Restrictive Lung Disease PDF

Created with Coconote - https://coconote.app Understanding Restrictive Lung Disease Morning. Today, we're gonna be discussing about restrictive lung disease. This is my 4th try. So if it doesn't work, we're going live next week. Outcomes for today is to explain the difference between restrictive a...

Created with Coconote - https://coconote.app Understanding Restrictive Lung Disease Morning. Today, we're gonna be discussing about restrictive lung disease. This is my 4th try. So if it doesn't work, we're going live next week. Outcomes for today is to explain the difference between restrictive and obstructive lung disorders, to describe the nursing assessment with a restrictive lung disorder, to determine the goals of therapy, and to discuss the nursing interventions that are recommended to treat this disorder, lastly, to recognize cues for respiratory failure and know when to take action. The over overarching concept here is gas exchange. And according to Giddens, the process, gas exchange is the process by which oxygen is transported to the cells and carbon dioxide is transported out. Important in that is to look at gas exchange being impaired. What's causing the impairment of ventilation? Now, again, for chronic lung disease, you're gonna have asthma and emphysema. You could have respiratory failure, pneumonia, pleural effusion, atelectasis, fibrotic lung disease, interstitial lung disease. But more importantly is to understand and and see that interrelated concepts such as mobility, fatigue, perfusion, acid based balance, anxiety, and nutrition are also affected. Just I just want to let you know that you need to review your lecture on COPD. What are the diseases that are associated with COPD? Again, COPD is the umbrella term, and you have emphysema. You have asthma. You have bronchiectasis. Those are some of the core basic diseases that encompass encompass COPD. What are the diagnostic tests that are done to diagnose those disorders? Well, again, you're gonna have a chest x-ray. You're gonna have a CAT scan. You may have a bronchoscopy. But, essentially, what you're gonna and you might have white count and sputum for CNS and so on and so forth. But the disorder these disorders are also accompanied with pulmonary function tests. These are tests that will help to classify these disorders as well as the disorders that we're gonna talk about in restrictive lung disease. So you need to go back and look at what is tidal volume, what is, total lung capacity, what is vital capacity, what is, forced expiratory volume. These are things that you need to learn and understand. What is residual volume? Because when we talk about restrictive lung disease and going into, respiratory failure, you'll be able to understand if you understand what the pulmonary function tests are. Can you identify the arterial blood gas analysis associated with COPD? Well, hopefully, you're telling me that they're in a respiratory acidosis. We're gonna go a little further than that because, you know, with restricted lung disease, again, you're gonna be in respiratory acidosis. But what you also have to understand is how the body is trying to compensate for that. So we're gonna go into partial, absent, or complete compensation. That's what we're gonna do for some of our class activities. Okay. So here you have a chart of obstructive disease and restrictive disease. Now in obstructive disease, the alveoli is expanding, but it's unable to deflate or it deflates ever so slowly in terms of internal gas exchange. Lung volumes increase in obstructive disease. People with obstructive lung disease have shortness of breath due to difficulty exhaling all the air from their lungs. So their total lung volume is gonna be high. The residual volume in their lungs are gonna be high, and residual volume is full of a lot of dead space where there's no in, internal respiration. Because of damage to the lungs or narrowing of the airway inside the lungs, exhaled air becomes out more slowly than normal. So inspiration is quick, but expiration is 3 or 4 times longer than inspiration, and you're still not getting it all out. In restrictive, the alveoli does deflate, but it's unable to inflate properly. And that's due to either lung scarring, fibrosis, or extra, parenchymal problems in the lung tissue. Lung volumes are greatly decreased in restrictive disease in restrictive cases because it can't stretch to allow the lungs in. The lungs have lost their elasticity, elasticity. So that'll be a problem. Most often, it results from a condition causing stiffness in the lungs themselves. In other cases, the stiffness of the chest wall or weak muscles or damaged nerves may cause restriction in the lung expansion, and we'll talk more on that. Another little chart. It shows restrictive versus obstructive, and it's 2 tests that are done, your forced expiratory volume and your, vital capacity. Forced expiratory volume in obstructive disease is definitely decreased vehemently. And in restrictive, it's it is decreased, but not as much as in obstructive. And your, vital capacity is slightly decreased or normal in obstructive, but in restrictive, it is greatly decreased. This is slide 5. We're gonna talk more on this slide later, and I'll give you some definitions so that you could see how it all works out. But this is a good thing to see the difference in the two diseases. Those of you that are visual people, I wanted to show you this slide. Look at the pneumonia that this patient has. Look at that, left side. There, it looks like the size of a foot a a softball. It's a real small area of lung, tissue that is actually participating in gas exchange. All below it is all white. That is a pleural effusion, which is obliterating the rest of that left lung, pushing it, squishing it down so it's lost its elasticity. With pneumonia, the other side of that lung doesn't look too good either. But with pneumonia, you have complications, which we'll get to the next slide. And these complications are causing restricted lung disease or restricted lung disorder. It's a temporary measure because pneumonia, hopefully, is a temporary condition, and the complications hopefully will be rectified. Once those complications are rectified, the restrictive part of the disorder is gone. So it's no longer apparent. This is how it's it's a transient thing for pneumonia. But for other disorders, it's restrictive lung disease is not gonna be transient. And this is what I'm talking about. The picture on the far right is your picture of the complication of pneumonia. It's pleural effusion. Look how much that left lung is obliterary obliterated. I'm sorry. You can't see it. And that's because pleural effusion, fluid seeped out from the lung, from the, pneumonia infected lung. It could either be transudative, meaning just fluid based, or exudative, meaning bacteria, pus, exudative. And that's caused an effusion in the pleura, which is putting compression on the bottom lobe of the lung on the left side and therefore not allowing that lung to expand. So reduction of volume of lung is restriction. So with your pleural effusion, you're having a restrictive lung disorder here. What's gonna happen? The doctor's gonna do a thoracentesis to relieve the pleura of the fluid, either transudative or exudative, and then find out if it if it is exudative to give the antibiotics to correct the problem, but then that lung that was compressed is going to be able to re expand and participate in gas exchange. The other picture on the on the left over here is an empyema. An empyema is pus exudate that seeped out of the lung and solidified. And I kid you not, with this solidification, sorry, it almost engulfs. It's like it's like an octopus and it engulfs the lobe of the lung where it is it's involved in and causes restriction. It's got all its tentacles around the lung. The lung is trapped, so it cannot expand and contract. You have a restriction. What they usually do for an empyema, they'll try to do a thoracentesis, but it's not gonna work because the exudate is is so thick. So what they're gonna have to do is the thoracotomy, open the patient up, remove the empyema, and peel off the tentacles of that octopus because it's so I mean, just peel the right decorticate the lung so that the lung is now free to breathe again, and then we put a chest tube in to help with the expansion of the lung. But these are good pictures to show you how restrictive lung disorders can work. Now restrictive lung disorders is any disorder that leads to or results in a decreased lung volume and decreased inflation, reduction in lung lung volume, decreased chest wall compliance. It could be either intrapulmonary or extrapulmonary. Intrapulmonary are diseases of lung tissue. For example, you could have interstitial, alveolar fibrosis, pulmonary fibrosis, which you could get from a lot of conditions, one being COVID 19. A lot of your people are finding results of pulmonary fibrosis after they had COVID. Intrapulmonary, you could have an atelectasis. Well, that's a, you know, it's a small collapse of a section of a load of a lung. You could have a lung reception. If you had a tumor resected or you had a lung, a lower lobectomy for cancer of the lung, guess what? You have restrictive lung disease because the total volume of air in your lungs is now changed because you're one lobe down. You could have interstitial, lung disease, which is, occupational exposure, asbestosis, farmer's lung, pneumoconiosis, sarcoidosis, and rheumatoid lung are immunologic. But those are diseases that can cause intrapulmonary restrictive lung disease. We'll talk more on that later. Extroverted. Ex extroverted. Oh my god. Extrapulmonary. Abnormality of the pleura. The pleura thickens. Maybe you had a pneumothorax where you had a puncture in the lung. The lung punctured. Pleural effusion. Abnormal chest wall. And I mean obesity. I'm talking morbid obesity, almost where you're pick Wikian, where you're the whole shape of the person is like an apple and 90% of their weight is in their chest. Ascites, pregnancy. But towards the end of pregnancy, 8th, 9th month, where the poor woman's carrying twins and can't breathe because obesity, ascites, pregnancies is pushing against the diaphragm and pushing against the lung volume so you have diminished lung volume. This can happen. Spinal deformities, such as scoliosis, kyphosis, lordosis. If you have definite spinal deformities, it will impair. It'll intrude on the volume of air by pressing against the lung and not allowing the lung to fully expand. Respiratory muscular weaknesses, neuromuscular diseases, Parkinson's, Guillain Barre, amylotropic lateral sclerosis, which is ALS, which we also call Lou Gehrig. MS, which is muscular, multiple sclerosis. You could have cystic fibrosis. You could have muscular dystrophy. These respiratory muscular weakness disease are going to affect the diaphragm and how well the person can can expand and contract the diaphragm, and that will affect them in terms of developing restrictive lung disease. Okay. A definition of restrictive lung disease. In physiological terms, restrictive lung diseases are characterized by reduced total lung capacity, reduced vital capacity, or reduced lung volume. Because something is happening to effect, whether they have a a rheumatoid disease, a connective tissue disease, sarcoidosis, they will affect loads of the lung. You know, here's a story. I don't know if I'm jumping the gun, but I had a patient in the ICU. She was 76 years old. She had a fractured hip. No. She didn't have a fractured hip. She had rheumatoid arthritis, and the rheumatoid arthritis wore down her hip joint, and she needed hip surgery. I'm sorry. She also had little COPD. So they kinda figured, you know, let's keep her in the ICU overnight just to be on the safe side. So, you know, she had the surgery and she was vented and she was in the ICU and we were taking care of her and the high pressure alarm kept going off on her ventilator. And I'm like now this lady was a big lady. Hey, I'm 5 foot 3 and a half, so anybody taller than me is tall. This woman was 6 2, a big lady. So for a woman that size, she has a good lung volumes. So they were they had her at maybe 50% oxygen on the ventilator, 20 respiratory rate. Tidal volume, they gave her about 550. And for somebody who's 62, that's a decent title volume. She's big enough to sustain that. So, you know, I came in and that high pressure went. And and and kept ringing, kept ringing, kept ringing. So I'm like, why? So my student said, is she in pain? I said, she's on Michael Jackson's propofol and Versed and fentanyl. I don't think she feels any pain. She's not awake. She's not aware. She doesn't respond to pain. Her blood pressure is good. Her heart rate is 82. So, no, I don't think she's in pain because she's not grimacing. She's not showing any change in her vital sign. She's not biting down on the tube. She's not coughing. I listened to her chest. I said her chest is clear. She has no bronchi. So what what is it that's causing this high pressure alarm to keep going off? And I'm thinking, I'm thinking, I'm thinking. And the pulmonary doctor walks in, and he goes, hi. And I went, just the man I wanna see. I said, she's she's, high pressuring. I said, she's not in pain. She's absolutely comfortable. Everything about her says not pain, no pain. Vitals are good, clear chest. I said, wait a minute. She has rheumatoid arthritis. Right? And he goes, yeah. Yeah. That's why we did the hip. And I said, do you ever do you ever check around for rheumatoid lung? And he said, no. She has COPD. I said, I'm wondering if she has rheumatoid lung 2. Rheumatoid arthritis is an immunological disease can cause changes in in the, the connective tissue in the lung. Lung has connective tissue. I said, do me a favor. I said, you have her at 550 for tidal volume, and and that would be adequate for a woman who's 62. I said, let's try her at 450, less of a volume. Sure enough, as soon as he put it down to 450, not a peep. The high pressure alarm didn't go on. And he said, son of a gun. I never thought of that. So, again, rheumatoid, these are things that are gonna reduce lung volumes if it affects the lung or any of your respiratory neuromuscular diseases can affect the lung. What are symptoms? Shortness of breath, especially with exertion, an inability to catch their breath or get enough breath in, a long term cough, a long term meaning forever. You know? Fatigue. Oh, gasping for breath, fatigue, which can be extreme. And it really affects their activities and daily living. It affects their lifestyle. So depression and anxiety go hand in hand with this poor patient. They really get very discouraged because they really can't do a lot without activity and tolerance and being short of breath. Again, I just wanted to give you an example of extrapulmonary things that could cause restrictive lung disease, which some of these could be a transient or temporary thing, but some not. Obesity. You know, maybe if they lost weight and exercised, that would decrease their restrictive lung disease. Neuromuscular disorders, which we talked about, your rheumatoid lung oh, well, it's not neuromuscular. Your, Parkinson's, multiple sclerosis, amytrophic lateral sclerosis, which we call Lou Gehrig's disease, myasthenia gravis, maybe. You'll get that next semester. MS, muscular dystrophy, cystic fibrosis, all of these things, Parkinson's, all of these things will affect the diaphragm, will affect the chest wall. Neuromuscular chest wall deformities, your kyphosis, scoliosis, pregnancy, ascites, empyema, atelectasis, pleural effusion. Your intrapulmonary are more interstitial lung disorders such as asbestosis, pneumoconiosis, sarcoidosis. Sarcoidosis can be anywhere in the body, but it does have an affinity for, the lung as well. And it can cause granulomatous lesions, which will hamper and impair the volume of blood that is associated with that lung. Volume of air. Sorry. Rheumatoid arthritis and lupus, are 2 immune, disorders that can affect the lung as well, but it's intrapulmonary. K. I just wanna kinda show you atelectasis. That's just a collapsing of a section of a lobe of a lung, not the whole lung. The whole lung would be a pneumothorax when there's the integrity of the aplura has been compromised. But atelectasis is collapsing of lung tissue, lung sections of lung. This can be micro or macro atelectasis. Micro, lung is not fully re expanded, diffuse collapse, especially at the basis. It's not usually visualized on chest X-ray. Very common in people who can't breathe deep. Examples of this would be patients who have neuromuscular diseases. So these people have little microadlectasis all at the basis of their lung. Macro, diffuse or local, and it can be visualized on X-ray. Cause could be immobility, inhaled anesthesia. Bing. Bing. Bing. Bing. Your post op patient. Every post op patient who's had anesthesia may have after this the the procedure or the surgical intervention is over may have, macroadyllectasis, and that is a form of restricted lung disease. So what do we do? We cough and deep breathe them. We get them out of bed. We walk them. We move them. We use and set a spirometer once, every hour, 14 times an hour, 10 to 14 times an hour. You know, immobility can do that as well. Abscesses, lung abscesses, tumor, bronchiectasis, abnormalities of the thorax, your kyphosis and scoliosis, overdose. Somebody overdoses on your opioids. Okay? They're not breathing. They're gonna have collapsing of air sacks and sections of the lung. Risk factors, shallow breathing, aspiration of foreign bodies, retained secretions. So what assessments would the nurse make on a patient with a macroadlyticis? I'm hearing the Jeopardy song play right now. Okay. Got it. Diminished breath sounds. Where are you going to hear diminished breath sounds? Not in the front. You're gonna hear them in the back. Because when you've got a shallow breathing, when you've got immobility, inhaled anesthesia, it generally hits the lower lobes of the lung first. Sorry. So you're gonna have diminished breath sounds. And what are you gonna do to intervene? To intervene, you're gonna cough, debreathe, get them out of bed, use the sense spirometer frequently. And what are the diagnostics? Well, first of all, you're gonna get a chest X-ray. You're gonna look for right ventricular hypertrophy because you're hypocapnic, you're you're, you're hypercapnic, I'm sorry. Hypercapnic. You're also, what's the word I'm looking for? Hypoxic. So when you have hypoxia, it's gonna make the pulmonary artery vasoconstrict. When that pulmonary artery vasoconstricts because of the hypoxemia, it's gonna cause little, pressure and strain on that right ventricle. So you're gonna have right ventricular hypertrophy. This can lead to another syndrome called cor pulmonale or heart lung disease, but we're not gonna talk about that now. CAT scan. CAT scan is gonna be done so that we can look to see how the lung tissue is. You might need to do a brow coloscopy. Go back to slide 6 now. They're going to do pulmonary function tests. They're gonna do a forced vital capacity. How do you do that? Patient inhales as much air as possible, then exhaling with as much force as possible. We're gonna do a forced expiratory volume in one second. That's an FEV 1. This measures how much air is exhaled at in the first second of a forced vital capacity, FVC. Now there's a third thing. The FEV 1 to FVC ratio. This compares the forced expiratory volume in one second reading to the total amount of air exhaled during the forced vital capacity test. The resulting ratio may be normal or high for a person with restrictive lung disease. Now based on these tests, you go back to what I showed you, and you can understand it a little bit better. That's why your forced vital capacity and your forced expiratory volume are essential tests to determine, for restrictive lung disease. Okay. What are the assessments? The assessments are the same for all the diseases pretty much in restrictive lung disease. The compliance and the elasticity of the lungs are damaged. Compliance may be like a balloon that's been blow blown up so many times that it's flabby, or the elasticity, it's just not there. So the compliance and the elasticity of the lungs are damaged. So the signs and symptoms are gonna be decreased vital capacity, decreased tidal volume, the amount of air you breathe in and you breathe out normally. Decreased total lung volume. Because restrictive, remember, either they've removed part of a lung or the lungs are being restricted. They're cramped so that the total lung volume is gonna be low because they just don't have that. If if they have interstitial lung or fibrotic lung or neuromuscular diseases causing atelectasis, that they're just gonna have a decrease in the total lung volume that they have. They're gonna be hypercapnic, high levels of CO 2. They're gonna be hypoxic, low levels of PO 2. They're gonna be short of breath, dyspnea on exertion. They're gonna have rapid shallow breathing patterns. They're gonna have a decrease of activity tolerance. They're gonna have a dry, persistent cough. I wonder why that is. Nonproductive. Why? You tell me. With interstitial fibrosis, there's really no cure. They're gonna treat symptoms. They're gonna there's really no cure. They're gonna treat symptoms. They're gonna put them on steroids. Sometimes they'll put them on immunotherapy, oxygen therapy, chemotherapy. With extrapulmonary obesity, with hypoventilation, there is a hormone that we use, progesterone, hypoventilation. There is a hormone that we use, progesterone, and it's a respiratory stimulant. So if you have somebody with what we call Pickwickian, which is hypoventilation related to obesity, and, they usually will put them on progesterone to help. What would be the nursing care for a patient with restrictive lung disease? Generally, it is somatic or symptomatic. You treat the symptoms depending on what is the cause of the restricted lung disease. Now as I told you, if it's a temporary measure because of an empyema or because of an atelectasis or because of pleural effusion, we can correct those issues so that they can breathe better. But if it's somebody with neuromuscular diseases, all the ones that are Guillain Barre, well, that's transient too. But Parkinson's, MS, ALS, muscular dystrophy. Those are diseases that can progress and get worse. Or if it's some of your immunological diseases, rheumatic, rheumatoid arthritis, lupus, and it's affected the lung, then you look at oxygen therapy. They might start with CPAP. They might go to BiPAP. And if there's been an exacerbation of something else, which makes their condition worse, then they might need to do mechanical ventilation. You wanna conserve energy. You wanna provide rest periods. They can't do a lot. You wanna try to maintain their PO 2 at around 55, 60, and their o two sat around 90%. What they use, though, there is a drug that they use, and I think I taught you I taught you about this before, pulmonary artery hypertension. You know, with hypercapnia and with, hypoxemia, you're gonna get, pulmonary artery, vasoconstriction, pulmonary artery hypertension, which is gonna cause that right ventricle to to kinda get swollen and thick and less less good at, pumping, so that they will try to treat that with Viagra. In fact, Viagra came out for pulmonary artery hypertension, and it was a side effect that they all discovered was much much more profitable than pulmonary artery hypertension. So they kinda reprocessed, and now you know it as as Sildenafil. They might put them on corticosteroids, especially if it's for immunotherapy or if it's for, immunologic problems, your, rheumatoid arthritis, your lupus. Sometimes the corticosteroids are good for sarcoidosis or the, occupational disorders, pneumoconiosis, asbestosis. They might use corticosteroids. But you know what? Then you have a problem with high risk for bleed, and so you put them on a proton pump inhibitor. And then you also have a problem with glucocorticoids. And it's a glucocorticoid, so it promotes the birth of new sugar. So, therefore, you gotta watch their blood sugars, and you may cause them to become over time a diabetic. Antibiotics. Well, you're gonna say to me, well, why antibiotics? I don't get that. Well, they have a restrictive lung disorder. They have another comorbid factor causing the restrictive lung. So they're an accident waiting to happen. So sometimes physicians or health care providers say, you know what? I'm going to be preventative. So I am gonna put them on low dose antibiotics end of fall beginning of winter. You know, I always know it's winter. My, COPD patients are there in my ICU from May from January until April March, April. And all your COPDs that aren't taking care of themselves because they have an exacerbation and they get sick, and that exacerbates it. And so, again, being on antibiotics is not such a big bad idea. The other thing I wanna really emphasize is health promotion. These people with restrictive lung. Alright. You know what you have, but you also have to understand what you can be susceptible for. So get the the the pneumonia vaccine. It's good for 5 years. Get the yearly flu shot. Get your COVID, vaccination. Get your shingles vaccination. Get RSV. It's another one. We don't want you getting sick because you cannot handle it as well as other people. Methotrexate, these are some really it's a chemotherapeutic type drug, but it's really good for rheumatoid arthritis. So if they have a rheumatoid lung, they're starting to use these kind of drug therapies to, just expand the person's life and give them more energy. Okay. Unfortunately, with restrictive lung disease and or COPD, you know, these people get exposed to somebody. They walk in the mall. They're not wearing a mask, and they come down with RSV or they come down with the flu because they didn't get their flu shot. And this is the the thing that's gonna throw the throw them over the edge, and it's gonna it's going to affect them in such a way that it exacerbates their underlying condition, whether it's emphysema, asthma, which is obstructive disease, or, you know, your lupus, your your rheumatoid arthritis, your immune disorders, diseases that, you know, or respiratory problems have, it could throw you into an acute respiratory failure. Acute respiratory failure is defined as a decrease in oxygen of below 55%. So the p02 is lower than 55%. Or and I think the books may vary, but still, we're circling the toilet with any of these numbers. An increase in p c o two, carbon dioxide, p c o two of 55 or higher. So you can see my little lady is on getting a breathing treatment. And if this isn't successful, they may have to intubate her and put her on a ventilator. Here you go. Now I already gave you the definition of acute respiratory failure and their causes. Alveolar hypoventilation. What in the same hell is that? We'll talk. Physiological shunting, alveolar dead space, alveolar capillary diffusion issues. So I gave you 2 pictures. 1 is a normal lung, and the other one are conditions causing respiratory failure. So a condition that affects the flow of blood to the lungs, a pulmonary embolus blocks the flow of blood and causes lung damage. So that whole section, the alveoli are are dead, and the space around them is dead. So that's like an alveolar dead space. Alveolar hypoventilation, that could be neuromuscular diseases that are not that are affecting the diaphragm, but also affecting the rate and depth of this person's respirations so that they're hypoventilating. Pain medication, anesthesia, this is alveolar hypoventilation. This physiological shunting, what's that? Well, you have your capillary, and you have your which is my cupped hand and my, alveoli, which is my fist. And they're a kissing cousin because they're doing internal respiration. So physiologic shunting. Okay. Now I have exudate coming in between my alveoli and my capillary. Maybe it's thick tenacious exudate from pneumonia, so that's gonna impair gas exchange so that the blood flow through that arterial and that capillary bed are gonna shunt. They're not gonna exchange c02 with 0 2. They're gonna shunt their CO 2 back to the heart. So that's what physiologic shunting is. Alveolar capillary diffusion, that could be several things. That could be, just, I was gonna say rails. Sorry. Crackles. When your alveoli gets pushed away from the capillary beds, there is diffusion of fluid, crackles. That could be heart failure. That could be renal failure that you had last week. That could be a host of thing, pulmonary edema. And it's not allowing the alveoli and the capillary to have good gas exchange, therefore, causing acute respiratory failure. And what are preventative measures that we can do that might reduce the risk of somebody going into acute respiratory failure? Maintain patent airway. How do you do that? Get them out of bed. Move them. I don't care if they're 96 years old. Move them. Get them up. Ambulate. Walk them. Have them do instead of spirometer 14 you know, every hour, 10, 13 times. Maintain patent airway. Listen to their lungs, not just in the middle of the beginning of the shift, couple of times a day. Minimize respiratory infections. Well, also with patent airway. If they have, cough and deep breathe them. Maybe they need a mucolytic. Maybe they need a respiratory treatment. You are the patient's advocate. Talk to your primary. Say, you know what? He's an at risk. He's post op. He's getting he's getting junky in the lungs. Can you give me a breathing treatment? Can you give me albuterol? Can you give me something to help clear up this mucus? You know, Tensilon pearls is a great, mucolytic agent. Mucamist, great mucolytic agent. So these are things you need to advocate for your patient to get. Minimize respiratory infections. Do not smoke. Do not be around people who do smoke. If you go to a large movie theater people go to movie theaters anymore. You go to the mall to go shopping. You go somewhere where there are people, wear a mask, especially in the fall winter when everything is flying around. Wear a mask. Get your your, booster shots. Get your immunizations, your flu shot, your COVID shot. I can't say that enough. Key clear airway secretions. If you need to, suction. If you also need to, chest physical therapy. We're gonna I'm gonna go over that with you in class and just practice it a little bit. These are things keeping patent airway, moving secretions. So these are things that we're gonna keep on working on so that these patients don't get a problem. Signs and symptoms of acute respiratory failure. Central nervous system. Okay. If you're hypoxic, how do you think that's gonna affect your mentation? They will have a change in in in AMS, altered mental status. They can become anxious, nervous, tech I mean, restless, irritable, confused. And, again, if you say, well, my guy is 86 years old, and he has dementia, you can tell the difference between dementia and being really confused. Cardiovascular, your pressure's gonna drop. You're gonna be tachycardic. I'm not gonna right now give drugs for that. You're tachycardic because you're hypoxic. We need to treat the lungs. Renal. Okay. Well, the kidneys, they're like, oh god. Blood pressure's down. I'm not getting perfused. You're gonna secrete renin, and here we go with the renin angiotensin aldosterone mechanism. But, you know, because of the perfusion, you're gonna have decreased urinary output. Gastrointestinal, let me tell you, the GI system, they're gonna say, you know what? I'm not really very important compared to the heart and the lung and the kidneys. So if you need the blood supply to keep them going, take mine. So GI, you're gonna have decreased, bowel signs. Hypoactive, you may even develop an ileus. Skin is gonna be cold and clammy. Your most common side effects are gonna be tachycardia, restlessness, headache, and confusion. What are gonna be the treatments? Somebody's in acute respiratory failure, depending if it's COPD or if it's restrictive, bronchodilators. You know, your prevental, your ventilent. Open up the airways. Steroids Because you wanna decrease the inflammatory reaction. And especially if it's, immunologic, if it's rheumatoid or lupus or some of the, intrinsic occupational lung disorders, you might wanna try it for that too. Antibiotics. And, again, because at this point, they're gonna start to develop a pneumonia, and you're gonna need it. Cardiac drugs, just hold off and be careful. We wanna treat the lungs first. I'm not saying we're not gonna use cardiac drugs, but we're gonna treat the hypoxia and the hypercapnia first. And if we can reverse that and there's still cardiac issues, we'll work on that. Sodium bicarbafirine and acidosis. We are gonna class activity, we're gonna go into, respiratory, acidosis, alkalosis. But we're also gonna talk about compensation, whether it's absent, whether it's partial, or whether it's complete so that you'll feel more comfortable about it. They may need to intubate and put the patient on a mechanical ventilator, which you're gonna get next semester, and put them on PEEP, which is a positive end expiratory pressure. And that is a pressure that is given to the patient at the end of expiratory so that their, bronchioles maintain patency, and it really kinda helps to push that alveoli into the capillary bed so that they're better, gas exchange. Chest physical therapy. I love this. Chest physical therapy is so important. Some of the beds up in the ICU are programmed that the beds do it. But either than that, I was taking the students 1 year down to West Orange to, Kessler. And it was about 9 o'clock, and I said, oh, jeez. You know? All the patients are still gonna be in bed. Oh, hell no. They were up. They were in their wheelchairs floating around. They had their ventilators attached to them. And I kept hearing, like, what's that thumping noise? And my my, nephew who's a physical therapist was with me. And he goes, NA, that's the cophalator. I'm like, the cophalator? I like that name. I said, what does it do? He said it's a vest, and they program it. And they program it to do percussion vibration for, like, 20 minutes. I said, god bless. That is amazing. And I because, you know, back in my day, we had to do it ourselves and not for anything, but it was exhausting to the patient, but it was so exhausting to me. And then to go and do it again to somebody else, And then to go and do it again to somebody else for 15 minutes, I was dead tired. So chest physical therapy is essential. It is crucial. It loosens the secretions. It forces them up the tracheal bronchial tree where you might be able to suction them, which comes to tracheal toileting. And if you have any questions on how to suction, we can go over that as well. Positioning. Positioning is paramount. You need to position them, turn them, move them. Even if they're ventilated in the ICU on a vent, we turn them every hour. Question. If I have a really bad pneumonia with consolidation in my right lower lobe, where am I gonna position them? How am I gonna position them? You'll position them on the left. You'll position them a little bit about on the back, but you're not gonna position them on the right. Why? Because that lung is a bad lung. It's got a really bad consolidated pneumonia causing restriction in airflow. We are not gonna match bad perfusion with bad oxygenation, so you're not gonna position them on the right side. You position them on the left or on the back. So positioning is you know, you're gonna learn about, adult respiratory distress syndrome maybe next semester. And one of the things that they talk about too is positioning them prone so that the back of the lungs have an opportunity to get better oxygenated. That's it. So this, can you think of how these diseases that I talked about can impact the different interrelated concepts that we talked about? What we're gonna do is we're gonna do some chest physical therapy. We're gonna do some blood gases, and we're gonna do some NCLEX style of questions. And maybe I'll make up a case study on a neuro, neuromuscular disease patient who comes in in acute respiratory failure, see if we can work it out. I'll see you on Monday. Have a good day.