Emphysema: Signs and Symptoms

00:00 it will be tympanoc. Obviously, I’m exaggerating but it will be tympanic, is that clear? Be careful, continue. So now, signs and symptoms of emphysema. You know that your FEV1 is already decreased, that is by definition. If it starts dropping below 30 percent, that is severe disease. Dyspnoea without exertion, most likely. Barrel chest, both the areas of the lung are now hyper-inflated, you have increase in AP diameter and you have depression of your diaphragm.

00:30 Diminished air sounds, can’t even hear your air sounds as much because you end up having air being trapped in your lung. Now there is something that I will bring to your attention here. It’s from physiology and you’ll find this to be interesting. You all know about the oxygen dissociation curve, but then we’ll take a look at the carbon dioxide dissociation curve. What does that even mean, Dr. Raj? You’ll see, I’ll walk you through it and you’ll be clear and you’ll see as to how to apply the physiologic concepts that you’ve learned in a setting coming up shortly.

01:04 Now, the cyanosis could be taking place and why are you pursing that lip, you’re pursing your lip so that you can add a resistor in a series so that you can do what to the pressure proximally? Increase it. Do you remember the silliness that I was doing a couple minutes ago? So, here you’ll find increased pressure and hence, you’re trying to keep this very flimsy alveoli and ducts and such open because otherwise it wants to collapse because you’ve lost radial traction. Why have you lost radial traction? Because the elastic tissue have been damaged. By whom? Elastase. How? Well, we talked about two patterns. What are they? Centrilobular. What’s the other one? Panacinar, are you good? Of course, you are.

01:47 Next, well the lungs are dying, when the lungs are dying and then what happens to the right side of the heart? It starts dying and it’s not a good thing, is it? This is called what please? Good, this is cor pulmonale. Let’s look at minimal V/Q mismatch due to septal loss now have you ever asked yourself this question, or if you haven’t then well you know what I’m referring to when I say pink puffer. What does “pink” mean? What does a “puffer” mean? Versus when you have chronic bronchitis where we shall take a look at and that patient is referred to as being a “blue bloater”.

02:17 Well, the pink, well, apart from the septal loss that might take place, you might have vascular supply that’s compromised as well and therefore, resulting in that “pink” type of effect. Next, well what about the “puffer” part? Literally here the patient can compensate just a little bit perhaps with hyperventilation or at least attempting to and so, therefore, the combination of the vascular supply being damaged and then also having the “puffer” effect gives you a pink puffer. Now, there’s an important physiologic concept that you very much want to keep in mind as you go through, the, well really the physiology of your emphysema. And by that I mean that it is possible for you to compensate a little bit. Not so much for the oxygen because once hypoxemia sets in, even if you are hyperventilating, so the “puffer” part, it does'nt mean that you will necessarily correct the oxygen.

03:16 However, you may not have a patient that has hypercapnia. Listen to what I said. That patient that comes in through the door, normally who has emphysema are usually a combination of emphysema and chronic bronchitis well then most likely will have hypoxia or hypoxemia and also have hypercapnia, wouldn’t they? Yeah, however is it possible physiologically in which there’s regional compensation in which your carbon dioxide levels might be either normocapnic or perhaps even hypercapnic? Yeah, interesting, why? Let’s take a look.

03:55 So, what we have here from physio is the all-important oxygen dissociation curve, something that you’re all so very comfortable with as far as that blue curve is concerned, isn’t it? So therefore, if you start at the upper-right plateau portion of your lung, well at this point you know on your Y-axis that you would have a oxygen content being quite high. Okay, so, if it is let’s say approximately 20.3 with your oxygen content which is equivalent to approximately 97 percent, this would mean that the haemoglobin here would be completely saturated at all four binding sites. What then happens when you leave the lung through your pulmonary veins and then through the aorta and it hits your tissue? You lose 1 oxygen. When you lose 1 oxygen this is equivalent to a haemoglobin of 75 percent which on your systemic venous side gives you a PO2 of how much please? Good, 40. So we're not going to walk through all that, that is something that you be quite comfortable with but now what if you were to hyperventilate? What direction of this graph are you moving in? Listen, if you’re hyperventilating what does the X-axis in boards and clinics all expect you to know that the X-axis represents what? PO2.

05:13 Which means what? Dissolved oxygen.

05:15 Okay, so, now, if you’re hyperventilating and you are at a PO2 of 100 which on the Y-axis represents a saturation of oxygen of approximately 97 percent, well now your PO2 might move up to 110, 120, right? But in terms of your saturation of oxygen, you’re still approximately 97 maybe a little bit more than 97 percent. So, point is you’re going to be on that plateau phase even if you’re hyperventilating. But if you’re hyperventilating on the right side of that graph I want you to now compare this to the red linear curve which on the right, the Y-axis says, blood carbon dioxide content. If you’re hyperventilating would you tell me as to what you’re doing with your carbon dioxide? You’re blowing it off.

06:05 If you’re blowing out or blowing off your carbon dioxide then you would expect that to be decreasing. Can you put everything together here for me please and on the right side if you’re hyperventilating you expect your oxygen content to normally be higher, maybe you have a PO2 of 120 and you expect your carbon dioxide level to be decreased. Now, this is something that you’ve seen in physiology, but then how do you put this into play when you’re dealing with pathology? Well, , let’s say that your patient has centrilobular type of emphysema. What is centrilobular emphysema mean to you? It means that this has nothing to do with alpha-1 antitrypsin deficiency, the patient is a smoker introducing neutrophils and elastase into the system abundantly, excessively, right? So now, at this point, the alpha-1 antitrypsin is overwhelmed and so therefore cannot properly handle a load. So, therefore you would have damage to maybe the upper middle portion of your lung but then could you have other portions of the lung that still might be working? Sure. Now, in centrilobular emphysema you’ve lost enough of your respiratory apparatus in which your oxygen is going to be depressed. And no matter how much you hyperventilate pathologically because you’re on that plateau phase or plateau region, you are not going to compensate for the oxygen, is that clear? So hypoxemia, is going to persist. However, because of linear fashion of your carbon dioxide, in this regional areas where compensation is taking place, is it possible that you might be blowing off the carbon dioxide even in emphysema or COPD where your carbon dioxide that you expect it to be higher would be perhaps normal or even perhaps hypocapnic? Yes. So from henceforth, clinically, you will then read in journals, in clinical vignettes, speak to pulmonologists in which emphysema could actually have with or without hypercarbia.

08:09 Huge point, but if your physio wasn’t strong which I’m hoping that through us, together we were able to bolster your education and really be able to integrate things.