or hypercarbia or it could be mixed between
Acute hypoxemia is where we are. We always have
to be a little bit more detailed. It’s a
V/Q mismatch, improves supplemental
oxygen. So, this, for example, gives you examples
such as pneumonia, COPD flares and PE. Remember
that no matter any time during a disease course
of your lungs that supplemental oxygen is
given, but you always have to utilise caution
because of that condition
that we called your hypoxic drive.
But, if it’s COPD flares, then you are left
with really not much of an option.
Now, something that you wanna keep in mind
and something that you very much want to understand
is the fact that what if your alveoli was
to collapse. This then brings us, take a look
at the abbreviations here, ALI stands for
acute lung injury or we have acute respiratory
distress syndrome. What these have in common
is the fact that ultimately, the alveoli
disappear. And when your alveoli disappear,
they’re no longer present. Understand that
this is called a pulmonary shunt. What does
a shunt mean to you? A shunt means that you’re
passing from one side to the other. You
all are extremely familiar with shunting in the
heart. So, why would you be so familiar with
shunting in the heart and maybe, well, at
some point, you’re not so familiar with
the shunting in the lungs? The only way that
you can get shunting of your blood from the
pulmonary arterial side, which is normally
how much of PO2? Approximately 40. To get
your PO2 of 40 to your pulmonary veins, you
shunt across an alveoli that no longer is
present. Is that clear? So, this is a intrapulmonary
type of shunt.
Now, if there is intrapulmonary type of shunt,
if you were to give this patient oxygen, if
that alveoli is dead, how in the world would
you expect there to be a significant response?
That’s my point. You don’t get one. Now,
the same thing can also be applied to intracardiac
shunt. For example, say that you had a right
to left shunt at some point in time.
A right to left shunt. If you did, then you
get deoxygenated blood into your left side,
from your right side, you’ve shunted your
lung and thus by giving oxygen, are you truly
having a response that you, well, expect?
No. Look for that particular clinical description.
Next, what else may cause acute hypoxemia?
Well, low FiO2. What does that mean? Now be
careful. You know me, at this point to be extremely,
or try to be, as accurate as possible every
single statement that I make. And so, therefore,
I’ve said earlier that FiO2 does not change
on planet, Earth, right? And by that I mean
what? Well, the fraction
that you’re breathing in of oxygen on planet
Earth is always going to be 0.2. "So, Dr. Raj,
why in the world are you seeing an FiO2 decreased
here, especially in the sense of high altitude,
does not contradict with what you say?" Well,
you’re thinking it and I absolutely accept
and welcome that question. But, the fact is,
if you’re going to high altitude, what is
it that truly decreases? Your barometric pressure.
Now, you tell me, ambient air, what’s the
simple equation of just ambient air?
It’s the fact that you take your barometric
pressure and you multiple by what? FiO2. So,
at sea level, if it’s 760 that you’ve
memorised, you multiple that by 0, what
do you get? 160. That’s normal. Sea level.
FiO2 in totality. However, if you
take the same equation and you put it in to
high altitude type of environment, where now
may be 250 times 0.2 then how low has that
FiO2 dropped to? Point is, you kept your 0.2
exactly the same. Ultimately, in high altitude,
you have low FiO2. Would that result in acute
high altitude sickness? Oh, yes.
What else? Impaired diffusion. Now things
become a little bit easier. What this basically
means is the fact that you’re not able to
properly cross your barrier. What barrier?
The barrier between the alveoli and trying
to get your oxygen into your pulmonary capillary.
Impaired diffusion, couple of important
points that we already discussed. A-a gradient widened
or normal, please? Good, widened. What are
some things that you wanna take in consideration
for A-a gradient? The age is a big one, right?
And the other big one is the fact that if
you were to then increase your FiO2 in hospital
setting. Okay. Now, the other big point to
test is going to be DLCO. Your DLCO laboratory
examination with the impaired diffusion would
find a decrease DLCO.
Hypoventilation can cause hypoxia, but this
occurs with (and due to) hypercapnea. So,
hypoventilation, if there isn’t enough
breathing, please understand that you’re
having a decrease in oxygen, but that you also
end up having an increase in carbon dioxide.
That’s not good. That displaces everything.
Acute respiratory failure is my issue. We’ve
walked through some important points of acute
hypoxemia. Let’s continue.
Now, the five possible physiologic causes
of hypoxia. Hypoxic respiratory failure is
almost always caused by a V/Q imbalance or
a shunt. And by V/Q imbalance, we’re referring
to something like perfusion defect, ventilation
defect and dealing with a diffusion defect
Continue forward. We have differentials now,
for acute type of hypercapnea. Ventilatory.