Reparative and Proliferative Phase (Nursing)

by Prof. Lawes

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    00:01 Now, let's move to the Reparative or the Proliferative Phase.

    00:05 I've got some cool pictures for you up there.

    00:07 Monocyte, lymphocyte, neutrophils, right? Those are the PMNs and the fibroblast.

    00:13 Okay, so this inflammatory process is continuing on and that reparative or proliferative phase.

    00:19 So you've got an influx of these critters, neutrophils, monocytes, lymphocytes and fibroblasts.

    00:26 Remember those fibroblasts make everything stiffer.

    00:30 So, the monocytes, lymphocytes, and neutrophils are responding to this infection and this inflammatory response.

    00:37 The fibroblast make things everything's differ because this is what happens in response to that initial injury in the first phase.

    00:46 So, this second phase is the reparative or the proliferative phase.

    00:51 Hey, underline the word, proliferative because I think this name makes better sense.

    00:56 Because of that initial injury that the lungs have gone through, the connective tissue and other structural elements in the lungs increase rapidly in numbers.

    01:05 Okay, so we got a lot of things going on.

    01:08 These particular cells are proliferating.

    01:11 That's why I like that name of the face to be included.

    01:15 Now, it's trying to repair things, that's why the other option is the reparative phase.

    01:19 But keep in mind, we got a lot of cells proliferating or rapidly replicating.

    01:26 So, there's some special risk to your patients in this phase.

    01:30 If you're caring for a patient with ARDS, now you got to know that there's an increased risk for pneumonia, sepsis, because of all of these going on they're limping along.

    01:40 So, if they didn't have sepsis before they could develop an pneumonia, sepsis are also at risk for their lungs rupturing.

    01:46 Remember these are fragile walls, and they've taken some major hits.

    01:50 So, we're at risk for these lung walls to rupture or these alveoli walls to rupture.

    01:56 If that happens, air which is supposed to stay right dissolved in the water supposed to orderly go across the alveolar membrane into the capillaries and into the rest of the body.

    02:07 But if air starts leaking into the pleural space, now we've got another emergency.

    02:12 Because air in the pleural space means I'm risking a lung collapsing.

    02:17 I can't breathe efficiently.

    02:19 I can't create negative pressure if that pleural space is not intact.

    02:23 So, that's why I'm very concerned about lungs rupturing and air leaking into the pleural space.

    02:31 We talked about pleural space and air but let's talk about the pulmonary vasculature in the whole syndrome of ARDS.

    02:38 The pulmonary vasculature is significantly damaged.

    02:41 Remember those fibroblasts and those other inflammatory cells, they do damage to the pulmonary vasculature.

    02:49 So, you end up with increased pulmonary vascular resistance.

    02:53 You have increased pulmonary hypertension.

    02:56 Now, the lung compliance keeps decreasing here because you develop instertitial fibrosis.

    03:02 Congratulations! I just gave you a lot of textbook words.

    03:05 But what does that even mean? Well, the reason the pulmonary vasculature becomes damaged is what cells? The fibroblasts and the other inflammatory cells.

    03:18 They damaged the vasculature.

    03:20 So we're talking about the blood supply in the lungs.

    03:23 Now, what do these three things have to do with it? Well, if you increase pulmonary vascular resistance, it means the blood is going to have a harder time getting through.

    03:34 Because the vascular referring to the vessels, the vascular resistance going to be higher.

    03:40 So, it's going to be harder for that blood to make it through.

    03:43 That's why you have increased pulmonary hypertension.

    03:47 It's the blood pressure within the lungs.

    03:50 Oh that can't be good, right? I've got increased pulmonary hypertension back it up.

    03:56 Where is blood going to backup? Which organ is that going to make extra work for? Yeah, your heart.

    04:03 So, now this is going to be really hard on your heart depending on how big a difference, how much increased you see in the pulmonary hypertension.

    04:12 But that right ventricle is trying to push blood through the lungs and it's going to have to work harder to do it.

    04:19 The more severe it is, the longer it lasts.

    04:21 You're going to see some changes to that right ventricle trying to compensate.

    04:26 Now, the lung compliance.

    04:28 It keeps decreasing, that's getting worse.

    04:31 The lungs are getting stiffer, look we got some fibroblast going on there.

    04:34 It's getting harder to get blood through it.

    04:36 It's getting stiffer.

    04:37 And that's why lung compliance, right? That tissue just can't accommodate air anymore like it used to and that's why lung compliance keeps decreasing.

    04:50 We have this increasing interstitial fibrosis.

    04:55 Think back to our picture.

    04:56 Remember, all those fibroblasts were building up, that interstitial space needs to be flexible, in order to have good compliance in the tissue with those fibroblast and all this going on, it is stiff and lung compliance will be worse.

    05:11 Those alveolar membranes are thickening.

    05:14 That's another reason why the hypoxemia becomes worse.

    05:17 You have VQ mismatch, which we already talked about and the role that hyaline membrane.

    05:23 So the diffusion of the gases is significantly impaired.

    05:26 Those alveoli are full of gunk, the walls are damaged in the alveoli and the capillaries you got dead cells, you got hyaline membranes.

    05:33 All this is going on top of in this phase.

    05:37 We have a lot more cells proliferating.

    05:39 This is why it's so problematic, fluid starts shunting because it just can't follow its normal pathways.

    05:47 Now, we have fluid in the lungs and secretions in the airways because of this inflammatory response.

    05:53 So, now it's just not a level problem at the alveoli and capillaries.

    05:58 It's actually causing excess secretion in the airways.

    06:02 So now the delivery model of air from my mouth and nose down to those alveoli, even become somewhat compromised.

    06:10 Now, we're at the end of the reparative phase.

    06:13 The lung tissue is replaced.

    06:14 Now this can go well for your patient or this can go not so well for your patient.

    06:19 We know that the lung tissue has been replaced and that is the end of the phase.

    06:24 That's what it's signals.

    06:25 But it might be replaced with dense and fibrous tissue.

    06:30 Yeah, this doesn't bode well for lung compliance.

    06:33 Now some people, they have these lesions but they can resolve if the reparative process stops.

    06:39 Other people, it doesn't resolve and they end up going into a fibrotic phase.

    06:44 Now, this is not a universal outcome.

    06:46 Thank goodness! For patients with ARDS, not all patients go through this phase.

    06:51 Because remember, this is the end of the phase, right.

    06:55 if the end of the reparative phase, if the lung tissue has been replaced some people bounce back from this.

    07:01 The lesions are resolved, the reparative process that proliferating stops.

    07:06 And they can go on with a relatively normal life.

    About the Lecture

    The lecture Reparative and Proliferative Phase (Nursing) by Prof. Lawes is from the course Acute Respiratory Distress Syndrome (ARDS) (Nursing).

    Included Quiz Questions

    1. Cells rapidly replicate to repair
    2. Cytokines arrive
    3. Hyaline membranes develop
    4. Lungs become fibrotic
    1. Impaired diffusion of gases
    2. Fluid in the lungs
    3. VQ mismatch
    4. Reduced vasculature resistance
    5. Increased workload of the left ventricle
    1. Lung tissue is replaced with dense fibrous tissue
    2. Lesions do not resolve
    3. Lungs become fibrotic
    4. Alveolus walls become thin
    5. Bronchiole spasms occur

    Author of lecture Reparative and Proliferative Phase (Nursing)

     Prof. Lawes

    Prof. Lawes

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