of sepsis and cardiogenic issues.
Moving on, we are still having deadening of
your alveoli instead of collapse of the alveoli.
However, this time, the age group that we
we are going to focus upon will be neonatal.
Now, in order for you to truly understand
neonatal respiratory distress syndrome, it
is imperative that we understand the normal
first. So, what we shall do is walk through
all of the important changes that are going
to take place from foetal life to birth, the
neonatal. What are some of these important
changes? Things that I wish to remind you
or re-inforce is the following. 90% of the
newborns will successfully make the necessary
changes of being in utero to being given birth.
This statement right here is important. Now,
you listen to me first, then you read this.
Okay; Just like we have been doing. In utero,
within the womb of your mother, there you
are, you are swimming in the
placenta, even had webbing of the fingers
and such and at this point, your lungs, for
all intented and purposes, are just bricks.
That is what they were. They were bricks.
They were completely non-functional, right?
Because the mother, through her and the foetal
placenta, was then providing you with the
oxygen and so forth. So, why would you need
the lungs? In fact, don’t you have all those
bypasses, right? All the shunts so that you
can avoid the lung including your foramen ovale,
including ductus arteriosus. Speaking of which,
go there. So, there is my ductus arteriosus.
The pulmonary arterial pressure is quite high
because the lungs are bricks, they are not
alive yet because obviously the foetus is
not breathing. So, therefore, the ductus arteriosus,
go there for me. It connects your aorta to
the pulmonary artery, doesn’t it? Here,
in foetal life, what is my direction of blood
flow? Good. Pulmonary artery into the aorta,
in that direction. It has to be so that you
can avoid the lung. But, Dr. Raj, I thought
that PDA was a left to right shunt. Yes. Who
is your patient of PDA? You are out of the
womb of your mother, aren’t you? So, you
are not in the womb anymore. So, of course,
it’s your aorta, the pulmonary artery left
to right shunt. However, as a foetus, it’s
right to left. Hmm, amazing! Now, what is
this that is occurring in terms of your pressures?
So, now, let’s say, let’s read this a
little bit now, 90% will make that necessary
adaptive physiologic change from PaO2 of 25
during intrauterine. Stop there. What’s
PaO mean to you? Oh, that means arterial.
A measly 25, do you understand this?
Why is it only 25 in utero or in foetal
life? Because your pulmonary pressure is so
high, it is then taking up blood, getting
it into the ductus arteriosus and your systemic
pressure is really low intrauterine. Is that
understood? So, now, what must it rise
up to with birth? Obviously, it has to rise.
What is your PaO2 right now? What is it? It’s
close to 100. In utero, what was it? Close
to 25. Are we clear how low this is? Okay,
now, what are you going to do? Birth has taken
place, delivery has taken place. You have
now removed a resistor from a parallel. My
goodness, Dr. Raj, you are so mean! How could
you talk about the infant as being just a
physiologic resistor? Because that is what
we are doing, we have to. That baby was a
resistor, that infant was a resistor. And
when you remove the resistor from the parallel
because the mother, pregnant, the foetus was
adding the parallel. Therefore, the systemic
pressure was low. What happens to resistance
when you add it to a parallel? Oh, it decreases
pressure, as referring to systemic side. Remember
that from simple physics way back in the day?
Physiology applied to your patient. Now, you
remove the child, you remove a resistor from
a parallel. What happens to resistance? It
increases. Take a look at your PaO2 here.
It increased, as it should. That is a
major change in a foetus, isn’t it? That
is point number 1. When does that occur?
Within minutes of extrauterine life. That
is amazing, isn’t
it? Do you understand what is happening here?
I mean, seriously, physics and physiology,
in terms of real life, to actually occur is
fascinating to me. I am sorry, I get excited.
That is point number 1. What about point
number 2? Wow, do you remember that lung
in a foetus? Intrauterine, it was a brick.
And the alveolar is filled with fluid. Dr.
Raj, is that reading right? Yeah, I told you.
In a foetus, there is no use for
the lung. So, therefore, the alveolar is filled
with fluid. What is it filled in right now
with you? I hope it is filled with air. The
fluid has replaced by air. That’s, oh my
goodness, that is point number 2, that is
Let’s keep moving. So, now, what happens?
Onset of breathing. So, why is that important?
The child is born. So crying is
taking place. You have to
introduce oxygen into the foetus.
You have to. Listen to this one. Ready? So,
what about that ductus arteriosus? Ductus
arteriosus is kept open by whom? The prostaglandin,
right? The prostaglandin. So, that keeps it
open, okay. And then after birth, what happens?
Oh, you remove the prostaglandin. Good. Then
what happens to ductus arteriosus?
It should close. And then now you have your
flow with increased pressure in systemic artery.
Oh, you tell me now. The pulmonary pressure,
what happens? Obviously, decreased. You don’t
want a lot of pressure to lung, right? You
don’t. You just want a little bit of pressure
so you can get the blood there, so then you
can have gas exchange. Just enough pressure,
so you can have oxygen exchange. Just enough,
okay? Not too much because then you damage
your lung, you don’t want that. Is that
clear? So now, you are going to then allow
for the baby to cry. There
is all this oxygen, what is it going to do
to the prostaglandin? It will remove it. It
has to, because what if you don’t remove
the prostaglandin? Oh, welcome to patent ductus
arteriosus. What is your method of treatment
there for management of PDA? Good. Indomethacin.
You are removing the prostaglandin. Let’s
Increase in pulmonary blood flow via increase
in systemic vascular resistance. Oh, we already
talked about that. So, we got through the
major points here, physiologically. Big time.
This must be understood. In the meantime,
though, also run what week were thinking
about surfactant synthesis? About 27 or 28
weeks, right? And that surfactant is
imperative. It’s absolutely mandatory for
it to exist so that you keep your alveoli
nice and open. So, guess what is going to
Now, we get into neonatal respiratory disorders.
Okay, we will take a look at three major issues.
Current day practice. These are the things
that you want to know. Let's first take
a look at what is in this transient tachypneic
or transient tachypnea of the newborn.
So, what is the baby doing after birth? Breathing
really fast, tachypnea. What happened? Well,
it’s caused by failure of adequate lung
fluid clearance. Really? Remember what I just
said. I just said in the foetus, what about
your alveoli? Oh, it’s filled with fluid.
Correct. And then like that, the fluid has
to be replaced by air. You really telling
me that is going to happen that quickly? May
not happen that quickly. So imagine,
this newborn now, and there is a little bit
of fluid in the alveoli.
That infant is not going to feel
very good. So, what do you think that infant
is going to do? Start panicking and tachypnea
is what we have. So, most frequently seen
in late pre-term. What if the fluid does not
get properly replaced by the air? Usually
about 34-37 weeks. Are we going to have enough
surfactant here? Yes, we are. Yes, we are.
But, distress? Sure. Why? Fluid. The onset
of TTN, what do you mean? The transient tachypnea
of the newborn, nasal flaring because of
it’s trying to breath real fast.
Breathing hard. And what about these accessory
muscles? Involved as well. Retraction, look
for that. Expiratory vocal cord grunting
with two hours after delivery. Look for that.
Big time. Okay. Important.
Now, the two impaired mechanisms could be
well, maybe there’s a problem with that
sodium epithelium channel. If I were you,
I would understand the concept at this point.
And then if you want to take a look at the
pathogenesis of why the fluid was'nt removed,
may be the sodium channel, which exists in
the alveoli, responsible for removing the
sodium. But, wherever sodium goes, yeah, food
goes. So, maybe there is impaired sodium channel.
Next, inability to adequately generate a transepithelial
hydrostatic pressure. So, anything that you
could possibly come up with in which the fluid
is not escaping the alveoli. So, another respiratory.
This is respiratory distress syndrome. And
this is the premature baby and less than 28
weeks. Why is that important? This is the
time in which the surfactant is being produced.
And so, therefore, if the surfactant is not
there, then you can only imagine that the
alveoli is then going to collapse. Welcome
to respiratory distress syndrome in a neonate.
The first one was a transient tachypneic,
right? And that patient was, how old was
that infant? Usually occurs in 34-37 weeks.
So, late-term. Here it is less than
28. Here, once again though there is going
to be respiratory distress. Decreased lung
compliance as you can expect. There is going
to be once again the grunting and preventing
end expiratory alveolar collapse. The baby
is actually doing this because here, there
is no surfactant. It’s not the fluid issue.
There is no surfactant, 28 weeks and before.
So, now, what do you think the newborn is
doing? Trying to keep the alveoli
open. Remember that pursing of the lips in
emphysema? You are not going to be able to
teach an infant who just got born, “Hey,
baby, purse your lips.” It’s not going
to happen. So, what is the baby going to do?
Right. So, he tries to keep the alveoli
So, what do we do here? Big time, pay attention.
You will do everything in your power to make
sure that you properly replace and
support this newborn. I can’t emphasise
how young this patient is. Preterm, my goodness!
So, tell me about the development of surfactant.
Okay, why do you need?
You need cortisol. Absolutely. And is pregnancy
stressful? I can only imagine. If I could,
I would be pregnant. I can’t, I am a male,
I don’t know what to tell you. But, I could
only imagine, if I had a baby right now, that
is rather stressful. So now, imagine if I
was to deliver. Oh my goodness, that is more
stress. So, what are you going to produce?
What is my point? With all that stress, what
is your stress hormone? Good. That is your
cortisol, isn’t it? So, anytime that you
feel stress, that is cortisol. So, now, during
pregnancy, that is a lot of cortisol that
that foetus is now being exposed to. Is that
important? Why here? Responsible
for proper alveolar type of development. So,
what is my therapy? Oh, take a look. Antenatal
glucocorticoid therapy, early intubation for
surfactant therapy. Fascinating! What else?
Well, may be that grunting. Why was the baby
doing that? Because trying to keep the alveoli
open. Obviously, you don’t want that to
occur for too long. It’s a neonate, for
pete’s sakes. And its muscles are going
to tire and it’s going to die. So, what
do you want to do? You want to keep the alveoli
open mechanically, well, not mechanically, excuse
me. By pressure. So, this is non-invasive.
So, this will be CPAP. Remember CPAP conversation?
And this is continued positive airway pressure.
You see this, you understand the pathology,
you understand the physio first with cortisol,
the weeks and such, then you know how to treat
your patient effectively. You have other things
that you can do. Do you remember the PEEP?
Positive end expiratory pressure? Oh, this
is going to then help you keep your? Good.
To keep your alveoli open. Next, in the mean
time, you give the oxygen. I am not done.
Neither are you. Pay attention. You have oxygen
here. You have to give oxygen, you have to.
The alveoli want to collapse. When you give
the oxygen, well, this is one of those catch
22 situations. You give the oxygen in the
newborn. At some point, there might be too
much oxygen and what may then happen? You
might then form free radicals. So, what is
this reactive oxygen species type of damage
taking place to a new born? Back here in the
eye, the retina. What is that called? Retinopathy
of prematurity, point number 1. Take a look
at this over here. We have bronchopulmonary
dysplasia. What is all this? What is causing
this? The oxygen that you are giving the new
born, you have to. You understand that. You
have to give the oxygen, but the things that
you keep in your mind is free radical damage
to your newborn.
Good topics. Move on. Now, we have... I am
going to quickly just mention this to you.
The two big ones were the tachypnea of the
new born and number 2, the surfactant deficiency
and then here, we have persistent pulmonary
hypertension in a newborn. Newborn, newborn,
newborn. This is a term infant, so there is
no prematurity here. There is going to be
increased pulmonary vascular resistance. Period.
Okay. Now, what you do need to keep in mind
and bring it to play here from physiology
is, please give me those things, those elements
that are being released by the endothelial
cell that are responsible for balance between
vasodilation, vasoconstriction. Endothelin
- vasoconstriction, nitric oxide - vasodilation.
There will be an imbalance between the two,
therefore giving you, persistent pulmonary
Let’s move on. Signs and symptoms of ARDS.
Pretty straight forward now. So, once we have