So let's continue with
this inflammatory response.
Now you end up with
a leaky membrane.
When you have a leaky membrane,
fluid starts shifting.
That's how we end up with an
extra fluid in the alveoli.
Now, look what you've got down
there, look proteases blink blink.
You've got some fibroblasts.
Yeah, that's not real good,
those are kind of stiff,
that interstitium, right?
That's now getting
widened and edematous.
That means we got fluid
building up there.
It's going to make it
hard probation to breathe
because they're going to
be able to get oxygen in.
They just can't get it
into the blood supply.
So these leaky membranes and fluid
shifting is really a big problem.
It's because of that
damage to the endothelium,
allows the cells in the fluids to
leak into the interstitial space
and that causes
the pulmonary edema
and then it continues to keep
leaking into the alveoli.
That is a ton of information,
so make sure you really have that solid.
Look at the picture,
what do you have there?
What are the names of those cells
that are migrating into the alveoli?
We know they make a lot of
havoc once they get in there.
What's happening to
It's getting wider.
It's getting full of fluids,
it's getting edematous
and that's what we mean
when we say pulmonary edema.
Okay, so that's how the
aveoli ends up filled.
We know what pulmonary edema is and we
see that interstitial getting wider.
We got the proteases
has the fibroblasts.
There are a lot of changes
happening on a cellular level.
Now one more thing I want to
tell you about this phase.
Patients in this phase are at
an increased risk for clotting.
Okay, so make sure you
have that written in.
You can see that this is a really delicate
system, things are getting out of control.
Now, if we add clots on top of that,
it's really going to be problematic.
It depends on how big the clots
are, where they're located.
But look down there, so you've got the
platelets in there just to remind you.
If the patient is at an
increased risk for clotting,
we could end up with some
very inconvenient clots.
You know pulmonary embolism can
cause immediate deaf for a patient.
So a patient in ARDS in this phase does
have an increased risk for clotting.
You're going to want to keep an eye
on that and the patient's lab work.
Now damaged and dying pneumocytes mean
poor oxygen-carbon dioxide exchange.
Okay just doesn't work.
So, why are these
cells being damaged?
Because of all this inflammation
that's going on there
and it's filled with all these
substances and it's just not working
the way it is intended to work.
So those cells that fragile one cell
alveolar wall membrane is getting damaged
and those cells are not just
damaged but they're dying.
We talked about these pneumocytes,
that's the type l and the type ll,
without those being intact we
know a long as not very compliant
and it doesn't exchange
O2 and CO2 very well.
Also, when these cells are
damaged, we have less surfactant.
And what we do have
is not very effective.
That puts us at an increased
risk the alveoli to collapse.
So, see how the inflammatory response
is good until it is out of control.
This is a very clear example
of when it is out of control,
and it is overwhelmed, the body.
Now we have this
alveolar collapse risk.
We know that it's
increased and we know why.
Because those cells are not able
to function and do their role.
We know that the type l and type
ll are damaged and they're dying.
They have inadequate surfactant and things
just aren't in the order they need to be
in order to have compliant lungs
and effective gas exchange.
Can you imagine trying
to breathe through this?
I mean, can you just stop for a
minute, just a really cool picture.
We're talking about a
lot of cellular stuff.
But stop and think about why this
is so brutal for our patients.
See this is why we can't
oxygenate them very well.
This is why their P/F
ratio is so low in ARDS.
Because we're trying
to get oxygen from here
down through all this goop
and it just doesn't work.
If you think this is bad,
I've got more to tell you about.