02.05 Nursing Care and Pathophysiology of Acute Respiratory Distress Syndrome (ARDS)

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Outline

Overview

Acute Respiratory Distress Syndrome

  1. Causes – anything causing inflammatory response in lungs
    1. Bacteremia, Sepsis
    2. Trauma, fat embolus
    3. Burns + Fluid Resuscitation
    4. Massive transfusion
    5. Pneumonia, Aspiration
    6. Drug overdose
    7. Near drowning

Pathophysiology: There are 4 phases within acute respiratory distress syndrome (ARDS). ARDS occurs rapidly and usually within 90 minutes of the body’s inflammatory response and between 24-48 hours of lung injury. In phase 1 there is an injury to the capillary endothelium of the pulmonary system. In phase 2 there is an injury to the basement membrane, interstitial space, alveolar epithelium. The damage to the lungs causes permeability so now fluid fills the alveoli (where it doesn’t belong) and this will impair gas exchange. In phase 3 there is damage to the alveoli because of the fluid that causes atelectasis and hypoxemia. In phase 4 the products of cell damage cause the formation of a hyaline membrane. This membrane is thick and will further prevent oxygen exchange. In this phase with impaired gas exchange, respiratory acidosis occurs. The damage to the lungs that occurs can not be reversed.
Nursing Points

General

  1. Inflammatory Response
    1. Cytokines
      1. Alveolar damage
      2. Scarring
      3. Decreases lung compliance
    2. Increased capillary permeability
      1. “Floods” alveoli
      2. Decreases gas exchange
  2. Early recognition improves survival

Assessment

  1. Symptoms of underlying condition
  2. Chest X-ray → diffuse bilateral infiltrates
    1. “White Out”
  3. Refractory Hypoxemia
    1. P/F Ratio (PaO2 / FiO2)
    2. Mild  <300
    3. Moderate <200
    4. Severe <100

Therapeutic Management

  1. Treat underlying cause
  2. Ventilatory Support
    1. High levels of PEEP
    2. Prone position – improve flow into lungs
    3. Special Vent Modes
      1. APRV
      2. Oscillator
  3. Prevent Complications
    1. O2 toxicity – keep sats 85-90%
    2. Ventilator Acquired Pneumonia – prevent infection
    3. Barotrauma – keep volumes 4-6 mL/kg
      1. Damage caused by too much pressure in noncompliant lung

Nursing Concepts

  1. Oxygenation
  2. Gas Exchange
  3. Infection Control

Patient Education

  1. Educate family on severity of condition and probable course
  2. Possible need for tracheostomy
  3. Purpose for endotracheal tube and ventilator
  4. Recovery time, may need rehab
  5. Infection control precautions
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Nursing Care Plan (NCP) for Acute Respiratory Distress Syndrome

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Transcript

Hey guys, my name is Brad and welcome to nursing.com. And in today’s video, what we’re going to be doing is we’re going to discuss acute respiratory distress syndrome. Also known as ARDS. We’re going to take a little look into the pathophysiology behind ARDS. What is causing this respiratory distress? How is this going to manifest through signs and symptoms and how are we going to treat these patients? Let’s dive in.

Now, discussing some patho surrounding ARDS. Essentially what we’re dealing with here, in acute respiratory distress syndrome, is a leaky blood gas barrier. Now, what are we talking about? You will remember that at the end of our respiratory tract, what we have are these alveoli, these little grape-like clusters of alveoli, where actual gas diffusion occurs, gas exchange occurs. So what we can see also on the superficial portion on the surface of these alveoli are all of these pulmonary arteries and pulmonary veins, right, actually wrapping around the alveoli itself. And this is where gas diffusion occurs, right? We have oxygen that we’re going to breathe in. That’s going to go down into that alveoli, that’s then going to pass into those pulmonary veins and be carried to the rest of the tissues of the body. And we’re also going to breathe out. We’re going to have diffusion of CO2 back into those alveoli so we can breathe it out. And this all occurs across this alveolar capillary membrane, right? This direct connection of these capillaries touching the alveoli is what causes the formation of an alveolar capillary membrane, also known as a blood gas barrier, right? Now, what occurs in ARDS is actually a breakdown in this barrier, right? For one reason or another, we now have an insult and an injury to this barrier. And this actually allows and causes the passage of fluid from those vessels into the alveoli itself. This is what is occurring in ARDS. And as this fluid seeps into the alveoli itself, we end up having fluid accumulating within the alveoli. This is greatly problematic, right? This is an insult and an injury to the lungs. So what ends up happening? We ended up having an inflammatory cascade occur, right? The release of neutrophils, going to this site of injury. This fluid then accumulates within the alveoli. You may remember from anatomy there is actually a homeostatic production of something called surfactant and surfactant is produced by pneumocytes cells. And the entire purpose of it is to basically lubricate the inside lining of these alveoli so that whenever you exhale and the alveoli collapse, they don’t remain stuck closed. They’re lubricated. They’re able to open and close with no problem as you inhale and exhale. The actual formation of fluid in those alveoli destroys surfactant altogether. So now whenever these alveoli collapse they’re stuck closed and they remain stuck closed. And it’s also important to remember as this is now an insult and an injury to the lungs itself, what actually ends up forming is basically scar tissue within the lungs, in the form of something called a hyaline membrane. And this actual permanent scarring in the lungs then greatly reduces your ability to oxygenate the body. 

So what are some causes of ARDS? So what we can actually see here, this is a really, really interesting image that we have here. What we can actually see is an actual blood vessel, right? When one of these pulmonary arteries or pulmonary veins residing within the alveoli itself, right? You can actually see all of these little caverns, if you will, these grape-like clusters, these actual alveoli. Look at how incredibly delicate that is, how friable that tissue is, how delicate it is. You can imagine that anything that’s going to cause ARDS is going to be a result of pulmonary injury, right? This could be something like a pulmonary infection, okay. This could be sepsis, a thoracic trauma, right? Actual trauma  to the thorax. What about drowning? This is something else that’s taught whenever we talk about ARDS, actual fluid, going down into the lungs.  Basically things that are going to directly disturb and disrupt that blood gas barrier, the alveolar capillary membrane, as we destroy that membrane fluid from within that capillary is going to begin to seep into all of these grape-like clusters, into all of these alveoli and all of that patho that we just discussed is going to ensue.

Some assessment findings that we’re going to see in patients with ARDS. Of course, we’re going to see symptoms of the culprit cause, whatever it is that’s causing our ARDS, right? Pneumonia, sepsis, thoracic trauma, massive blood transfusion, near drowning, whatever it is, we’re going to see symptoms related to that cause.  Now, of course, recalling that our alveolar are filling with fluid. They’re just filling up with fluid in the O2 is having a much greater distance to cross that alveolar capillary membrane. As a result, we’re now chronically low on O2. We’re starving for oxygen. As a result, our respiratory system tries to compensate in the form of tachypnea.  Our heart tries to compensate, to pump more oxygen to those lungs in the form of tachycardia. Hypoxemia requiring mechanical ventilation, right? This is actually an ET tube that ends up, an endotracheal tube, that ends up going into the patient’s lungs to try and help them ventilate and breathe when they cannot do it themselves, right? Fluids filling up these lungs. So our surfactant is getting crushed and dissolved. We have an inflammatory response. All of these neutrophils coming to this new site of injury, the formation of this actual scar tissue, this hyaline membrane. All of these things are going to decrease our body’s ability to get O2 in. And as a result, our patients are going to need assistance breathing. PF ratio, less than 300. Don’t concern yourself with the ins and outs of that. Just know that a normal PF ratio is less than 300. We’re also going to be looking at chest x-rays, right? Over here we may see a more normal chest x-ray with these black lung spaces, but over here on the left, we can see heavy fluid accumulation in the form of this white, what we would sometimes call white out chest X-ray. All of this white appearance is fluid within the lungs. And what are we going to auscultate whenever we actually listen to those lungs, right? These bronchioles, these alveoli all have fluid in them. And so air is passing in and out across all of this fluid. We’re going to hear rhonchi, rales,crackles are very common.

 So how are we going to treat a patient with ARDS? Well, of course, we’re going to treat the culprit, right? If a patient has massive pneumonia that is now causing sepsis, we’re going to treat the sepsis. We’re going to treat the cause. And the source of whatever has led to this pulmonary insult. We’re going to again, have patients on mechanical ventilation, artificially ventilating the patient when their lungs are too damaged to do so on their own. Proning patients, right? Proning a patient simply means putting a patient face down in the bed, right? Instead of a patient being supine, we prone them chest down to the bed with the entire idea of allowing these posterior areas of the lungs to be able to expand, right? These posterior areas of the lungs are pointing up to the ceiling, right? We need to allow expansion of the lungs. Whenever a patient is laying on their back, flat in bed, their gravity is pulling these lungs down. It’s basically preventing the posterior portions of the lungs from expanding. So if we prone them, we can allow areas of the lungs that are otherwise collapsed to hopefully expand and begin to oxygenate better. And supportive therapies. Usually whenever patients, we experience it in the ICU all the time, whenever they’re mechanically intubated and mechanically ventilated, there’s going to be all sorts of supportive therapies that are going to go along with that, right? Vasoactive medications to keep their blood pressure up, sedation to keep the patient asleep. You know a lot of things that we’re going to be doing that are kind of critically care based, but that go along with the inclusion, whenever we’re caring for patients who have ARDS. 

So summarizing some key points from acute respiratory distress syndrome, remember that with ARDS, what we have is a leaky blood gas barrier, fluid is passing from those capillaries across that alveolar capillary membrane into those alveoli, leading to a lot of different problems. A lot of those different causes make sure that you familiarize yourself with those. Also the assessment findings, all of this as a result of fluid in those lungs, inflammatory response scarring in those lungs, et cetera. And all of the therapeutic management that we just discussed. 

Guys, that was acute respiratory distress syndrome. It’s a very intricate pulmonary process that is applicable across a wide range of causes, but it’s something that you may very well end up encountering in your patients. And it’s one that you’re certainly going to end up being tested on. So I hope this helped. I also hope that you guys go out there and be your best selves today. And as always, happy nursing.

 

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