Hyaline Membranes – Changes in the Exudative Phase (Nursing)

00:01 Now, all this cellular debris, you've got dead cells, you've got protein-rich fluid.

00:06 Remember those proteases is all that is accumulating.

00:10 So in the picture, you can see we've got debris just to kind of remind you what that is.

00:15 We've also got fibrin.

00:17 All this stuff is building up in the alveoli and it's got to go somewhere.

00:22 So what do you think happens? This is where the waxy hyaline membrane forms.

00:28 So see it there in your picture.

00:30 This is what we were talking about earlier when I said remember hyaline membrane.

00:33 Now, I want you to actually see it.

00:36 This hyaline membrane forms from all this cellular degree.

00:41 So it's thick, its waxy.

00:42 It is not like our beautiful one cell of alveolar membrane.

00:47 It's horrible for CO2O2 exchange.

00:50 This is what makes you see that opacity is called crushed glass.

00:55 Yes, these are actual quotation marks live and in person.

00:59 But when we talked about opacities, we talked about crushed glass findings on chest x-ray.

01:05 This is what you're looking at.

01:06 This is what the alveoli looks like.

01:08 If we could zoom in on a cellular level that chest x-ray, that's what the alveoli likely looks like.

01:15 So what is that hyaline membrane made of? Yeah, it's all the junk, the debris in the dead cells and that alveoli build up and make a membrane that makes it even harder.

01:28 You're not just breathing through all this fluid.

01:30 Now you're trying to get gas exchange through a hyaline membrane with type l and type ll cells at just can't do the job like they used to.

01:40 So let's do a quick review.

01:42 You got an underlying cause that occurs.

01:44 We know it is direct or indirect, because we're smart like that.

01:48 Remember, you are smarter than nursing school makes you feel.

01:53 I promise.

01:54 Stay with us, keep engaging with the videos, you're going to be okay.

01:59 So let's do this quick review and you're going to be amazed at how much you know.

02:03 So the underlying cause occurs boom now, it's either a direct one or an indirect one.

02:08 We know sepsis is the most common.

02:10 It could also be severe pneumonia, major injury, pancreatitis, toxic inhalation.

02:16 Whatever it is, that happens.

02:18 Now these cytokines release which starts the process of this intrapulmonary shunting.

02:24 This is going on right inside the lungs.

02:27 Now the fluid shifts into the alveoli that's cost because the lymph system is overloaded.

02:32 Remember how that interstitium is full and edematous, the lymph system can't get rid of it quick enough.

02:38 So that's why we end up with the edema.

02:40 End result is poor O2 CO2 exchange.

02:44 Those pneumocytes have been damaged both type l and type ll.

02:49 We don't have enough surfactant and what we do have doesn't work very well.

02:53 So we have decreased lung compliance.

02:56 I've lost the ability to take oxygen in and breathe it out.

03:03 Everything in here is getting full and gunky and really kind of stiff.

03:09 So remember that hyaline membrane, what is it made of? Let's review.

03:15 Good, dead cells debris.

03:19 Nice.

03:20 You got it.

03:21 Now look at how that membrane is going to prevent oxygen from getting if we can get it into that alveolus.

03:29 That's going to be like putting a cap right on it, right? We can't get it down to that capillary very well at all.

03:36 Remember, it's necrotic cells, its protein and fibrin.

03:40 That's what makes up the hyaline membrane.

03:42 Hey, didn't we just talk about this? Yes this the third time I'm talking about it in this video, because it's critically important that you understand what this is.

03:52 Necrotic cells, protein and fibrin, and that's what makes the hyaline membrane.

03:58 It's also what makes ARDS so difficult to treat.

04:03 Okay, we can't go in just scrape that membrane off.

04:06 These are the types of lungs that were dealing with.

04:09 So they're deposited on that epithelial basement membrane.

04:13 Aha now, I hope it's making sense to you.

04:16 Remember we introduced the alveolus again? And I said, I want you to pay attention to that membrane.

04:22 Well this hyaline membrane deposits itself on the stripped or the denuded epithelial basement.

04:30 I love that word.

04:31 Denuded, yeah just means it's been stripped, it's damaged.

04:36 So, all that debris is landing down there right on that basement membrane.

04:42 And that is going to stick there, be waxy.

04:45 And almost impenetrable in the alveolus.

04:49 So you've seen how wicked these hyaline membranes look, right? Now, just thinking through logically.

04:57 We know that alveoli are one cell thick.

04:59 They are delicate.

05:00 The capillaries one cell thick, they have this close interaction with each other.

05:05 If we slam the concrete that is the hyaline membrane in there.

05:10 Things are not going to go well.

05:12 And that's why hyaline membranes contribute to pulmonary fibrosis.

05:17 Now pulmonary fibrosis is never a good thing.

05:20 My lungs need to be compliant, right? They need to be able to inhale to get larger and filled with air and then recoil and get smaller when I exhale.

05:30 That's what I need my lungs to do.

05:32 If they're full of this hyaline membrane stiffness, they just can't do that, like they normally would.

05:39 And because of that with this decreased compliance, loss with an increased risk for atelectasis.

05:45 That means collapse of the alveoli.

05:48 And you know that a collapsed alveoli absolutely can't exchange CO2 or O2.

05:54 So we know that the membrane can put you at risk for collapse, but it can also really impair the exchange diffusion of oxygen over these waxy membranes that are full of debris.

06:07 So the hypoxemia, remember the low oxygen in your blood can become severe or even refractory.

06:15 Yeah, that's why I wanted to bring our friends.

06:18 Well, they're not our friends.

06:19 That's why I wanted to bring the hyaline membranes back, because refractory hypoxemia is a hallmark sign of advanced ARDS.