00:02
Moving on.
00:03
We're still having
a deadening of your alveoli.
00:06
We still have collapse
of the alveoli.
00:08
However, this time, the age group
that we're going to focus upon
will be neonatal.
00:13
Now, in order for you
to truly understand
Neonatal Respiratory
Distress Syndrome,
it is imperative that we understand
the normal first.
00:19
So what we shall do
is walk through
all of the important changes
that are going to take place
from fetal life to birth.
00:30
The neonatal.
00:33
What are some of these
important changes?
Things that I wish to remind you,
or reinforces the following.
00:39
90% of newborns was successful make
the necessary changes
of being in utero
to being given birth.
00:47
This statement right here
is important.
00:49
Now, you listen to me first,
then you read this, okay.
00:51
Just like we have been doing.
00:54
In utero,
within the womb of your mother,
that you are
swimming in the placenta,
even at webbing, and the fingers,
and such.
01:02
And at this point, your lungs,
all intent purposes,
or just bricks.
01:08
That's what they were.
They were bricks.
01:11
They were completely
non-functional, right?
Because the mother through her
and the fetal placenta
was then providing you
with the oxygen and so forth.
01:22
So why would you need the lungs?
In fact, don't you have
all those bypasses?
Right?
All those shunts
so that you can avoid the lung,
including a foramen ovale,
including ductus arteriosus.
01:33
Speaking of which,
go there.
01:35
So there is my ductus arteriosus,
the pulmonary arterial pressure
is quite high.
01:41
Because the lungs are bricks,
they're not alive yet.
01:44
Because obviously,
the fetus is not breathing.
01:48
So therefore, the ductus arteriosus,
go there for me.
01:52
It connects your aorta,
to the pulmonary artery, doesn't it?
Here in fetal life,
what is my direction of blood flow?
Good. Pulmonary artery,
into the aorta, in that direction.
02:06
And asked to be
so that you can avoid the lung,
when that arise.
02:10
I thought that PDA
was a left to right shunt.
02:14
Yes. Who's your patient?
PDA.
02:16
You're out of the womb
of your mother.
02:18
Aren't you?
So, you're not
in the womb anymore.
02:21
So of course, it's an aorta
the pulmonary artery,
left to right shunt.
02:26
However, as a fetus,
it's right to left.
02:29
Hmm, amazing.
02:30
Now, what is this?
It's occurring in terms
of your pressures.
02:35
So now, let's read this
a little bit now.
02:38
90% will make that necessary
adaptive physiologic change
from PaO2 of 25 and
during interuterine, stop there.
02:46
What's PaO2 mean to you?
Oh, that means arterial.
02:52
A measly 25?
Do you understand this?
Why is it only 25 in utero
or in fetal life?
Because you're pulmonary pressure
is so high,
is then taking that blood,
getting it into
the ductus arteriosus
in your systemic
pressure is really low.
03:11
Intrauterine.
03:12
Is that understood?
So now what must it
rise up to with birth?
Obviously, it has to rise.
03:19
What is your PaO2, right now?
What is it?
It's close to 100.
03:25
In utero, what was it?
Close to 25.
03:28
Are we clear how low this is?
Okay, now,
what are you going to do?
Birth has taken place,
deliveries taken place,
you have now removed
a resistor from a parallel.
03:40
My goodness, Dr. Raj,
you're so mean.
03:42
How could you talk about
the infant
as being just a
physiologic resistor?
Because that's what we're doing.
We have to.
03:50
That baby was a resistor,
that infant was a resistor.
03:54
And when you remove the resistor
from a parallel,
because the mother pregnant,
the fetus was adding to parallel.
04:02
Therefore, the systemic pressure
was low.
04:03
What happens to resistance
when you add it to a parallel?
Oh, it decreases pressure,
as referring to systemic side.
04:11
Remember that from simple physics
way back in the day?
Physiology applied to your patient.
04:17
Now you remove the child,
you remove a resistor
from a parallel.
04:21
What happens to resistance?
It increases.
04:24
Take a look at your PaO2 here.
04:27
It increased as a should.
04:30
That's a major change in a fetus,
isn't it?
That's point number one.
04:35
When does that occur?
Within minutes of
extra uterine life.
04:39
That is -- can you met?
That's amazing, isn't it?
Can you understand
what's happening here?
I mean, seriously.
04:45
Physics and physiology
and in terms of real life
to actually occur
is fascinating to me.
04:51
I'm sorry, I get excited.
That's point number one.
04:53
What about point number two?
Wow! Do you remember
that lung in a fetus, into uterine?
It was a brick.
05:02
In the alveolar
it's filled with fluid.
05:05
That right.
Did that reading right?
Yeah.
05:07
I told you. In a fetus,
there's no use for the lung.
05:13
So therefore, the alveolar
is filled with fluid.
05:15
Was it filled in right now
with you?
I hope it's filled with air.
05:20
So the fluid has replaced by air,
that's... oh my goodness.
05:24
that's point number two.
That is a miracle.
05:27
Let's keep moving.
05:28
So now, what happens
onset of breathing.
05:30
So why is that important?
The child is born, right.
It starts crying taking place,
you have to introduce oxygen
into the fetus,
you have to.
Listen to this one.
05:41
Ready?
So what about
that ductus arteriosus?
Ductus arteriosus
kept open by whom?
The prostaglandin. Right?
Prostaglandin.
05:49
So that keeps it open. Okay.
And then after birth, what happens?
Oh, you move the prostaglandin.
Good.
05:57
Now what happens to
ductus arteriosus?
It should close.
06:02
And then now
you have your flow
with increased pressure
and systemic artery.
06:06
Oh, you tell me now.
06:07
The pulmonary pressure,
what happens?
Obviously decrease.
06:11
You don't want a lot of
pressure to your lung, right?
You don't.
06:14
Just want a little bit of pressure
so you can get the blood there.
06:16
So then you can have gas exchange,
just enough pressure.
06:19
So you can have oxygen exchange.
Just enough, okay.
06:23
Not too much, because then
you will damage a lung.
06:25
You don't want that.
Is that clear?
So now, you're going through then
allow for the baby to cry.
06:31
There's all this oxygen.
06:33
What is it going to do
to the prostaglandin?
It'll remove it.
It has to.
06:37
Because what if you don't move
the prostaglandin?
Oh, welcome to
patent ductus arteriosus.
06:44
What's your method of treatment
there for management, a PDA?
Good, indomethacin.
You're removing the prostaglandin.
06:51
Let's continue.
06:53
Increase in
pulmonary blood flow
via increase increase in
systemic vascular resistance.
06:56
Oh, we already
talked about that.
06:58
So we got to the major points here,
physiologically, big time.
07:02
This must be understood
in the meantime, though.
07:05
Also, Ron, what week are you
thinking about surfactant synthesis?
About 27-28 weeks, right?
And that's a fact
and is imperative.
07:14
It's absolutely mandatory
for you to exist
that you keep the alveoli
nice and open.
07:19
So guess what's going to happen?
Now we get into a
Neonatal Respiratory Disorders.
07:24
Okay, we'll take a look at
three major issues.
07:27
Current day practice,
these are the things
that you want to know.
07:31
At first, take a look at
what's in this transient tachypnic
or transient tachypnea
of the newborn?
So what the baby doing after birth?
Breathing really fast. Tachypnea.
07:42
What happened?
It was caused by failure of
adequate lung fluid clearance.
07:48
Really?
You know what I just said?
I just said in a fetus,
what about your alveoli?
Oh, it's filled with fluid.
07:53
Correct.
07:54
And then...
07:56
like that, the fluid has
to be replaced by air.
07:59
You really tell me
it's gonna happen that quickly?
May not happen that quickly.
08:04
So imagine this newborn, now.
08:07
And there's little bit of fluid
in the alveoli.
08:10
Excuse me.
08:11
That infant is not going to
feel very good.
08:14
So what do you think
that infants going to do?
Start panicking and tachypnea.
So we have.
08:19
So most frequently seen
in late preterm.
08:23
Or the fluid doesn't get properly
replaced by the air.
08:26
Usually about 34-37 weeks.
08:29
So we're going to have
enough surfactant here?
Yes, we are. Yes, we are.
But distress? Sure. Why? Fluid.
08:37
The onset of TTN. What do you mean?
The transient.
08:40
Tachypnea of the newborn?
Nasal flaring because of...
08:44
trying to breathe, real fast.
08:48
Breathing hard.
08:49
And what about these
accessory muscles?
Involved as well.
08:52
Retraction, look for that.
08:54
Expiratory vocal cord grunting
with two hours after delivery.
Look for that. Big time.
09:01
Okay, important.
09:02
Now, the two impaired mechanisms
could be
well, maybe there's a problem
with that sodium epithelial channel.
09:08
If I were you, I would understand
the concept at this point.
09:12
And then if you want to take a look
at the pathogenesis
of why the fluid wasn't removed?
Maybe the sodium channel,
which exists in the alveoli
responsible for
removing the sodium.
09:23
But wherever sodium goes?
Yeah.
Food goes.
09:27
So maybe there's impaired
sodium channel.
09:30
Next, inability to
adequately generate
transepithelial
hydrostatic pressure.
09:35
So anything that you could
possibly come up with
in which the fluid
is not escaping the alveoli.
09:42
So, another respiratory.
09:44
This is the
Respiratory Distress Syndrome.
09:46
And this is the premature baby.
09:48
And less than 28 weeks.
Was an important.
09:52
This is a time in which
the surfactant is being produced.
09:55
And so therefore,
if the surfactant is not there,
then you can only imagine
that the alveoli is then going to...
10:01
collapse.
10:02
Welcome to respiratory distress
syndrome in a neonate.
10:07
The first one,
was transient tachypnic, right.
10:09
And that patient was
how old was that infant?
Usually occurs in
34-37 weeks.
10:15
So late, late term.
Here is less than 28.
10:19
Here once again though, there is
going to be respiratory distress,
decreased lung compliance
as you can expect.
10:24
It is going to be once again
the grunting,
and preventing and expiratory
alveolar collapse.
10:30
The baby is actually doing this.
10:32
Because here
there is no surfactant.
10:34
It's not the fluid issue.
10:37
There is no surfactant
28 weeks and before.
10:40
So now, what do you think
the newborn is doing?
Trying to keep the alveoli open.
10:47
How about that pursing of lips
and emphysema?
You're not going to be able to teach
an infant who just got born.
10:55
"Hey baby! Purse your lips."
It's not gonna happen.
10:59
So what's a baby gonna do?
Alright. So he tries
to keep the alveoli open.
11:05
Fascinating.
11:06
So what do we do here?
Big time, pay attention.
11:09
You will do everything
in your power
to make sure
that you properly properly replace
and support this newborn.
11:17
You can emphasize,
how young this patient is.
11:19
Preterm. My goodness.
11:21
So tell me about
the development of surfactant.
11:27
Okay, what do you need?
Any cortisol?
Absolutely.
11:31
And is pregnancy stressful?
I can only imagine.
I if I could, I would be pregnant.
11:39
I can't I'm a male.
I don't know what to tell you.
11:41
But I couldn't imagine,
if I had a baby right now.
11:44
That's rather
stressful.
11:47
So now imagine, if I was to deliver,
oh my goodness, that's more stress.
11:52
So what are you going to produce?
What's my point?
With all that stress?
What's your stress hormone?
Good. That's your cortisol.
Isn't it?
So anytime that you feel stress,
that's cortisol.
12:03
So now, during pregnancy,
that's a lot of cortisol
that the fetus
has not been exposed to.
12:09
Is that important?
Mm hmm.
12:11
Why here?
Responsible for proper alveolar
type of development.
12:15
So what's my therapy?
Oh, take a look.
12:19
Antenatal glucocorticoid therapy.
12:22
Early intubation
for surfactant therapy.
12:25
Fascinating.
12:27
What else?
Well, maybe, that grunting?
Why was a baby doing that?
Because trying to keep
the alveoli open.
12:37
Obviously, you don't want that
to occur for too long.
12:39
It's a neonate for Pete's sakes.
12:41
And its muscles are going to tire
it's going to die.
12:44
So what do you want to do?
You want to keep the alveoli open.
12:49
Well, I'm mechanically,
excuse me, but pressure.
12:52
So this is non invasive.
12:54
So this would be CPAP.
I'm a CPAP conversation.
12:57
And this is continued
Positive Airway Pressure.
13:01
You see this.
13:01
You understand the pathology.
You understand the physio first.
13:05
With cortisol, the weeks and such.
13:07
Then you know how to treat
your patient effectively.
13:10
You have other things that you can
do to remember the PEEP,
Positive End Expiratory Pressure.
13:14
This is going to then
help you keep your...?
Good.
13:18
You keep your alveoli open.
13:20
Next, in the meantime,
you give the oxygen?
I'm not done.
13:23
Now there are you.
Pay attention.
13:25
The oxygen here,
you have to give oxygen.
13:27
You have to.
13:28
The alveoli want to collapse
and give the oxygen.
13:30
Well, this is one of those
catch 22 situations.
13:33
You give the oxygen in a newborn.
13:36
At some point, there might be
too much oxygen.
13:39
And what may then happen?
You might then form free radicals.
13:42
So what's this reactive oxygen
species type of damage taking place
to a newborn?
Back here in the eye.
The retina.
13:49
What's that called?
Retinopathy of prematurity.
Point number one.
13:54
Take a look at this over here.
13:55
We have bronchopulmonary dysplasia.
13:57
What is all this?
What's causing this?
The oxygen that you're giving
a newborn.
14:01
You have too.
You understand that?
You have to give the oxygen
but the things that you're
keeping in mind is
free radical damage
to your newborn.
14:10
Good topics. Move on.
14:12
Now we have, I'm going to quickly
just mention this to you.
14:15
The two big ones were the
tachypnea of the newborn.
14:18
And number two,
the surfactant deficiency.
14:20
And then here we have
Persistent Pulmonary Hypertension
in a newborn.
14:25
Newborn.
14:26
Newborn.
14:26
Newborn.
14:28
This is a term infant.
14:29
So there's no prematurity here.
14:31
There is going to be increased
pulmonary vascular resistance
period. Okay?
Now, what you do need
to keep in mind
and bring into play here
from physiology
is please give me those things,
those elements,
that are being released
by the end of the
endothelial cell
that are responsible for balance
between
vasodilation
vasoconstriction.
14:52
Endothelin, vasoconstriction.
Nitric oxide, vasodilation.
14:56
There'll be an imbalance
between the two,
therefore, giving you
Persistent Pulmonary Hypertension.
15:02
Let's move on.