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CHEST 2023 On Demand Pass
Obesity Hypoventilation Syndrome: Case-Based Accou ...
Obesity Hypoventilation Syndrome: Case-Based Accounts of Outpatient and Inpatient Management
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All right, I guess we're going to get started. I think it is just about 1.30 now. So welcome, everybody, to this very special session on obesity hypoventilation syndrome. So we're hopefully going to give the full spectrum of management of obesity hypoventilation syndrome. First, we're going to have Dr. Zarabian talking about a case of acutely decompensated OHS in the ICU. Then we're going to have Dr. Kha talking a little bit more about management of OHS in the inpatient setting and perioperative setting. And then Dr. Moklisi is going to be giving some examples of a couple of difficult OHS cases. And so hopefully you'll learn a lot of things from these talks because we're very lucky to have these experts with us today. So with that, I'm going to bring up Dr. Zarabian, and hopefully I can load her presentation here. All right, well, good afternoon. Thank you all for joining us today. My name is Dr. Zarabian. I'm a second-year pulmonary and critical care medicine fellow at the Mayo Clinic working with Dr. Dupuis. And so thankful for the opportunity to be here and speak with you all today. And so the objectives for at least my portion of the talk today is first provide a brief overview of obesity hypoventilation syndrome as a distinct clinical entity. And then using a case-based approach to first highlight important characteristics for detection of OHS in the ICU, describe some of the pathophysiology of OHS, and then look at management strategies of OHS in the critically ill patient. And so obesity hypoventilation syndrome is defined by awake hypoventilation really in the absence of other causes. And so it is a diagnosis of exclusion. But it is formed by three very important characteristics. One is patients need to have an elevated BMI of more than 30. Two, they need to have a confirmed sleep-related breathing disorder. Most often it's OSA. And then lastly, confirmed daytime hypercapnia. And so that's shown with an arterial CO2 of more than or equal to 45. And then the most important part is to exclude other causes of awake hypoventilation. So obstructive lung disease, restrictive lung disease, neuromuscular weakness, and metabolic alkalosis from for example a loop diuretic are probably the most common causes. And so to emphasize again that obesity hypoventilation syndrome really is a distinct clinical entity just from obesity is that we see more ICU admissions, greater need for invasive mechanical ventilation, and then a greater proportion of people requiring long-term care facilities at discharge. And as well as increase in hospital and post-discharge mortality in patients with OHS in comparison to the same degree of obesity. But in patients that are eucapnic. And so those with OHS who are discharged and prescribed non-invasive ventilation after their hospitalization, there is a marked reduction in all-cause mortality. So to start with our case, this is a 56-year-old female with class 3 obesity. And so BMI more than 40. She also has a history of type 2 diabetes and hypertension. She presents with increased lethargy and somnolence noted by significant, noted by her significant other and then brought to the ED. So not an unusual medical ICU admission. And so she presents. She's afebrile. She's tachycardic to 110, a respiratory rate of 24. She's requiring 4 to 6 liters via nasal cannula to maintain a pulse oxygen saturation of more than 80%. And she has a BMI of 42. And so she awakens with repeated questioning and physical stimulation, but very drowsy. She's tachycardic. Breath sounds are clear, no adventitious breath sounds, but she does have some pitting adena bilaterally. On her laboratory data, she has a PaCO2 of 55, a pH of 7.25, and a bicarb level of 32. She has a chest x-ray done in the ED. They confirm low lung volumes, but otherwise clear. And so she's transferred to the MICU for initiation of noninvasive ventilation. And so most patients with unrecognized obesity hypoventilation syndrome really encounter health systems in one of two ways. Either in crisis for acute on chronic respiratory failure. And so admitted to the ICU or a hospital ward. And then second is usually in the outpatient setting and evaluated by a sleep medicine physician. And so because of this, they often present in the fifth to sixth decade of life. And unlike OSA, there's really no observed male predominance in this patient population. About 50% of ICU hospitalizations involve patients with an elevated BMI of more than 30. And then another single study of consecutive adult hospitalizations of patients with a BMI of more than 35 confirm OHS at 31%. So a significant proportion. And so characteristics to note, generally they have a very elevated BMI and so more than 40, so class three obesity. But you can really find it in the full spectrum of elevated BMI. Their AHI is generally in the severe range with very classic descriptors of OSA. They're hypersomnolent. They also may have signs of dyspnea with signs of cor pulmonoli, which is generally absent in people with eucapnic OSA. On exam, they may have facial plethora, polycythemia, firm chronic hypoxemia, enlarged neck circumference, and perhaps a loud P2 on cardiac auscultation. And so with obesity hypoventilation syndrome, the vast majority, about 90%, have a concomitant sleep breathing related disorder, specifically OSA, and the other 10% in non-obstructive sleep hypoventilation disorder. And so often we'll cite using a bicarbonate level to screen for patients with OHS, but this might not be the best tool to use in somebody who's admitted and critically ill and coming in with acute decompensated respiratory failure. And so awake ABG on room air, their, again, PACO2 should be more than 45 or equal to 45 to confirm daytime hypoventilation. And although they may have an elevated bicarb, that might not be the most clinically significant or prognostic finding in an acute decompensated situation. And so wakeful hypoxemia is not common in obstructive sleep apnea. Its presence really should lead clinicians to inquire into OHS and patients with OSA. And so, you know, we've confirmed awake hypercapnia. We've confirmed a sleep-related breathing disorder and an elevated BMI, and so the next step is if there's pulmonary function testing available, if they've had that done in the past, and then, of course, imaging to exclude other causes of hypercapnia. So PFTs and imaging are helpful for exactly that reason, to exclude other reasons. And so with PFTs, you generally see a significant decline in their functional residual capacity and their expiratory reserve volume, and that often parallels the severity of obesity. Part of the pathophysiology of OHS also includes a decrease of their total airway compliance, increase of airway resistance, and then also an increased work of breathing with a described associated weakness in their respiratory muscles. So back to our case here, this is our lady with 56-year-old, a 56-year-old female with class 3 obesity, and so we've ruled out a precipitating event. She has no pneumonia, no heart failure based on the workup she's had so far. And so we decide to initiate non-invasive ventilation, either using a pressure-limited or a volume-limited mode. And so, importantly, there really are no guidelines for pulmonary management of critically ill OHS patients, and really no clear benefit with using either BiPAP or AVAP, so either a pressure-limited or a volume-limited mode. Much of the knowledge we have on using positive airway pressure and obesity hypoventilation has been performed in the setting in outpatient sleep medicine clinics and not in the ICU. And so a common algorithm we'll see in the outpatient is to initiate CPAP and then switch to non-invasive ventilation with either a bi-level positive airway pressure or AVAPs, but I would really caution using CPAP in somebody who's critically ill with OHS. They tend to present with acute respiratory failure, and so a mode that can both relieve upper airway obstruction and promote ventilation is the most suitable. And so our practice really is to start with a pressure-limited mode using a full face mask. And so we'll use expiratory positive airway pressure to relieve their upper airway obstruction. And that difference between their inspiratory and expiratory positive airway pressure helps support ventilation and CO2 clearance. And so what we generally do is start with an EPAP between 6 to 8, and then we'll titrate their EPAP based on the severity of their upper airway obstruction. And then start with a delta of at least 6. Generally, this patient population requires elevated positive airway pressure than you would expect in somebody else coming in with acute decompensated respiratory failure starting on non-invasive ventilation, really due to the high thoracic impedance with these very elevated BMIs. And some things that we've done that's been helpful in trying to A, make it more palatable for people to remain on positive airway pressure. And then, of course, to treat their hypoventilation is to use longer rise times and inspiratory times. And what that really does is to help facilitate recruitment of adalactatic lung, specifically in this patient population that have a marked reduction in their functional residual capacity and expiratory reserve volume. And so while they're on BiPAP, we'll monitor them periodically in the ICU. And so we'll continue them on non-invasive ventilation while awake and asleep until their blood pH completely normalizes. Periodically, we'll monitor vital signs, their alertness, their respiratory patterns, their tidal volumes, most importantly on whatever set of pressures we've decided, and then their blood gases. Once their blood gases have normalized, then we can take them off BiPAP and allow them to just use BiPAP while sleeping at night. And then lastly, sometimes it's a little bit tricky to find the optimal pressure settings using bi-level positive airway pressure. And so what we've done in the past is use a volume-limited mode, such as AVAPs, to trend their pressure supports throughout the night to help guide reasonable bi-level positive airway pressures to get to a targeted tidal volume that can achieve adequate ventilation. And so the American Thoracic Society recommends that hospitalized patients with respiratory failure and suspected OHS should start on non-invasive ventilation before being discharged. And until they undergo outpatient markup and titration of PAP, ideally within the first three months after hospital discharge. So it's really important that once this patient population is identified in the inpatient setting and in the ICU, that they do get set up with sleep medicine in the outpatient setting. But even more importantly, before they get sleep medicine evaluation, once they leave the hospital, is to be sent home with a device like a ResMed so that they can support their ventilation during the night. So I'll stop there for now. All right. Thank you very much, Dr. Sarabian. So we've talked about this in other sessions already today, and it's been a hot topic. Giving someone non-invasive ventilation in the hospital is a wonderful idea, but it's not always easy to do in practice with the insurance guidelines. So I don't know if anyone else has experienced the frustration of trying to get someone qualified after they have been acutely decompensated with their OHS. I guess we have a positive response there. So anyway, but that's another story. But thank you very much for your good summary of hospital management of OHS. All right. All right. Next up we have Dr. Kha, and he is going to talk about inpatient management of OHS. Thank you all for being here today. My talk is about inpatient management which is a non-ICU setting, and also perioperative and surgical setting. I'm a hospitalist with interest in perioperative medicine, so this will be a slightly different angle. This is my disclosure. And my objectives are basically actually in a big way to highlight how widely chronic hypercapnic respiratory failure is under-recognized on the medical and surgical wards. I'm personally appalled when I see diagnosis of chronic hypoxic respiratory failure in a lot of these patients. I hope that's not a reality everywhere else. Also discuss a model for ICU to ward transition of patients with OHS, optimizing discharge, and reducing readmissions. So we have a pilot that I want to discuss here at the Clinic Connect, and then discuss how we can do safe perioperative care of patients who have obesity hyperventilation syndrome. So I have some, I don't have any difficult cases to present, but I have some questions related to some scenarios. So if they populate on your cell phones, you might want to choose the right answer or the most incorrect answer depending on what the question says. So here's the question number one. That's what I expected from this audience, obviously. Is that good or bad? So it saves me some time. I don't have to go through the explanations of any of this stuff. But out of this one, I might want to say again that I see barely any cases coming through the ER. If they are coming with obesity hyperventilation syndrome, they usually have another admitting diagnosis. Most of the times, that's correct provisional diagnosis. And they have OHS going on in the background. Most cases that come to us come from the ICU. In the surgical setting, this disease is unknown. So if you're consulting any of those patients, I happen to do a lot of those. So it's a relatively newer thing in those patients. And then I want to talk at the end about how supplemental oxygen makes things difficult, especially in the surgical setting with these group of patients. So you guys spotted the correct answer. OHS stands under-recognized for a very, very long time. So amongst the diagnosis that these patients are usually billed for is basically morbid obesity, nine times more likely, and interestingly, congestive heart failure, which there is an interesting connect there, which I want to talk about also as we keep moving on. So to basically identify this disease on the medical and surgical floors, the ATS made things easier by defining where we could exactly do the ABG instead of having to do it in every patient with suspected OHS. That would make things a little easier. In other words, if the patients have a very high probability of having OHS, which the ATS defined mostly as patients who are very morbidly obese and have more than 20% chance of having OHS, like BMI is upward of 35 to 40, then essentially we should always get a blood gas in those patients to make the diagnosis of OHS. However, if they happen to be low or moderate probability for OHS, which is less than 20%, then we might use a screening serum bicarbonate level, and if that happens to be less than 27, we do not need to get any ABGs in these patients. They're less likely to have OHS. However, the serum bicarbonate level has to be viewed in light of other things that affect serum bicarbonate, which is like if a lot of these patients, like I said, have PEP and we are using Lasix, or if they're having intractable nausea, vomiting from some reason. So that makes the accuracy of serum bicarbonate as a screening test questionable. So needless to say that patients that, you know, like I said, a lot of patients are IC as a hospital as they come through the ICU, obviously if they come through the ICU, their diagnosis is limited compared to the ones that are admitted to the floor and they happen to have OHS also going on in the background. This is one of the old and probably the only study of patients who were diagnosed on the medical floors. It's a series of patients basically who eventually ended up having diagnosis of OHS down the road. And only 23% of these patients got the diagnosis of OHS the first time. And only 13% of these patients got PEP therapy for OHS at discharge. And when they looked at mortality, the eight-month mortality was 23% in the OHS group versus 9% in simple obesity. So obviously we all know that this is a very morbid condition. And sometimes it can have like a very terminal prognosis within 18 months or so. So to that, ATS recommended that hospitalized patients with respiratory failure with suspected OHS should be started on NIV therapy before being discharged. Now I want to emphasize here, this is not for patients where we know they have OHS. Obviously they will have something in place depending on whether or not they're using it in the first place. But the patients that are coming as suspected cases through the ICU should always be, we should make an attempt to discharge them on some sort of NIV or PEP therapy at discharge so that that previous slide that showed the high morbidity and bad outcomes are mitigated in some way. And then outpatient PEP titration study at the sleep lab, ideally during the first three months after hospital discharge. So then with the same guideline statement came a study which basically looked at patients that were discharged with empiric non-invasive ventilation. And this study looked at how it affects the mortality in patients where NIV was used at discharge versus the ones that didn't get NIV. So a total of about 1,100 plus patients were looked at. And interestingly, in this individualized patient data meta-analysis, about 90 plus percent of patients were discharged on NIV. So that's sort of a little issue right there. But however, the meta-analysis showed that the patients who were discharged had reduced mortality at three months, nine months, and 12 months compared to those who were not discharged on NIV if they had acute and chronic hypercapnea vascular failure as their advent diagnosis. So some of the limitations of this meta-analysis need to be mentioned, that these were mostly non-comparative studies. You would think that these studies were comparing patients discharged on NIV versus those that were not. Only two of them were studies like that. And obviously, there were no randomized controlled trials. So there was some selection bias based on non-consecutive enrollment and variable inclusion-exclusion criteria for obesity hyperventilation. And as is not uncommon in these studies, about 50% of patients did not have spodumetry data. And also, there was no mention of the process of PAP discharge, the settings, or adherence data. So what we do in these patients where we may want to say that these patients, they come from the ICU, they have not had a previous diagnosis of OHS, and they need to be discharged on some sort of PAP therapy, we have a pilot where the objectives of the pilot are that to increase the recognition of these patients that are transitioning from the ICU to the general medical floor with a diagnosis of hypercapnic respiratory failure. Then optimize the transition of these patients from MICU all the way through the sleep disorder center post-discharge, and try to reduce hospital readmission rates. This is a very laudable objective. So here is the pilot. If a patient is transferred out of the medical ICU with hypercapnic respiratory failure, and obviously the suspicion is based on their BMI being 30 or more, and arterial hypercapnia. Obviously in this setting, we cannot exclude other reasons for hypercapnia unless they have been previously excluded. So they are just suspect. The primary team on the floor, which is the hospitalists like me, will order a sleep consult for suspect OHS or OSA for this patient. And then the sleep medicine team will come, and they will give recommendations whether they can send this patient on PAP at discharge, or whether they will do an in-house sleep study or like a portable sleep apnea study. And if the patient qualifies for an IV without sleep study, then it's not done. Usually in all these cases, we'll have arterial blood gases from the ICU, so we'll cover there. And then a PAP setup process is initiated with the help of the DME through our case managers, and sometimes we succeed. So this is happening not with enormous success, but sometimes we're able to send patients with a device who were previously not having diagnosed OSA and are suspected OHS through the MICU. So now in that, I have to say that, and I haven't looked at this whole data in a granular way, but a lot of these people are going out on CPAP and not anything more than that. And the qualifiers from a DME standpoint are that we're doing their sleep study in-patient, and they have hypercapnia. And we haven't succeeded in getting patients out on BiPAP with qualifying criteria for hypovalidation, actually. So that still is the next step. We thought of introducing some in-patient spirometry criteria to help us qualify for that, but that process is still in the works. And obviously, as you can see, this is a team effort, a lot of stakeholders. The Sleep Center is involved, primary team, in-patient care management, DME, floor nursing, and what have you. I'm going to skip these two slides in the interest of time, and here is the next question. So you're asked to evaluate a 50-year-old obese man who is a non-smoker for a preoperative consultation with a BMI of 42. He uses three liters of oxygen at home. He has no idea why and how long he has been on it. A physical exam is very difficult to assess his JVP, but he has a 3-plus spitting edema, and his chest X-ratio is no cardiometally, infiltrate, or effusion. So these are the choices here. You can read them and cast your votes. All right, we'll discuss this a little bit. So I guess I hope that the trick part was not the reason. We wanted to choose the statement that is most inappropriate and makes little sense. So there's no way we can go back now, but we'll discuss this question as we move on. So a few years ago, we tried to do this study where we tried to identify a cohort of sleep apnea patients that are at the highest risk of post-operative events, complications. And in that, my interest was to find out how bad is obesity hyperventilation as a perioperative risk factor, since it's already bad as a qualifying diagnosis with limited prognosis to begin with. And yes, exactly, that's what we found. We compared hypercapnic OSA to OSA patients, not controls. So there's no way that in the OSA patients that will have ABGs in all these patients. It's not humanly possible to do any of those studies, at this point at least. So the OSA group where no ABGs were done, and the hypercapnic OSA group where ABGs were done and they were hypercapnic. So that's the comparison. But regardless, we found that there was a higher incidence of post-operative respiratory failure in the hypercapnic OSA group, and higher incidence of heart failure after surgery, and tracheostomy and ICU transfer. So hypercapnic OSA is definitely a perioperative risk factor, much worse than OSA itself is to begin with. And the reason we don't have pure OHS here is for obvious reasons, because a lot of these patients did not happen to have spirometry data. So that was a limiting factor. So that's why we call it hypercapnic OSA. And then also, some patients were overlap patients. So that was a very small fraction of this whole group. They were COPD and OSA combined. So how do we go about it if you call for such a consult? So this is sort of a little working figure to assess that, is that if you have patients' prior sleep data, that makes things obviously easier. And they have known sleep apnea. And you check the serum bicarbonate. And if it is less than 27, like we said, it's unlikely to be OHS. You simply use OSA precautions. Anesthesiologists are very familiar with what OSA precautions mean. So they kind of naturally follow that in their practice mode. But if the ABG shows a bicarb more than 27, more than 45, sorry. Yeah, sorry, bicarb more than 27, you've got an ABG. And if it's more than 45, then you have confirmed obesity hyperventilation syndrome preoperatively. But most cases are going to be where you don't have a prior sleep study. So you're kind of stuck. Now, I would encourage you that look at OHS in a slightly different light. If you consulted for a preoperative consultation for medical clearance, then how you look at OSA, you may want to get a sleep study. You don't have to cancel the surgery, disappoint the surgeon or the organization. But if you have enough time, you might want to do this. We strongly consider that. In fact, this was part of the Society of Anesthesia and Sleep Medicine Guidelines also that such consideration should be given. This is not necessarily that you can't do surgery. But if you have time, try to get those things done. But if you can't, then you just use the STOP-BANK score if it's more than 3. And then again, same, bicarb more than 27. And then if the OHS is confirmed, then they have to use OHS precautions. If not, then probable OHS. There are three main tenets to preoperative management of OHS. One is secure airway management, which is preoperative. This is for the anesthesiologist. What this means essentially is that, as you know, the regular sleep apnea patients are also oftentimes difficult to intubate. And the OHS patients are particularly difficult to intubate. So the second thing is that, so we try to avoid intubation in OHS patients if they're undergoing non-cardiac surgery electively. We try to do that under regional or local anesthesia if possible, depending on like the extent of the surgery. But for minor procedures, like minor, not like a proper surgery, but minor procedures like endoscopies and stuff like that, and some of those can get very nuanced, like taking a long time if it's advanced. So for minor procedures where you're going to use deep sedation, that's the patient where you have to have a secure tube in place. So it's like, where is the tube problem and where is it necessary? So you might want to think of it in that light. So at our institution, most of these people get minor procedures under general anesthesia if they're having deep sedation. You can't do deep sedation without knowing where the airway is. The second one is intraoperative. The main thing that we use here is pre-oxygenation, PEEP, and recruitment maneuvers. And there is still debate on optimal patient positioning, and we won't go into those controversies at the moment. Most people know what the right position is, and they use it, and it works. And post-operatively, like we already covered that piece with how to use BAP post-operatively. So I'll briefly talk about this concept of diffusion oxygenation or using high-flow oxygen during the intubation period. The way it works, and I'm sure a lot of you know that already, is that even if the ventilation is compromised, you can increase the pulse ox by giving high-flow oxygen. And the way that works is that by giving very high-flow oxygen, 100%, for example, you're creating a gradient across the airway up to the alveolar level, where the oxygen is rapidly diffusing into the blood, and it just keeps pulse ox up for a while, which helps to mitigate analytics down the road from induction of anesthesia, and many other issues that can happen post-operatively. The catch here is that your patient is apneic, technically, pre-intubation or during that period, so you might cause severe respiratory acidosis. Anesthesiologists sort of know how to do this, and a lot of them are very good at pre-oxygenation in these patients. So here's the sum total of all the recommendations. I think I have covered most of them. And at the top, you can see that in patients with known or suspected OSA, consider additional preoperative evaluation when there is evidence of hypoventilation. This is what I was talking about earlier, that if you have evidence of hypoventilation in this patient, don't think of it as in the same realm as OSA. You might want to do something. Particularly pulmonary hypertension and or resting hypoxemia, that's not attributable to other cardiopulmonary diseases. So that's one I want to mention. The rest of the stuff may be mostly for the anesthesiologist folks here, but I think the main points for this audience I think I have covered. The correct choice for the question that might have been tricky, because we were supposed to pick up the least appropriate answer, was actually that you shouldn't go to ambulatory surgery even if the anesthesiologist at the ambulatory center is a strained and difficult intubation protocol, which most of them are anyway. These patients don't belong in the same day care, same day surgeries bucket. They have to be done in the main hospital. And they have to be admitted after that. So as far as the other choices are concerned, recommending local or regional anesthesia except for patients who undergo procedural sedation, and that I already explained. Recommending pre-oxidation to increase safe apnea time, we already talked about it. And the PEEP question may not be as accurate here, because after the pro-obese and pro-willow studies, the high PEEP versus low PEEP question still is not settled. So it doesn't have to be about eight. But it's not a totally inappropriate choice compared to the one at the top. So then I want to talk a little briefly about, and I know I'm running into Babak's time, but about supplemental oxygen. And we're looking at this in many ways in the post-operative state. And it's kind of interesting. And this becomes even more interesting when you have patients with OHS. So essentially, if a patient is in room air, they basically cannot hyperventilate sufficiently to elevate their carbon dioxide levels more than 70 without desaturation. In other words, if you're not giving any patient post-op any oxygen, if they are retaining CO2, they will desaturate once the CO2 crosses 60 to 70. But if you give them small amounts of supplemental oxygen, then they will maintain their pulse ox. And that's your only thing on the post-op ward after they are out of the vacuum, or the medical ward. We have lots of surgical patients on medical wards at our organization. So hence, pulse oximetry may be useful to monitor for hyperventilation patients who are only in room air, but not on supplemental oxygen. And as you know, a lot of surgical patients are on supplemental oxygen, period. I mean, they mostly are for a certain amount of time. And so if you look at this mathematical model that explains that, it basically gives you on the y-axis the PaCO2 and the PaO2 values. And then it gives you three different types of FiO2 and how the PaCO2 responds to that. So if you look at the room air situation, as the PaCO2 rises, the PaO2 starts falling. And it can go up to 60. And that's the desaturation that happens in a patient breathing in room air. And if you look at the top one, FiO2.30, when you're giving supplemental oxygen, they can still maintain their PaO2 at 100 while their PaCO2 keeps going up. So that's the best slide I have found so far to explain this situation. And at the end, like I said, there was nothing new I told you, because a lot of this stuff is not evidence-based at the moment. It's very hard to do studies of this nature, particularly in OHS patients. And the primary problem is identifying OHS patients to begin with. So I have some challenges, too, basically, that I mentioned, and then some reflections. One of the ones is that ICU transfers, even with known diagnosis of OHS, do not consistently come to the floor with that diagnosis. And I don't know why. And there's almost no data to guide the management. We already talked about that. And rarely, any patients get admitted for OHS, like admitting diagnosis of OHS, from the ED. Now my thought is that obese patients with repeat admissions for HFPAF and then discharged home on oxygen therapy may represent that missed pool. But we need to look more into this. There's a study that came out of the ICU patients recently where there was a high prevalence of CHF patients in the ICU who had OHS. So this still needs to be untangled in many ways. And then also, the last thing I want to emphasize particularly is that it's not uncommon for OHS and even PH pulmonary hypertension to be diagnosed for the first time in the post-operative patient. I come across this a lot. So thank you. All right. Thank you, Dr. Cobb. Before you go anywhere, actually, oh, sorry, everyone can clap. As you can tell, I'm dying to ask you a question. So you mentioned in your protocol that you are qualifying people for NIV before hospital discharge with the hypoventilation pathway. No. Oh, OK, not the hypo. OK. Not the hypoventilation. All right. So I might have misspoken, but we qualify them on the basis of their sleep study. And then obviously, they have the ABG criteria, but they don't get the full qualification of hypoventilation. And I've heard from other places, too, that it's very hard to push that. But you can at least send them out with CPAP. Now knowing that people who need NIV at the time of discharge, you know, this is not going to be great for them. But at least they have something, computer. You know, most of these patients are going out with nothing. And then a lot of the patients that need NIV are going to, if they aren't turning around from the ICU standpoint, they shouldn't be coming to the floor that soon to begin with. I hope that's. No. That answers my question. I just thought either I'm hanging out with some nefarious characters who aren't playing by the rules, or you discovered some secret way to. No, no, no. I think we're in the same boat. OK. Yes? So my question is, when you were talking about some studies doing hospitalization, in some form, a four-channel study. Yeah. It's a limited story. Considering you're in hospital. I mean, clinically, they're not sleeping, or you've sedated them so much that their upper airways are going to collapse no matter what. It's a good thing that we can qualify them, but are these studies actually the true reflection of... Not as much in the surgical patients. We don't do this a lot in the surgical patients, like inpatient sleep study. In the surgical group, I mentioned that if you have time, you might want to do it beforehand. Because most of these surgeries are elective surgeries, and if you have like two weeks before surgery, you might as well want to do that, a full lab PSG. But this was for the medical patients. The medical patients are on the floor, and the ones that have come out of the ICU with suspected OHS are now on the floor and should go out. So this is mostly for those patients. Since we know that sleep apnea OHS plus COPD equals greater mortality unless fully treated, why didn't the groups do in those 44% subgroup analysis? I got that question a lot in the communication as well as during the review. But honestly, if I had the bandwidth to do that and come up and think that this was going to be a good one, I would have done it. I still have the data, but I would have loved to do it. But it wasn't going to be a meaningful subgroup analysis. I think we should actually move on to Babak's talk. I don't want to cut too much to his time. But we'll take more questions at the end. We'll stay here for questions. Yeah. Thank you. All right. Thank you for inviting me. I was telling Bahari it was great to have a fellow present. So thank you for doing that. And I don't have any conflicts. I always tell people as I was doing the ATS clinical practice guidelines, one of the criteria was to chair it. I had to give up conflicts. And I couldn't have conflicts for two years. So now I'm actually looking for conflicts. So feel free to approach me if you have anything. And this was the easiest one. I had to come up with my objectives. So here it is. This is a challenging case. So there was no QR. So we'll just do the quick question. For sake of time, I removed some of them. So here's a case of a 55-year-old woman who you saw in clinic and suspected she had OSA and OHS. She underwent an in-lab PSG that confirmed severe OSA, significant sleep hypoxemia, and transcutaneous CO2 monitoring demonstrated hypoventilation going from baseline of 55 to 66 millimeters of mercury. But her sleep was very fragmented. So there wasn't enough time to do a titration study. So now she returns for a pap titration study. And I'm going to show you this is a real case. So here it is. This is a two-minute window here. And what you can see is, let me see if the mouse works, okay, here. So this is a hypnogram. The red bars are REM. So this is at the beginning of sleep onset where she's going from wake to sleep, right? And you can see the transcutaneous CO2 is around 48, 49, 50. CPAP is at CPAP of 8. And here's your oxygen saturation. So I'm just going to jump to the next slide. Now we're in this REM. She had early onset REM. And you can see the transcutaneous CO2 is 71, 72 millimeters of mercury, CPAP of 8, in REM sleep, good eye movements, good respiration. Respirate here is around 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, around 18 to 20 breaths a minute roughly. And then the technician running the study, of course, seeing that transcutaneous CO2 made some changes. And now we're in this REM portion, you're with me? And here's a pressure signal. So you have flow, pressure, you can see is around 19 over 14 or 20 over 14, transcutaneous CO2 is 100. So I guess my question is, since we were going to do difficult cases, what do you guys think? What would you do at this point? I gave this talk yesterday. So if some of you heard it, don't feel bad. You can say the answer. But if you don't know, what would you do? Your technician, the technicians start calling people, of course, they start getting nervous, right? Luckily, I was not the one who was called. So I was a Monday morning quarterback. Indeed, it was a Monday morning I was reviewing this study with a fellow. No, no, no, this is just on room air. Wake them up. That's one answer. Sure, you can do that. Raise IPAP. Raise IPAP. IPAP what? Backup rate. Backup rate is an option, but be mindful that a patient is already breathing around 16, 17, 18. So if you want to increase the backup rate, you have to go above them, right? Lower the EPAP. Lower the EPAP. So do you give more pressure support? You can do that, yes. But that wouldn't make the tech less nervous. So here I'm showing this to you because it was a challenge for the technician, of course, and it was a challenge for us because I want to go over physiology with you. The alveolar gas equation. And I apologize for bringing some medical school nightmares here. And I bring this up because when I, two years ago, when I moved to Rush University, one of the pulmonary critical care fellows asked me, I don't understand what's the point of the alveolar gas equation? I'm like, are you kidding me? As a pulmonologist? Well, here's the reason. So here's the alveolar gas equation that many of you are familiar with, right? So I'm not going to belabor this, but, you know, you can go to Google if you don't want to do the math. And you input room air, PCO2 of 40, C level, respiratory quotient of 0.8. That means the amount of oxygen that gets into your alveoli is around 100 millimeters of mercury. And then if you have healthy lungs, that diffuses quickly into the red blood cells and into your body. So the big A versus a small A, the A and A gradient is small. Here is this patient. Let's assume for a second that the transcutaneous CO2 signal was accurate. And this patient had a transcutaneous and arterial gas of 100. So let's input 100 on room air, barometric pressure, C level, respiratory quotient the same. You would get an alveolar oxygen level of 25 millimeters of mercury. Now, more pain for you. Here it comes. Yeah. And the oxyhemoglobin dissociation curve. And I'm going to plot for you where 25 is. 25 would correspond to an oxygen saturation of less than 40%, which begs the question, how is it possible for a patient to have a transcutaneous CO2 of 100 and on room air and have an oxygen saturation of 97%? The answer is it's not possible. So this is an error. So if you want to run transcutaneous CO2 in your lab, you have to be aware of the limitations. And the alveolar gas equation is actually helpful, particularly if you're on room air, because it makes the math easy. So this was a lab error. And actually, we tried to scramble and figure out the next day, again, the Monday morning error backing, what was going on in that room. We identified what room it is. And we talked to our chief technologist who was sitting there, Mr. Henry Arantes. And we said, Henry, what's going on here? And he said, oh, yeah, we have one faulty transcutaneous CO2. And was the patient ran in room seven? I'm like, yeah. I'm like, well, that's it. Anyway, but the poor tech who was doing this study was getting very nervous. And so was my fellow who was interpreting the study. And I looked like the hero. And I said, nah, let's just give this guy CPAP. And we're good. So let's do this question quickly. A 42-year-old female, history of severe obesity, class 3 obesity, hypertension, dyslipidemia, referred for outpatient split night. And with these symptoms that are described, there was a blood gas that had a PCO2 of 50. And the split night shows an AHI of 54, so severe ulcer. Significant hypoxemia. And you can see there that significant percentage of sleep was spent below 80%. 25% of the night was below 80%. And the transcutaneous CO2 went up by more than 10 millimeters of mercury. Loading. All right. So CPAP titration up to 15 was done, which led to resolution of OSA. And the SPO2 improved to 90%. Transcutaneous CO2 became uninterpretable in the middle of the night, which sometimes happens. And the sleep technologists performed a brief trial of bi-level of 20 over 10. And OSA was also resolved on bi-level with a mean SPO2 of 92% on that setting. So what would you recommend for this patient? CPAP of 15. Bi-PAP of 20 over 10. Give him supplemental oxygen. Or additional full night PAP titration. Yada, yada, yada, yada. Remember they always say the longest answer on the boards is the correct one? Well, I'll give you a hint. Not in this case. All right. For sake of time, I'm just going to, because some of you are hesitating to vote. You know, I'm from Chicago. We vote often and early, right? So the correct, so many of you picked, I think both answers are correct, you know. But one of the things we did in the clinical practice guidelines was to look at the data of comparing CPAP versus non-invasive ventilation, in this case bi-level without a backup rate, in patients who are ambulatory, like this patient, who have severe obstructive sleep apnea. And the data suggests that there's not that much of a difference between CPAP and NIV. So in this case, the titration actually looked pretty reasonable with CPAP of 15. So you could justify giving this person just CPAP of 15. And here are a couple of studies that informed the clinical practice guidelines. These were two studies from Australia that compared CPAP with bi-level spontaneous mode and CPAP to bi-level ST mode. These were medium-term studies with two, three months of follow-up, and there was no difference in terms of gas exchange. And the longer-term study that also informed the clinical practice guideline was a PICWIC study in which you can see people with OHS, ambulatory patients with OHS, who had severe OSA, which is 70% of them, were randomized to CPAP versus NIV with three years of follow-up. And those who had less severe OSA were randomized to NIV versus lifestyle with three years of follow-up. But again, this is a much smaller study. And the bottom line is that in people who are ambulatory and have severe OSA, there was no difference between CPAP and NIV in terms of adherence, six hours of use median, and outcomes such as hospital admissions, incident cardiovascular events, and mortality. And you can see the average pressures that they were getting was around 11 for CPAP, and this is volume-targeted pressure support. But on average, the patients were getting around 20 over 8, so around 12 of pressure support with a backup rate of 14, so no difference. And here's the Kaplan-Meier survival curve. So if you have an ambulatory patient who has severe OSA, I think it's reasonable to give them CPAP. And here's an example of a patient that was done in our lab at Rush University, I want to say in late June, early July, 48-year-old, BMI of 48, severe OSA. You can see the pattern of oxygen desaturation. This is just to orient you. The line here is 50%. I will tell people if this is happening on a general medicine floor, guess what? The patient gets transferred to the ICU with this level of hypoxemia. But these patients live like this, unfortunately, for many years. And you can see here the average HI was around 77. This is a split night. CPAP was initiated. You can see that the patient had a nice REM now that they don't have any stimulus to arouse because they're not occluding their airways anymore. And bi-level titration was also performed here. So this would be a good example of somebody who would, whether you give them CPAP or BiPAP or NIV, it probably doesn't make that much of a difference, right? That's what the clinical practice guidelines say. Here's another example. This is a 40-year-old with a BMI of 67 who also has severe OSA, daytime hypoxemia, and hypoventilation. And had a recent admission to the ICU. This study was done six weeks after ICU admission. And the ICU admission was acute on chronic hypercapnic respiratory failure, like the one that the prior speakers were talking about. So if you read this, look at this study, and quote me my own paper to me, and you say, well, hold on. You said this patient is ambulatory and has severe OSA, HI of 77. Why don't you give him CPAP? Well, I think this is a little bit different, and I'll tell you why. And I'll tell you what my bias is. So here CPAP titration is performed. This is up to around like 15 or so, 16. You can see hypoxemia is profound. Again, this is like consistently around 70%. Oxygen is at 3 liters per minute right here. Then they switch to bi-level. Crank up the bi-level towards the last few minutes to above 25 over 10 or so. Significant amount of pressure support. And a backup rate. And 5 liters of oxygen. And this patient is still profoundly hypoxemic. So it didn't work. Now, part of it is because there wasn't enough time. The poor tech feel bad for the techs. They're trying to squeeze many things in the same night. So the reason I think this patient, although if you read the paper and the guidelines, you say, well, he's ambulatory. He's six weeks out of ICU. Why don't you give this person CPAP? Is because, well, he had a recent hospitalization. And all the patients who were enrolled in the PICWIC trial had no recent hospitalizations. The average BMI in PICWIC was around 43. Look at the BMI here. There was no patient like this in the PICWIC trial. So I don't think this case, you can apply the PICWIC trial to this case. So, of course, we were very nervous about this patient. So we called the patient. And in three days, we opened up space in the lab. Thank you, Henry. He's sitting back there. And we squeezed him in. And before I show you the next study, I want to show you. This is a five-minute window of these patients. You can see it's apnea after apnea after apnea. Significant hypoxemia that is sustained and intermittent on top of it with significant hypercapnia. And in five minutes, he's only taking 16 breaths. So you can appreciate why they're hypoxic and hypercapnic. So then he comes for an IVAPS titration. This is a volume-targeted pressure support. So essentially, it's a pressure mode. But the machine is looking at, if leak is low, is looking at estimation of exhaled tidal volume. And if it senses that the tidal volume is going below your target, it cranks up the pressure support. So you can see here, as they were at the beginning, I'm not showing you the pressures here. But essentially here, they're cranking up the EPAP manually until the airway is open. And then it looks better after that. And what ended up happening with this patient is EPAP got titrated from 6 to 8, pressure support min, pressure support max, backup rate of 15. They started with target alveolar ventilation of 5.1 liters, and it was cranked up to around 6.0 mLs per minute, which is around 9.4 mLs per kg of predicted body weight. For those of us who practice in the ICU, you start getting nervous. And I always tell people, and I ask myself, are we causing harm in some of these patients? And anybody who tells you 100% no, they don't know what they're talking about, because I have no idea if we're causing harm in the long term. Are we causing alveolar inflammation here? Are we causing potentially lung injury in the long run? Nobody knows because nobody has looked into it. But it's something to think about. Nonetheless, if you want to get the CO2 normal or get some improvement in your CO2 because of so much adiposity that they have, you really need to provide high levels of pressure support to these patients to lift the chest up. And you can see that this study looks substantially better than this study. Right? And this is three days of difference between the two cases, the two studies. So the clinical practice guidelines, as the name suggests, is just a guideline. You should not replace your clinical judgment all the time. Now, if you're going to be doing – how much time do we have? Okay. Well, I'll just close with this slide. If you're going to be running noninvasive ventilation in your lab, I encourage you to monitor several things from your PAP devices. So, of course, everybody looks at C-flow, your CPAP flow or PAP flow. But look what else we're monitoring here. We're monitoring pressure. You can see EPAP, IPAP, EPAP, IPAP. You have tidal volume. You have leak down here. And then you have this channel, if it's a ResMed device, it's called cycle trigger. So just to orient you, this is the trigger. That means this is a backup rate. It just happens before the pressure goes up. And this is a cycle. It's a tick mark going down. That's at the end of the breath. That means the patient reached TI max, and the machine is now cutting off the breath and cycling from IPAP to EPAP. So if you have these channels on your display, on your montage, you will be able to then correctly label respiratory events when a patient is on noninvasive ventilation. And then I'll wrap up with this slide to say this is a three-minute window showing an event that, would you guys say, does it look more like central apnea or obstructive apnea? Anybody? Don't be shy. Central or obstructive? It looks central. It looks central. But look at the cycle trigger here. It goes from 10 to 15, 10 to 15, achieves no flow. This is a patient who has no drive to breathe with an occluded airway. You can have two problems at the same time. And the only way you can diagnose this is by giving a backup rate because without a backup rate on CPAP, this is treatment immersion central. On full polysomnography, it's a central apnea. With the device that gives you a backup rate, and you would notice if you're displaying pressure and cycle trigger, then you have to label these as obstructive apneas. This is an obstructive apnea. The treatment of choice is crank up the EPAP to open up the airway. The treatment, that's the only thing you can do for this patient. So I'll just leave you with that. If you're going to do noninvasive monitoring, please add these on your montage because they're important. Thank you. All right. Thank you. Those were great cases. Thank you to all the speakers. ♪
Video Summary
The presenters discussed various aspects of obesity hypoventilation syndrome (OHS) management. Dr. Zarabiyan provided an overview of OHS as a distinct clinical entity and discussed the diagnostic criteria. She emphasized the need for diagnosis of exclusion and highlighted the importance of confirming elevated BMI, sleep-related breathing disorder, and daytime hypercapnia to diagnose OHS. She also mentioned that OHS patients have higher ICU admissions, greater need for mechanical ventilation, and higher mortality rates compared to patients with the same degree of obesity but without OHS. Dr. Kha focused on the management of OHS in the inpatient and perioperative settings. He discussed the challenges in recognizing OHS on medical and surgical wards and emphasized the importance of starting non-invasive ventilation before hospital discharge. He also discussed the perioperative management of OHS patients, including airway management and pre-oxygenation strategies. Finally, Dr. Co showed two challenging cases of OHS. He discussed the use of transcutaneous CO2 monitoring and emphasized the limitations of such monitoring. He also shared recommendations on the use of CPAP versus non-invasive ventilation in ambulatory patients with severe OSA and discussed the importance of monitoring pressure, flow, tidal volume, leak, and cycle trigger during non-invasive ventilation. Overall, the speakers provided valuable insights into the diagnosis and management of OHS in different clinical settings.
Meta Tag
Category
Sleep Disorders
Session ID
1055
Speaker
Kara Dupuy-McCauley
Speaker
Roop Kaw
Speaker
Babak Mokhlesi
Speaker
Baharan Zarrabian
Track
Sleep Disorders
Track
Critical Care
Track
Respiratory Care
Keywords
obesity hypoventilation syndrome
OHS management
diagnostic criteria
daytime hypercapnia
ICU admissions
mechanical ventilation
inpatient management
non-invasive ventilation
transcutaneous CO2 monitoring
OSA
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