Pathophysiology of COPD

Alright engineers, in this video we're going to talk about COPD or chronic obstructive pulmonary disorder, so let's go ahead and start, so let's go ahead and start with COPD, so there are two conditions with COPD, chronic bronchitis and emphysema. The two big ones that we're going to talk about here, sometimes people will consider chronic asthma to be part of COPD, but again we'll keep it separate, so the main ones that we normally classically associate with are chronic. bronchitis and this will classically be seen with, you know, that mucus production, that productive cough, which is one of the hallmark signs of chronic bronchitis, we can usually diagnose it based on the clinical diagnosis, how much sputum they are producing, how often.

For a long time, that kind of thing and the other condition we're going to talk about is emphysema, emphysema is usually described as structural changes and we'll talk about why, okay, now what are the causes of COPD, so let's go. to review. In the

pathophysiology

we are not going to go into a lot of detail, but we are going to try to address the most important thing, you know, what are the main risk factors associated with COPD. Well, the one I want you to know. Remember it's the biggest one, the most important one because 90 to 95 percent of COPD cases is smoking, so let's draw a little sign here, look at that nice little sign, little uh, pleated there, then here, this guy is burning it right now at the end. and then here we're going to have some smoke coming out of this, again, don't smoke, let's not promote that, okay, smoking, it's the number one cause, the number one cause of COPD, we'll talk about how, what is this? real? reaction that causes COPD, but again this is the most common, don't forget another one that is less common but still important to mention will be environmental exposure, so what do I mean by certain things where you are exposed to a a lot of dust, you know, maybe silica and another one are even just air pollutants, okay, so air pollutants from the exhaust gases of different types of things within the atmosphere, another big one will actually be a condition genetics and this is called alpha one antitrypsin.

Deficiency We're going to put a down arrow here, so alpha 1 antitrypsin deficiency is now the least common type, but it can happen, it's an autosomal dominant disorder. One of the things with this one is that there are usually those who have a family history of COPD, some unknown underlying reason why there is liver disease, and they usually have to be under 45 to 50 years old for deficiency to be taken into consideration. of alpha-1 antitrypsin, but again it is the most common. smoking now, how does all this influence? What are these risk factors like? These things we believe are the cause that lead to chronic bronchitis, emphysema.

Another point I want to make sure you realize here is that COPD is not always clear cut. It's not always the feeling that you just have chronic bronchitis or just emphysema. One of the important things we need to understand is that these things often coexist. It is an important point to remember. Now let's first review chronic bronchitis. the

pathophysiology

we'll talk about some of the things that can develop from that and then we'll go over emphysema, first things first, chronic bronchitis. I want you to think that mucus buildup is okay, so we have these mucous glands, they're actually located if guys, remember a little bit about your anatomy, we have a mucosal lining which is your epithelial tissue, maybe a lamina propria and then, Outside of that, you have a submucosa which is a kind of loose connective tissue and you will have these submucosal glands.

They are producing mucus naturally. Okay, they naturally produce mucus to humidify the airways, trap certain types of pathogens, and help keep the airways moist and humidified, but in situations with chronic bronchitis the problem is mucus production. increases significantly and is the result of exposure to smoking dust, generally these irritants, and what happens is that this mucus plugging causes narrowing of the airways. We have to remember that there will be hypertrophy and hyperplasia of these mucinous glands and it is because the respiratory tract comes into contact with all these irritants, the smoke, the dust, the silica, the pollutants and it is causing this agitation of the mucosa and the way that our actual body goes about stimulating these mucous glands to produce more mucus to cover that area, so one of the classic things that we're going to look at here is hypertrophy and hypertrophy is just an increase in the size of the glands. mucinous glands that are going to grow, the second thing is that they are going to produce more, that is called hyperplasia and these are the classic signs of these mucous glands, it is okay now because we also have other cells that are important for the production of mucus there.

There are a couple of them scattered throughout the airways, we have these special cells and they are called goblet cells. The goblet cells are also responsible for producing that mucus and it's more of that, again, that alkaline mucus that helps to be able to line the airways helps to humidify the air humidifying the air helps to be able to filter out any pathogens, that's important, so that because of these different risk factors there will be hypertrophy, hyperplasia of the mucous glands and goblet cells, so again we go Having mucous glands and goblet cells is okay, that's important, so there will be a lot of mucus production.

Unfortunately, the next thing that happens is smoking, especially there's so much irritation in this area that it can actually cause destruction of the cilia, so there can be ciliary shortening and they're also going to have less motility, so what's going to happen now It's going to be that you're going to have so much mucus accumulating in your airways and this mucus is going to be very, very difficult to get to. Because of that, you're going to have what's called ciliary dysfunction, so there's going to be some ciliary dysfunction and again the ciliary dysfunction is because the cilia are getting shorter, they're becoming less motile and they can't overcome that. mucus accumulates because that is one of the functions of the cilia, they help eliminate mucus, we can spit it out or swallow it well, but because there is so much mucus and the cilia do not work properly, what is going to happen that the mucus just flows away? stay still? there in the airways and it clogs the airways and causes obstruction to the airways, narrowing of the airways, that's the problem with this one now imagine, take a second and imagine that here I clog these airways, right here, here it goes to be a mucus plug so here's a mucus plug here let's say here's a mucus plug here what's going to happen think about this both ways here our airways are responsible for bringing oxygen to the actual alveoli so O2 is supposed to be able to reach the alveoli, but because very little oxygen is going to come down from this mucous plug, a large amount will not, it may have to be diverted to other areas where there are more patent airways, so one of the important things is here is that not a lot of oxygen is going to come in, on the contrary, we want to exhale CO2, so what will happen now is that the CO2 that we are trying to exhale will get stuck or trapped, so one of the most important things What you'll notice with chronic bronchitis is that we can't get as much air in terms of oxygen and we can't get as much air out, but more specifically getting air out, that's the most important thing.

So one of the biggest things that you'll see in patients who have this chronic bronchitis is that they have what's called air trapping, and this air trapping is basically again, think about it as you try to exhale as you try. to exhale, your actual bronchi get a little bit smaller when you exhale, you have elastin to keep them open, but overall they get a little bit smaller, so if you already have this mucous plug that narrows your airways and then you're exhaling and that Real airway becomes even smaller, will you be able to get that air out?

No, a lot of that air starts to settle in these airways and a lot of it builds up, especially CO2, so very little oxygen goes in and you get very little CO2 out and this causes that classic air trapping to now go away because to that air trapping effect. Think again. You have little oxygen getting in because of that mucous plug. Here we will remove that mucus plug again. Here's this mucus plug, okay? This mucociliary dysfunction increases hyperplasia, hypertrophy of mucinous glands, goblet cells and cilia dysfunction causes the accumulation of mucus causing air to become trapped, in addition to less oxygen reaching the airways due to this plug. mucociliary, but the most important thing is that you will accumulate more CO2 because again remember the CO2 exchanges here, but because of this mucus plug that occludes the airways, especially during expiration, because as we exhale the airways become a a little smaller, this will cause a lot of CO2 to accumulate.

Now, these are two things: CO2 will start to build up in the blood, okay, and less oxygen will reach the airways and be perfused into the tissue. This is a VQ imbalance, this can cause hypoxemia and another one that is really bad here, hypercapnia and hypoxemia is the low partial pressure of oxygen and hypercapnia is the high partial pressure of CO2, so this is one of the great common findings that we will see in patients with chronic bronchitis. Well, again, hypertrophy, hyperplasia of the goblet cells of the mucous glands because of these irritants they produce more mucus to compensate for the irritation.

Mucus starts to clog the airways, on top of that especially due to smoking and again those air pollutants also the cilia are shortening and becoming shorter. it will become less efficient and be able to overcome mucus, so now you have increased mucus and can't even get the mucus out that builds up and causes mucus plugs. These mucous plugs cause less air to come in, but specifically more of The real problem will be that less air comes out, especially CO2, so you will have a buildup of CO2 in particular and this is called hypercapnia, but you will also not be able to get as much oxygen into the lungs because to that actual obstruction and that's going to cause hypoxemia, another thing that we have to think about with chronic bronchitis and I want you to think naturally if you remember in our pneumonia video we talked about how chronic bronchitis or COPD puts people in risk. of developing infections, lung infections, especially due to mucus obstruction.

If you remember, there are two bacteria that are commonly seen in COPD patients that can actually cause this increased risk of demonia, so there will be an increased risk of pneumonia and again this. It was due to two types of bacteria, one is called hemophilus influenza, let's give it the flu, and the other is called merexella cataralus. Well, these are the ones that are going to increase the risk of that pneumonia and again when we talk about this. In general, this could be pneumonia. from strep or it could be low bar pneumonia so here there would be a um this right here could be low bar pneumonia where there's actually what's called a consolidation forming and then this one here on the left side could be be a bronchopneumonia where there is actually a diffuse spread, particularly in the bases of the lungs, so there will be an increased risk of pneumonia, okay, because that mucus is building up and because that mucus is building up, it will lead to that flu and that Marxian catarrhalis. basically feeding in that area, which can then lead to infection, so these are the important things that I want you to look at, especially with chronic bronchitis.

Well, again to summarize, hypertrophy, hyperplasia of the mucous glands and goblet cells that cause mucus buildup. Ciliary dysfunction because smoking and pollutants destroy cilia and cause a decrease in the number of cilia, as well as shortening of cilia and reduced motility leading to mucus buildup. This accumulation of mucus can form plugs. Plugs can cause air to be trapped. Okay, which is a classic sign again because of the mucous plugs, less oxygen can get in, causing hypoxemia. Less CO2 is expelled, which causes hypercapnia and another complication that can develop due to chronic bronchitis is that the risk of developing pneumonia increases, especially with chronic bronchitis due to the buildup of mucus and particularly influenza H and morexotic caloralis are the etiological bacteria responsible for that.

Well, that's chronic bronchitis. We're going to talk about another complication that is extremely common and is a bad diagnostic sign in patients who have chronic bronchitis and we'll get to that when we get to this part. Well, let's go to emphysema for a second and then again we'll talk about the complications that can develop from these two, the biggest one with emphysema again.which should be the lower part of the lungs and then the distal astiner has effects near the actual alveolar, they also call it periceptal emphysema and again it affects the distal alveoli and that goes they are usually close to the pleura and again, these can actually form small blisters that can rupture in the actual pleural space and that air in the pleural space is called a pneumothorax, we call it spontaneous pneumothorax, but it's secondary because they have an underlying lung disease, okay.

Well, those are the important things that I wanted to make sure we mentioned here with emphysema. Now remember I told you that there was a big complication that can develop with emphysema and chronic bronchitis and it was related to this hypoxemia in this hypercapnia and again, I can't emphasize enough: hypoxemia and hypercapnia are much more common in the chronic bronchitis, emphysema can occur, but it is usually in the later stages, how does this work? If you remember a little bit about your physiology, what happens is that over time you have this hypoxemia, if you remember a little diagram here of a little diagram.

Let's say here we have an alveolus and then here we have a blood vessel. If you remember we said that as long as there is low ventilation, low ventilation, low v, based on that vq ratio which is equal to 0.8, that's fine, and again, this is what we learned. In physiology, well, we say that vq is equal to 0.8 if you decrease ventilation to the alveoli, what do you need to do with the denominator to make it at least equal to 0.8? Well, if you decrease the top number, you will get the small one, the total number is smaller, so we have to make the profusion smaller as well, so as a result, we have to decrease the perfusion so that we can bring the general number back to 0.8, so as long as you have low ventilation at a specific level. point of the airways is going to decrease perfusion and you can remember because they called that hypoxemic vasoconstriction, it is a normal self-regulatory mechanism of the lungs, so with hypoxemia it is going to result, I'm sorry, with this situation of low ventilation, it will to lead to hypoxemic vasoconstriction now, that's fine if it's just a small part of the airway, but imagine if this is affecting multiple parts of the actual lung, so imagine that there are actually several of these types, multiple alveoli within the lungs that are eventually having so much vasoconstriction.

These pulmonary vessels are going to develop a really very high pressure, so that's why imagine it like this, imagine this type of diagram, imagine here that there is an artery and this artery branches into multiple different small terminal arteries and these guys go to the alveoli. I will draw some small alveoli here some small alveoli here some small alveoli there imagine that this one had little ventilation, what do you do? You contract it right now, so now this area here as a result will contract if there was poor ventilation. Send it to the other. areas, but what if these alveoli also have poor ventilation?

So I'm going to restrict that one as well. What happens if these alveoli also have poor ventilation? I'm going to restrict that where this blood is going to go. back and it will increase, what that will do to the pressure in this area, it will increase it and cause what is called pulmonary hypertension because there is so much generalized vasoconstriction that it causes the blood pressure to increase so much in the pulmonary arteries, so this vasoconstriction Hypoxic over time can lead to pulmonary hypertension and now think about it this way, if the pressure in the pulmonary arteries is high, then the ventricle, the right ventricle, will have to increase its workload. pump and pump and pump against high pressure so they can push the same card.

Sorry, the same stroke volume because of that will put so much workload on the right side of the heart that it can eventually lead to what is called right ventricular hypertrophy, but unfortunately over time it fails and this is what we call pulmonary nucleus, it is a complication that can develop due to chronic obstructive pulmonary diseases and how can you tell if someone has right ventricular failure or right-sided heart failure? the fluid returns to the superior and inferior vena cava, so what will they have an increase in jugular venous pressure? They'll have apatomegaly, splenomegaly, maybe they'll have peripheral edema.

All of these things will be common signs that someone has a right ventricular heart. fails, again, that's something we want to take into consideration as a very serious complication of chronic obstructive pulmonary disorders. again you'll see this more specifically with chronic bronchitis or the later stages of emphysema, okay and again ruling out right ventricular heart failure, obviously, you have to know that it checks your bmp levels, it's called brain natretic peptide, it's produced by the ventricles, you can do an ultrasound to see if there is a decreased ejection fraction and if you really want you can check for what is called a swan gonz catheter, that's right. ventricular catheterization and the pulmonary capillary wedge pressure is checked and checked to see if it is greater than 18 millimeters of mercury.

Those are generally ways we can see if a person has right-sided heart failure. Okay, but again, the gold standard would be the Swansen catheter, that's what we would need to know about all of this for our chronic bronchitis and the pathophysiology of emphysema.