COPD, or chronic obstructive pulmonary disease, is a common respiratory condition involving the airways and is characterized by airflow limitation. Exacerbations and comorbidities contribute to the overall severity in individual patients. Let's look at the signs and symptoms of COPD.
So patients with COPD present usually with three cardinal symptoms, and these are dyspnea, chronic cough, and sputum production. Less common symptoms include wheezing and chest tightness. Risk factors for COPD include smoking in 95% of cases, so it's a big risk factor. There's also air pollution, low birth weight, recurrent lung infections and cannabis smoking.
Low socio-economic status and alpha-1 antitrypsin deficiency are also risk factors for COPD. COPD again stands for chronic obstructive pulmonary disease. and encompasses a variety of diseases.
The big three COPD chronic obstructive pulmonary diseases are chronic asthma, the blue bloaters which is the chronic bronchitis, and the pink puffers which is emphysema. In this video we will mainly focus on the blue bloaters and pink puffers, but before looking at these two let us quickly revise asthma. And I have a video that actually looks into more detail on asthma if you're interested. So asthma, it's a chronic inflammatory disorder of the airway in which many cells and cellular elements play a role. Recurrent episodes of wheezing, breathlessness, chest tightness, and coughing are only some signs and symptoms of asthma.
So now we will talk about the blue bloaters and the pink puffers. And here I am drawing a diagrammatical, I guess, representation, a stereotypical representation of patients that presents with chronic bronchitis as well as emphysema side-by-side, blue bloaters and pink puffers. We will use this to compare the difference between the two chronic obstructive pulmonary diseases, beginning by looking first at the blue bloaters. So the blue bloaters, they These are patients that look very cyanosed, blue, bloaters, possibly potentially due to the dyspnea, severe dyspnea, and lack of exercise. So in chronic bronchitis, you have inflammatory change leading to mucociliary dysfunction and increased goblet cell secretion and numbers, which leads to excessive mucus production.
So if we look at a normal alveoli, It has oxygen coming in and carbon dioxide going out. Normal ventilation and perfusion. These are alveoli and it has elastic fibers surrounding the alveoli which is important for basically the air recoiling during expiration.
So when you exhale, it recoils back, pushing the air out and we breathe this carbon dioxide out. Now if we look at an alveoli, and the bronchioles of a chronic bronchitis patient, we can see big differences. In the bronchioles and bronchi, we see bronchoconstriction and mucus hypersecretion. The mucus hypersecretion leads to the productive cough in chronic bronchitis. The airways obstruction from bronchoconstriction and mucus leads to wheezing.
And we hear wheezing during expiration typically. When we have airway obstruction this also can mean that we have alveolar hypoxia because oxygen is not getting through to the alveoli efficiently. This leads to a VQ mismatch. The VQ mismatch leads to hypoxemia and hypercapnia. Hypercapnia means respiratory acidosis.
A decrease in oxygen in the blood means the body will try to make more red blood cells to compensate. This is known as polycythemia, where we get an increase in hemoglobin. The respiratory acidosis and polycythemia with the decrease in oxygen contributes and basically means cyanosis, the blue color.
And this is why these patients with chronic bronchitis are known as a blue bloaters. So just recapping, chronic obstruction means that during respiration, less oxygen comes in and less carbon dioxide goes out, which leads to decrease in oxygen in the blood and increase in carbon dioxide in the blood. Because in chronic bronchitis, oxygen is not properly getting into the alveoli, we get alveolar hypoxia. When this happens, the pulmonary vessels will constrict so that it can shunt the blood flow. to healthier alveoli.
But when you get pulmonary vasoconstriction, you can get an increase in pulmonary vascular pressure, so pulmonary hypertension. When you get pulmonary hypertension, this can cause backflow of blood to the right side of the heart, and this can cause right-sided heart failure, which causes your core pulmonale, leading to the increase in jugular venous pressure. If that, I hope that makes sense.
Now going back to the alveolar hypoxia again, remember that, you know, the pulmonary vasoconstriction of some vessels leads to the pulmonary hypertension. So pulmonary hypertension leads to less blood going to the left side of the heart, which means there can be a decrease in left ventricular cardiac output. And this means a decrease in circulatory volume. Now a decrease in circulatory volume results in the activation of the renin-angiotensin-aldosterone system which causes more fluid retention despite still having fluid piling up in the lungs.
And of course this is in more severe cases. So I hope that all made sense. So that was for the blue bloaters, chronic bronchitis, and they are they are they are sinus, they present with wheeze. and also productive cough.
Not productive but very prominent cough. Now let us look at emphysema. Emphysema are known as the pink puffers.
Very skinny, muscle wasting, but prominent thoracic cage, barrel chested, and we will see why. So emphysema is an inflammatory response which leads to elastic fiber breakdown and destruction. of the alveolar walls, which means loss of alveolar integrity, and so we lose alveolar recoil as well. This leads to a phenomenon known as air trapping, which is typical of emphysema patients.
So if that all did not make sense, we'll look at it in a diagram. So let's draw the same diagram as before with the bronchiole and the alveolus here and its pulmonary supply. Now within the alveolus, there are macrophages normally residing in there, helping to keep the place clean and sterile.
And normally, again, oxygen comes in and carbon dioxide goes out. Now with emphysema, due to smoking or inhalation of pollution or other toxic substances, the macrophages can become stimulated and begin secreting proteases and cytokines, which lead to a number of things. The cytokines released attract neutrophils from circulation to move into the area.
The neutrophils as a consequence begin secreting a special protease called elastase, which specifically targets the elastic tissues. So elastase secreted by the neutrophil leads to loss of elastic fibers around the alveolus, which would mean loss of elastic recoil, which means decrease in ventilation. The proteases secreted by macrophages and the neutrophils also lead to the destruction of the alveolar wall and capillary beds. The destruction of the capillary beds leads to a decrease in perfusion.
And so as you might realize, we have a big problem with the ventilation and perfusion ratio. The loss of elasticity and destruction of alveolar wall leads to air trapping. Air trapping is basically when you still have a lot of gas trapped in the alveolus after you expire, after you exhale.
So you have oxygen and carbon dioxide trapped there still after you exhale. This means you have an increase in end-expiratory volume. So because you have an increase in N-expiratory volume, this leads to one of the clinical signs of emphysema, which is barrel chest. Because you are not emptying your lungs, you still have gas trapped, and you're using accessory muscles and a lot of effort in breathing, all these together lead to the barrel chest.
Okay, so the decrease in perfusion and the decrease in ventilation, which we talked about earlier, leads to a matched VQ deficit. As a result of this deficit, in the blood, you see similar things to chronic bronchitis. a decrease in oxygen, and an increase in carbon dioxide in the blood. So recapping what we just drew on the diagram, the protease is released by macrophages and neutrophils damages the elastic fibers leading to decrease in elastic recoil, which means a decrease in ventilation.
The protease also destroys capillary beds, which means a decrease in perfusion. Decrease in ventilation and perfusion means we have a matched VQ deficit. As a result of this VQ match deficit, we get hypoxemia and hypercapnia.
I think that's what you said. Hypoxemia and hypercapnia in the blood becomes more severe in late stage. The loss of elastic recoil is due to the loss of alveolar integrity and the destruction of the alveolar walls.
And so the person needs to work a lot harder to breathe in. As a result, we get dyspnea and also cachexia. Now, Alpha-1 antitrypsin deficiency is a hereditary condition, which means that if you are deficient in antitrypsin, you cannot defend against proteases, and so you have a net too much protease and less anti-protease, which means you get a net damage to your lungs, essentially.
So I hope all that makes sense about emphysema. So emphysema are your pink puffers, chronic bronchitis are your blue bloaters. Now let's...
proceed to investigations. What sort of investigations would you perform if someone presents with difficulty breathing, sputum production, as well as a cough?