00:01
This should look
familiar to you.
00:02
But let's do a quick review
because there's some additional
key structures.
I want to point out.
00:07
So I know that this is repetition
and that's in there intentionally.
00:12
Remember you're studying
with me as we go,
so I can minimize the time you have
to study outside of the video series.
00:19
Okay, so start the
top tray set around.
00:23
That's the alveolar wall,
one cell thick has two
types of cells in the wall.
00:29
Type l, those are the ones
that do the CO2O2 exchange.
00:33
Type ll, those are the short and
squatty ones that squirt out surfactant.
00:38
Good deal.
00:39
Now inside the alveolus you see the other
cell that's involved in ARDS, Macrophage.
00:45
Remember these are the cells if you
have a direct injury to the lung,
they're going to squirt
out those cytokines.
00:52
Now keep moving down.
00:54
Now you see the capillary that is
just snug around the single alveoli.
00:59
You know in real life there are
multiple alveoli all squished together,
but we extracted just one to show
you so we could really break down
and focus on the parts of it.
01:10
So you see the capillary, right?
It's also a one cell
thick membrane so that
O2 and CO2 can exchange
easily over that.
01:18
But two things I
want to point out.
01:20
You've got an epithelial basement membrane
and an endothelial basement membrane.
01:25
See their job is to kind of keep
things all in the right place.
01:30
But look at that little space in
between the alveolus and the capillary.
01:34
What's it called?
Interstitial space.
01:40
Yeah, so when your patient
has pulmonary edema,
you got a lot of
extra water in there.
01:45
It makes it really hard
for them to breathe.
01:50
Can you see why?
Well, if you feel that
interstitial space with
water and fluids and
all this stuff in there.
01:59
You can't have the gas exchange
between these two very good friends,
the alveoli and the capillaries.
02:06
Okay, but let's look at
that basement membrane.
02:08
Remember it's a thin
extracellular matrix, right?
Cool word.
02:13
Just means it kind of helps keep
things where it's supposed to be.
02:17
Now, this gets damaged.
02:19
We got a havoc, okay?
If the basement
membrane is not intact,
we're going to have some real
problems in the oxygen exchange.
02:27
So I want to look at the
changes in the exudative phase.
02:30
Let's take a look
at what happens.
02:32
I forgot to point out here
want you to take a look at,
what are those little
fellers in the bloodstream?
Those are what we call PMN's -
Polymorphonuclear White Blood Cells.
02:45
Cool, you got it.
02:46
Now if we filled in
all the blood cells,
you know,
what other ones would be there.
02:49
There's five types
of white cells.
02:52
You've got red cells,
you've got platelets,
but we're keeping it
straight forward and clean.
02:56
I want it simple.
02:58
So your brain can focus
on the key players.
03:01
But you know in real life, what would
be flowing through that capillaries
are all of the blood cells.
03:07
Okay.
03:07
So there's a healthy alveolus.
03:09
I wanted you to compare it too.
03:11
Yes, here's what goes on
and something that
is experienced ARDS.
03:16
I mean, how did we end up here?
Well, look at the difference.
03:21
Now, you've got type
l on both sides.
03:24
We've got type ll on both sides.
03:26
We've got a macrophage right in the middle
to remind you there on both sides but,
look at the difference,
see that term alveolar flooding.
03:35
Whoa.
03:36
That is full of a lot of fluid.
03:39
There's no way this is
going to be able to function
as effectively as the
healthy alveoli on the left.
03:46
Look at the difference in
the interstitial space,
and the healthy one
is tight and even.
03:53
In the one that's in trouble.
03:54
It's starting to get bigger.
03:57
Look at that endothelial
basement membrane on the left.
04:01
It's intact on the right.
04:02
We've got problems.
04:06
What is that PMN doing?
What is that?
Little guy is not supposed to be
migrating, that's what they call it.
04:13
So this responder is migrating
up through into the alveoli.
04:19
He does not belong there.
04:22
So let's walk through
what happened?
What is the process that we end
up going from a healthy alveolus
to this problematic,
not efficient alveoli?
So ready.
04:35
Let me walk you through step-by-step
how we end up in this mess we call ARDS.
04:41
Now after the cytokines arrived,
remember if it's a direct lung injury.
04:46
Who squirts out the cytokines?
Right, the macrophages
released the cytokine.
04:52
If it's an indirect lung
injury, how do they arrive?
Right, the cytokines
arrived in the bloodstream.
05:00
So we're all on the same page.
05:01
The cytokines are here, right?
That's what we're talking about.
05:04
Now, I want you to put your
finger on the endothelial cells.
05:09
Where are those?
So put your finger on the
drawing on the endothelial cells.
05:14
So when these cytokines arrived,
these cells are going to secrete some
additional inflammatory molecules.
05:22
Now what these molecules do
is they cause circulating immune
cells like the neutrophils,
to stick to the
endothelial cells.
05:33
Got it.
05:34
Cytokines are there.
05:35
The endothelial cells from
here in real close contact
with the alveoli also got
things in your bloodstream.
05:42
So what happens is those endothelial
cells, it's their job.
05:46
They're doing the right thing.
05:48
They start secreting these
other inflammatory molecules
that cause the circulating
immune cells to stick to them.
05:54
So see the neutrophils.
05:56
Those are some of the
circulating immune cells
that will stick to that
endothelial membrane.
06:03
Now when the neutrophil stick
to the altered endothelium,
they can start to begin to migrate
through that damaged capillary wall
and into the alveoli.
06:13
That's how the PMN's
get from the bloodstream
into the alveoli.
06:19
Remember cytokines arrived,
the endothelial cells start
excreting the sticky substance.
06:24
So circulating immune
cells stick to them.
06:27
It's damaging the walls
when that wall is damaged.
06:31
Now this endothelium
has been altered
and now those cells
can migrate through the
damaged capillary wall
and into the alveoli.