 Hello and welcome to Nursing School Explained. Today's topic is COPD or Chronic Obstructive Pulmonary Disease. As always, let's look at the pathophysiology first. When chronic obstructive pulmonary disease, we always have to distinguish between two different pathophysiological mechanisms that are going on here. One of them is emphysema and the other one chronic bronchitis. So let's look at emphysema first. So emphysema is caused by inhaled pollutants and most commonly that is smoke or any kind of other environmental pollutants such as smoke living close to factories, a lot of agriculture, those kind of things. And these inhaled pollutants over time destroyed the elastin that the alveoli are made of. Therefore, when the elastin is destroyed, the alveoli lose their recoil ability after exhalation. So basically what that means, I've drawn it out here. So you have the airway and on the alveoli at the end and typically the air comes in, the O2 comes in, gas exchange happens at the alveoli and then CO2 is exchanged. Well, when the alveoli here lose their elasticity, that elastic recoil, they're kind of a little bit more distended to begin with. And because they can't really kind of contract as they're trying to get rid of the CO2, they're not able to exhale or eliminate the CO2. And that means that the CO2 gets trapped here in the alveoli. And that's right here, the small airways then collapse and leading to alveolar distention and that air trapping that I just explained over here. Which means that the CO2 can't exit and the O2 can't enter and therefore the patient will become hypoxemic. So less oxygen concentration in the blood. In comparison, chronic bronchitis is also a chronic obstructive pulmonary disorder, but it works a little bit differently. The causative organism or mechanism, again, is chronic exposure to smoke or the environment. But in chronic bronchitis, the bronchi and bronchials get inflamed. Now this inflammation, as we know typically anywhere, especially in the lungs, causes increase in mucous production. And therefore the airway walls thicken causing an airway obstruction. So now we're having the problem where the air also can't escape because of the mucous and the thickened airway walls. And a chronic bronchitis diagnosis is usually made if there's a daily productive cough for three months for two consecutive years. So that's a long time exposure to any of these pollutants or smoke that cause all these things going on over time. And keep in mind, both of these are chronic diseases. So nothing happens really quickly here. This is a chronic exposure and these changes happen very slowly over time. Now this would be in comparison, let's say, to acute bronchitis, which like an upper respiratory infection can lead to acute bronchitis, but today we'll stick with these chronic respiratory disorders. Now if we come back to emphysema, signs and symptoms because the CO2 can't exit and the O2 can't enter, the patient will have shortness of breath and they'll have increased work of breathing, as well as they might have accessory muscle use. A lot of patients because of this physiological mechanism that's going on here, it will be easier for them to breathe in the tripod position. And what that means is that they will usually lean forward if they're sitting in a chair. Sometimes they'll put their hands on their knees and they'll be a tripod. So their arms will be two parts of the tripod and then their head will be the second. So basically leaning forward allows them for more expansion and to easier excrete that CO2. A lot of times patients with emphysema, they will be thin and they will have what's called a barrel chest and then increase an AP diameter and that means anterior posterior diameter. Usually our torso is shaped where the diameter from anterior posterior here is would be a one and then the lateral diameter would be a two. So our torso would be shaped, if I look at it from the top, would be shaped like this. So this is a one and then this dimension here would be a two. So it's a two to one diameter. But in somebody with a barrel chest because this happens over time, these aviola, every single aviola this patient has gets distended. So that takes up space. So over time the chest, the shape of the chest reconfigures and instead of this two to one, we now have a one to one ratio. So the diameter, anterior posterior and lateral is the same. This is not the best drawing here, but their chest diameter will increase and now be the same as kind of like the shoulder to shoulder measurement. So they will have that barrel chest as the description. A lot of times they'll have a reddish complexion and they also are called pink puffers. And the reddish complexion happens because now we are hypoxemic and the body's compensatory response is to produce more red blood cells because now we need more oxygen carriers to be able to perfuse the tissues that need the oxygen very direly. And so the patients will have increase in red blood cells and they'll therefore look a little bit pinkish. And the pink puffer is because a lot of times they'll do personally breathing and we'll talk about that later in nursing considerations, which helps them with that recoil of the aviola to kind of exhale that CO2. It helps with that. And on physical assessment findings, patients with MPCM a lot of times will have diminished breast sounds because there's just no air movement, no air movement happening at the aviola. And they will have a hyper resonant chest on percussion. So if you put your finger and you percuss their chest because there's so much more air in there because of this air trapping, their chest wall will be hyper resonant when a normal finding would be just resonant. Okay, now moving on to signs and symptoms of chronic bronchitis in contrast to patients with emphysema, these patients might be obese. Again, they have hypoxemia. They might be cyanotic. So these pink poppers over here are more reddish in complexion where the chronic bronchitis patients are also called the blue bloaters because they'll appear cyanotic. They'll have excessive mucus production. And that is because of all this destruction that's happening and the inflammation that they have going on chronically. So they have excessive mucus production. And a lot of times you can hear that in their cough, the kind of a wet sounding cough. And with that goes bronchi or wheezing. Remember whenever you have mucus moving around in the airways, it can be heard as lung sounds as bronchi. They might have some wheezing because this inflammation kind of like in asthma patients. They will also have an increase in their hemoglobin level and chronic bronchitis because all of this obstruction going on. So now we have something that's obstructing the blood flow to the lungs because we're just not really perfusing well and the oxygen exchange can't happen. So that can lead to right-sided heart failure. And whenever right-sided heart failure occurs because of a pathology that's originating in the lungs, it's also called core pulmonar. So because of a pulmonary mechanism that's causing it. And with that, think of right-sided heart failure, patients will have peripheral edema as well. Now risk factors for COPD, either one of those two are smoking and environmental exposure for both chronic bronchitis and emphysema. And then for emphysema here in pink, it color codes, it matches. There is something called an alpha one antitrypsin deficiency. That's a pretty rare disorder. And the patients don't produce this alpha one antitrypsin and then they will lose that elastic recall just like in patients with emphysema. Now diagnosis is usually made based on symptoms, but of course we might also want to visualize their chest with a chest x-ray or CT of the chest. And pulmonary function test, I put a star here. That's the golden standard for diagnosing these respiratory disorders. Of course, if the patient is in distress or has an exacerbation, we might want to look at an ABG, see how they are doing. A sputum culture, if they have an acute infection and we want to see if there's maybe a bacterial or viral infection going on. And then at alpha one antitrypsin test, if we are suspicious, that they have emphysema because of this deficiency. Complications. So remember, these are very chronic, these conditions happen over years and years of chronic exposure. So these patients are at higher risk for respiratory infections because their normal protective mechanisms of the lungs, the cilia that propel the any kind of inhaled irritants out or all this mucus production puts them at higher risk for respiratory infections. Now they're also at risk for pneumothorax because now if the alveoli are so distended, they can burst and then the air escapes in the pleural cavity and now a segment of the lung can become basically open causing a pneumothorax which is also a collapsed lung. Certainly it can use to cancer, smoking specifically, and then right-sided heart failure, respiratory failure and eventually death. Excuse me. Now treatment for these patients, stop smoking or stop the exposure to the environmental pollutants is really the number one goal here. Now for medications, they will use beta adrenergic agonists which is basically the albuterol, a bronchodilator, because if we have airway constriction and obstruction and these airways collapse, we want to make sure that we dilate the bronchioles so that more air can travel to the alveoli and perform that gas exchange. And they might also be using anti-cholinergic medications. Keep in mind that cholinergic usually pertains to the parasympathetic nervous system. So now if it's anti-cholinergic, we want to block the parasympathetic nervous system so we want to allow the bronchioles to open up and dilate. And I put here, there's a combination which is called a combi-vent, hence combination, which is a combination between the albuterol and the atrovent and a lot of patients will need that. Now the difference is that adrenergic works on the sympathetic nervous system, cholinergic on the parasympathetic nervous system. So sympathetic response is a little bit faster versus parasympathetic slower, but these patients might be needing both nervous systems to be helping with the bronchodilation for these chronic conditions. Now they might also need an ICS, an inhaled corticosteroid, if they have frequent exacerbations that require hospitalization or they just, maybe it's winter season and there's a bad cough and cold season. And they might even require oral steroids if the exacerbations happen very frequently or it's late in their disease. And then certainly they might also be needing O2 at home and it's okay for them to have an O2 sat that's between 88 and 92 percent. So don't panic if you see a patient with an O2 sat of 90 percent for example and they're actually looking at they're okay. It's always okay to ask them, do you have any kind of lung disorders and then they might tell you, yes I have emphysema, yes I have chronic bronchitis and you might even want to ask them the normal O2 sat level and then they say, oh it's usually 90 and they look perfectly fine at that O2 sat. Now let's look at nursing care for patients with chronic obstructive pulmonary disease. So first of all we want to encourage them to stop smoking and keep in mind this is not going to be an easy task because a lot of times these patients have been smoking for decades or you know many many years that is a very difficult habit to stop doing. So they're going to need a lot of encouragement maybe all kinds of other disciplines have to be involved to help with that. And then we're going to have to help them with some breathing retraining and I wrote down here per sleep breathing and diaphragmatic breathing and so the way that the per sleep breathing works is basically you ask the patient to exhale through per slips as if they were exhaling through a whistling. So they would inhale and then exhale and what that does because of the narrow oral cavity now there's increased pressure that is needed to exhale the CO2 which will help deflate that blep that are violas that is so distended and help them get rid of some of that CO2. And then diaphragmatic breathing the diaphragm is the major muscle of breathing and we really want to encourage them to strengthen that so that they inhale by using kind of like the muscles of the belly to to inflate the kind of like the belly button which helps to bring the diaphragm down and allows for lung expansion and then as the diaphragm recoils it allows them to help to expel the air. Now coughing and deep breathing certainly will help as well as chest physiotherapies specifically in patients with chronic bronchitis who have a lot of that mucus production that we talked about. Now nutrition think about if somebody has these chronic disorders they might be chronically short of breath and all their energy goes into breathing so they're not even gonna have time or the effort to really be hungry because just eating the motions of eating will make them so tired that they can't breathe. So now we have to focus on how can we get nutrition into these patients that are really chronically ill. So recommendation would be resting 30 minutes before the meal so no activity at all and also using a bronchodilator right before the meal so that the lungs can expand and then there will be less effort to breathe while eating. They might need an increased protein and high calorie diet as well as to consume small frequent meals because again they get tired very easily and then there's a specialty called pulmonary rehab and that's basically where specifically trained nurses and respiratory therapists work together to work on all these techniques with the patient. Now I also wrote down here the hypoxic drive because that's always something that comes up in discussion when we're talking about COPD and there's a saying that if you give a patient with COPD too much oxygen they will stop breathing and so I want to discuss the mechanism behind that. So in a normal individual without any lung disorders when the blood pH decreases or the CO2 level increases or the PAO2 decreases that's what stimulates us to breathe and that's accomplished by central chemoreceptors in the medulla ablongata as well as peripheral chemoreceptors in the carotid arteries that kind of provide feedback and then remember that the pH balance helps or takes place when the respiratory and the renal system work together to excrete bicarbonate, hydrogen ion and CO2 which is our acid here in the respiratory system. So in a normal patient what stimulates ventilation is a decrease in PO2, an increase in CO2 or a decrease in PAO2. Now the problem that we discussed over here is that these patients with emphysema already have too much CO2 in their system so that kind of becomes their new normal. So they are CO2 retainers and because of that inc that continuous chronic increased level of CO2 they're in a constant state of respiratory acidosis but their kidneys have adjusted so their kidneys are now used to helping getting rid of some of that hydrogen ion and absorbing more of the bicarbonate to balance their pH. And now this normal mechanism where a decrease in O2 or increase in CO2 stimulates ventilation is no longer valid in patients with COPD but now if we give them O2 because of these receptors react a little bit differently by administering O2 to these patients it might decrease their respiratory drive and it might decrease their respiratory rate and therefore they stop breathing. Now I'm not saying that if a patient presents who has a history of COPD and they come to you and all of a sudden they have an O2 sat of 65% and they are struggling to breathe they can barely talk they're using accessory muscles that you shouldn't give them oxygen. I'm not saying that this patient most likely the way that I just described him or her will need a lot of other measures and maybe even be put on mechanical ventilation if that's within their wishes. But keep in mind the mechanisms of normal what drives the respiration and gas exchange in COPD are not like in anybody with healthy lungs and therefore we want to be cautious with O2 administration and a lot of times they only be on one to maybe three liters of oxygen per nasocannula if they need it for home care and then anything else has to be discussed very much in detail with their physician or their pulmonologist to regulate that. So I hope this has helped you clarify the concepts of emphysema chronic bronchitis and how it applies to our patient population. Thanks for watching. I'll see you next time.