00:01
Now, let's move to the Reparative
or the Proliferative Phase.
00:05
I've got some cool
pictures for you up there.
00:07
Monocyte, lymphocyte,
neutrophils, right?
Those are the PMNs
and the fibroblast.
00:13
Okay, so this inflammatory
process is continuing on
and that reparative or
proliferative phase.
00:19
So you've got an influx
of these critters,
neutrophils, monocytes,
lymphocytes and fibroblasts.
00:26
Remember those fibroblasts
make everything stiffer.
00:30
So, the monocytes, lymphocytes,
and neutrophils are responding
to this infection and this
inflammatory response.
00:37
The fibroblast make
things everything's differ
because this is what happens in response
to that initial injury in the first phase.
00:46
So, this second phase is the
reparative or the proliferative phase.
00:51
Hey, underline the word,
proliferative because I think
this name makes better sense.
00:56
Because of that initial injury
that the lungs have gone through,
the connective tissue and other
structural elements in the lungs
increase rapidly in numbers.
01:05
Okay, so we got a lot
of things going on.
01:08
These particular cells
are proliferating.
01:11
That's why I like that name
of the face to be included.
01:15
Now,
it's trying to repair things,
that's why the other option
is the reparative phase.
01:19
But keep in mind, we got a lot of cells
proliferating or rapidly replicating.
01:26
So, there's some special risk
to your patients in this phase.
01:30
If you're caring for
a patient with ARDS,
now you got to know that there's an
increased risk for pneumonia, sepsis,
because of all of these going
on they're limping along.
01:40
So, if they didn't have sepsis before
they could develop an pneumonia, sepsis
are also at risk for
their lungs rupturing.
01:46
Remember these are fragile walls,
and they've taken some major hits.
01:50
So, we're at risk for these lung walls to
rupture or these alveoli walls to rupture.
01:56
If that happens, air which is supposed
to stay right dissolved in the water
supposed to orderly go across the
alveolar membrane into the capillaries
and into the rest of the body.
02:07
But if air starts leaking
into the pleural space,
now we've got another emergency.
02:12
Because air in the pleural space
means I'm risking a lung collapsing.
02:17
I can't breathe efficiently.
02:19
I can't create negative pressure
if that pleural
space is not intact.
02:23
So, that's why I'm very
concerned about lungs rupturing
and air leaking into
the pleural space.
02:31
We talked about pleural space
and air but let's talk about
the pulmonary vasculature in
the whole syndrome of ARDS.
02:38
The pulmonary vasculature
is significantly damaged.
02:41
Remember those fibroblasts and
those other inflammatory cells,
they do damage to the
pulmonary vasculature.
02:49
So, you end up with increased
pulmonary vascular resistance.
02:53
You have increased
pulmonary hypertension.
02:56
Now, the lung compliance
keeps decreasing here
because you develop
instertitial fibrosis.
03:02
Congratulations!
I just gave you a lot of textbook words.
03:05
But what does that even mean?
Well, the reason the pulmonary
vasculature becomes damaged is what cells?
The fibroblasts and the
other inflammatory cells.
03:18
They damaged the vasculature.
03:20
So we're talking about the
blood supply in the lungs.
03:23
Now, what do these three
things have to do with it?
Well, if you increase
pulmonary vascular resistance,
it means the blood is going to
have a harder time getting through.
03:34
Because the vascular
referring to the vessels,
the vascular resistance
going to be higher.
03:40
So, it's going to be harder for
that blood to make it through.
03:43
That's why you have increased
pulmonary hypertension.
03:47
It's the blood pressure
within the lungs.
03:50
Oh that can't be good, right?
I've got increased pulmonary
hypertension back it up.
03:56
Where is blood going to backup?
Which organ is that going
to make extra work for?
Yeah, your heart.
04:03
So, now this is going to be really
hard on your heart depending on
how big a difference, how much increased
you see in the pulmonary hypertension.
04:12
But that right ventricle is trying
to push blood through the lungs
and it's going to have
to work harder to do it.
04:19
The more severe it is,
the longer it lasts.
04:21
You're going to see some changes to that
right ventricle trying to compensate.
04:26
Now, the lung compliance.
04:28
It keeps decreasing,
that's getting worse.
04:31
The lungs are getting stiffer, look
we got some fibroblast going on there.
04:34
It's getting harder to
get blood through it.
04:36
It's getting stiffer.
04:37
And that's why lung
compliance, right?
That tissue just can't accommodate
air anymore like it used to
and that's why lung
compliance keeps decreasing.
04:50
We have this increasing
interstitial fibrosis.
04:55
Think back to our picture.
04:56
Remember, all those
fibroblasts were building up,
that interstitial space
needs to be flexible,
in order to have good
compliance in the tissue
with those fibroblast
and all this going on,
it is stiff and lung
compliance will be worse.
05:11
Those alveolar membranes
are thickening.
05:14
That's another reason why
the hypoxemia becomes worse.
05:17
You have VQ mismatch,
which we already talked about
and the role that
hyaline membrane.
05:23
So the diffusion of the gases
is significantly impaired.
05:26
Those alveoli are full of gunk,
the walls are damaged in the alveoli
and the capillaries you got dead
cells, you got hyaline membranes.
05:33
All this is going on
top of in this phase.
05:37
We have a lot more
cells proliferating.
05:39
This is why it's so problematic,
fluid starts shunting
because it just can't
follow its normal pathways.
05:47
Now, we have fluid in the lungs
and secretions in the airways
because of this
inflammatory response.
05:53
So, now it's just not a level problem
at the alveoli and capillaries.
05:58
It's actually causing excess
secretion in the airways.
06:02
So now the delivery model of
air from my mouth and nose
down to those alveoli,
even become somewhat compromised.
06:10
Now, we're at the end
of the reparative phase.
06:13
The lung tissue is replaced.
06:14
Now this can go well
for your patient
or this can go not so
well for your patient.
06:19
We know that the lung tissue has been
replaced and that is the end of the phase.
06:24
That's what it's signals.
06:25
But it might be replaced with
dense and fibrous tissue.
06:30
Yeah, this doesn't bode
well for lung compliance.
06:33
Now some people, they have these
lesions but they can resolve
if the reparative process stops.
06:39
Other people, it doesn't resolve and
they end up going into a fibrotic phase.
06:44
Now, this is not a
universal outcome.
06:46
Thank goodness!
For patients with ARDS,
not all patients go through this phase.
06:51
Because remember,
this is the end of the phase, right.
06:55
if the end of the
reparative phase,
if the lung tissue has been replaced
some people bounce back from this.
07:01
The lesions are resolved,
the reparative process
that proliferating stops.
07:06
And they can go on with
a relatively normal life.