Chronic Obstructive Pulmonary Disease (COPD) | Clinical Medicine

Summary

Highlights

• The video covers the two types of COPD: chronic bronchitis and emphysema. 🤓
• Chronic bronchitis is marked by a persistent productive cough, often due to mucus accumulation. 🟢
• Emphysema is noted for breathlessness due to large, overinflated lungs. 🌬️
• Smoking is the primary instigator of COPD, causing chronic airway inflammation. 🚬
• Managing COPD involves stopping smoking, vaccinations, and medications like bronchodilators. 💉
• COPD can lead to severe complications like pneumonia and right heart failure. 💔
• Diagnostic tools include chest x-rays, PFTs, and assessment of lung volumes. 🔬

Key Takeaways

• COPD is a complex respiratory disease consisting of chronic bronchitis and emphysema. 🌬️
• Smoking is the primary cause of COPD, triggering chronic inflammation and airway obstruction. 🚬
• Chronic bronchitis is characterized by a productive cough and mucus overproduction. 🤧
• Emphysema leads to dyspnea and large, hyperinflated lungs, often seen with barrel chest. 🫁
• COPD management involves lifestyle changes, bronchodilators, corticosteroids, and sometimes surgery. 💊
• Complications include pneumonia, respiratory failure, and sometimes heart issues in chronic bronchitis. 🏥
• Early diagnosis and treatment can significantly improve quality of life for COPD patients. ⏳

Overview

Chapters

• 00:00 - 00:30: Introduction to COPD The introduction to COPD kicks off with a warm greeting to the audience and an invitation to engage with the content by liking, commenting, and subscribing. The video is part of the clinical medicine section and aims to provide comprehensive information about COPD. Viewers are encouraged to explore additional resources on the Ninja Nerd website, including notes, illustrations, and exam prep courses for various medical exams.
• 00:30 - 03:30: Chronic Bronchitis Pathophysiology Chronic Bronchitis is a type of Chronic Obstructive Pulmonary Disease (COPD). Patients with this condition typically present with a productive cough, which is one of the most common symptoms. Additionally, they may exhibit signs of dyspnea. These are the primary clinical presentations observed in patients with chronic bronchitis when they visit the clinic or hospital.
• 03:30 - 05:30: Chronic Bronchitis Symptoms and Physical Exam Findings This chapter focuses on the symptoms and physical examination findings associated with chronic bronchitis. Key symptoms include a productive cough and dyspnea. During a physical exam, practitioners should be attentive to wheezing and rhonchi, which are indicative of mucus in the airways. Wheezing results from airway obstructions, while rhonchi, which often clears after coughing, is a sign of mucus presence in the air passages. These auditory signs are classic indicators of chronic bronchitis.
• 05:30 - 09:30: Inflammation and Airway Obstruction in Chronic Bronchitis This chapter explores the main features of chronic bronchitis, focusing on the sounds heard during lung auscultation such as snoring, wheezing, and rhonchi. These sounds often improve temporarily after coughing. The primary reason for symptoms such as a productive cough and wheezing is significant inflammation within the airways, which may lead to obstruction and, in some cases, irreversible fibrosis.
• 09:30 - 18:00: Emphysema Pathophysiology The chapter focuses on the pathophysiology of emphysema, particularly the development of chronic inflammation. It explores how chronic inflammation arises, specifically within the bronchial sections, emphasizing the presence of massive mucus accumulation in the airways. This heavy mucus production leads to a productive cough, as the body attempts to expel the excess mucus. The chapter provides a detailed look at these processes and their contribution to the symptoms observed in emphysema.
• 18:00 - 28:30: Emphysema Symptoms and Physical Exam Findings This chapter discusses the symptoms and physical examination findings of emphysema. It explains that narrowing of the airway lumen makes it difficult to get air in and especially out, leading to hyperinflation of the lungs. This causes the diaphragm to be pushed out, restricting deep breaths and resulting in dyspnea. Additionally, patients experience inflammation, loss of mucus production due to damaged goblet cells, and undergo fibrosis.
• 28:30 - 47:00: COPD Complications The chapter 'COPD Complications' discusses the issue of fibrosis in the airways, which is characterized by the activation of fibroblasts that deposit collagen fibrous tissue. This process leads to the narrowing of airways, rendering the disease irreversible and particularly problematic in terms of airflow. While both inhalation and exhalation are affected, the text highlights a greater difficulty in exhaling.
• 47:00 - 56:00: Diagnosis of COPD Chronic Obstructive Pulmonary Disease (COPD) is characterized by excessive mucus production due to inflammation by goblet cells, leading to the formation of fibrous tissue. This results in irreversible destructive lesions and chronic illness, as patients cannot regain their normal bronchial airway function. Progressive fibrosis contributes to the irreversibility of the disease.
• 56:00 - 66:00: Treatment of COPD The chapter discusses the treatment of COPD, focusing on the obstruction in the airways caused by a combination of bronchospasm, mucus production, and fibrosis, which makes it particularly difficult to expel air from the lungs. COPD is classified under obstructive lung diseases, sharing similarities with asthma, though asthma does not involve fibrosis.
• 66:00 - 76:30: Acute Exacerbation of COPD The chapter discusses the acute exacerbation of Chronic Obstructive Pulmonary Disease (COPD). It points out the main characteristics of COPD, including fibrosis, mucus accumulation, and bronchospasm. Unlike asthma, bronchial wall edema is less prevalent in COPD patients. However, the combination of these factors results in significant airway obstruction. This obstruction is a defining characteristic of COPD and greatly influences the presentation and symptoms in these patients. The chapter aims to elaborate on these physiological changes and their impact on patient appearance and health.

Chronic Obstructive Pulmonary Disease (COPD) | Clinical Medicine Transcription

• 00:00 - 00:30 foreign what's up Ninja nerds in this video today we're going to be talking about COPD this is a part of our clinical medicine section and if you guys like it please support us and you can do that by hitting that like button commenting down the comment section and also subscribing I also suggest if you guys have the opportunity to go down the description box below there's a link to our website where we have amazing notes illustrations we're developing exam prep courses for those of you taking your step one your step two your pants Etc and we have some great merchandise that
• 00:30 - 01:00 I suggest you guys check out all right let's start talking about COPD with COPD chronic obstructive pulmonary diseases there is two types but oftentimes most patients kind of present with a mixture of the two we're going to start with the first one that being chronic bronchitis so chronic bronchitis the primary way that these patients present when they come into the clinic or they come into the hospital they'll usually present with a productive cough that's by far I would say one of the most common presentations they may also present with some signs of dyspnea so we could also you know suggest that that would be another particular finding
• 01:00 - 01:30 the other thing is the physical exam findings so whenever you have them come in they have a productive cough maybe they have some dyspnea you go to the bedside you examine them what are some of the things that you'll actually appreciate on their exam one of those things is that sometimes when you get your stethoscope out you listen you hear a lot of wheezing and rhonchi that's very classic of patients who have chronic bronchitis so listen for any type of wheezing usually due to a Airway obstruction from mucus and also listen for rhonchi which is again mucus within the Airways but clears when you have the patient kind of cough so it sounds like
• 01:30 - 02:00 a snoring type of sound on auscultation you have them cough clears a little bit sounds a little bit better that's usually suggestive of these particular two now the thing that I want you guys to think about with chronic bronchitis is why do they present with a productive cough why did they present with wheezing and ronkai well the process here is super super interesting one of the things that we see with these patients is they have a lot of inflammation within their airways and that is the key thing and there may also be some irreversible fibrosis from
• 02:00 - 02:30 chronic inflammation we'll talk about the means by which chronic inflammation develops when we take a section out of these guys bronchials and we zoom in on it what does it look like one of the big things is that there is a massive amount of mucus within the Airways so tons and tons of mucus within their airways and therefore if you think about that if they have lots and lots of mucus within the Airways guess why they're having a productive cough a cough that's containing a lot of this mucous kind of material that is the reason why so heavy heavy mucus within
• 02:30 - 03:00 the Airways what would that do well it narrowed the airway Lumen and so that would make it really difficult to get air in and get air out more particularly getting air out right and if your lungs get super hyperinflated my diaphragm is pushed out I can't take a deep breath in that's usually one of the reasons why these patients also present with dyspnea the other cool thing about this patient population is that they also have because of the inflammation loss of mucus production from their goblet cells but they undergo a lot of fibrosis this
• 03:00 - 03:30 activates a lot of fibroblasts and they laid on a lot of this collagen fibrous tissue which unfortunately Narrows the airway as well so having this fibrosis makes this two things one it makes this disease irreversible but it also Narrows the Airways and by default that will make it difficult to be able to again get air in and get air and get air out and again I would stress that it's more difficult in getting air out than it is getting air in
• 03:30 - 04:00 again mucous production excessively from inflammation by gobble cells playlists laying down a lot of fibrous tissue which makes this irreversible destructive lesions that's why it's chronic and these patients usually don't have the ability to come back to their normal bronchial Airway function usually there's Progressive fibrosis that makes this an irreversible disease the last one's a really big one from inflammation this is bronchospasm these patients also develop a ton of bronchospasm and again inflammation activates leukotrienes it activates
• 04:00 - 04:30 histamine molecules and this bronchospasm also really Narrows the airway so combine bronchospasm combine mucus and fibrosis you have a super obstructed Airway and again common theme Here difficult getting air in and out but I would stress more on the difficulty of getting air out now with all of these combinations of things we say that COPD is a part of what's called an obstructive lung disease in combination with asthma you'll notice a similar theme against these with asthma there was no fibrosis
• 04:30 - 05:00 though right with COPD you'll notice fibrosis and mucus and bronchospasm more bronchial Walla demon asthma less of that present within the COPD patients but what you'll see here is that the combination of these three things the airway is super obstructed and that Airway obstruction is really the Hallmark of why these patients look the way they look let me explain that in another way
• 05:00 - 05:30 if I have an increased Airway obstruction that I form within this alveoli so here's a little bronchial here's going to be some smaller bronchioles and then an alveoli here's normal all of a sudden I decide to have some mucus some fibrosis of this bronchial I bronchospasm this area what's it going to do now it's going to make it really difficult to get Co2 out of the lungs that's going to be impossible so now I can't get Co2 out as I can't get Co2 or air out of the
• 05:30 - 06:00 lungs the CO2 will build up but in general the lungs will get bigger and bigger and bigger so what we notice here is we notice that these patients develop a lot of air trapping and as they air trap because of this Airway obstruction what do we notice the alveoli will get bigger and bigger and bigger and eventually the patient's lungs will become hyperinflated so that's another potential finding that we can see with these patients is they have hyperinflation of their lungs now
• 06:00 - 06:30 you're like okay isn't that a good thing don't we want them lungs to be big no because if they're too big imagine taking a deep breath in hold it now try to take a deep breath on top of that how difficult would that be that's why it's so difficult for these patients to take a breath in because their lungs are already filled as much as they possibly can because of Airway obstruction so we're taking a patient with normal lungs causing Dynamic hyperinflation via air trapping and then from that increased
• 06:30 - 07:00 hyperinflation making it difficult to take a breath in this is usually the pathophysiology that progresses in patients with chronic bronchitis the type of COPD the question comes what in the heck is causing all of this process I already told you it was something that's really really really jacking up a lot of inflammation and this inflammation is not a one-time experience like you have an asthma that it comes around every now and then
• 07:00 - 07:30 this is something where these cells your lymphocytes your macrophages your neutrophils these are releasing tons and tons of cytokines massive amounts of cytokines and growth factors and things to that effect and these guys are really amplifying your inflammatory response and as they do that they stimulate these things that we see here gobble cells to make a lot of mucus platelets to make a lot of fibrous tissue and smooth muscle starts really becoming
• 07:30 - 08:00 hyper responsive and and starts narrowing the Airways we obstruct and we precipitate the findings that we see here which is the patient air trapping and dynamic hyperinflation is what the heck is causing these these immune system cells to become hyperactive well the primary cause here is smoking smoking is by far going to be the biggest trigger for this immune system activation
• 08:00 - 08:30 particularly neutrophils cd8 lymphocytes and macrophages that's it so now we have an understanding of chronic bronchitis let's come down now and talk about the next part of the COPD picture which is the patient who exhibits findings of emphysema so emphysema again is a little bit different and it only differs a Teensy bit within the pathophysiology but again the concept exists as the same COPD can be a mixture of these two
• 08:30 - 09:00 patient populations it's just on exam and when learning it you want to be able to have some differentiations of it let's talk about emphysema emphysema these patients will not really present with a productive cough usually what makes chronic bronchitis very specific is that productive cough for a long time I'm talking like three plus months for like two consecutive years emphysema is way more likely to cause things like dyspnea and particularly dyspnea on exertion
• 09:00 - 09:30 but Disney in general is going to be by far I'd say one of the most common features so if a patient come in with dyspnea and a cough again it could be a mixture of the two but if you hear Disney I think a little bit more for your exams about emphysema the other thing is that these patients lungs are super huge and we'll talk about why they're much much more hyperinflated than the chronic bronchitis picture so because of that these patients usually have this like big big chest like I'm talking like a barrel chest so
• 09:30 - 10:00 sometimes you'll see what's called a increased AP diameter which means that they just have these huge lungs they have they have what we call this barrel chest and because their lungs are so huge and Hyper aerated and hyperinflated the breath sounds sound very diminished and the reason why is because their lungs are so huge it's really hard for them to take air in and that's why I feel like I'm short of breath all the time right so this sometimes you'll see this concept of the breath sounds being like
• 10:00 - 10:30 somewhat reduced or diminished so if I see this increased AP diameter a barrel chest type of presentation and decreased breath sounds in combination with a dysnic patient I definitely starting to think a little bit more about emphysema and the chronic bronchitis patient either way what's the pathophysiological difference in this one it was inflammation of fibrosis and this one is tissue structure tissue destruction secondary inflammation and fibrosis let me explain
• 10:30 - 11:00 here's a zoomed in portion of the airway you don't notice any mucus that's one of the big highlighting features of chronic bronchitis and here here's the airway and on the outside of them is this elastic tissue what happens in this disease is they have a decrease in the elastic tissue now if you decrease elastic tissue within the bronchials this will cause the bronchials to not be able to keep to stay open essentially
• 11:00 - 11:30 so with decreasing elastic tissue the bronchioles will begin to collapse a bit a little bit so that's one Downstream effect out of this is that with decreasing elastic tissue one of the things that you'll see as a result of this is bronchial collapse the other thing that's really interesting is that in these patients they also have destruction not just of the elastic tissues look this thing's getting chewed
• 11:30 - 12:00 up here I'm going to kind of like chew it up a little bit chewing up the elastic tissue and now these bronchioles can't stay open and they start collapsing the other thing is that they start having destruction of some of the elastic tissue and the SEPTA that are present between alveoli so now I'm going to chew up some of this elastic tissue here and then I'm going to start breaking down the SEPTA between alveoli and then what happens is is you end up with these gargantuous like alveoli these big big sacks of alveoli so the
• 12:00 - 12:30 other one is you're going to get alveolar SEPTA septal destruction and the combination of that leads to these like massively large Airways so you have increased alveolar septal destruction decreases in elastic tissue and what's the other last thing that you can see here fibrosis all right making this an irreversible type of disease so we have a combination of fibrosis
• 12:30 - 13:00 alveolar septal destruction and decreased elastic tissue because I'm destroying that what fibrosis does it leads to bronchial collapse so now I have bronchial collapse here as well because I'm not able to kind of like keep this Airway kind of open it's now narrowed and this is a scenario here that's again a problem getting air in and out but if I have the combination of bronchial collapse from fibrosis and decrease elastic tissue within the bronchials that's one thing and the second thing is I'm going to
• 13:00 - 13:30 have these gargantuous Airways so with the bronchial collapse this is where you'll get Airway obstruction okay that's where the airway obstruction comes into play all right so we're going to get Airway obstruction from the bronchial collapse from elastic tissue that's being destroyed within the bronchial walls and thumb from fibrosis what happens with the alveolar septal destruction is a little bit different and this is what makes emphysema a tiny bit different
• 13:30 - 14:00 here we have a normal lung tissue right with some normal elastic tissue as I start causing alveolar septal destruction destruction of elastic tissue and fibrosis these bronchioles start collapsing if they collapse now CO2 can't get out if CO2 can't get out air stays Within These alveoli and it makes them bigger so there is the concept of air trapping just the same as it was with chronic bronchitis that's why these two are very very difficult to differentiate sometimes
• 14:00 - 14:30 but here's the big difference I've destroyed the elastic tissue and then on top of that I've caused alveolar septal destruction so not only do I have air trapping but I have very large alveoli so now I have these massively enlarged Airways so air trapping and enlarged air sacs so I have these enlarged air sacs from Air trapping and alveolar septal
• 14:30 - 15:00 destruction these things get huge these lungs and this is what leads to this classic hyperinflation if I can't get air out it's going to cause these alveoli to get bigger and bigger and bigger and bigger and then that's going to lead to the lungs getting bigger and bigger and bigger and these guys have these huge like big big lungs and now if their lungs are super hyperinflated they can't take a deep breath in above what they're already at all right that's the classic presentation that you're going to see is
• 15:00 - 15:30 enlarged air sacs causing air and air trapping leading to increased hyperinflation in this patient population question comes here this was chronic inflammation guess what it's the same thing it's just a Teensy bit different neutrophils all right and scenarios two scenarios one the primary causes here is going to be the same smoking well we're going to add one more to spice it up a little bit their disease called Alpha One anti-trypsin deficiency so two of these
• 15:30 - 16:00 can cause this let me explain what I mean neutrophils and exposure to smoking will cause neutrophils will actually release a molecule called elastases so the release molecule called elastases now what's supposed to happen is when smoking is present smoking will actually lead to this process where it'll actually kind of
• 16:00 - 16:30 lead to increased inflammation so it'll help to be able to stimulate unfortunately these neutrophils and that'll increase the elastasis so that's one downside of this but the other thing is that there's an enzyme there's an enzyme here and it's called Alpha One anti-trypsin and what alpha-1 antitrypsin is supposed to do is is it supposed to degrade or inhibit these elastases so it breaks them down
• 16:30 - 17:00 what smoking in alpha-1 antitrypsin deficiency do is they decrease the presence of alpha-1 antitrypsin because smoking will lead to the degradation of this enzyme and alpha-1 antitrypsin deficiency will lead to the deficiency of this enzyme and now we have less of these to inhibit elastasis and so this pathway is lost and elastasis build up and build up and guess what they like to break down
• 17:00 - 17:30 elastic tissue and this is where they will start causing destruction of elastic tissue propagating inflammation which lead to fibrosis and they'll destroy some of the alveolar SEPTA all of these things lead to Airway obstruction hyperinflation and enlarged air sacs that's the big big thing to remember one of the things that can come up that they try to test you with is smoking is definitely going to affect more of the upper lobes of the lung whereas a patient with alpha-1
• 17:30 - 18:00 antitrypsin deficiency this will affect more of the lower lobes of the lungs so if I were to compare here let's say red is going to be smoking this will affect the upper lobes and if I were to say here in this uh uh let's use this pink color here this was alpha-1 antitrypsin deficiency this will affect more of the lower lobes of the lungs so that's the predilection here is red will be smoking
• 18:00 - 18:30 and then the pink here will represent the Alpha One anti-trypsin deficiency that's another thing that they like to kind of like throw onto the exam that I don't want you guys to miss okay my friends so at this point we have covered the pathophysiology the causes the history the physical exam findings that are suggested by patients with COPD what I really want to do is talk about what are the complications that can arise in these patients who have COPD alright guys so now COPD we have to talk about
• 18:30 - 19:00 what are the potential complications one of the big ones I'd say especially with chronic bronchitis is pneumonia this can happen generally patients who have pneumonia you definitely want to be thinking about potential causes such as chronic bronchitis the primary process behind this is that there's obstruction of the Airways and so if you can't clear bacteria out of the Airways they'll build up and if they build up with inside of the actual alveolar or the bronchi they can definitely start precipitating colonization infection destruction of
• 19:00 - 19:30 cellular debris white blood cell infiltration and then you end up with a pneumonia so again primary process of ocean pneumonia occurs is because of Airway obstruction and even obstruct the airway not only is this preventing CO2 from getting out in oxygen from getting in but it also decreases the clearance of bacteria because naturally what happens here is that you should have cilia that beat
• 19:30 - 20:00 the actual bacteria up you know what else is interesting and patients who smoke so again we know that Airway obstruction can actually decrease clearance of bacteria but the other concept here is that smoking destroys cilia so if you have cilia destruction or dysfunction because of smoking which is common in patients who have chronic bronchitis or emphysema what happens you lead to decreased clearance of bacteria if you can't clear them they stay there they colonize and if opportunities arise
• 20:00 - 20:30 they will cause infection then patients will present with things like fevers mucopril and sputum hypoxemia potential signs of respiratory distress so that's one of the big things there second one is respiratory failure patients with chronic bronchitis are very very common to decompensate this could be due to an acute exacerbation of COPD or this could just be chronic what I want you to think about with respiratory failure is there's usually a trigger so sometimes we refer to this as sometimes a let's actually put this in parentheses
• 20:30 - 21:00 here this is a cute exacerbation of COPD and this can present as respiratory failure I'd say by far one of the most common triggers is a viral upper respiratory tract infections right so if a patient develops for example a viral upper respiratory tract infection what that's going to do is is that's going to increase the inflammation within the Airways right now if I increase the inflammation within the Airways I'm going to cause more bronchospasm more
• 21:00 - 21:30 muco purulent type of production within the Airways and that's going to cause Airway obstruction if I get an increase in Airway obstruction now what happens is it makes it even more difficult to get Co2 out of the lungs so CO2 getting out of the lungs is going to be very very difficult because of the airway obstruction so CO2 will build up in the bloodstream as a result that's called hypercapnia right now the other concept here because CO2
• 21:30 - 22:00 can't be cleared is that the Airways actually get a little bit more air trapping and hyperinflation so if you have hyperinflation your lungs are super super expanded what happens it's difficult to take a deep breath in so your tidal volumes drop and if your tidal volumes drop then you have difficulty in being able to get air into the lungs and so as a result the O2 delivery to the alveoli can also reduce and if that happens
• 22:00 - 22:30 there's a reduction in O2 delivery this can also lead to less oxygen getting into the bloodstream and what's that called that's called hypoxemia so now these patients can potentially have a low oxygen oops son of a gun they can have low oxygen and elevated CO2 when this happens when you have these patients this is more likely to be the presentation of what we call a type 2 respiratory failure so this can cause a type 2
• 22:30 - 23:00 we're going to put RF respiratory failure which is classified by an elevated CO2 and a low oxygen this is super common especially in acute exacerbations of COPD is elevated CO2 because of Airway obstruction and hypoventilation causing decreased ventilation and decrease oxygenation what happens in these patients is a viral upper respiratory tract infection is usually the big trigger because it propagates an increase in inflammation and therefore an increase
• 23:00 - 23:30 in Airway obstruction and that's where all of this kind of just runs downhill is you have some particular trigger there is other triggers besides the viral upper respiratory tract infection another one because you're just not taking your medication so you're non-compliant with your Albuterol inhalers or your steroid inhalers and that could definitely worsen the airway obstruction so it also could be due to medication non-compliance but I would say by far
• 23:30 - 24:00 the more common etiology is the viral upper respiratory tract infection and this is why we actually tell people who have COPD hey make sure that you get vaccinated against influenza or other viruses because again you get an infection you would worsening Airway obstruction you could decompensate and cause these problems now if a patient has these problems or they have elevated CO2 in low oxygen one of the other big things that will actually happen here is that they will work really hard they'll work really hard to try to take
• 24:00 - 24:30 a deep breath in blow off their CO2 take in more oxygen so what will happen is the respiratory rate will start to go up their work of breathing will start to go up and they will look like they are in extremis and that could be a potential sign of an acute exacerbation of COPD Okay this may be picked up off the blood gas but this may be the signs that you see or the patient may complain of dyspnea this is extremely common in chronic bronchitis here's one big thing I want to add on this drop in the O2 is extremely more
• 24:30 - 25:00 common in chronic bronchitis than it is in emphysema patients with emphysema will generally not drop their O2 until they're in the severe severe stages of emphysema chronic bronchitis though they will that's a big thing to remember okay pneumonia respiratory failure due to an acute exacerbation of their COPD from these particular etiologists what else can happen all right because these patients develop irreparable damage to their lungs they develop so much fibrosis and
• 25:00 - 25:30 inflammation and all of these processes what's the recurring theme that they can develop hypoxemia all right this hypoxemia due to this lung disease leads to what so because of their COPD they have hypoxemia hypoxemia is a potent pulmonary vasoconstrictor so what it'll do is it'll actually cause pulmonary vasoconstriction look at these blood flow is supposed to be going on here and then just like wow clamp down
• 25:30 - 26:00 what does that do to the pulmonary vascular resistance it's going to go up so now because these things are clamped down because of the hypoxemia your pulmonary vascular resistance will go up so your afterload will go up that's another way of saying it the resistance to blood flow will go up what happens to the right heart pressure it'll have to rise more and over time what that'll do is that will cause the pulmonary artery pressure will become so high that the right heart has to work really really hard what's it called whenever the pulmonary artery pressure is really high pulmonary
• 26:00 - 26:30 hypertension so these patients can over time because of this High Resistance lead to what's called type three pulmonary artery hypertension and over time the right heart will have to hypertrophy it'll try its best to start thickening and because of that eventually it'll fail so these patients over time because of this pulmonary artery hypertension will develop features of what's called right heart failure how's that classified
• 26:30 - 27:00 elevated central venous pressure right so they have a hard time getting blood in to the right heart and getting blood out of the right heart so this is impaired difficulty getting in difficulty getting out so because of that what happens to their central venous pressure it arises and if you develop increased central venous pressures what does that look like jugular venous extension this can cause hepatic congestion or we call hepatomegaly this can cause elevated pulmonary artery
• 27:00 - 27:30 sorry a portal venous pressures which we call ascites whenever it causes portal hypertension hypertension and it can also cause swelling of the lower extremities which we call pedal edema these are classic findings of right heart failure and again I want you to understand something my friends if you see hypoxemia as the big factor here what did I tell you what was the primary COPD ETI type or subtype that caused hypoxemia chronic bronchitis you
• 27:30 - 28:00 will not see right heart failure as commonly in patients who have emphysema okay so that's very very specific there we come to the last scenario here polycythemia again because patients develop these terribly low oxygen levels in chronic bronchitis they drop their oxygen levels and you know what happens whenever you drop your oxygen levels because of this underlying lung disease you tell your kidney hey Oxygen's low what your kidney thinks is is that oh
• 28:00 - 28:30 there's maybe less number of red blood cells so what I'll do is I'll tell the body to make more erythropoietin and if I tell them to make more erythropoietin that'll say hey bone marrow increase the production of red blood cells and so that's what it'll do it'll tell hey hey bone marrow we got to get more oxygen so we probably need more red blood cells go ahead and pump me out some more and it increases the number of red blood cells and whenever you increase the number of red blood cells within the bloodstream this is classic of a patient who has polycythemia so look for an elevated
• 28:30 - 29:00 hemoglobin an elevated hematocrit and more red blood cells and if they have an underlying history of chronic bronchitis it could be due to that okay so now that we've covered chronic bronchitis with the primary findings that we've discussed what about the complications that can arise in emphysema with emphysema again you can see pneumonia I would say it's not as common as you can see in chronic bronchitis but you can't see it and again it's a two-factor process
• 29:00 - 29:30 you're having difficulty with clearing bacteria and it's twofold one is because of ciliary dysfunction what's causing the ciliary dysfunction it is smoking smoking destroys cilia and the other one is Airway obstruction if your Airway is obstructed not only having difficulty in moving air but you're going to have difficulty in clearing some bacteria through that Airway and so both of these
• 29:30 - 30:00 will lead to a decreased clearance of bacteria they'll colonize the Airways and then over time if they're given the opportunity they will cause inflammation infection and precipitate pneumonia so this is something to think about and then again patients may present with signs of worsening mucopril and sputum worsening cough worsening dyspnea maybe fevers leukocytosis other constitutional symptoms that would be concerning that now they have pneumonia secondary to their COPD all right respiratory failure it's the same concept as we talked about up here
• 30:00 - 30:30 in emphysema this could be due to again an acute exacerbation of COPD and it's the same concept a patient has some trigger that puts them to get worse something that increases Airway obstruction it's a viral upper respiratory tract infection or we're going to put med non-compliant so they're not taking things that are supposed to prevent inflammation and bronchospasm or they're getting infected by something that's going to cause
• 30:30 - 31:00 worsening bronchospasm and if you cause worsening bronchospasm you're going to cause increased mucus maybe more inflammation bronchospasm a lot of that process and this will worsen the airway obstruction now the airway obstruction that these patients develop is not as severe as compared to the patient with chronic bronchitis they have lots of mucus and they have lots of like bronchospasm
• 31:00 - 31:30 that's occurring and here they'll get some bronchospasm they'll definitely get a little bit of mucus but not a lot so with that being said they're not going to have that crazy problem with massive massive Airway obstructions but nonetheless it does occur and so same thing exists CO2 is really hard to get out and if I can't get Co2 out it'll build up within the bloodstream okay and that's because again why their airways are super super hyperinflated because of the airway obstruction that
• 31:30 - 32:00 they can't take a deep breath in so they can't generate a good tidal volume so they hypoventilate and if that's the case they can't actually get the CO2 out so it builds up what's that called again hypercapnia now here's the thing that you would think you would think that the because of that they would also have difficulty being able to properly ventilate they don't have that problem as much so they're problem rarely ever exists as hypoxemia it's primarily hypercapnia so these patients usually
• 32:00 - 32:30 will exhibit a respiratory failure but it'll usually be a classically a type 2 respiratory failure and this one will be classified by a elevated CO2 and a relatively normal oxygen so their oxygen sometimes will be very normal and their CO2 can be elevated all right that is the classic findings that we will see in these patients but again because their problem is they can't take these deep breaths in they'll work really really hard because
• 32:30 - 33:00 they're going to have to keep trying to generate a good title volume and so because of that they will show signs of respiratory distress sometimes and they'll increase their respiratory rate and they'll increase their work of breathing and this is unfortunately a finding that we can see in these patients with COPD now again you'll pick this up off the blood gas that you'll see findings of respiratory acidosis findings of respiratory acidosis you'll see findings of increased respiratory rate tachypnea
• 33:00 - 33:30 increased worker breathing sensation of dyspnea but the big findings that are really different here between chronic bronchitis and emphysema is the oxygen is usually relatively normal it usually doesn't start dropping until you get to the severe severe cases of emphysema okay that's that concept now we come to the last one that really is a big feature that separates emphysema from COPD and that is the presence of these emphysemidis boole right so you can get these boulay that form so this is a boulee
• 33:30 - 34:00 and this one right here is a boole now what happens is is this is because of hyperinflation whenever the lungs and patients who have COPD get hyperinflated they get like these like big bulbous portions of lung tissue these are those those big alveolar sacs you know how you destroy alveolar SEPTA and elastic tissue and so you cause these Airways to get big and massive this is classic of it so they get all these bulay and the problem with these dang things is that they can
• 34:00 - 34:30 rupture and decompress right into the pleural cavity and if they decompress into the pleural cavity boom you got air that decides to present itself into the pleural cavity and there you go a pneumothorax but the big thing to understand here is what kind of pneumothorax this patient will have is it a primary spontaneous a secondary spontaneous or traumatic it's a secondary spontaneous pneumothorax so look out for a secondary spontaneous pneumothorax that's one of the potential complications and this can happen in
• 34:30 - 35:00 certain patients who have emphysema they have an underlying lung injury or disease process that leads to their pneumothorax that's the concept so if you have a patient who has an underlying history of COPD particularly maybe the emphysemidis predominant type and you go and you listen and you hear decrease your absent breath sounds on one side you see potential signs of tracheal deviation to other things think about a potential pneumothorax all right my friends that covers the complications of COPD particularly covering chronic bronchitis emphysema now how do we go about
• 35:00 - 35:30 diagnosing these puppies well how do we go about diagnosing a patient with COPD well if they come in they're a little bit older they're a smoker they're coming in with dyspnea productive cough wheezing rhonchi on auscultation decreased breast sounds increase AP diameter or barrel chest kind of appearance and they're presenting with respiratory failure or features of right heart failure and pneumonia things to that effect I think it's really important to start thinking about COPD so how do we do this and any patient who comes in with dyspnea I think it's always
• 35:30 - 36:00 important to get a chest x-ray ECG and ABG the chest x-ray may show some potential signs that are suggestive of pneumonia look at this huge AP diameter so anterior to posterior diameter is massive the apple is called an increase AP diameter and a barrel chest they also are super hyperinflated you can almost see all their ribs that's really a big sign here their diaphragm is relatively flat relatively flat and there's really increased loosens here darkness in the
• 36:00 - 36:30 actual lungs that are a little bit more evident and suggestive of again a patient having something of a COPD like picture ACG could show right Axis deviation this is just telling me that we have a lot of right heart strain from pulmonary vasoconstriction and again right ventricular hypertrophy again from a lot of pulmonary vasoconstriction and core pulmonale developing and ABG is somewhat helpful because again these patients trap air they trap air and they trap CO2 which can cause respiratory acidosis to develop so
• 36:30 - 37:00 that's one thing to also look for in a patient who has a COPD kind of disease this may be chronic for them or it could be much much higher if they're having a COPD exacerbation with that being said if I find these things and I really want to diagnose COPD the best test is pfts so pulmonary function tests I want to look at my fev1 FEC ratio again suggesting obstructive I have to have a really low fev and a low FEC so the ratio is less than 70 percent the next thing is that would be more suggestive of COPD but how do I rule out asthma well I check the fev1 and again
• 37:00 - 37:30 this helps me to determine the degree of severity of their COPD but I use this as a tool after I give them a bronchodilator if I give them a bronchodilator and I recheck their fev1 and it's less than 12 percent increase that's more suggestive of COPD than it is asthma now if I really want to confirm that this patient has COPD I can add on some plasmography or lung volumes because total lung capacity functional residual capacity and residual volume should all be elevated and patients who have COPD because it suggests a lot of
• 37:30 - 38:00 air trapping and if I looked at their flow volume Loops it would show that it shifted to the left now the last thing is I really wanted to go the extra distance and say which predominant COPD do I have if it's a low dlco it's because the surface area is reduced that's emphysema if the DLC is normal though then that would be more suggestive of chronic bronchitis now real quick talk about emphysema emphysema that is usually due to smoking affects more of the upper lobes of the
• 38:00 - 38:30 lungs and we call this Century lobular emphysema again more associated with smoking but if I have a patient who has pan lobular or the lower lobe emphysema on boole that's a little bit more likely associated with alpha-1 antitrypsin deficiency now if that is the case I'd also want to remember that patients who have alpha-1 antitrypsin deficiency also have underlying liver disease and so I would also expect their asts and alts that would be elevated so that's one big thing and I would also see this in a younger patient someone
• 38:30 - 39:00 who's not of that greater than 60 65 year age range so I really think it's important to screen for Alpha One and third trips in efficiency if they're young have liver disease and have pan lobular emphysema and again going back if they have a normal dlco they have no change in their surface area no change in the thickness of the respiratory membrane so that's more suggestive of chronic bronchitis okay that's how we would diagnostically approach COPD all right guys let's move into the treatment of COPD so whenever we treat a patient with COPD It's always important to Institute things that will reduce mortality and there's a lot of
• 39:00 - 39:30 things that can do that and I think one of the biggest things is smoking cessation you're not going to stop the disease but you're at least going to kind of prevent the progressive fibrosis and mucous accumulation of bronchospasm and all that chronic inflammation so that's a really really important one Institute the second one is you should always make sure that these patients are up to date with their flu and pneumococcal vaccination the reason why if you go back to that pathophysiology that we talked about they could have that stable emphysema or stable chronic bronchitis but if you introduce an infection like a pneumonia or you introduce like a viral infection
• 39:30 - 40:00 like influenza or streptococcus pneumonia then you increase the risk of them developing an acute exacerbation of their COPD which can cause them to again increase the risk of death on top of that you can also increase the risk of pneumonia which also increases their risk of death so these are important things to Institute the other thing is oxygen therapy this may reduce the risk of development of right heart failure or at least the progression of right heart failure so whenever you give a patient auction you're doing it because again oxygen whenever it's really really low it causes pulmonary vasoconstriction elevator right heart pressures and then
• 40:00 - 40:30 eventually the right heart can fail if they start developing signs of core pulmonality they need to be on oxygen because it's again a very very big risk factor for them is that chronic hypoxemia when you give them oxygen though you don't want to aim to go too high you only want to aim for like 88 to 92 percent because as you go greater than 92 percent there's two theories one is that it may suppress the respiratory drug you'll lose the support the the respiratory drive because whenever a patient has like a pao2 that's less than 60 it's the primary driving stimulus for the patient to breathe at least a little bit faster and
• 40:30 - 41:00 deeper but if you take that away you may lose that intense Drive the other thought is that if you increase their oxygen it may kind of alter the pulmonary vasculature and potentially lead to worsening VQ mismatch so those are the concepts that you guys have to understand so I think you always want to ask yourself if the patient needs oxygen what are the reasons why one is the SP2 is chronically less than 88 they have features of core pulmonale which is the right heart failure or they have polycythemia plus an spo2 of less than
• 41:00 - 41:30 90 so I'll increase the threshold to start oxygen if they have polycythemia so these are the things that you want to think about here after I tell them to stop smoking make sure they get vaccinated consider when they need oxygen then I'm going to say do they need bronchodilator therapy or inhal corticosteroid therapy so then I ask myself the question have they had two plus exacerbations in their experience if the answer is no okay well then I'm going to move to the next step how symptomatic are you if your mmrc which is a scale that determines how symptomatic you get is it
• 41:30 - 42:00 you know whenever you're really walking upstairs is whenever you're kind of like walking flat is it when you're getting dressed or doing some of your daily activities or if it's at rest we can get that score off of the mmrc if it's not greater than or equal to 2 then I would say that you're kind of in that low group so you're in what's called a gold group a and really this is mild we can actually kind of do like a Sam or a Sab a bronchodilator therapies so a sap is like Albuterol and you do that when you kind of feel short of breath or Sama which is like hypertroprium and we can do that also when they're short of breath so it's one
• 42:00 - 42:30 of the other however if their symptomatology is a little bit worse and we can actually kind of give them a scale of greater than or equal to two then we might need to up their actual bronchodilator therapy so we'll do either again a salmon or a Saba right but we'll add on a lab so we'll add on something like salmeterol or fomotorol now if they're two plus exacerbations is yes then one what's called gold Group C so then we have to ask two questions is there eosinophil count greater than or equal to 300 and have they been hospitalized for their COPD if the answer to that is no
• 42:30 - 43:00 it's still pretty bad COPD all right and so we definitely need to treat them with a Sam or Saba again which either one but now what we're going to do is we're going to escalate the long-acting bronchodilator so we're going to continue with the lava but we're going to add audit we're going to add on a lamba so a lamma is going to be something like thaiotropium so they could be on let's say for example if they're in this point I put them on Albuterol plus their diatropium plus there's a salmeterol and they would be on that they would use the sabba whenever they're distic and they would
• 43:00 - 43:30 continue daily Lama lab of therapy if their eosinophils are greater than or equal to 300 or they have been hospitalized for COPD this is really bad because this patient is really going to be in need of inhaled corticosteroids the more exacerbations they have the more there is the need for inhaled corticosteroids to reduce the inflammation and so I would continue the samura the Saba but I would add on and inhaled corticosteroids so they would be on a Saba for example albuterol when they're disc
• 43:30 - 44:00 and then daily Lama diatropium daily salmeterol and daily inhale corticosteroid and this would be example like budesonide or fluticasone that is the last thing that we would do for the bronchodilators but if the patient is still symptomatic still refractory you could consider in this last stage here adding on something like a pde4 inhibitor this is more of an experimental drug and this would be things like refillu Mass if that's failed and you're at the last Point here you can consider things like lung reduction surgery as well
• 44:00 - 44:30 now the last component that I want to talk about here in a patient who has COPD is the treatment of an acute exacerbation of their cop when a patient has a tree or an acute exacerbation of their COPD you really want to try to treat these patients with massive bronchodilation and so generally this is going to be the combination of a sama and a Saba so we call this a duaneb it's ipertroprium which is the Sama and albuterol which is the Saba the next thing I want to do is really reduce Airway inflammation this Probably
• 44:30 - 45:00 sounds a lot like asthma doesn't it it's pretty similar the only thing that was different than asthma is that we had IV magnesium and then again you had a samosaba for execute exacerbation of COPD say I'm a Saba no IV magnesium but guess what you're going to do to reduce Airway inflammation corticosteroids so you're going to give systemic steroids like Po or IV steroids the next thing is to reduce the work of breathing what did we do for asthma it was BiPAP what am I going to do here bypass BiPAP is really interesting because against the same concept as we talked about with asthma is that there's air trapping which leads to
• 45:00 - 45:30 hyperinflation hypoventilation and you build up your CO2 and you develop hypoxemia what if I throw a BiPAP in here what does it do it since the Airways open allows for me to deflate my lungs allows me to reduce my work of breathing and again clear the CO2 improve my oxygenation and reduce air trapping that's a really cool concept so the last thing that I would actually think is important to for remembering for the treatment of acute exacerbation of COPD is that these patients again they kind of have a lot of bacterial colonization in patients who have bronchial collapse or lots of mucus they
• 45:30 - 46:00 lead to a lot of bacteria that can't be cleared and so they can colonize and they can build up to levels where they can actually cause destruction of the tissue inflammation and so you really want to reduce bacterial colonization and oftentimes one of the things that we throw on for these patients is Azithromycin or doxycycline so again bronchodilate them reduce inflammation BiPAP to reduce the work of breathing and antibiotics like azithromycin or doxycycline that's how we would treat an acute exacerbation of COPD all right my friends that's COPD I hope it made sense I hope that you guys enjoyed it and as always until next time
• 46:00 - 46:30 [Music] thank you [Music]