilocks. I just want just right. And everybody's just right is a little bit different. And some of those things like your eye time is super individual. Cause you can even have a patient, for example, that has a neuromuscular disease and the next one has similar disease, but what they want for an eye time, for example, is very individual. It can also be driven where they are in the process of their neuromuscular progression. My ALS patients progress really fast. Some of my SMA people can go really slow over years. And so that's the other benefit about being able to monitor their CO2 over time is some of these folks may just have really subtle clinical symptoms and they're not like, oh, I feel terrible in the morning, but it just happened over months to years. And they're like, I didn't notice. It was just how I thought things were gonna be. So again, looking at that trigger rise cycle, tidal volume and inspiratory timer key. So these are some of my favorite questions and you can do versions of this, but I ask them, is the breath or airflow too fast or too slow? Then think about adjusting that rise. And you can do that while you're sitting in clinic or do that at the bedside. You can ask, are these breaths too big or too small? You can adjust that cycle, the pressure support and the eye time. Does the breath end too soon or too late? And then thinking about that cycle and eye time. I always remember when I was a fellow, back what seems like forever ago now, sitting in the ICU with your COPD or knowing that they want a really long time to exhale. So I gotta make that eye time real short. And then we're looking to see how those changes impact that patient. And then is it just hard to take a breath? Do you get the breath when you want one? Do you get the breath before you want one? And then again, depending on your site, your device, literally going in and figuring out how you have that trigger set and then adjusting that trigger. And sometimes I'll adjust it harder, adjust it easier, and then just sit and watch what they're doing and then continue to adjust as needed. So these are some of my favorite questions just to kind of narrow down, which things should I play with while they're in the clinic? And then additional settings to think about. Your neuromuscular folks may be pretty weak. And then so during the daytime, I will think about their backup rate for nighttime settings, thinking typically less than two based on their baseline rate, but you can adjust this. And then thinking about the RAD device guidelines, which devices have an auto rate. So that also might be something to key into if you feel like they're hypoventilating that that rate may not be set adequately if it's an auto rate. Again, monitoring their CO2, whichever method you have, I'm lucky to have transcutaneous CO2. One of the ways actually that was kind of creative that we were able to get the Syntec at my institution was that we have a neonatal ICU and we routinely use these transcutaneous setups for the tiny babies, right? Because you don't want to keep poking them and they can be on for long periods of time to monitor their CO2. So for our respiratory therapy department, they were already maintaining these devices. So me adding one or two to the 10 we already had was no big deal. The other aspect is there's disposables of cost. And even though, unfortunately, we haven't yet been successful to get a CPT code for measuring CO2 outside of an ABG, we're really arguing that this is a much more functional way to get this data and it makes a big difference in how we're able to take care of folks. The other thing though, speaking of it, is again, adjusting positions. If I have a patient that's like, I feel fine when I'm sitting up, but I can't breathe when I lay down. In clinic, I have the luxury of actually having beds in my clinic rooms, which is kind of a unique feature. But sometimes even in their motorized wheelchair, I'll just tip them back because I want to see what it's like when that pressure of their chest is really on them and they're really at a mechanical disadvantage because gravity is working against them. And then this takes some time. I'll be realistic. I'm very lucky and I've structured my clinic to do this. But sometimes what I'll do is if I have an extra clinic room, I will stick them off in that extra clinic room for half hour, an hour, and just keep adjusting things. But there is actually a CPT code. So you're aware to do these prolonged visits beyond 55 minutes. So at least you can get some compensation for this. I work with my respiratory therapists and my other multidisciplinary team as well during that time, so it works out for us. But I realized those in more of a community or private practice setup may not have that luxury, but these are some of the things that you can do to kind of tweak this. And then just because I went to the University of Michigan for residency and fellowship, I always thought this was funny when we called it EMing. Some of these new ventilators are actually pretty cool. Frankly, they have as many options as our ICU ventilators, but the newest one is like six pounds, which just blows my little mind. But being able to actually look at the waveforms, because many of us are trained from our ICU background to look at the waveforms and spot the dyssynchrony. And this EME gave you an extra clue though in this case, the M waveform, you have a flow time waveform and that they basically got flow starvation here. And then you have a spontaneous pressure supported breath, which is the second hump of the M, that person's trying to trigger that. And so being able to then adjust this to support the patient the way that they want. And then additional factors to consider again, depending on the underlying disease, how fast may they progress? One quirk of our system here in the United States is that hospice is a bundled payment. If I have a patient that is on a ventilator, they may have difficulty getting hospice coverage when they transition to more of their end of life. So again, having those goals of care discussions about what kind of support do you want? What kind of goals do you have for going towards hospice may be an important factor in your practice depending on the patient. And then nocturnal use versus progressive daytime use. I'll have people, nights and naps is always what I tell them but if I find they're on 16 hours a day, 18 hours a day, then it may be time to really go up to your ventilator status. And then the other thing is, is I have a huge catchment area that may have not so great power supply sometimes. If you try to say, well, they need a backup ventilator because they're out in the middle of nowhere, most insurance won't buy that. But if you say they need a backup ventilator for mobility, and I'm using that in quotes there, some insurance will actually cover that. There's gonna be some real big quirks, writing your notes about why you're justifying these devices can be really important. And then home ventilators, again, for mouthpiece ventilation is another justification piece. And then in follow-up, the settings, questions, the mask fit, checking their CO2, whatever way you have, comfort, and then again, goals of care. And so I'm gonna share with you right now a very lovely QR code that Dr. Greer put together. I like the little dinosaur in the middle. But this is actually a collection of some of our dot phrases that we use in clinic. And documentation sometimes makes me crazy. It makes me wanna run away. But the reality, this is how we get our patients, their devices. And like, for example, one day someone called me and said, well, they don't have a NIF, and I'd written MIP. And I'm like, that's the same thing. But the problem is the person calling me has no medical background. They're just a bean counter for some insurance company. So sometimes the way you structure the things you write will make it much easier to jump through the hoops and get your patients the device they need. So this is a link that you can go to that has some of the dot phrases. And we'll continue to update this with hopefully things like appeal letters and templates that we've put together as well. So thank you, Meredith. And then in summary for my session, patient comfort is key. Ask these questions to be able to adjust these comfort settings, and then looking at your efficacy with CO2 monitoring, and then thinking about your underlying disease and progression. And then thank you to my lovely folks in Utah that helped me do fun things with my patients too. We do a lot of adaptive recreation as well. And then these are our summary points for our session.

non-invasive ventilation

patient settings

timing

physiology

oxygenation

mean airway pressures

ventilation augmentation

CPAPs

bi-levels