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Neonatal Respiratory Distress Syndrome: TTN, RDS and PPHN

by Carlo Raj, MD

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    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.


    About the Lecture

    The lecture Neonatal Respiratory Distress Syndrome: TTN, RDS and PPHN by Carlo Raj, MD is from the course Disorders of the pulmonary circulation and the respiratory regulation.


    Author of lecture Neonatal Respiratory Distress Syndrome: TTN, RDS and PPHN

     Carlo Raj, MD

    Carlo Raj, MD


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