Neonatal Respiratory Distress Syndrome: TTN, RDS and PPHN

by Carlo Raj, MD

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    00:01 of sepsis and cardiogenic issues.

    00:01 Moving on, we are still having deadening of your alveoli instead of collapse of the alveoli.

    00:06 However, this time, the age group that we we are going to focus upon will be neonatal.

    00:12 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.

    01:09 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.

    02:49 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.

    03:19 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.

    04:26 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.

    05:00 And the alveolar is filled with fluid. Dr. Raj, is that reading right? Yeah, I told you.

    05:07 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 a miracle! 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.

    06:04 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 continue.

    06:51 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.

    07:02 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 happen? Now, we get into neonatal respiratory disorders. Okay, we will take a look at three major issues.

    07:25 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.

    07:35 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.

    07:53 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.

    08:09 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.

    08:32 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.

    08:46 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.

    08:59 Big time. Okay. Important.

    09:01 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.

    09:11 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.

    09:28 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.

    09:42 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.

    09:54 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.

    10:06 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.

    10:37 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 open. Fascinating! 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.

    11:25 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.

    12:51 So, this will be CPAP. Remember CPAP conversation? And this is continued positive airway pressure.

    12:59 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.

    14:08 Good topics. Move on. Now, we have... I am going to quickly just mention this to you.

    14:14 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.

    14:55 There will be an imbalance between the two, therefore giving you, persistent pulmonary hypertension.

    15:00 Let’s move on. Signs and symptoms of ARDS. Pretty straight forward now. So, once we have

    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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