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I see. Ok. Real life. Ok. Uh hi, good evening. Everyone. Can someone just let us know if you can hear us, please? You just drop a message in the chat and then as soon as you guys give us a confirmation, we will get started. Yeah, hoping people can hear us. Yeah. Ok. Someone please just drop a message in the chat just to let us know you can hear us. Yes. Ok, lovely. All right. So welcome everyone to our teaching today on Asthma and COPD. Uh My name is Harish. Um and we have, yes, I'm I uh I'm 1/5 year medic at UCL. Yeah. So we're both fifth year medical students at UCL and we're going to be teaching you today on asthma and COPD. So we have we get side ok, just a quick introduction to teaching things. So we do weekly tutorials. Um It's run by medical students for medical students and we um keep you updated on the medal um via group chat and on emails as well. So just a quick reminder to follow us on meal page if you haven't already. So starting off with asthma, we're going to start today with a case study. So we have a 35 year old woman who's presenting to her GP with shortness of breath and chest tightness. You go to take a history. So what do we want to know? Just write in the chart? Anything that you would want to take a history from, for this woman? Any questions you'd like to ask? Can you see anything in the chat so far? Yeah. So we've got some good, good answers so far. So, when did it start? Yeah, definitely very important. Um, uh, does it happen at rest or with exercise, onset of symptoms? What she was doing before it started? Has she taken any medications? Uh, anything that makes the shortness of breath better or worse? Yeah. Really good stuff. I agree. Yeah. So in terms of having a structured history, starting with her history of presenting complaint, um, we learned from her that she has recurrent episodes of shortness of breath that's been ongoing for the past few months. Um, and she describes it as difficult to breathe, struggling to get enough air in and she also describes a feeling of her chest tightening. Um, she also comments that she has an, a cough that comes on when she has these symptoms and absolutely, in terms of things that make it worse, she notices it's worse when she goes for a run, but she also notices that it's often worse in the morning and sometimes it wakes her up during the night from her sleep in terms of a broader history. So her past medical history includes hay fever, which she's had since childhood and treats with antihistamines. She doesn't have any drug history, no known drug allergies. Um, her father has hypertension and in terms of her social history, there's nothing particularly of note. So what is asthma? Well, it's a chronic condition and as our patient has, it's um characterized by recurrent episodes of efl obstruction, that's mostly reversible bronchial hyperresponsiveness and an underlying inflammation. It's a really common condition and leads to a lot of disease burden worldwide with an estimated 5 to 10% of the global population affected by asthma. Um It's also a potentially fatal condition with about 1000 people dying every year in the UK alone. So it's a really, really important condition to diagnose correctly, to manage correctly. So what causes asthma? Well, we know that there's quite a significant heritability. Um estimates vary, but we know that um asthma can run in families. And we also have um something called the atopic triad where patients often present with sort of this triad of hay fever, eczema and asthma. You don't have to have all of them. But we know that they're quite closely linked in terms of their pathophysiology. We also have environmental factors, um certain triggers that might make your symptoms worse. Uh but also being surrounded by these uh factors might in fact be uh make it more likely that you have that you develop asthma in the first place. So certain allergens um having respiratory infections, especially in childhood, um being surrounded by tobacco smoke, air pollution and certain occupational exposures. Um And these are all things that are quite important to get in your um in your history taking to sort of to understand a bit better about what your patient, how to manage your patient appropriately, especially avoiding these triggers. And then we also know that there are certain immunological factors that are involved in the development of asthma. Um They're quite complex. We'll go into a little bit of detail about it, but they're not fully understood at this stage. So asthma is a type one hypersensitivity reaction. I've just got a picture to remind you of the different types of hypersensitivity reactions on the side. Um So that means it's IgE mediated, it means it's really fast onset and it recurs. Um we also know that we've got airway inflammation. Um So it's largely t helper cell two cell mediated, but we know that there's a whole host of other proinflammatory mediators that are involved in asthma. Um and together they lead to airway inflammation and over time, this can then lead to airway damage. We have airway hyperresponsiveness. So your airways in a normal person might um be able to cope with these certain triggers that I mentioned before. Whereas in asthma, if you're exposed to a trigger, whichever one it might be, your airways are more likely to narrow in response to the to that. And in terms of the narrowing or bronchoconstriction, um the mechanism is that we have smooth muscle in the airways and they um as because of the hyper responsiveness, they're more likely the smooth muscle is more likely to contract, but we also have impaired bronchodilator mechanisms. So that means that in a normal person, you've got mechanisms to help your airways relax again, which in asthma is impaired. Um And this narrowing of the airways then leads to obstruction of airflow, which leads to the symptoms that patients describe. And then over time, we've got increased mucus production and remodeling of the airways. So there are certain structural changes in the airway walls itself. Um And that can then lead to irreversible changes and irreversible airflow, sorry, irreversible airflow obstruction, which then leads over time to a decline in lung function. Um And in overall, so the extent of remodeling is associated with the severity of the disease, the duration of the disease and how well controlled it is. So how often patients are having experiencing symptoms? Here's just a quick overview of the structural changes that patients with asthma might have. So, um we know we've got angiogenesis or um creation of new blood vessels in the airway walls. Um We've got a change in the epithelium, increased smooth muscle, which is due to this hyperresponsiveness, it's more likely to um contract you might have more mucus and um a fibrosis as well, scar tissue forming. So how does asthma present? There's a complete variation between patients. So some patients might complete uh might present with very mild symptoms and barely noticeable symptoms, whereas other patients might have very severe, very recurrent symptoms that massively impact on their quality of life. So, some of the common symptoms patients present with include a wheeze which is widespread and bilateral. So if you hear a wheeze only in one part of the lungs, it's unlikely to be due to asthma. But in medicine, of course, nothing is ever always or never. Um And in terms of the wheeze, it's specifically high pitched whistling sound that is occurs during expiration. This expiration is very important. It's not an inspiratory wheeze, it's specifically an expiratory wheeze and it's caused by airflow that's passing through the narrowed airways that becomes turbulent and that's what we can hear in the wheeze, but wheeze is not a specific sign. So there are other symptoms that come together, um, a cough can be dry or productive. Um And as our patient presented is often worse at nighttime or in the early morning, which we call dienal variation and it can be bad enough to disrupt sleep. It can also be in response to a trigger, which I mentioned before. We also have dyspnea, shortness of breath, which is largely due to the constriction of the airways and can be again, as a result of a trigger during exercise or can occur at rest as well. Um, and similarly to the cough, it might be worse in the mornings or late at night. And then we also have chest tightness, um, which is this feeling that you can't breathe enough and that your, your chest muscles are tightening. Um, that's because you're working harder to breathe in and you've got this because of the airway obstruction. So based on our history, we're considering a diagnosis of asthma. Can you write into the chart? What investigations we might consider doing on our patient? Good. So we've got peak flow. Good. Fantastic. Yeah. Anything else we could consider? Yeah. So we've got feno testing, blood eosinophils, uh spirometry. Very good. Brilliant. Yeah. So we started with peak flow. Um peak flow is useful in two kind of settings. So in an acute asthma attack, we might consider using a peak flow. Um But very, very commonly people use what we call the peak flow diary, which is where you measure your peak flow over the course of two weeks, um measure it in the morning and evening, see if there's that diurnal variation. Um And noting um whether there's any patterns or any triggers um in terms of your um peak flow, in terms of your lung function, um importantly, with peak flow, your technique is really important and can massively impact the results. Um So often patients might have a learning curve where they, it takes them a few tries to learn how to use the peak flow meter, which you can see in the bottom left. Um But especially with young Children, it might be quite difficult to get them to do, to use proper techniques. The peak flow is quite a, you might, might call it a subjective test. And uh just in the top right, you can see um that your ex your estimated peak flow changes depending on whether you, you're a woman or a man, what your height is. So, again, it's not the most objective test that we can use, but it's a fantastic one we can use in primary care or it's very quick to use. And then someone mentioned pheno. Um So in terms of what pheno is measuring, we have nitric oxide um that's just naturally produced by our bodies and we have different types of nitric oxide synthases. Um So, pheno specifically looks at inducible nitric oxide or inos um which is produced by eosinophils. And so the levels of inos or the levels of nitric oxide correlates directly with the level of inflammation in the lungs and the airways. Um notably, smoking might give a falsely low result. So do be aware of that. But in general, feno is quite a good, more objective test than peak flow. Um and what we consider diagnostic of asthma or it um contributes to the diagnosis of asthma in adults is a feno reading of above 40 parts per billion and in Children above 35 parts per billion, someone also mentioned spirometry. Um So we have two main readings that we at least at medical school that we look at um which are F EV one and F PC. So F EV one is the forced expiratory volume. So what that means is if you can see my cursor, um it's that initial volume that you can exhale in the 1st 2nd of force exper expiration. So breathing out as hard and as fast as you can, the volume that is exhaled in that 1st 2nd. And this is the one that in asthma is usually the most affected, we then have the forced vital capacity, which is the maximum volume that you can exhale after full, full inspiration, full exhalation, how much can you exhale? And in asthma, usually this is normal. So in terms of the numbers that we look at something that's really important in asthma diagnosis is looking at the ratio between FEV one and FVC. So a ratio below 70% indicates there's an obstructive pathology. Um It's not completely diagnostic for asthma because we can't necessarily distinguish between an obstructive COPD and an obstructive asthma. Um But just to show you on the graph, you can see that in a normal person that fev one should be normal. Whereas in asthma, um it's reduced here. So, further diagnose diagnostic tests that we can use is what we call BDR or uh bronchodilator reversibility testing and what that is, it's, it's using the spirometry meters. Um But we use spirometry first without anything and then you repeat the spirometry having used a bronchodilator. So something like a salbutamol which aims to open up your airways. And if there is a significant difference between the two, then we can assume that this person has this reversibility, which is one of the core features of asthma. And that can help us to distinguish between asthma and COPD in patients where the diagnosis might not be so clear. Um There are certain cutoff criteria for diagnosing asthma with broncho bronchodilator reversibility. So, in adults, um more than 12% improvement in fev one or a more than 200 mL increase in volume is diagnostic and in Children, only 12% improvement is enough to diagnose. Um So you can see here in the graph, the red line is um the spirometry reading before using the bronchodilator. And then the green reading is once they've used it, their lung function improves. We also occasionally use a diagnostic test called bronchial challenge, which is effectively inducing an asthma attack in patients because one of the hallmarks of asthma is that you might develop an asthma attack in response to a trigger. And in this case, we use a drug that's known to irritate the airways. And in a normal person, you might have a very high threshold for developing or for your airways constricting, whereas in someone with asthma, your threshold is a lot lower. And so you can tell how sensitive someone's airways are. Um But obviously a big risk comes with this in a patient with potential asthma, you don't necessarily want to induce a life threatening asthma attack. And so it's not necessarily done for everyone. It's usually done in those cases where it's not quite clear whether they have asthma or don't have asthma in terms of diagnostic criteria. Um it varies between adults and Children. So all patients above five years should have objective tests according to nice. Unfortunately, the NHS doesn't necessarily work like that. And so often patients are diagnosed on a clinical judgment uh clinical basis. Um for Children under the age of five, all diagnoses should be made on a clinical judgment alone. That's just because Children under five are quite, it's quite difficult for them to go through the mechanisms of doing spirometry and understanding um how to do those diagnostic tests because they don't necessarily have the um the coordination to do those tests. But in Children between five and 16 where their coordination is a bit better, we can start doing spirometry. We can also use the Bronchodilator reversibility. And if they have a normal or obstructive spirometry picture with a negative BDR test, we can also consider using the FENO test. And then in all patients over 17 years old. So adults, all patients should have spirometry with bronchodilator reversibility and feno um and in the back of your mind, in especially in adults, you might want to consider occupational asthma if their symptoms are better when they're away from work. For example, if they're on holiday and they notice their symptoms get better. So going back to our case, um our patients spirometry results have come back and show an EV one to F EC ratio of 67% and a 12.7% improvement in F EV one following bronchodilator use. So my question is what conservative measures might improve her outcome. So we're not talking about medication or treatments for her. We're just talking about conservative management to help her improve her outcomes. If you want to write in the chart, any ideas that you might have that might help her? Any ideas, guys, smoking cessation? Fantastic. Yeah. Absolutely. Hm One, any other ideas, uh removal of any other triggers says? Yeah, exactly. So if you have, you know, if you have um, a dust mite allergy and we know that you're more likely to have an asthma attack. If you've got a, um for example, a dust mite allergy, you might want to make sure that you keep your home as dust free as possible. Ok. Is there anything else in the chart? Otherwise, I that'll be fine. No, there's nothing else at the moment that come in. Ok. That's, that's ok. Um So something that's really, yeah, absolutely. Vaccines are really important. In patients with asthma. Um so they should be offered their flu vaccines and COVID vaccines every year as well as a one off pneumococcal vaccine to help with um pneumonias. As you mentioned, smoking cessation is really important in patients who smoke or patients who are exposed to smoke. So for example, if um a child's parents smoke, it's important to educate people on, on the risks of that. Um and talking about patient education. So every patient should have an asthma action plan. Um And that involves what to do in certain situations. For example, if they notice that their breathing is getting worse rapidly, what what to do and at what point to seek help also attending regular reviews of their asthma control. Um this can be done either in primary or secondary care depending on what's most appropriate for that patient. And as you mentioned, avoiding triggers absolutely really important. Um and then managing associated conditions that we know exacerbate asthma. So these are things like rhinitis or hay fever, which I mentioned before or allergies or things like acid reflux can worsen people's asthma as well. So now we're talking about medical management. Can anyone name any drugs that we commonly or or rarely use in asthma management? Yeah. Sabas such as um s really good. Perfect. Yeah. S um leukotriene receptor antagonist. So Yes, brilliant. Yeah. OK. Stuff guys and las Yeah, for me. Yeah, perfect. Yeah. So I'll go through um just some of the more common drugs, um and a little bit about them. So, Sabers, as you mentioned, short acting beta agonist, um examples include salbutamol, which is really commonly used at the moment. People often refer to it as either their relief inhaler or their blue inhaler. Um And it's generally used acutely when a patient develops symptoms right here right now. Um As the name suggests, it's short acting, so it doesn't have any long lasting impacts. Um and it works by relaxing that smooth muscle of the airways, but it doesn't really have an impact on any of the underlying inflammation. Um So generally, it's only used for either an acute situation. So acutely, patients have symptoms or um if patients have very mild asthma, I'll talk more about that later. One of the important side effects of um salbutamol is having a tremor. So that's why in our respiratory examinations, we might look for um whether a patient has a fine tremor, as you also mentioned, the inhaled corticosteroids or ics. Um Examples include um beclomethasone and people will often refer to it as their preventer or their brown inhaler. Um This one is taken every single day, regardless of symptoms or rather it's meant to be taken every single day. Um And it's meant to prevent symptoms from occurring. Um So the mechanism of this is this one, the, the ICS acts on the inflammation aims to reduce it um because it is a steroid, it can lead to oral thrush um and in Children potentially stunted growth. Although because it's inhaled, the steroid isn't as systemic as taking um you know, um oral tablets every day. You also mentioned laba so long acting beta agonists and that um examples of that include salmeterol, formoterol. And again, these are taken every day regardless of symptoms. And you also mentioned the leukotriene receptor antagonists such as Montelukast, which are taken orally, they're tablets that are taken every day. And finally, this is very recent. So in November, the guidelines were updated and this now includes a term called air therapy. So, anti-inflammatory reliever therapy um which includes a low dose ics and Formoterol. So a laba combination inhaler and that one is meant to be taken for symptomatic relief. And then we have something called ma or maintenance and reliever therapy, which is a combined ics and LABA and a single inhaler, which is similar to the air therapy. But the doses and specific labs that are used might vary. Um and these ones are used for daily maintenance therapy and the relief of symptoms as required. So it's meant to be all, all uses in one inhaler and finally, in really severe um almost uncontrollable asthma, um people can now potentially be eligible for biologics. Um So these might include Benralizumab and Mepolizumab. So as I mentioned, the guidelines were updated in November and so previously, all the different bodies so nice, the British Thoracic Society and s which is the Scottish Society, all had different guidelines suggesting different things. And so asthma management used to be very complicated and quite, um, it was up to the physician's judgment. And if you're, you know, if you're a respiratory physician, um specializing in asthma management, that's great. You, I'm sure you know your stuff, but if you're your typical GP, it was quite confusing and so different people were on different medications and to combine that to make things easier for, for us, um they combined the guidelines into one guideline, which I'm not going to go through the reason why I'm talking, I'm even mentioning that the guidelines changed is because because a lot of patients will still be on the medication from the previous guidelines. And so it's important to be aware that there has been a shift very recently. So can anyone tell me what should be given in newly diagnosed asthma? So like our patient. Yeah. So just to answer your questions have so we have a question about the change in guidelines to therapy the therapy as far as the second dose, second line. And yeah, we will go through that very shortly. It is coming up in a moment. So yeah, if you just write in the chart, what do you think might be given for newly diagnosed asthma? If you don't know, that's also ok, I'm, I'll go through it because as I said, the guidelines have changed. So it is a bit confusing an answer saying, uh, low dose ics and for, for mo uh therapy. Fantastic. Yeah. Um, perfect. And that's purely for symptomatic relief. So, in our patient where they're presenting with the occasional symptoms, that might be all they need. Um, so then the question is if that isn't enough. So if they've got, they're on air therapy but they're still getting symptoms or they've got, and, and they're still getting persistent symptoms or they're newly diagnosed, but they have symptoms more than three times a week or they're waking up in the night because of their symptoms, we'll put them on a low dose mark. So that's just step one. As, as I said, the doses will be different um in terms of the um the LMA that's used. But again, the I CS will be a low dose I CS in terms of step three, all that changes is the dosage. So it's again a marked, but a moderate dose mark in step four, we then go on to check the pheno and the eosinophil count in the blood. And if either of them are raised, we just refer straight to the asthma specialist. If they're both normal, we'll then put the patient on keep them on the moderate dose ma but add either the Gluco tren receptor antagonist or Alama. And finally, step five, if that's not enough. If patient's symptoms are still not being controlled on that, then we refer to an asthma specialist. So in terms of converting the old guidelines to the new guidelines, because I know this is quite confusing. Um previously step one would have included only a cyber, so only salbutamol and so those patients who are previously on cyber should now be put on to air therapy patients who were previously on a Saba and either a low dose I CS with Alaba or with a leukotriene receptor antagonist will all be put on to a therapy. Now, patients who were previously on the Saba with a moderate dose I CS with any of the others will now be put on to a moderate dose of mark therapy. And finally, anything with a high dose I CS will be referred to asthma specialists. So hopefully, this is um I think the aim of all of the guideline changes is to make it sorry, make it a bit more understandable, a bit more straightforward and hopefully improve patients outcomes um by having the straightforward guidelines and also to answer your questions, the biggest difference between the air therapy and the ma therapy is almost kind of in the name. So air therapy is antiinflammatory reliever. So it's taken as and when similar to a like Emma just mentioned, whereas the ma is maintenance and reliever. So that's something you take, you take it every day, even if you have don't have an asthma like wheeze or anything, you will still be taking it. Yeah, again to, to prevent the symptoms from happening. Exactly. Um, something that's important to comment on with management. Ideally, patients should be, um, what we classify as having complete control of their asthma. And what that means is that they should not be having any daytime symptoms. They should be not, they should not be waking up in the middle of the night due to their symptoms and they shouldn't need rescue medication or any SABA, um, medication because they're feeling acute symptoms. Um So in an ideal world, a patient, even I'll go back to, to this, a patient on any of these therapies shouldn't really be noticing that they have asthma symptoms on a day to day basis. They should be, if they, they're on a therapy, they might have symptoms less than three times a week. Um Any of the others, they should not be noticing that they've got symptoms. And if they do, they should be increased. If they're on step two, they should be increased to step three or step four, et cetera. Um And again, if there's any complications, any um anything that makes their asthma complicated to manage, refer to asthma specialists, that's the, the aim. And so the aim of having complete control of their asthma is to improve their quality of life and improve their functional status so that they can do more. Um but also it's a risk reduction. So we know that patients with poorly controlled asthma are at higher risk of death because of all of the acute attacks and needing emergency care. For example, if they've got an, um, uh, pneumonia and they've got asthma, they're more likely to need, um, emergency care. However, if the asthma is well controlled, they're more likely to do well in the community. And finally, me, all of these medications have side effects. And so what we want is to not over medicate all of our patients by putting them immediately onto the highest dose of whatever we want to keep them on the lowest dose that can control their asthma sufficiently. Ok. So going back to our case, our patient has been started on air therapy a few weeks ago and she's now presenting to A&E with sudden onset shortness of breath, a widespread wheeze and a cough. You can see her observations. So her heart rate is 100 and four. Her BP is 100 and 10/65 her respiratory rate is 26. Her sats are 94% on room air and her temperature is 37.7 degrees. So what diagnosis should we, should we be suspecting here if you want to write it in the chat again? Anyone got any ideas? If not? That's ok. Ok. We should carry on and yeah, in the interest of time I'll move on. So this patient is likely to be presenting with acute asthma or an asthma attack. So it's um, what we call a progressive worsening of asthma, which is over this acute or subacute period over a few hours or minutes. Um, of the patients who have asthma diagnosed asthma, um, about 8.4% of them present every year with an acute asthma attack. And as I mentioned before, asthma can be fatal. Um, and absolutely is still fatal in the UK. Um, there are certain factors that might increase your risk of presenting with acute asthma and increasing your risk of fatality from acute asthma. Um So we know homelessness, drug, alcohol use is a big factor. Um, over using salbutamol can be a factor. We also know that having a lack of a personalized asthma plan and re uh representing with asthma attacks or having a near fatal asthma attack is a big risk factor for fatality in terms of how it presents, as I mentioned, it's a short onset over a few hours or, or minutes with the typical asthma symptoms. So the shortness of breath, cough, wheeze chest tightness, um you might also have a fast heart rate or a fast breathing rate and inability to finish your sentences with one breath and very rarely what we call a silent chest. So where you listen with your stethoscope and where you would normally hear breath sounds, there is no breathing. Um How we classify asthma or rather acute asthma is based on four main, uh four main factors. Um So the peak flow, as we mentioned before in diagnosing asthma is really useful in acute asthma. Um we also look at the O2 saturation. So, in our observations, and then we use the arterial oxygen, partial pressure and carbon dioxide partial pressures. Um and ultimately, all of those together determine which management is most appropriate for our patients. So there are different criteria for the different classifications. So, in moderate acute asthma, we've got the symptoms, increasing symptoms, we've got a peak flow rate of between 50 75% of the patient's best or predicted score. And we have no features of severe acute asthma. In severe acute asthma, the peak flow is between 33 and 50% of the patient's best or predicted score. They might have. So none of these, you don't need to have all of them. Just one suffices to be categorized as severe acute asthma. Um So respiratory rate of 25 per minute. A heart rate of over 100 and 10 BPM. And as I mentioned before, this inability to complete your sentences in one breath will indicate a severe acute asthma attack. Now, lifethreatening acute asthma attack is categorized by either a peak flow rate of below 33%. So a third of the patient's best or predicted score, um A set of below 92% AP O2. So partial pressure of less than eight. So reduced oxygen saturation in the blood, as I mentioned, the silent chest. So there are no breath sounds when you listen with your stethoscope, cyanosis of the lips, exhaustion or reduced respiratory effort. So, whether the patients get these breathing, working so hard to breathe that they're getting physically exhausted and are struggling to continue to breathe. Um And then some sort of sly, so a new onset arrhythmia, reduced awareness or um as it, it says here, reduced G CS and hypotension. So low BP and then a neo ftal asthma attack is indicated by a raised P CO2. Um So that means there's more carbon dioxide in their bloodstream. Um And in this case, that that's one of the indications for mechanical ventilation. So note on PA CO2, um because it can be a little bit confusing in terms of moderate and severe asthma, we're expecting a low PC two and that's because the patient is working harder to breathe and they end up actually breathing out more carbon dioxide. And so they've got a low P two in life threat asthma, they're breathing hard, they're working hard to breathe, but they're starting to not compensate for the um the, so they're starting to not decompensate effectively. And so more CO2 is being retained and finally in near fatal asthma, they'll have this increase in CO2 because they're struggling so much to breathe, that they're not breathing out enough. And that means that the CO2 just rises in their blood. So, in terms of investigations that we should consider um as we mentioned, the peak flow is one of the ways of classifying what severity of asthma attack the patient is having, we can also do an fev one. but in most cases, especially in the more severe or life threatening categories, it's unlikely that the patient is going to be able to do a spirometry correctly. And so peak flow is often more appropriate, especially if they have established asthma and know how to do a peak flow equally even in, in many. So, particularly in severe and life threatening or neo ftal asthma, even a peak flow might not be appropriate because a patient is struggling to breathe so much that you just want to manage them. Um rather than waiting to categorize which which severity of asthma they're in, of course, in all of our acute situations, we're going to take our observations. Um And as I mentioned before, they can help us categorize which severity of asthma your patient is presenting with an ABG. So this is how we get our PA O2 and P AC two is usually indicated in more severe asthma. So if the oxygen saturations are below 92% or if the peak flow is below 30% we'll consider doing an ABG. And so just to, just to help remind you the lower the PA O2, the more severe the asthma attack because they're not able to oxygenate their blood enough. Um Another note on PA CO2 apparently um uh sorry, a raised P CO2 correlates, I forgot to add it on the side. A raised P CO2 correlates with an F EV one of about 20% of their predicted F EV one. Um so indicates of significant reduction. Um And in terms of the ABG most patients, you're going to expect to see a respiratory alkalosis. So if you'd like to write in the chart, a brief explanation of why we're expecting to see a respiratory alkalosis on most of our patients presenting with acute asthma. This ties in with the P CO2 and P two. Po two got hyper hyperventilation. Perfect. Yeah. Um So it it's the this hyperventilation and then um breathing out so much CO2 that you end up becoming alkalotic until you become acidotic with increased CO2 in your blood in near fatal asthma attacks. Um A quick note in terms of the practicalities, we prefer doing an ABG because we get this um idea of the blood oxygen levels. But if that's not possible because they're a lot more invasive, we can also use a VBG to get a, a basic idea of what's going on. And then finally, we might do a chest X ray. If there's an underlying diagnosis that's suspected, for example, we might have a pneumonia that might be causing the acute asthma attack in terms of managing our patients in lifethreatening or near ftal acute asthma, all patients should be hospitalized in severe acute asthma, they should be admitted to hospital. If they're failing to respond to the initial treatment, we'll definitely consider using oxygen to support the pa the patient's breathing. So either if they're unwell, um acutely unwell or if we know their sats are below 92% we'll absolutely give them oxygen. So, can you write in the chart any ideas you have of how we can administer oxygen? What uh what methods, what masks will it be used? Yeah. So you've got 15 L via a non rebreath mask? Amazing. Fantastic. Yeah. Is there any other ways of administering oxygen that you can think of? Not necessarily for all patients but just different options that we can consider? Yes. Yeah. Brilliant. Yeah. Ok. So I'll show you these three pictures. So we've got the non rebreed mask on the left. We've got the nasal cannula on the right. Does anyone know what the middle picture is showing? What type of mask? Yeah. So we've got ventura. Perfect. Yeah. Yeah. And so the ventura mask um we can titrate specifically to what percentage of oxygen we want to administer to the patient? The non rebreathing mask, as you mentioned, the 15 L through the non rebreathing mask is a um sort of initial um initial resuscitation for the patient to give them as much oxygen as we can. And then we can always titrate it down and the nasal cannula, you can only give a small amount of oxygen 5 to 10 L. Um And so yeah, we give, we give the nasal cannula if they're just about not um not able to meet the 92%. So now patient visit, our patient, forget that question. So um in terms of going back to our acute asthma management, so we consider hospitals admission, we consider oxygen therapy. The next thing that we consider is giving them saba. Um So that's it, that would be a high dose, inhaled salbutamol if they already have a diagnosis of asthma and they already have saber at home, it's highly likely that they will have already taken some. Um And often that's one of the ways patients know that they're having an acute asthma attack is because the cyber is not um not doing enough to help their symptoms and that's what makes them present. Um We can either give it as the standard pressurized um meter dose inhaler, which the patient will have at home or we can give it as a nebulizer, which is usually indicated in more severe lifethreatening or neo ftal asthma attacks um notably in acute asthma because we're giving high doses of sa we need to monitor our patients for the two main complications. So, hypokalemia can happen and that's why we want to do our um ABG S ideally or we can do use and es so doing regular blood tests and the patient might also have a tachycardia. So we need to keep doing regular obs on them and that then might develop into lactic acidosis over time. Next on our list of what we need to give. Our patient is prednisoLONE, 40 to 50 mg for at least five days. Um But it might be more until the patient is completely recovered. While they're taking the prednisoLONE, they should continue taking their normal medication even if that includes an inhaled steroid. If at the beginning, they are unable to swallow tablets, if they're so breathless, we can also give IV hydrocortisone every six hours. Next on our list is Ipratropium bromide, which is a summer short acting muscarinic antagonist. This one is given if the first few um our first few um management options haven't worked. We'll then consider giving tropium bromide. And then we have to where the evidence is not clear on whether they actually help. But these are two management options that are often considered in again, more severe or non, non responding. Asthma is magnesium sulfate, which can be either given IV or via a nebulizer and aminophylline, which again is given IV. And finally, if our patient is still not responding and is still struggling and is at the point of exhaustion, we'll consider mechanical ventilation. Um So it's a clinical decision that isn't really based on any hard facts and that can make it a really difficult decision to make. Um certain indications might make it more likely a patient will have, will require mechanical ventilation. So if they're really, really fatigued, if they've got any kind of cardiovascular compromise, especially hypotension, if, of course, if they're in a coma or if they've got cardiac arrest, they're in cardiac arrest, we'll, we'll definitely consider mechanical ventilation. Um, one of the things that makes it a difficult decision to make is that it's got a really high rate of complications. So, um, one of the studies found that in, um, patients who had mechanical ventilation, more than 50% of their um, complications came from the mechanical ventilation itself rather than from the acute asthma exacerbation. And one of the things this is not necessarily PG, but I think it's a really useful way of remembering the order of the management of asthma of acute asthma is um, the, I don't know if it's a mnemonic, but I should, I hate my asthma. Um It just helps with the memorizing the order of what we give things in. Um So we'll give oxygen, salbutamol, ium bromide hydrocortisone or prednisoLONE, magnesium, sulfate and aminophylline. So, going back to our patient, she had treatment in A&E and is now feeling better. She's breathing more comfortably and is able to consistently maintain her sats above 94%. So, what do we do? Now? Does anyone want to write in the chat, any ideas you have that we can do for our patient before we discharge her or any advice we can give her while we discharge her or anything the GP could do perhaps. OK. Is, is there, are there any answers? Uh No, not at the moment. OK. OK. Just in the interest of time I'm going to move on. Um OK. Um So three important things to do, as you rightly mentioned, right at the beginning is identifying any triggers. Um That means that we can prevent this from happening again. In terms of inhaler use, many, many patients have been given inhalers and have been given a five minute introduction to using inhalers and then don't get any follow up. And so it's really important to check what is their inhaler use. Um in terms of what's their technique and how often are they using it? Are they using it appropriately? Um and ultimately optimizing the treatment. So seeing if we need to change them to a higher dose of any of their medications. Um And in terms of inhaler use, one of the really big drives in the past few years has been to go from, as you can see the picture in the bottom, um with the patient using the inhaler directly to using a spacer. So we know that that massively improves outcomes just because it's so much easier to correctly take the drug. Um So if you're not using your inhaler correctly, the medication isn't going to actually reach your lungs and so it's not going to have much of an impact. Um, so I'll give you this SBA there should be a poll. So a 16 year old presents for an asthma review. She demonstrates her inhaler technique and does the following steps. When administering her salbutamol, she removes her cap and shakes the puffer. She breathes out gently. She puts a mouthpiece in her mouth and presses a canister when she breathes in and inhales deeply. She holds her breath for 20 seconds and then she repeats the process immediately for the next administration. So what are the issues if any with her technique? So we're starting to get some responses. So we've got most people going for Option B at the moment. B, let's see if there's a couple more that will come through. Yes, please answer the poll if you can see it. If not. That's OK. So we've got 100% of people going for option B Perfect. Very good. Um So something, the reason why I've got an SB on this uh topic in particular is because every um every presentation where a patient is coming for an asthma review or an acute asthma exacerbation is an opportunity to check their technique and to make sure that they're using it correctly. Um OK, I'll hand it over to you. Amazing. So guys, um I will be posting this again at the end, but please do fill out the feedback forms so you can a claim your attendance certificates and ba gives us very useful information about how we can improve. OK, so now we're gonna talk a bit about CO PD. So we, first of all, we've got a case here. So you've got a 67 year old man who's come in with dyspnea or shortness of breath. Um, so similar to before, what more would you like to know? But also more importantly, what differentials are you initially thinking of straight away? So if someone says Disea, what could be going on imagining this isn't AC O PD tutorial. So what might, what do you think might be going on? So if you just drop those in the chat, please, that would be great. Any ideas guys in the interest of time, I'm just gonna move on because I know it's getting delayed. So if we, so I've got a diagram here um in this next amazing. So we've got pneumonia pe Yeah, really good guys. Yeah. So as you can see on this diagram, dysnea is a very, very, very common presentation in A&E and GP and everything and it can be caused by a great number of things. Um You can use things like your surgical, serve your vitamin CDE type things to categorize them. Um As you can see, there's a massive number of pulmonary things. So like you guys have said rightly, pneumonia, pe um heart failure and other cardiac causes, there's a great number of things. And so what we wanna do is we obviously wanna take a detailed history and when you're taking a history on dysnea, uh yeah, a great thing to use is actually your Socrates. So obviously, as a lot of you will know Socrates, we use primarily for pain and it everything you need to know about a pain history. However, you can actually use this for any kind of symptom and just omitting things as necessary. So in this case, the site not really relevant, the onset, when did it start? When does it come on? Is it with activity? And if it is a really, really important thing is always to know about their baseline. So for example, the patient may say I used to be able to walk a kilometer every day, no problems at all. And now I get really short of breath after 100 m. You wanna know how much has this changed? If they say, oh yeah, this is normal for me, then you're not gonna be as worried that things have gone worse. Ok. Character you don't really need radiation, you don't really need associated symptoms. Now, there's a great ton of associated symptoms which I'm gonna go through in a moment. Time, time is really important. Like Emma mentioned earlier with asthma, is there things like dal variation? And also this is also time is also about the progression. Has this gotten worse over time? Like, so let's say they've said, oh, it's been going on for six weeks and I'm getting worse and worse and worse. Ok. Exacerbating factors, any triggers, does anything make it better and then severity. How bad is it um affecting you? How bad is it affecting your day to day life? Like, are you struggling to do your daily activities? So Socrates is really, really useful for any kind of symptom. So you can cover all your bases and then I find it really useful when you like, if you're just get like asking about a symptom that you're maybe not as aware of. Ok. So now talking about the associated symptoms, there is a great number of associated symptoms here. Ok. So these can be things like infective. So, fever, productive, cough, wheeze, et cetera. Um We've got chronic respiratory distress. So things like reduced exercise, tolerance, nonproductive cough, chest tightness, finger clubbing, there's a great number there, neoplastic changes. So weight loss, fatigue, night sweats, pulmonary embolism. So tachycardia, hemoptysis, pruritic chest pain and things like your traumatic and cardiac causes. So other club, so edema in the legs, um traumatic might be, you know, wheeze pruritic chest pain, et cetera. So there's a great number of associated symptoms and it's always important to ask about these. Ok. Um So I've got a quick question here if you guys could ans take a go and answer this. So you've got a 59 year old patient who's come to the GP with dyspnea and cough upon further questioning. She has lost 7 kg of weight over the last two months and wakes her very sweaty at night feeling generally quite fatigued during the day. She's unable to go to the shops and do her daily activities of living. And she tells you she is an ex smoker with a 20 pack year history. What should you do? Ok. So I just give it 30 seconds or so good. So, we're getting a few answers coming in and we've got kind of a 5050 split at the moment of referral to the emergency department and a two week wait, referral for suspected lung cancer. Ok, cool. So there's a couple more people going for two week. Wait, good. So yeah, you guys are right. So in this case, the answer here is two week wait, referral for lung cancer. And now I've highlighted some of the big red flags here. So they've got 7 kg of weight loss. Now we class this as unintentional weight loss. Um And you can tell it's unintentional because she's unable to do her daily activities. So she's not moving around, she's not exercising. So you're not, you can't say oh, she's been going to the gym, so she's lost 7 kg. That's not what's going on here. She's waking up at night sweating and, you know, always you want to characterize this is like a drenching sweat. In this case, it most likely would be. And she's generally quite tired during the day. These are all your very classic bee symptoms and you're worried very much about lung cancer and in the UK as a GP, if you're worried about some kind of cancer, it's always a two week wait, referral. This goes to the, um, dedicated teams and they will see this patient within two weeks for appropriate investigations. So, within the UK, two week wait is always important. And on the next slide, I've just got a other couple of red flags to look out for. So chest pain hemoptysis, which is unexplained, um, that might not necessarily mean lung cancer might do. But these are important red flags where you're very worried and you either wanna do things like two week wait or referral to the emergency department. Ok. So other important questions in a additional history, any past medical history, you wanna know if there's anything else that might be going on, whether it's cardiac pulmonary, et cetera drug history. So some medications can precipitate a cough and interstitial lung disease. So things like methotrexate, uh nitrofurantoin amiodarone, these can actually cause pulmonary fibrosis. So you wanted to ask, it's really important to know about their history and obviously with their allergies as well, family history for um, any kind of conditions that run through in the family. Um, you know, things like cystic fibrosis and all of those. Although in older patients, you're not gonna be suspecting that travel history is actually really, really important when it comes to dysnea, especially for things like TB some kind of atypical pneumonia. So, you know, legionella is commonly found in places like Spain. So you wanna ask about, have they been traveling around recently and especially also for things like pulmonary embolism. Have they been on a, a really like a 12 hour flight? Right. These are big risk factors, you wanna ask? And then of course, your social history is always really, really important. Um What do they do for work? Are they exposed to allergens or asbestos? And obviously one of the biggest things is always gonna be smoking history. And you wanna know how many of they're smoking? How long have they been smoking for? It's always good to ask, have they tried to stop? Because when it comes to things like smoking cessation, you, it might give you an idea of if this is gonna be working for them or how you might go about that and pack years. So pack years is kind of this thing you can calculate to see what their risk of risk of developing lung problems might be and the greater the number of pack years, the greater the risk, ok. And obviously always things like alcohol housing is really important in terms of their accommodation. If they are getting, you know, disn or on exertion, you wanna know, do they have to climb loads of stairs? Cos that's obviously gonna pose a big risk and always im important to ask about their support and their independence. Ok. So in our case, our 67 year old man reveals he's had this on and off dyspnea for the last six months, which has been getting progressively worse with a slight productive cough. He's got reduced exercise tolerance and he used to be able to walk to the shops every day, but now is becoming quite short of breath and wheezy. After a few 100 m, there's no significant past medical history, drug history or drug allergies. And he's a smoker of the last 40 years, smoking one pack a day. So this equates to a 40 pack year history. So one pack a day for 40 years is a 40 pack year history. Um and he's a social drinker lives out with his wife in a two story house. So our top differenter in this case is most likely going to be if anyone wants to drop it in the chat. So I will move on just because of time. So our top differential here is most likely CO PD. Ok. So what is CO PD? So chronic Obstructive Pulmonary disease, this is one of the most commonly seen respiratory diseases, especially in the older population. And it's actually responsible for, I think it's the third most common respiratory disease in or third most common in the world for in everything. Ok. So it's a combination of both chronic bronchitis and emphysema. And it's so it's actually this umbrella term of the two and it's caused by chronic irritation of the lung, parenchyma. So the lung tissue which leads to inflammation and structural lung damage and this causes airway narrowing, which is your bronchitis and reduced lung elasticity, which is your emphysema. Ok. So when and who is the most commonly seen in? So, it typically affects adults greater than a above the age of 40. And obviously, the prevalence increases with age and of course, things like your smoking history is a massive risk factor and it's the third most common cause of morbidity and mortality in the world. So it's a very, very prevalent thing and it's a huge state disease that is um very common across the whole world. And as, as I've said, the most common cause is tobacco smoking, especially in high income countries in your lower income countries. There might be other things like asbestos or other exposure, environmental causes. Um So yeah, other causes environmental and occupational um such as air pollution, cold cotton, et cetera, and then alpha one antitrypsin deficiency. And this is an inherited condition which I'm gonna talk about in a few moments. So, how does this happen and what's going on? So you get repeated injury and repair of um your lung because of exposure to things like tobacco smoke. And this causes things like oxidative stress and these like protease antiprotease imbalances. Um So your protease antiprotease. So these are things, it's kind of like you have this balance of when you have infection or inflammation, you have uh recruitment of macrophages and neutrophils and other inflammatory mediators, these secrete things like proteases to destroy the bacteria. Um However, when you get repeated inflammation and irritation, you don't have enough of this antiprotease to stop this protease from now attacking things like your alveoli. So in emphysema, you have excess proteases, it destroys the alveoli, typically central ana which is kind of like not your really, really distal alveolar, it's more a bit further back and it, it destroys the elastin that's found in your alveoli. And as we know, alveoli expands massively to increase the surface area for oxygen exchange and then it recoils. So without this elastin, the there is no more recoil, it leads to a at least can cause airway collapse during exhalation. And it also impairs your gas exchange. So you get reduced um oxygenation, you have increased um carbon dioxide which remains in the body, it remains in the lungs. So that's your emphysema. So it's the destruction of alveolar alveolar air sacs, your lungs cannot expand as much and collapse as much as they used to be. And you also have chronic bronchitis. So this is a narrowing of the airways. And again, it's this irritation which leads to hypertrophy and hyperplasia of your mucus secreting cells. So your goblet cells in the lungs and also the smoke can damage the cilia itself. So it's really ineffective at removing that excess mucus. So overall, you have narrow airways, you have a lot of mucus build up which causes that kind of crackles, wheeze sounds that you might find on examination and it causes really difficulty in breathing and again, poor gas exchange. So I've just got a couple of diagrams to show what's going on here. So as you can see tobacco smoke, oxygen species, tissue damage and this kind of emphysema picture. And then on the next page uh on the next slide, you'll see kind of more the bronchitis. So again, this narrowing of airways, um you kind of get this irregular shape going on and a lot of excess mucus production. Ok. Amazing. So the other common cause, well, not as common is alpha one antitrypsin deficiency. Now, if you have a patient who's presenting with signs of CO PD and they're quite young and they say they've never smoked in their life. There is a good chance that they have alpha one antitrypsin deficiency and it also commonly presents with jaundice. So what's going on here? So this is an autosomal recessive condition. Um It's a gene that's located on chromosome 14 and it presents commonly with an associated liver injury. So, alpha one antitrypsin is this protease inhibitor produced by the liver and it protects your cells from those protease enzymes released by neutrophils. Ok. So it's kind of the antiprotease that I was talking about before and without alpha one antitrypsin when you have a deficiency, um that neutrophil elastase remains in the lungs and it targets those alveoli alveoli and it breaks them down, you lose all this alveolar recoil and it causes emphysema. And this is a plan a scenario. It attacks all the alveoli everywhere in um frequency of the lower lobes. OK. And also because you have a misfolded enzyme which builds up in the liver, it leads to cirrhosis and which gives you your jaundice picture. And it also increases your risk of hepatocellular carcinoma. Please. If you guys, if that doesn't make sense at all, please do ask. And I will try and repeat. OK. So this diagram kind of just shows that a little bit. So you have this destruction of the um alpha one antitrypsin. So it stops, it leads to tissue disruption and put of the alveoli. OK. So moving back to our case. So what do we see on examination? So he's got increased work of breathing. He's got, he's coughing, he's using excessive muscles. Um You know, he's got personal breathing, nasal flaring. Uh He's got tar staining on his hands, reduced chest expansion, hyper hyper residency, percussion and bilateral wheeze. What else might you see? Well, so let's see. So, on general inspection. So as we've said, they might be coughing, mucus product excess mucus production, they might be using accessory muscles and tripoding, er a sign of respiratory distress. They might be quite cyanotic. You might see blue lips, you might see er blue peripheries or they might also be quite flushed or be quite pale and this might suggest that they've got really severe CO PD and their heart is now starting to fail because of that increased pressure in the lungs, causing strain onto the right side of the heart. And that's known as Cor Pulmonale, they might be flaring their nostrils to increase the volume of inhaled air or they might be personal breathing. So this is kind of when you, you, you kind of bend your lips inwards, um, and then you blow against it. And if you do this yourself, you'll notice that it's quite hard to exhale. And what's do, what you're doing here is slowing down the expiration and it produces a small amount of positive end expiratory pressure. So what this is doing is it's kind of, it's trying to maintain your airways to stay open, especially some of those kind of distal bronch um bronchioles and it maintains them to stay open. It supports the patency and this increases the surface area of alveolar for slightly longer for gas exchange. And it's to allow that increased clearance of CO2. And this is really, really important. And the, yeah. So these are some of these, some of the diagrams that show that. So on the bottom, you can see this tripoding position and on the top B and C, you can kind of see how he's kind of pursing his lips together. OK? On the hands, like we said Tar staining. So it will show that they've had significant smoking history. They might be cyanotic, they might get clubbing and now clubbing you'll see like thickening of your fingers. Um Some people use shamrocks windows of putting your fingers together like this. I find that this is really difficult in elderly patients because they usually quite have a bit of a tremor. So it's a good way to do it is just look at the fingers at the level of your eyes and see. Are they really thick? Have I lost that kind of uh c convexity of the, the nails? They might have asterixis. So this is because of CO2 retention. And what's happening here is you get toxicity at the kind of motor centers in the brain which are usually responsible for these muscles and because of chronic CO2 retention which I'll get onto um it causes this kind of flapping motion. They might also have c er cool hands and their pulses might you might find a bounding pulse, which again is to do with CO2 retention. And always it's a good idea to measure the respiratory rate at the same time. So you might see tachypnea, which is gonna be quite common. OK. So now looking, so we've got some photos here. So the top left shows that kind of star tar sailing and the bottom left is quite severe clubbing. It's probably not gonna be that obvious, but you will see something similar to that amazing. So moving on to the face and neck. So in the face. Again, central cyanosis, you might see oral candidiasis, so like white spots all over the tongue. And this is very common with inhaled corticosteroid use. And it's why you should always counsel patients to rinse their mouth out with water to prevent this from happening. And again, you might see this raised JVP on the left, which again is suggesting right heart failure in the chest, you're gonna find reduced chest expansion and you're gonna find this kind of hyperinflation of the chest. It used to be called barrel chest. But I think we're trying to get away from that a little bit. Some people call it dynamic hyperinflation. They essentially mean the same thing. And these photos again, obviously, it's not the most advertising to look at. But the top left oral candidiasis, this kind of bluish looking tongue to suggest central cyanosis. I don't know if you guys can see clearly, but that black hour is pointing towards a raised JVP. Yep. And then you can see this chest is quite hyperinflated. Um And this is just at rest. OK. And percussion and auscultation are hyper resonance. So there's increased air staying in the lungs. So you're gonna have hyper resonance in this air trapping. You're gonna find wheezing because of this narrowing of airways. And you may listen and find some crackles because of a lot of excess mucus, especially if they're having infective and exacerbations, there's probably some consolidation going on. So what kind of investigations do we wanna do? So, our first line investigations are always spirometry, chest X ray, pulse oximetry and an FBC. So I've got a question here. So if you guys can have a go at this, so we've got a 67 year old patient who's undergoing. So our 67 year old patients undergoing spirometry, which of the following best represents his likely results. So if you guys can have a go at this, please. Amazing. Yeah, so a couple of you have responded and we've got 100% of people you choosing C uh So C is the right answer. So we've got a reduced F EV one to F EC ratio of less than naught 0.7. And the importantly, this is post bronchodilator. So like Emma mentioned earlier in with asthma, if it's reversing, then you're not really considering CO PD because CO PD, it maintains even post a bronchodilator. So less than 0.7 is an obstructive picture. And in the case of CO PD, this is diagnostic for um CO PD. It's showing this chronic obstruction, you may also find this decreased diffusing capacity of the lungs, which basically is just showing that they have impaired gas exchange and the F EV one itself. So the amount of air you can blow out within one second is really useful for the staging of the disease. So if it's, so if we go to the next slide, so if we see us about, it's, it's still greater than 80% of predicted. It might be quite mild and you may even, you, you would have to see symptoms to say that they have CO PD 50 to 79%. It's quite moderate stage 2, 30 to 49 it's getting quite severe and less than 30% is very, very severe CO PD. Um and requires a lot of therapy. Now in the chest X ray, you might see hyperinflation and you see this with flattened diagrams. So if you see these red arrows, you can see the diaphragms are quite flat. Um You don't really see that curvature as nicely and you might see also these bullet and so bullet is basically air spaces. And this is again because of emphysema. And at this stage, it's always important to check for lung cancer and to rule that out if you're worried about that. Ok. So other investigations, so pulse oximetry are they hypoxic? It's quite likely and it's always good to look for secondary polycythemia. So if you're consistently hypoxic, your body's gonna respond by being like, oh maybe we need more red blood cells. So it triggers this increase in ep O. So erythropoietin leading to increased red blood cells. Bye-bye and other investigations for exercise testing. It's good to now determine a baseline of how far they can walk before they get um short of breath. It's always important to rule out your alpha one antitrypsin co PD can commonly cause sleep apnea. So you may wanna consider a sleep study. Um always great to monitor for ischemic heart disease and checking for right heart failure. And then ABG and this is more used in acute exacerbations, but it's good to monitor their levels of hyper. OK. So talking a bit about hypercapnia and this can be quite confusing to understand. So if we first look at ourselves, the majority of us here and the majority of people on a day to day rely on a hypercapnic drive to drive their respiration. So what this means is if you have raised levels of CO2, usually from some form of hyperventilation. So if you've been running for two kilometers and you're quite short of breath because you're hyperventilating, you're gonna increase that CO2 like Emma mentioned earlier, you're gonna give yourself this respiratory alkalosis and what this is gonna do, it's gonna trigger your body to sorry, you're gonna get a respirator, yeah, respiratory alkalosis and it's gonna increase um your I see CO2 that's maintained in your sorry respiratory acidosis, cos you're maintaining CO2 and this is gonna cause you to uh breathe more and expel with the CO2 in emphysema and airway narrowing. When you have reduced ventilatory capacity. CO PD patients tend to retain more CO2 and over time, this leads to hypercapnia and respiratory acidosis. And as time passes because they've got this chronic maintaining of um increased CO2, they lose this hypercapnic drive and they become these things that we like to call as CO2 retainers. So in these situations, they rely on a hypoxic drive instead. So we have baroreceptor chemoreceptor and baroreceptors in the aortic arch and your carotid bodies. And they monitor this O2 level instead of a CO2 level. And this in. So w when they detect low O2, this then drives their respiratory rate, increases their depth of bleed ventilation so that they can get rid of more CO2. However, when we give supplemental oxygen and this is really important for um when you're kind of treating an exacerbation, these chemo receptors then detect a rise in O2 levels and it kind of in because they have this hypoxic drive, they think, oh great. We've got loads of oxygen, we don't need to breathe as much. So it actually causes them to breathe a lot less and this causes a build up of CO2 further and a respiratory acidosis and makes everything worse, could send them into like er shock. Ok. So what, how do you find out if a patient is CO2 retainer? So this is really, this is why an ABG is really, really important. First, you're gonna see a raised P CO2, that's as expected. But importantly, you wanna look at the bicarb. So the HC 03 and this, if they're a retainer of CO2, it will show metabolic compensation which is a raised HC 03. And if it's normal it shows that there's not been much compensation and therefore, they might not actually be a retainer of CO2. And the reason we can say this is because it takes the body quite a while to adapt and compensate for this er raise in CO2 in the body. So if it's just, you know, you're acutely um not breathing as much and you've got a build up of CO2 in your body, your bicarb isn't really gonna change that acutely. It takes quite a while. It takes days, weeks, months to adapt and raise. Ok. So it's really, that's why ABG is really, really important. Ok. So back to our patient. So we've investigated him and we can confirm that he's got diagnosed, he's diagnosed for CO PD. So, first of all, how do we wanna manage this patient? So I'm gonna put an SBA up now. So what management options do you want to consider? First, that are very highly cost effective and really beneficial to reduce disease progression and risk of complications. So what do you guys think are really, really useful for this? Good. So we're getting some responses coming in now. So yeah, so all of you so far have gone for option C and this would be correct. So, option C smoking cessation vaccines and pulmonary rehabilitation. Now, these three, obviously you have your medical management, but as conservative management, these three are very, very, very important. Smoking cessation is really, really necessary to reduce this progression of disease. Um And you wanna always counsel them on trying to, you know, stop smoking, maybe giving them like buPROPion or varenicline to um if like nicotine replacement therapy, those kind of things, vaccinations are really important to reduce the risk of catching infections. As we know, obviously, if they have damaged lungs, they're likely gonna catch uh pneumonia and pulmonary rehabilitation, which I'll guarantee now. So if we go to the next likely. So just the slide before amazing. So pulmonary rehabilitation, this is kind of for functionally disabled people with CO PD. So where they're really struggling to do their day to day activities and it involves them as a group with other CO PD patients, they do various exercises which kind of helps them to have deeper breaths and improve their ventilation. So they can, you know, get rid of more CO2 and if you look at this pyramid here, so this is some research that was done and they showed that cost effective wise, these things are incredible for um CO PD like management and interventions. So as you can see the vaccinations at the, at the bottom, they're for, for the quality adjusted life you gained, it's, it's really, really cheap and then stopping smoking rehabilitation. And then after that is when you go to your medical management. So what medical management are we going through? So, first of all, so you have your Saba or your Sama. So your kind of salbutamol, your bronchodilators. These are gonna be your first line to help reduce their wheeze and open up the airways and then we're gonna check for asthmatic or steroid responsiveness features. So he's looking for things like, have they got a history of asthma or at P so things like eczema, have they got a high eosinophil count which is again significant to asthma diurnal variation or just variation in your fed one. Now, if you do, you're gonna want to give, so sorry if you don't have those things after the saber or s you're gonna wanna add a laba or lama. So you kind of for meter to those kind of things and if you are on the arm, you wanna switch to the. So I know these saam can be really confusing, but I hope it makes sense on the slide itself. If you do have asthmatic features, that's when you wanna start adding your inhaled corticosteroids and then if it still continues to be worse after that, you wanna move to your triple therapy. So that's an IC sa laba and a lama altogether. And at, at this point, you always wanna just make sure they're not on a Sama and they're on a saba instead. OK. So how about and yeah, so here it is a nice little diagram which you guys can look at afterwards just to remind yourself. OK. So after that, you wanna look at things like oral theophylline, but you have to make sure you do bronchodilators and then you're gonna think through, think of things like prophylactic antibiotic therapy. So, Azithromycin is typically used in this case. Um They might, they, they can't be continued smokers. They have to have optimized standard treatments and have exacerbations. But you should always rule out uh QT prolongation. So, macrolides, as we know is a risk factor for Long QT syndrome. So you wanna make sure you probably want to do an EKG to make sure that this isn't happening. OK. Other things you wanna consider is kind of like a rescue pack. So stand by a short course of oral steroids and antibiotics if and but you wanna make sure that the patient is aware of these risks and benefits like that, you need to know that they're safety netted, well, that they're not just gonna use this and then all of a sudden be in really severe exacerbation and need it support. So they will know when to come in when they realize things aren't working. And you have things like your phosphodiesterase inhibitors such as PDE four to reduce the risk of exacerbations. But these kind of things that are always very, very senior management, you're gonna, this is gonna be in AC O PD clinic with a very experienced respiratory physician who is gonna be assessing and gi giving all these treatments, ok. Saved back to our case. So our patient returned six months later. So they've had some investigations side on some, um, probably a Saba. Um, they've come back six months later with an increase in dyspnea cough and wheeze and he's brought in by ambulance with increased but production and seems slightly confused. So, what do we think is going on here? And what do you want to do first? Does anyone wanna suggest something in the, in the chat? Ok. Yeah. Amazing. So, we've got an answer here for infective exacerbation of CO PD in. Yeah. Amazing. So, yeah, this is what is going on. So we have an infective exacerbation of CO PD. So if we get the next slide, please. Yep. So, acute exacerbation with the most common thing being a infective and what's the first thing we wanna do is always gonna be a two E examination. This is an emergent setting. You wanna do an ATV examination? So we do this and what do we find? So, of course, you wanna do your danger response. So he's responding to your voice. So he's not fully alert. His airway is patent and you see some sputum in the mouth which you suture out. You find that he's got an increased work of breathing. He's using accessory muscles and he has reduced ex chest expansion. You find dullness to percussion with some wheeze and crackles as well. And you have, you do some observations, you find his O2 SATS are 84% and his respiratory rate is 34. He's sweating he has a slightly prolonged capillary refill time. He's quite dry. He's got dry mucous membranes. His BP is hypertensive. He's 85/45 with a raised heart rate. Um and I haven't put it on here, but they find that his temperature's also 38.2. OK. So he's responding to voice. His pupils are OK. His blood glucose is OK? And he has no DVT or anemia. So I'm gonna put another pole up here. So what should be your first step in the management of this patient if you guys could take a go at this, please. So we got a bit of a split right now. If we get maybe a couple others, that would be great. So in this case, our answer is gonna be e so the most important step here is start supplemental oxygen. Now, you've got to remember this is an A two E examination and I know I've given you all the information here. But in real life, you're, you're assessing A then B, then C and you're treating as you go, right? So in this case, we've done a, he's completely his, his airways patent and we've gone on to breathing and we find that he's got an oxygen saturations of 84%. So, you know, that's our first alarm bell has been like, OK, he's hypoxic. The first thing you wanna do therefore is start supplemental oxygen. And if we go through the others it you and getting a bed. Yeah, you might wanna do this later on and it probably is quite relevant but not your initial step. A chest X ray again is important. We're probably worried here that he's got some kind of pneumonia. So you probably do. You will wanna do a chest X ray to identify the location, but again, not the first step. A bolus of 1 L of normal saline. Now, this isn't a bolus, this is more of a long, longer infusion and this is something you probably do in something like DK A. So diabetes ketoacidosis, they need aggressive fluid resuscitation, uh a 500 mil bols of normal saline. Now, yeah, this is important and this is probably gonna be your second step when you realize that he's hypotensive but not the first and always remember in a two E it's assessing in the order of what's gonna kill the patient first. Now, hypoxia kills. So you want to assess and treat that as soon as possible. So you need that supplemental oxygen. OK. So again, so going a bit further on to the management now with breathing and oxygen in CO PD. So I mentioned earlier about this hypercapnia, CO2 retainer thing. And in a lot of cases, you know, you might find, you might find a patient who you have no idea who they are. You don't know about their past medical history and you don't know they have CO PD, you they might, you, they might, you might know they have CO PD, but you might not know that they're a CO2 retainer. So you have this kind of dilemma of what do I do? I know that I've been taught always all through medical school that co PD patients, their target saturation should be 88 to 92%. But I've got a patient here. I have no idea about them. So in those cases, you're always gonna start 15 L, non rebreed mask as you would with any other patient and you would do a target of 94 to 98% as you would with any other patient. OK. Obviously, always remember to, you know, ask for immediate senior support, check your trust guidelines. Always there are always gonna be er things that are available to you, but in most cases, you're gonna start the patient on 15 L of oxygen with a target of 94 to 98%. And this goes back to what I was just saying, hypoxia is going to kill the patient first. So if you can't be waiting to assess whether they, whether they are a CO2 retainer, you just wanna start them on high flow oxygen. And whilst you're doing that, you're gonna do OK, I've started the patient on high flow oxygen. Let me get an ABG and let me get this, let me find the results straight away ABG S for and I'm sure most of you are aware, are you get the results within seconds? You take the blood, you take it to the machine, it gives you the results within seconds and you have your information. And then like I mentioned before, you check the bicarb, is the bicarb raised or is it normal if it's raised? You can be like, ok, I know this patient is, is a CO2 retainer. I can see they have a high P CO2 and therefore I'm now going to reduce my oxygen, my supplemental oxygen 4 L per minute by a 28% ventral mask with a target of 88 to 92%. And then you can just be like, OK, I'm gonna titrate this up or down as I feel necessary. Does that? I hope that all makes sense to all of you guys. And please do, let me know in the chat if um you're confused at all. But importantly, start the patient on high hypoxia kills first. So once you confirm they're a Co2 retainer, you can reduce as necessary. Ok? Now, we also can t hear that they have a wheeze. So you wanna start, you kind of nebulized salbutamol and ipratropium bromide. So you're kind of like burst therapy type thing that you might do an asthma as well. And also you can hear crackles, you know that they have a high temperature. So you might wanna think, ok, let me start some broad spectrum antibiotics. So something like amoxicillin or Clarithromycin or Doxycycline. Now, looking at their circulation, they're hypotensive. So let me give a fluid bolus. And now you're actually thinking, oh, wait. So they're hypotensive hypoxic and they have a raised temperature. I'm actually very worried about sepsis. So you're gonna immediately call for help and start your sepsis six. So you're gonna wanna take your blood cultures, um, measure your lactate, which you would have got with the ABG. Um, obviously, uh measure your urine output, start your fluids, start oxygen and start broad spectrum antibiotics. So you wanna make sure you're covering that. It's very, very important. OK. And then other things. So, so that's your kind of management. And then from there you're gonna get senior support. So, infective causes of se exacerbations. So we have bacteria, which is probably the most. So the most common bacterial cause is haemophilus influenza and then other things. So, streptococcus pneumoniae and Moraxella. Um I don't think I can pronounce that second word. So I'm gonna leave it and then respiratory viruses. So these account for about 30% of exacerbations with human Rhinovirus being the most important. Ok. So how do you manage these if they don't have admission? Well, we know that they present with increased symptoms. So, sputum production, hypoxia confusion. If you find that they might not need admission, like they just have a bit of a cough, but otherwise they generally, well, they're not hypoxic, they don't seem confused. You would wanna tell, tell them to increase the frequency of their bronchodilators, maybe consider a home nebulizer. A lot of patients will have those always wanna give oral prednisoLONE for 30 mg for five days. And this is two patients both in and out of hospital. But without admission, if oral prednisoLONE, 30 mg for five days and give oral antibiotics and it's one of the three I've put there. And if you wanna, if you're worried about, you know, they're really bad, bad and you need to admit them, this is a criteria you look for. So have they got severe breathlessness? Is their respiratory rate in the thirties? Have they got acute confusion or impaired consciousness? Are they cyanotic? What's is the oxygen? So that's really low. Are they living alone? And therefore you're worried that no one will be around to notice if it gets really bad and they won't be, they won't have the capacity to take themselves to hospital or do they just have really significant comorbidities such as cardiac disease? And therefore you're worried that this could escalate very quickly. And in those cases, you wanna admit them to secondary care and offer them oxygen therapy, nebulize, salbutamol, ipratropium bromide. And in this case, your steroid therapy is more likely gonna be IV hydrocortisone um because they probably won't be able to swallow things and it's just easier to give them IV drugs and then things like IV theophylline. But again, this is senior support level and in some cases, you wanna consider noninvasive ventilation. So in CO PD, the most common one you can use is BIPAP. So this is a bi level, positive airway pressure. And this is much better in CO PD because it is much better for the removal of CO2. And this is important if you get type two respiratory failure, which is when you have high CO2. Um and you only really do this if the PH level was around 7.25 to 7.35 less than 7.25 you're gonna have a lower threshold for intubation and ventilation with high dependency unit or ITU admission. So it's 7.2 fives to 7.3 fives um is bipap less than that intubation and ventilation. Ok. Complications of CO PD. So there's quite a few here. So one of the most common ones is gonna be Cor Pulmonale. So this is right sided heart failure. So, like we mentioned before, you have increased pressure in the lungs. This causes pulmonary hypertension which increases the strain on the right side of the heart. Um and it develops into symptoms of RJ BP Hepatomegaly. And this is because your IVC is connected straight to your liver. You have a loud P two and you have sorry you have the sneeze is not coming. Ok? Excuse me. And you have peripheral edema. You treat this with furosemide to reduce the edema and you wanna optimize your CO PD treatment and consider this thing called long term oxygen therapy. You also can get lung cancer. Obviously, CO PD and smoking history is a very big risk factor for lung cancer and something which is actually gonna be quite common is depression. Obviously, patients who have developed CO PD, it's probably come on quite out of the blue. It's probably gotten worse over time. You know, they probably don't see their friends as much or are able to go out as much. And they might need some psychiatric evaluation and some support there. They may get recurrent pneumonia, which obviously with lung disease, they have increased risk of that and they may get pneumothorax as well. Ok. So a bit about long term oxygen therapy, I don't think the slides have are refreshed on there. If you could maybe go off, it might refresh. Um Oh, there we go. So what is long term oxygen therapy? So this is when patients will be breathing supplemental oxygen for at least 15 hours a day. And you assess a patient for this in a few few scenarios. So you're looking at have they got very severe airflow obstruction. Um So that F ev one of less than 30% which we said was very severe. Are they cyanotic, do they have that secondary polycythemia, um peripheral edema? So, signs of the right heart failure, however, you will never offer this to a patient who continues to smoke and that's only as continue to smoke despite being offered services to help them stop. So advice treatment, specialist services. Ok. So if you think, ok, this patient needs oxygen therapy, you wanna assess them for it. So the criteria for this is first looking at two APG results and they have to be at least three weeks apart. And within that time, they can't be having exa exacerbations, they must be stable, they must be optimally managed with the medical treatment. And you're looking at in this case, you're looking at their po two. So seeing how hypoxic they are, if they're less than 7.3 that's a alone, that will be criteria for them to start this therapy. If they're between 7.3 and eight, you wanna see if they have one of the following. So secondary polycythemia, peripheral edema or pulmonary hypertension. So those are the kind of criteria for this and always it's great to do a risk assessment. So, obviously, this is a lot of machinery that's gonna be in their house. So are there a risk of falling over from this equipment? And is there a risk of burns and fires? Obviously, we know oxygen is very, very flammable and because it supplements oxygen, they have these like concentrates concentrators of oxygen to maintain a specific saturation. So if there's someone who's smoking, including ecigarettes, you want assess for this and make sure that this patient will be safe and it for their house to be safe. Ok. So thank you all for coming today. There was obviously a lot of information the slides will be available um on med all itself. Um I'm gonna again send this feedback form and please please do fill this out. You can get your certificates and also it gives us a lot of useful information of how we can improve for the next, for next time. But otherwise, thank you so much for coming guys. We will stay on for a few minutes if you do have any questions. Um and yeah, we really appreciate you being involved as well. Thank you. Absolutely. Thank you very much for coming. Ok, I'm gonna stop broadcasting now.