For the 30 million adults in the U.S. with COPD, effective care requires providers to have an up-to-date understanding of treatment options as well as the ability to respond to changes in a patient’s status. This guide from pulmonologist Julia Maheshwari, MD, reviews diagnostic steps (including tips on spirometry) and offers tools for assessing severity and knowing when to step therapy up (or down). Hear about pulmonary rehab’s proven benefits and a wearable programmable ventilator; plus, learn criteria for advanced care referrals.
My name is Julia Maheshwari. It's lovely to meet all of you this afternoon. I am a pulmonologist and a critical care physician at UCSF, University of California, San Francisco. Um, my main clinical foesci in the pulmonary world or COPD and the intersection of advanced COPD and lung transplantation. So I spend most of my time I'm looking at people and helping patients with advanced COPD think about whether or not they are coming into the window for lung transplantation. That is not the topic of today's talk. And today I'd really like to focus on outpatient COPD management steps and the workflow to managing patients with COPD and how I can help you help these patients. So I will go through. So, a workflow thinking about various diagnostics and therapeutics, and I absolutely welcome questions and thoughts at the end of today's conversation. I would love to speak through and answer any questions that I can for you. So I'll go ahead and get started. So COPD, as we all know, COPD stands for chronic obstructive pulmonary Disease, which is characterized very specifically by incompletely reversible expiratory airflow limitation. The burden of this disease is very large. There are 30 million adults in the US with COPD right now, and it's become the 4th leading cause of death in the country. Every year, COPD causes approximately 126,000 deaths and 3.2% of all physician office visits, as you know, and hence why we're sitting down together today to talk. So the clinical presentation of COPD, just to review, symptoms for of a patient with COPD can include dyspnea, cough, sputum production, wheezing, chest tightness, chest congestion, or simply a complaint of decreased exercise tolerance. History that can be important to obtain is often exposure to tobacco smoke, in 75% of US cases for COPD. But it's important to remember as well that patients with occupational or environmental particle exposure, diesel exhaust, or smoke from indoor cooking can also contribute to the development of COPD. It just doesn't just have to be cigarettes. And on physical exam, even through Zoom, we can see patients with COPD presenting with a barrel chest, a prolonged expiratory phase, diminish diminished breath sounds, accessory muscle use, and tripod posture. So how do we diagnose COPD and what exactly do we need to say firmly someone has COPD? Well, spirometry is key. This is one part of pulmonary function testing, the, the most important part for diagnosing COPD. And the question to ask is, on the spirometry, is obstruction present? Let me walk through that. This portion of the pulmonary function test is the spirometry. This is the breathing out that a patient is doing during these pulmonary function tests. And what you're looking to see is if the ratio of FEV1, which is the expired volume in the 1st 2nd of a forced expiration, the initial burst of expiration that patient gives over FEC, the entire exhaled volume. is less than 70% in absolute value. So you can see here the predicted value, the best value, and the percent predicted. You're actually looking at this absolute number here, and it's 63.72 here, but we refer to that as a 0.63, so that it's a ratio, that FEV1 is 0.63 of FEC. So it's a yes no. Is obstruction present? Is the FEV1. Over FPC ratio less than 0.7 in absolute value. The other clue you can have is on the flow volume curve, on the expiratory portion of the flow volume curve, when patients are breathing out, that's this portion. This is what it looks like for someone to breathe out normally, starting to pick up flow and breathe out with effort and then effort independent portions. Patients with COPD start to breathe out and immediately drop their flows and have a concave loop of the expiratory portion of their flow volume loop. So if you're wondering if someone has COPD and they happen to have a history of PFTs somewhere in the system, you can look for either of these clues to tell you that someone has obstruction, meaning Impaired expiratory airflow limitation, which is your strongest clue that someone is presenting to you with COPD that might contribute to their systems symptoms. If you see somebody who presents with obstruction, it's a very good clue to someone coming to you with COPD. But COPD is not the only disease that person may present with, and I want to talk you through just a few differentiating factors, if you see PFTs like this, to think, well, it could be COPD or it could be one of two other entities. Let's talk through those now. One is asthma. A patient with asthma can have obstruction on PFTs. They don't have to, but they may come to you in an asthma exacerbation, or they have been tested when they have more exacerbating features, and they may have spirometry that shows obstruction, like a person with COPD. But what might point you in the direction of an asthma diagnosis. I if someone feels dramatically better with albuterol, that's a good clue that asthma is very sensitive to albuterol, and if they really profoundly respond to it, perhaps you're looking more at asthma than you are at COPD. If they have significant eosinophils on their CBC and their differential in the past. When I say significant, I'm thinking anywhere upwards of 150, maybe 200 or 300. Elevated IgE, immunoglobulin E, is also going to make me think about asthma for somebody. A patient who's presenting with these symptoms and obstruction, who's younger, who's not very old, doesn't have a significant smoking history, or has other comorbidities, like significant allergies or eczema, that gives you the sense that someone has an allergic profile, that might point you towards thinking about asthma for someone. And finally, if they tell you, I'm waking up all night, and it comes in bursts that come and go, come and go, and they wake me up, I just feel like I can't stay asleep. That is a little more sometimes of an asthmatic profile than a COPD. I'll move to this part relatively quickly, but if you have somebody where you suspect suspect COPD because of the obstruction on spirometry, or you happen to have a CT scan that shows they have emphysema, it is worth thinking about evaluating for alpha one antitrypsin deficiency as well as a cause of their obstruction and or emphysema. The direct recommendation from the World Health Organization, the goal guidelines, the COPD Group, or the COPD Foundation, is to screen all patients with COPD for alpha-1 antitrypsin deficiency. And the reason is because only 5% of alpha-1 patients currently in this country have been diagnosed with the disease. There's a very large portion of folks that haven't been diagnosed, and it's important because giving appropriate patients alpha-1 antitrypsin enzyme replacement therapy can slow the progression of their emphysema. So there is action that can be taken if that diagnosis is made. Some providers do screen every patient with COPD for alpha one, they just send it off. The testing is free through the Alpha-O Foundation, so you could send it on anybody, just to see if that's playing a role in addition to COPD. But I tend to, um, my practice is evolving on this, and I tend to screen patients who present with what looks like COPD at a younger age, who have more emphysema in the bases of their lungs because that's where alpha-1 tends to show up or have a very strong family history of emphysema. So I'm a little more discriminatory in sending that testing, but you don't have to be. When you do think someone has COPD, how do you assess how severe it is? What are the metrics? How can you communicate to other providers? How bad do you think the disease is? Well, there are two ways that we go through it, and they are guided by the gold guidelines, the Global Initiative for Chronic Obstructive Lung Disease. So this term, gold grade 4 Group D, you might see this in Care Everywhere in the charting, you might think, what does that mean? It's evolved recently to take a couple of different forms. Let's just walk through that so that you can actually grade it up front and get a sense of where that patient might need to be seen and how bad their disease is. The grade 123 or 4 depends exclusively on the post bronchodilator FEV1. And it's broken down into these categories you can see. Gold 1 being the mildest, gold 4 being the most severe, simply an FEV1 cutoff. The severity, the letter is a mixture of the symptom burden and exacerbation frequency. It's relatively new that the severity of COPD comes to account for the exacerbations in the symptoms. It used to be all about the FEV1 on spirometry, but now we think more holistically about what that patient's disease. Profile is like when categorizing the severity, we think about the number of hospital admissions they have and how bad their symptom burden is. So if someone has mild symptoms, these scores, which I'll go through in a second with lower numbers, and 0 or 1 admissions, they end up in the A category, which is less severe. If they have a higher symptom burden, which again I'll walk through, and 2 or more admissions or more, 1 or more admissions that landed them in the hospital, then they're in a more severe category like a D, and that's a universal communication to talk about the severity of COPD. I'll step through these symptom markers. The MMRC is one symptom scale that we use to categorize and to monitor COPD. It's very straightforward, 0 through 4, and 0 is that a person is not troubled by their breathlessness at all. They are not limited by their symptoms in the slightest. A person with an MMRC scale of 4 is too breathless to leave their house. They will tell you, I don't even go to the grocery store because I feel that bad. The COPD assessment tool, or CAT, is a couple more questions. You can see here, I never cough, I have no phlegm, all the way through, I cough all the time, and my chest is completely full of phlegm, and they rank how many, how severe their symptoms are. A CAT or CAT score greater than 10 is what we tend to consider more severe and bumps up their severity of COPD. Just in terms of a broad sense of mortality for COPD, I will go through this relatively quickly, but the BA index is what we use to look at someone and say, well, your chance of mortality is extremely high or not, and it depends on these four variables, the FEV1, percent of predicted, unlike the spirometry, that's the percent of predicted, a 6-minute walk distance, the dyspnea scale we just referred to in their body mass index. A higher bone score is a sicker patient with a higher chance of mortality. So what can we do for these patients once you've confirmed that they do have COPD, once you've got an I got an idea of how severe their disease is, what can we do now, and where do we need to go in terms of treatments and then escalating to higher levels of care or specialty referrals? Well, smoking cessation again and again and again. Of course, we know that smoking cessation done through both behavioral therapy and pharmacotherapy is more effective than either therapy avenue alone. So referring somebody to a quit line or a group, in addition to starting medications for them, is a more effective strategy than trying one pathway or the other. Behavioral therapy can include quit lines, counseling, support groups. I like 1-800-Obus because it's very easy to remember. I also think that the smoking cessation leadership, um, profile at the smoking cessation Center that we have at UCSF I use a lot for my patients, and I think it's quite a good resource to direct them to. There was a really interesting study out of the UK about 10 years ago that talked about um how to discuss patient age, lung age when they're smoking, and how to give patients a sense of how much damage smoking is causing to their lungs as a motivator for smoking cessation. And what they did was, if a patient was, say, age 52, they, and they were smoking, they would find their lung function of the smoker, this FEV1 of the purple line here. Then they would draw out the same lung function to somebody who had never smoked, it's red dashed line, and they would say, well, this 52 year old smoker, you have the, the lungs of a seventy-five-year-old who doesn't smoke. And so that method actually resulted in 7.2% more quitting and the higher rates of smoking cessation than not using that graph. I thought it was a very interesting and helpful study to give us some tools for smoking cessation. To talk briefly through pharmacotherapy. Nicotine replacement therapy is, of course, a crux of smoking cessation tools that we can use. But one interesting tactic to think about is to send somebody out on a long-acting form, a patch, for example, and short-acting. They're not going to overdose on nicotine nicotine through this mechanism. They will titrate the amount of. Nicotine to curb their cravings, it is not dangerous to do both long-acting and short-acting. But doing something like a nicotine replacement patch, and then giving them gum or a lozenge for when the cravings break through in the moment, can be really helpful. You lower the baseline and you manage the symptoms as they come about. Beennolin or Chantix is a very common medication that we use for smoking, uh, smoking cessation. It's a partial agonist at the nicotine acetylcholine receptor. So because it's a partial agonist, it actually blocks nicotine withdrawal when not smoking. But when someone does smoke, part of the receptors are taken by the agonist, and it prevents the reward from smoking from becoming too great. It's a middleman, and it tempers the extremes of withdrawal and euphoria that patients get from smoking. In studies, it's 2 times as effective as placebo for smoking cessation. So it really does work. It is contrain indicated in severe CKD, but otherwise, it is safe to think about. Wellbutrin or bupropion increases, increases quit rates by 65%, so also very, very effective. It's an atypical antipsychotic that increases dopamine release, and the contraindication here is for seizure disorders or patients with a predisposition to seizures. It's worth thinking as well about, um, sometimes we hear about Chantix and patients with, um, Anxiety or depression, being at higher risk for suicidal or depressive episodes with Chantix. That came about because there was some concern um in 2009 for the safety of Chantix, that actually spurred the FDA to run a trial called the Eagles trial that was a head to head directly of Vennolin, bupropion, nicotine patch, and placebo in 8000 smokers, half of whom had no psychiatric comorbidities. Half of whom had mild anxiety or depression, and it was a safety trial. It primarily looked at the rate of psychiatric side effects, and they saw no difference in 8000 patients in psychiatric side effects with Verennolin compared to placebo. And with that, in 2016, the FDA removed the black box warning. So the concern about Vereniclin in patients with psychiatric issues shouldn't be too much of an issue and shouldn't hold back initiating that therapy, which is relatively effective. That's the eagles's trial there. In addition, baseline things like making sure someone has gotten their influenza vaccine, their pneumococcal vaccines, and their COVID vaccination could be helpful steps for patients with COPD when seeing them to stabilize them, when referring them on to other care, or for a longitudinal primary care. And lung cancer screening, the guidelines for lung cancer screening recently changed. They liberalized, and ages adults aged 50 through 80 with a 20 pack year smoking history, who currently smoke or quit within the past 15 years are eligible for lung cancer screening. And in the lung health study, the lung cancer screening reduced relative all-cause mortality by 6.7% and lung cancer-specific mortality by 20%. So it's very effective if done. Other things that we can ask for help with, in addition to smoking cessation, vaccinations, and lung cancer screening, pulmonary rehabilitation, regular review and correction of inhaler technique, and long-term oxygen therapy for resting hypoxemia are all critically important. I'll move next to bronchodilators, and I won't go through this in nitty-gritty detail, but I work on questions on specifics at the end. So, bronchodilators can be thought of by receptor, beta2 agonists, which promote promote bronchodilation or muscarinic antagonists, which prevent bronchoconstriction. They can also be broken down by duration, short acting, a short-acting beta agonist or SAA, short-acting muscarinic antagonist, or SAMA. I put the names here, I won't read them out loud. But the other category we think about are the long-acting, the long-acting beta agonists or lamas, and the long-acting muscarinic antagonists like lamas, teotroprium or Spiriva, for example. So, thinking practically about management. Where do we start with inhalers? Well, most of us start with a PRN rescue inhaler, a short-acting bronchodilator, albuterol, for example, or ipratropium for limited or activity-related symptoms. But when someone's on that rescue therapy, when do we add a maintenance inhaler, inhaler? When is it appropriate? Well, if a patient tells you they're using their short-acting bronchodilator 2 to 3 times a week for rescue, start thinking about a maintenance inhaler. If they have a high symptom burden to begin with, an MMRC of greater than 2, so the more severe half of those patients on that scale, or a CAT score greater than 10, like we mentioned. If they have a history of prior exacerbations or an FEV1 of less than 60%, think about adding a maintenance inhaler. And which long-acting maintenance inhaler do you choose? Well, both long-acting muscarinic and beta2 agonist monotherapies decreases exacerbations and they decrease dyspnea, but long-acting muscarinic antagonists, like teotroprium or Spiriva, which is my personal go to, more effectively reduce exacerbations and hospitalizations in studies compared to lava therapy. So I tend to start people on Spiriva, and I like the Spiriva Respimat, which is an inhaled inhalation mist and can be more calming to patients. They feel the sensation of the inhaled mist actually going into their lungs, so I tend to preference Spiriva after they need more than just a rescue. And if I'm doing Spiriva, I'll try to get them the Respimat therapy, a newer delivery device that patients have found very helpful. If on monotherapy, on Spiriva alone, it's not enough. They still have exacerbations, they still have uncontrolled symptoms when they exercise, for example, then you can give them dual long-acting therapy, a llama-LABA. And that will increase lung function, decrease symptoms, and decrease exacerbation risk. Alternatively, you don't have to step your way through rescue inhaler, Spiriva, and then um llama laba. You can go straight to a llama lava likes Stioltoe for a high initial symptom burden or exacerbation frequency. I tend to find it really helpful to have one of the charts with all of the inhalers, so I can reference in my own practice, but also have patients point to it, because there are so many names and so many colors, and I just think having copies on the wall, and then right at my desk, I have about 3 in my room at any time, and that's really, really helpful. Inhaled corticosteroids are the next step, but they're not without risk. So what are the benefits of adding ICS to a patient with COPD? Well, they're proven to reduce exacerbations, so they do have effect. They improve symptoms, and they improve lung function, but there is a risk of thrush, which is why we have people rinse out their mouth after using the medication, bacterial pneumonia and hoarseness. So with the risk and benefit, which patients should we add the inhaled corticosteroids to? Well, there are a couple of hints for a patient who's on llama laba therapy, but still having severe symptoms or exacerbations. Add on the inhaled corticosteroids. Put them on what we call triple inhaler therapy. If patients have an elevated blood eosinophil level on their differential on their CBC, I put more than 150 here, that's from trials. I again look more like 200 or 300 to add ICS to somebody, or if somebody has a profile of having both COPD but some asthma. They're really responsive to bronchodilators, they have a history of allergies. Maybe they told you they were diagnosed with asthma when they were a kid. OK, add it on, they might respond. This is a proposed treatment algorithm here. I walked through this with you, so I won't go through it, but I just wanna put it all together and I'm happy to share slides for a stepwise algorithm if that would be beneficial. After stepping up, which patients do you step down? Well, the only thing I think about really when stepping down is withdrawing inhaled corticosteroids. That's because of the bacterial pneumonia, thrush, and hoarseness risks that I laid out, and I think about that when someone's been for 2 or so years without an exacerbation, or they really don't have a profile that would suggest they would be responsible to inhaled corticosteroids. They don't have eosinophilia on their CBC. They don't have an asthmatic profile. They're not significantly bronchodilator responsive, for example. This, um, section on recurrent exacerbations, I find really helpful. So if somebody's on triple inhaler therapy, a beta agonist, long-acting, a muscarinic agonist, long-acting, and an inhaled corticosteroids, but they're still having exacerbations, it can feel like you don't know what to do to keep that person out of the hospital. Try one of these. The first medication is Reflumalast. It's an oral PDE4 inhibitor. We really use it for the anti-inflammatory inflammatory properties. I think about using reflumalast in patients with chronic bronchitis symptoms. A COPD patient with hacking cough and frequent mucus mucus production, who's having a lot of exacerbations, try reflumalast. It decreased exacerbations by 14.3% in clinical trials and improved lung function. Um, we do look for and watch out for adverse effects that are mainly GI, nausea, diarrhea, weight loss, and we do check to make sure that anyone with a predisposition to depression or anxiety is tolerating it OK from a mood standpoint. We start at 250 mics for a month and then we go up to 50 mics daily. Azithromycin is another medication for recurrent exacerbations. It's a different profile. So I think about, do they need reflumalast or azithromycin. I don't put this one person on both, it's one or the other, generally. Again, for anti-inflammatory properties. The biggest thing to think about for azithromycin is if someone is an active smoker, azithromycin is not effective in reducing their exacerbation, so they have to be a former smoker. It does decrease exacerbations. We do think about adverse effects like reversible hearing impairment, like we see with the macrolide class of antibiotics generally, arrhythmias, and antibiotic resistance. For that reason, with the arrhythmias, I obtained a baseline EKG to check their QTC and if less than 500, safe to start azithromycin. And the dose is 250 mg daily or 500 mg Monday, Wednesday, and Friday. Those are the two dosing regimens that have been clinically proven in trials to be effective. Sometimes patients will end up on 250 mg Monday, Wednesday, Friday. Some providers do that to mitigate the side effects of azithromycin, but we don't have proven efficacy. That that works. So if someone comes to you on azithromycin 250 mg Monday, Wednesday, Friday, it might be worth boosting them up to 500 mg Monday, Wednesday, Friday to see if it actually does a better job of keeping them out of the hospital and not having exacerbations. I'll touch briefly on theophylline for recurrent exacerbations, but we're really not using this medication much anymore. I almost never use it. It's a phosphodiesterase inhibitor, really as a last resort therapy, and that's because the therapeutic index index of, of theophylline is so narrow. Adverse effects like headache, nausea, insomnia, heartburn, seizures are really problematic, and the peak level has to be monitor monitored 3 to 7 hours after the a.m. dose to make sure that patients don't suffer from toxicities of theophylline. I find this so troublesome, and the liver hepatic metabolism. And the clearance that gets worse with age and the prone, the predisposition to toxicity to be too much of a burden, I almost never use it. It's pretty rare to come across people on theophylline. To touch briefly on an exacerbation, of course, what that looks like, which we've all seen, and where to go, I'll go through it briefly. Free to feel free to ask any questions. Patients will present with increased respiratory symptoms, dyspnea, cough, sputum production, or purulence, exacerbations we know, worsen quality of life, precipitate decline in lung function. Every exacerbation drops lung function that doesn't come back again, so it's worth preventing everyone. So we can tell patients, well, increase your albuterol or relieve albuterol use. And then we use tools like prednisone, as we know, for 40 mg for 5 days. That's been proven to be equally as effective as 10 to 15 days of steroids, but has fewer toxicity, so we do 5 days. And then an antibiotic such as azithromycin or doxycycline, which we're mainly using for anti-inflammatory properties. When do we send patients who are exacerbating to the ED? Well, if they have persistent symptoms, their dyspnea is not going away despite trying all of these things. They have new or worsening hypoxemia, aidemia, tachypnea, altered mentation, accessory muscle use, respiratory distress, a history of frequent exacerbations, and you're worried they'll tip easily. Insufficient home support, serious comorbidities, so that their overall organ systems may not tolerate the exacerbation well, just send them to the ED. I think a solid follow-up plan that we do in our clinic is to discharge patients from the hospital, for example, and do a phone call 48 hours later and see them in clinic, in person, within a week. I'll touch briefly on long-term oxygen therapy. The two studies on the right here are from several decades ago. They show that um supplemental oxygen is proven to improve survival in patients with resting hypoxemia on room air. That is a sat on the pulse ox of less than or equal to 88% on room air sitting at rest. Or if they have RV dysfunction or polycythemia, your threshold to start oxygens lower, they can have a set of 89% at rest on room air. The LOT trial looked at patients who have resting hypoxemia, so patients who are sitting at rest and have a sat that's a little bit higher of 89 to 93%, and oxygen does not provide a survival benefit for them. But for some patients who are in that zone who tend to walk and feel very dyspneic, we know that exertional hypoxemia managed with oxygen can help improve their dyspnea, but won't help their survival. I give it to patients who feel better walking with oxygen. I just tell them it's not going to prolong their life, but it may make them more functional, and that's how I approached, um, that patient profile. And then I'll say briefly that there's no guidance on patients who DSAT overnight in the setting of their hypoxemia and hypoventilation, but I tend to give supplemental 02 if they DSAT below 88%, um, and then many providers do, even if though there's no clear guidelines. Pulmonary rehabilitation, I mentioned earlier, as something that is essential as a baseline to managing patients with COPD. So why do patients need pulmonary rehabilitation? Well, they have a cycle, decreased activity results in muscular deconditioning, cardiovascular deconditioning. They become frail, they become isolated, they become depressed and less active, and it spirals and continues. Pulmonary rehab brings in many tenants, strength training, endurance training, dedicated patient education sessions, nutritional counseling, and psychosocial support. Many patients who go to pulmonary rehab tell me their favorite part of rehab is the friends who also go to rehab. So that community can be really rewarding. Less than 5% of eligible patients in this country currently receive pulmonary rehab, so it's worth referring people. And after patients are hospitalized for a COPD exacerbation, if they start pulmonary rehab within 4 weeks, and I count that as even referring them because we do what we can, that has been shown to improve mortality and reduce readmissions. So it's effective to get them into PR if they come to you after an exacerbation. Patients go to the sessions for 2 to 3 hours a week, different sessions, Monday, Wednesday, or Monday, Wednesday, Friday, generally for 6 to 12 weeks. Contraindications to safe participation are unstable cardiac disease or cognitive impairment. But patients who do have and undergo PR have been shown to improve their dyspnea, their exercise tolerance, and their quality of life. I find Livebetter.org to be a really great resource to find pulmonary rehab programs near where patients live, and then I refer them to the programs that are near their homes because in order to go a couple of times a week, it needs to be convenient, so I almost always refer locally if I can. Looking at advanced COPD therapies like BiPAP and then endobronchial valves, surgical valves, and lung transplantation. This is where I spend most of my time practicing, and In the Bay Area, we have a clinic where patients can be referred and we just think about all of these therapies for you. We just take severe disease and we go down the line and think about what patients could be um amenable to or what might be appropriate. So BiPAP first. Why do we use BiPAP for advanced COPD? Well, it's thought to provide respiratory muscle weak rest and decrease the work of breathing, so just make it easier to breathe. The key with BiPAP is to initiate it when patients are hypercarbic during the daytime. When stable, After, say, an exacerbation, give them a couple of weeks to cool off, have them come see you when they're stable, then do a daytime ABG. If the CO2 is greater than or equal to 52 millimeters of mercury, insurance will cover a BIPAP, and that's when it's useful. Patients, of course, are often sent out of the hospital on BiPAP after a hospitalization, and that's a common initiation. Um, and I will skip the other portions here, but it's worth noting that that patient profile of just hospitalized for COPD cooled off, stabilized out, but still hypercarbic with a PCO2 greater than 52. Using BiPAP in those patients may improve hospitalization-free survival in that profile. So it's worth initiating. I tell them to do it at night, and if I feel that it's not good enough, they're feeling cloudy in the morning, or they're still feeling groggy in the day, we do it overnight and with any naps, they wear BiPAP. Initiating BiPAP can be done in the hospital following a COPD exacerbation because respiratory therapy can set the settings there, or in a sleep lab where they can undergo polyssonography to exclude sleep apnea, but also titrate the settings at that time. And I think it's worth mentioning that there are many different masks for BiPAP. So, patients come to us all the time and say, I hate my BiPAP mask. I won't tolerate it, and that's the reason why I stopped using my machine. Same with CPAP. This goes for CPAP too. This particular mask here covers the nose and the mouth. But there is this little triangle that goes exclusively over the mouth. If a patient is a mouth or over the nose, apologies, if the patient is a mouth breather, then you can imagine everything they're getting in through their nose, they're breathing out of their mouth, so they can have a chin strap to make sure the mouth stays closed, but patients do find this a lot more comfortable. And there is the nasal pillow as well for BiPAP and CPAP that can make these machines just much easier to tolerate. If patients come to you and have difficulty tolerating the masks, you can always send them to sleep medicine, and they will go through all of the different types of masks to find something that works for the patient. The data on whether BiPAP actually makes a difference in COPD is conflicting, but the, I won't go through the details of all of this, but the bottom line is, in the 3 clinical trials in which BiPAP was used at higher pressures, regular pressures to breathe in bigger breaths, it showed that it was effective, and it actually reduced mortality and readmissions. When they used BiPAP with lower settings, and it wasn't as impressive, they didn't deliver great breaths, it didn't make much difference. That makes complete sense to me. Bitter pressure. So I think it makes sense to send them to the sleep lab if they're an outpatient and have it titrated so you get effective settings that make a real difference for that patient. When patients are enrolled in pulmonary rehab, and they add on BiPAP, studies show that patients in quality of life, functional status, and gas exchange all improve. So anything you can add of all these different tools, they complement one another to enhance the patient outcome. Another thing that I'll bring up is what I think of as a walking BiPAP. So this is a portable ventilator. On the newer side, um, it's a wearable, non-invasive ventilator. So if someone needs BiPAP, but they want to be mobile, they need help taking deep breaths because they want help with offloading the work of breathing. But they want to be portable and they want to be ambulatory. This is a 1 pound mask-free device that clips onto their belt, and it delivers through nasal pillows. I'll just highlight the little dial here, which is what you can set. The breaths per minute, you can set bleed-in oxygen, so you can get supplemental oxygen for when they're ambulating, and if they need help pushing in breaths, they have Settings, which I think are really fun. They give a volume of delivered title volume when they're lying down, a little more support when they're sitting up, and a little more support when they're walking, and the patient just hits their activity level. This is something you could send to the COPD clinic and they would titrate and go ahead and set up for them with um the companies that run this. Hillrom is one of them, for example. These ventilators decrease dyspnea, work of breathing, PCO2, and improve exercise tolerance, but they don't change mortality, and they don't affect readmissions. It's about patient comfort for them. So some patients find it helpful to know that these things exist, um, if you're having trouble convincing someone that BiPAP would help them, for example. I'll talk briefly about endobronchial valves, both because it's helpful to think about which patients might benefit, but also because you might see patients who have these. So this is the spiration umbrella-shaped valve. This is the Zephyr duckbill-shaped valve. These are both approved for use in the US. There is no data about which valve to use the over the other. It's proceduralists preference. How do they work? Well, they serve as a one-way valve that goes into the airway. So during Exhalation. They allow air to escape from the lung through the airways and out of the body, but on inhalation, they shut, so it does not allow air into the lungs and allows air only to escape. The valves are placed into portions of the lung, and allowing air to escape over time, but no new air to enter, allows for the lung to collapse, and you put them in the most emphysematous ballooned out parts of the lung and slowly collapse down those portions of the lung. That allows the rest of the lung and the respiratory muscles to work more effectively and for their oxygenation and ventilation to improve through that mechanism. I have a nicer photo on how that works in an image that I can show you in just a couple of slides. It makes it a little easier to wrap your head around. As I said, the goal of these valves is to induce atectasis of the most emphysematous portions of lung. And the two very baseline requirements to think about whether this might be good for somebody is if they have heterogeneous emphysema, so portions of the lung that are a lot worse than the others, cause that's what they'll target when they place the bowels, and no collateral ventilation. That just means that there's no ventilation. Between the lobes of the valves of the lung, I'm sorry. So you don't have ventilation from the right upper lung seeping into the right middle lung because you can imagine if you're trying to collapse a lobe of the lung, it's not helpful to have ventilation from other parts of the lung continuing to circulate back into that lung. These parameters and looking at this part of the lung requires specific software and a discussion with the interventional pulmonary team. And this is what the report looks like, that looks at where the portions of emphysema are, dark gray is the worst, and how complete the fissures between the lobes of the lung are to prevent the collateral ventilation, to get a sense of whether someone might be a good candidate. This is just another tool that assesses whether or not there's collateral ventilation. And this is the image I walked through earlier. It just shows that on inhalation, air comes in but is not allowed to pass into the lobe of the lung where the valves are, but on exhalation, all of the air can escape out and gradually induce analectasis of the most emphysematous portions of the lung, thereby allowing the lung mechanics, the respiratory muscles, and the hyperinflation of the rest of the lungs to work better. Through various studies, bronchial valves have been shown to improve dyspnea, lung function, exercise tolerance, and quality of life, but they're not going to prolong someone's life. They don't have any benefit in terms of mortality. They make them more functional in the meantime, but they don't change someone's overall mortality. Very briefly, surgical lung volume reduction achieves the same goals as endobronchial, you're just wedge resecting the most emphysematous portions of lung. And in the National Emphysema Treatment Trial in 2003, they showed very clearly that a subgroup of patients, those who have upper lobe emphysema and a low exercise capacity, those are the patients who have a mortality benefit from surgical LBRS, and those are the patients you should think about sending to cardiothoracic surgery for an evaluation to see if LVRS, lung volume reduction surgery, would be appropriate for them. And then finally, lung transplantation. This is my world. The goals of lung transplantation are, 1, increase survival, but also reduce disability and improve health-related quality of life. And we transplant people specifically for goals 2 and 3. They don't have to have The goal of increasing survival. They can know that for some reason their survival is not great, but they have terrible quality of life, and they want that to be the reason to go through all of the work of a transplant. If they think their quality of life is bad enough, they're willing to undergo transplant, we'll do it. People patients to be referred for lung transplant. Well, I walked through the bode score with you, and abode score of 5 to 6 is a good threshold to refer someone for lung transplantation. The bode score, you can go, there's online calculators that you can use all the time. I use them all the time to. Calculate a number for you, super straightforward of those four metrics. If their lung function is less than 25% predicted, the FEV1, send them over for a lung transplant eval. If they're hypercarbic or hypoxemic on room air, they should also be referred for a lung transplant. The listing criteria for lung transplantation is a bit in the weeds, but the bottom line is, if it's worse than the referral, we should think about listing. There's not that much room between the referral criteria and when they're bad enough, you need to think about going on a list, and I think about that. Contraindications to lung transplants. So I bring this up just because it's used to know, worth, it's useful to know if someone is actively smoking, they can't have a transplant for 6 months. If they have an active cancer or renal failure, or extremely unstable cardiac disease, for example, then they're not an appropriate candidate for a lung transplant evaluation evaluation. So there are some barriers we know off the bat it's not a good idea, but we can always refer and think through it. And palliative care. How can palliative care help COPD? Many, many ways. Palliative care specialists can manage dyspnea through pulmonary rehab, relaxation technique techniques, opioid use. They can address anxiety and depression, which are extremely prevalent in patients with COPD and undermanaged. Using cognitive behavioral therapy or pharma therapy, they can talk about advanced care planning or transition to end of life care if needed. And now I'll just transition and talk a little bit about the advanced COP COPD clinic that we have at at UCSF and what we can do and how we can partner when patients are referred over, who to send and how we can help them. So this advanced COPD clinic is a clinic that I helped to found at UCSF. It's multidisciplinary. So we find, we, um, deliver multidisciplinary emphysema care, medical evaluation, but I also have an in-clinic respiratory therapist who does walk tests, supplemental oxygen therapy, non-invasive, uh, BiPAP settings, inhaler teaching, and airway clearance. We have physical therapy in clinic to initiate pulmonary rehab and educate patients, and a nutritionist on staff. We can also in the same visit, think about advanced therapies and whether that would be appropriate for patients like lung transplant and a bronchial valve. This is reframing and rephrasing what I just told you. The 3 goals of the clinic are to optimize medical management, evaluate for advanced emphysema therapies, and address common comorbidities. I bring this up because this is the structure that we've established at UCSF, but that's not the only place that this type of care model is available. For example, UC Davis in Sacramento has a great multidisciplinary COPD clinic that thinks about all of the same things and we partner with them a lot, and they, um, can basically take anybody who's moderate to very severe COPD and run through any possible appropriate management strategy for that patient, which we hope serves as a great resource. Who should be referred to such a clinic? Well, any of the following an FEV1 of less than 50% predicted on any baseline spirometry. Patients who are hypercarbic or hypoxemia, who've had two or more COPD exacerbations within the past year, a bone score of greater than or equal to 5, or mean pulmonary artery pressure of greater than or equal to 20, so the beginning of pulmonary hypertension. And if you're referring someone with the intent that they be evaluated for advanced therapies like endobronchial valves or lung transplantation, it's beneficial if they've quit smoking greater than or equal to 6 months before they're going to be evaluated in clinic. To be very granular. We do referrals or we accept referrals to the UFCSF Advanced COPD clinic. It's through the pulmonary practice, you can specify advanced COPD or you can specify my name, and we do in-person and telehealth. And then it's helpful if patients have PFTs. If you just order all three tests on the PFTs when recording them, so body plethysmography, spirometry, and diffusion capacity. If you have questions, ordering all three is easier for the evaluation we'll do down the line. And I put here the specific protocol of CT that's helpful for endobronchial valves, but we can always chase this up and get the right protocol if needed or reformat the CT if we can do so. And with that, I will stop and thank you for your time and I'll welcome any questions.
