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.