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Unpack the evolution, pathophysiology, and modern treatment approaches of ARDS (Acute Respiratory Distress Syndrome). Join us for this enlightening episode of the CSPA Podcast as Dr. Jeremy Heiner, an esteemed educator with over 16 years of experience, dives deep into ARDS complexities, offering invaluable insights for ICU nurses and nurses pursuing CRNA.
Whether you’re a seasoned ICU nurse or a nursing student eager to expand your critical care knowledge, this episode is packed with essential information that will enhance your understanding and skills in managing ARDS. Tune in for a masterclass in respiratory care and gain practical knowledge that could be crucial in your next shift in the ICU.
Join the Free CSPA Community! Connect with a network of Aspiring CRNAs, Nurse Anesthesia Residents, practicing CRNAs and CRNA Program Faculty Mentors here: https://www.cspaedu.com/community
Get access to application & interview preparation resources plus ICU Educational Workshops that have helped 1,000s of nurses accelerate their CRNA success. Become a member of CRNA School Prep Academy: https://cspaedu.com/join
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Book a mock interview, resume or personal statement critique, transcript review and more: www.teachrn.com
Dr. Heiner has an extensive background in clinical anesthesia and is the co-author of several textbooks including Emergency Management in Anesthesia and Critical Care (EMAC), Critical Events in Anesthesia, & Nurse Anesthesia, the main textbook used by a majority of Nurse Anesthesia Programs.
Learn More about The Nurse Anesthesia: https://thenurseanesthesia.com/
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Watch the episode here
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Understanding ARDS with Dr. Jeremy Heiner: An In-Depth Look
Welcome back to the CSPA podcast. I’m so excited for today’s episode. It’s going to be taught to you by Dr. Jeremy Heiner, who has over 16 years as an educator. He is a passionate advocate for both student and CRNA education, and he has created dozens of clinical anesthesia trigger films, and he also hosts an anesthesia podcast, which you can find at thenurseanesthesia.com/podcast. It’s intended to advance CRNA learning and practice. He continues to work on the AANA, COA, NBCRNA and State Association Committees. He is also one of the primary authors and editors of the textbooks Nurse Anesthesia, Critical Events in Anesthesia and Current Anesthesia Practice, and today he’s going to teach you the pathophysiology process behind acute respiratory distress syndrome. So let’s go ahead and get into today’s show.
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Hello everyone. I am super excited to talk to you today. My name is Jeremy Heiner and I’m with The Nurse Anesthesia. But first before I get going, I want to thank Jenny and all the folks at CRNA School Prep Academy for this opportunity to speak on their podcast. They do great work and I’m very excited to be here with you today. So what I’m going to talk to you about today is something as an ICU nurse you’ve probably dealt with in the ICU, the condition called acute respiratory distress syndrome or ARDS. So get ready, get fired up because it’s go time! Now I’m going to start by asking you all a question. What was ARDS initially known as? Idiopathic pulmonary edema, shock lung, adult respiratory distress syndrome, anesthesia rocks during surgery, or acute respiratory distress syndrome? Well, the answer is idiopathic pulmonary edema.
We know of more than 60 possible causes for ARDS and we're still finding out more. Share on X
Believe it or not, back in 1821, this was what ARDS was first known as. Now over the years it’s been known as other things in World War I, world War ii. Even in the Vietnam War, it was termed shock lung because all the medics noticed some severe respiratory distress in combat veterans who experienced shock and significant hemorrhage. In the 1960s there was a series of case studies where physicians were noting respiratory distress and they termed it adult respiratory distress syndrome, and that’s the first known acronym where we see ARDS. Now, in 1994 there was an American and a European Consensus Conference where they revised ARDS and instead of adult, they turned it acute respiratory distress syndrome because it can happen in adults and in children. Now I feel like D could be an answer and it probably should be because it’s true.
Anesthesia does rock during surgery. Alright, so what is ARDS? Well, its an inflammatory form of lung disease. It’s acute because it’s serious and it happens pretty fast. It has a quick onset and it’s diffused, meaning it’s dispersed all over the lung, throughout the lung, and it’s associated with a variety of causes and etiologies. Now this type of lung insult leads to severe and rapid onset of dyspnea, hypoxemia and diffuse pulmonary infiltrates. So what’s the incidence of ARDS? Well, within intensive care units, we’ve seen that approximately 10 to 15% of admitted patients, up to 23% of mechanically ventilated patients meet the criteria for ARDS. And this condition is certainly higher in the elderly as compared to younger patients. Now, as I mentioned, it can be caused by a variety of insults. We know of more than 60 possible causes for ARDS and we’re still finding out more.
For example, during covid we found out that was a cause, but there are a few common causes and we can see them here in this chart. They’re the bolded ones, and as ICU nurses, you know that even there are more specific causes that lead to ARDS. So the majority of cases of ARDS cases are actually the result of sepsis or pneumonia. Now, ARDS can be caused by either a direct or an indirect lung injury. So we’ve already talked about pneumonia as a direct lung injury, sepsis would be considered an indirect lung injury. Other direct lung injuries of course would be aspiration of gastric contents, trauma to the lung such as a lung contusion, an inhalational injury, a near drowning reperfusion after cardiac bypass, and of course pulmonary embolism. Other potential indirect lung injury causes could be transfusion related acute lung injury. So these hematologic causes shock any form of shock drugs that affect the lungs such as chemotherapeutic agents or even drug overdoses and major surgeries such as cardiac bypass or even transplants and other known conditions such as acute pancreatitis.
What Is ARDS: ARDS can be caused by either a direct or an indirect lung injury
The Pathophysiology of ARDS Explained
So what’s the pathophysiology of ARDS? This is pretty interesting. Now to set the stage, normally healthy lungs, in healthy lungs, there is a regulation of fluid movement and this regulation keeps fluid out of the alveoli and a small amount in the interstitial space essentially keeps the alveoli dry. Now when ARDS happens, this flow of fluid is interrupted and part of what happens in ARDS is edema, but overall the pathophysiology of ARDS is essentially a result of either a direct or indirect lung injury, which is followed by an overactive inflammatory response. So the initial precipitating cause whether that be direct or indirect injury, causes an activation of our inflammatory mediators, the body’s own inflammatory mediators and the release of pro-inflammatory cytokines such as tumor necrosis factor and interleukins. Now these cytokines, they recruit neutrophils and platelets to the lung and what happens is when they become activated, they release toxic mediators such as reactive oxygen species and proteases.
Now these toxic mediators, what they do is they damage pulmonary epithelium and capillary endothelium. So essentially that avular capillary membrane that sits there and is very, very important for ventilation and the exchange of oxygen and carbon dioxide. So essentially it’s these neutrophils and platelets that are the primary culprits responsible for the inflammatory mediated damage that occurs in the alveoli and the capillary endothelial linings. Now ultimately this damage is important because these membranes, when there is damage to them, there is an increase in fluid into the alveoli. And essentially what ultimately what happens is an influx of protein rich fluid and inflammatory cells into the alveoli. What does this do? It causes airflow obstruction, a dysfunction of surfactant and the cells that produce surfactant and ultimately alveoli collapse. So here on this image we can see a picture of what happens in the pathophysiology of ARDS.
Now on the left is a normal alveoli and what we see here is a type two cell which produces surfactant, a surfactant layer, helping to keep the alveoli open, an active alveoli macrophage. We see bronchial epithelial cells up at the top that are tightly bound together and we don’t see any edema in the alveoli. Now when ARDS occurs and platelets neutrophils are activated, it’s very difficult to turn off the immune response once it’s activated. So once they’re activated and then they enter the alveoli, they promote that inflammatory response again, which is difficult to turn off and we can see some of the consequences of this overactive immune response. So what we see here is damage to the capillary endothelium and leakage of cells into the interstitium and then ultimately into the alveoli themselves. We see edema, micro hemorrhaging inflammation and inactivation of surfactant and essentially a breakdown of the alveoli cells.
Eventually, what we’ll see here at the bottom of this alveoli and what can happen all over the alveoli is the formation of what’s known as a hyaline membrane. This occurs from cellular debris, dysfunctional pulmonary surfactant and plasma protein aggregates. And when this hyaline membrane forms, it makes it very, very difficult for gases to be exchanged from the alveoli to the pulmonary capillary space and essentially oxygenation suffers. What are the consequences of ARDS? Well, we see this in the ICU, someone who is really difficult to ventilate because of a decrease in lung compliance. We’ll see high peak airway pressures and low tidal volumes, we’ll see a decrease in saturation. And when we look at ABGs arterial hypoxemia, this is a result of impaired gas exchange from VQ mismatching and pulmonary shunt. We’ll also see pulmonary hypertension a lot of times in these patients, and this can happen from a whole host of reasons, which you can see here on this slide.
Now the development of progressive pulmonary hypertension is not a good sign and it’s associated with a poor prognosis. So if we’re seeing pulmonary hypertension get worse and worse, that’s not a good sign. In terms of the signs and symptoms of ARDS, certainly we’re going to see severe arterial hypoxemia and many times this is resistant to increases in FiO2 concentrations. One of the reasons for this is because of pulmonary artery vasoconstriction and certainly some of those causes that were just noted in the previous slide from pulmonary hypertension. What happens within the lung is VQ mismatching and pulmonary shunt. The signs and symptoms we see would be before they’re intubated, dyspnea, respiratory distress, tachypnea, tachycardia. When we do chest x-rays, we’ll see infiltrates and you can see an example here on this slide, a normal lung on the left and a lung in the acute phase, the exudative phase of ARDS. Now once these patients are mechanically ventilated, they become very difficult to ventilate and we see high peak airway pressures.
The Stages of ARDS and Their Implications
ARDS does have a set of stages and not every patient will progress through these stages. They may. So we’ll talk about these stages here. So here in this image on the left, we have a healthy individual and a healthy alveoli, but what happens is some type of pulmonary insult, so whether that be a direct cause such as pneumonia or an indirect cause such as sepsis. And then what happens over a period of time is something known as the exudative phase. This is the first phase which consists of about the first seven to 10 days after exposure to a precipitating ARDS risk factor. The patient experiences the onset of respiratory distress and those respiratory symptoms we just talked about and many times it doesn’t take seven to 10 days and can actually happen within hours- within 12 to 36 hours after the initial insult.
Now if a patient, and of course the exudative phase here, we talked about in the pathophysiology of ARDS with the recruitment and overactivation of the immune response ending up in pulmonary edema. Now if a patient does not recover from the exudative phase, they enter what’s known as the proliferative phase after about the first 7 to 10 days. In this phase, there is very prominent interstitial edema and early fibrosis. Now the good news is that approximately three weeks after initial pulmonary injuries, most patients do recover and if we see a normalization of pulmonary artery pressures, that’s a good sign. It’s a good sign because it indicates that the syndrome is resolving and the alveoli are getting better. Now some patients end up going through until the fibrotic phase and this is a pretty rough phase. It can occur anytime after day seven of injury and onset of ARDS and it’s characteristic with a significant and substantial amount of fibrosis both within the alveoli and within the pulmonary interstitial space.
Now the degree of fibrosis can range from minimal to severe, and generally if a patient is in the fibrotic phase of ARDS, they’re going to require long-term ventilation. And these are just those tough patients that you have in the ICU that are just there for weeks on end and end up having all the complications, which we’ll talk about coming up. Certainly complicate pulmonary complications such as pneumothorax and other end organ complications as a result of hypoxemia the chronic hypoxemia that’s happening. So a lot of times these patients will have acute renal failure and even cardiac dysfunction. Now when the patient begins to recover from ARDS and they begin the recovery phase, this is characterized by a gradual resolution of hypoxemia. So the hypoxemia begins to get better, thank goodness, and we’ll start to see improvements in lung compliance. They become easier to ventilate and their chest x-ray starts to look better.
We start to see the alveoli open up and less pulmonary infiltrates. Now the reason that this occurs is because there begins to be a repopulation over here on the left in this image, a repopulation of the bronchial epithelium alveolar type one cells, and very importantly tight alveolar type two cells. These alveolar type two pneumocytes, which are super important for the production of surfactant fibrosis begins to break down alveolar macrophages become a lot more active and they start eating up cellular debris and dead neutrophils and there begins to be a reabsorption of the protein rich edema fluid within the alveoli. So it starts pumping that out of the cell, out of the alveoli and becomes much easier to ventilate these patients. Alright, so what are the treatment goals, the ARDS treatment goals? This is what you guys do all the time in the ICU when you’re caring for these patients.
Well, first and foremost, we need to take care of the initial insult. So if it’s sepsis, we need to give a broad spectrum antibiotic that’s broad enough to cover the suspected pathogens. Same with pneumonia, we got to treat that. So whatever the cause is, we need to figure it out and fix it. We’re also going to need to correct the hypoxemia and we’re going to do this with a protective lung strategy and we’ll talk about that in the next slide. One of the most important things we can do with an ARDS patient, many times we have to provide fluid restriction. And you’ve probably seen this in the ICU, a conservative fluid strategy, maybe targeting a CVP of four or less. Very common because we don’t want to give too much fluid and have a worsening in edema. Now if the initial insult is the result of trauma and hypovolemia, well we’ve got to correct that first.
And so yeah, there may be an initial amount of fluid and blood products that are given, but once that’s stabilized, usually when a patient experiences ARDS, we’ll have some type of fluid restriction. Now, many times these patients are on multiple vasopressors and vasoactive infusions, so you’ll see a lot of pumps and different vasoactive medications. ARDS patients have multiple risk factors for venous thromboembolism, and this is because of prolonged immobility and because of the activation of the coagulation pathways. So prophylactic strategies for those certainly would be to provide compression stockings or pneumatic compression devices and giving different variations of heparin, low molecular rate heparin or even heparin itself. Other potential complications can occur if they’ve been intubated and are in the ICU for a while, they could have pressure ulcers or GI ulcers. There is the risk of pulmonary aspiration from prolonged intubation and certainly if they have invasive lines in order to administer the vassopressors, we got to keep those lines clean to help prevent infection.
What is ARDS: Many times these patients are on multiple vasopressors and vasoactive infusions, so you’ll see a lot of pumps and different vasoactive medications.
Ventilator Protocol for ARDS
Now the evidence for providing steroids has historically been mixed, but there are newer studies that suggest that there is some benefit for low dose corticosteroids early in patients who experience moderate or severe types of ARDS. Let’s talk about this ventilator protocol here. As I mentioned, lung protective ventilation has unequivocally proven to reduce the mortality of patients with ARDS. And here’s the protocol. This was essentially based from a 2000 study known as the ARDS network study and in this study they found that lower tidal volumes and limiting inspiratory pressures was beneficial for ARDS patients, which seems obvious for us today, but back then it wasn’t so much. We used to give higher tidal volumes to these patients, but now we’re giving the recommendation is about six milliliters per kilogram of predicted body weight and sometimes even lower than that down to four milliliters per kilogram.
We definitely want to limit plateau pressures. Plateau pressures, less than 30 centimeters of water. In terms of ventilation goals, we’re going to target a PaCO2, we’re going to use that as a ventilatory guide and try to keep that within the physiologic norm. We can allow a small degree of hypercapnia, so this is known as permissive hypercarbia or hypercapnea, and we’re going to increase the FiO2 because of the hypoxemia that occurs. So inspired FiO2 concentrations, they’re adjusted, we adjust them to maintain a PaO2 of greater than 55, usually between 55 and 80 is pretty typical and an SaO2 of 88% to 95%. Now we want to do serial blood gases in order to look at these, and I have SpO2 on here as well because that’s just an easier one to look at all the time. So a lower SpO2 is okay in the lower area of normal.
Now it’s not uncommon to provide a lot of PEEP for these patients, so as the FiO2 is increased because of the degree of hypoxemia, a ventilator strategy will be to increase the amount of PEEP given. And recent studies have shown that patients with severe ARDS definitely benefit from these higher levels of PEEP. Here’s a chart that is showing all the predicted body weight and the tidal volume that you can give. So for example, if you have a patient who is 5’10”, it gives you the number for six milliliters per kilogram of 440. So that would be your tidal volume for an ARDS patient and for a female, a little bit less so just a chart to simplify, figuring out what kind of tidal volume you need to give. Now there are additional therapies that we do in the ICU to take care of these ARDS patients, prone positioning.
When we put a patient in the prone position, it helps improve functional residual capacity. It helps with diaphragmatic excursion and it repositions the heart. Share on XIt helps with recruitment of the alveoli, especially in the dependent lung zones. When we put a patient in the prone position, it helps improve functional residual capacity. It helps with diaphragmatic excursion and it repositions the heart. So a lot of times we’ll get an increase in an improvement in cardiac output. Now the prone physician has its challenges, no doubt about it. Our patients are intubated and we certainly risk extubation when we’re flipping these patients prone. You can see here in this image a patient with a lot of vasoactive drips who likely has an invasive line, so we risk pulling those out as well. We got to be really careful with that. And this patient is pretty skinny in this image. That’s not always the case, which can complicate things. Sedation and paralysis are frequently used for ARDS patients. Now, currently, in terms of other types of ventilation such as high frequency oscillatory ventilation, or even inverse ratio ventilation, we don’t have complete data for that and more studies really need to be done.
Now I do know that some intensivists use these ventilation strategies, but they’re typically reserved for a very severe ARDS patients and reserved for rescue ventilation therapies rather than primary ventilation therapies. Now, some patients with severe hypoxemia and hypercapnic respiratory failure may need to go on ecmo and I’m sure as ICU nurses, you’ve seen some of these patients moved on to ecmo. The goal of this therapy is to help overcome that severe hypoxemia and respiratory acidosis that’s occurring and letting their lungs rest. Other treatments that may occur or that may be initiated could be in inhale nitric oxide or prostacyclins. These are pulmonary vasodilators and they have shown to improve oxygenation, but their effects are transient, so they don’t last that long and they really haven’t shown overall an improvement in mortality because their effects don’t last that long. So it really depends on the intensivist comfort level as to whether or not they’re going to institute these therapies.
About The Nurse Anesthesia
Alright, everyone that does it for ARDS, Acute Respiratory Distress Syndrome. Now, before I go, I want to talk to you just a little bit about who I am and some of the fellows I work with and The Nurse Anesthesia. I partnered with two other individuals, Sass Elisha and Mark Gabot. We’re based in Southern California and we created The Nurse Anesthesia. We are nurse educators and we’re also clinicians. We still work in, every single one of us still works in the operating room. Together, we have over 50 years of teaching experience and it makes me feel really old to say that. We currently write many of the books that you will use in anesthesia school though. For example, Emergency Management in Anesthesia and Critical Care, like to call it EMAC. Critical Events in Anesthesia. And the main textbook used by the majority of nurse anesthesia programs, Nurse Anesthesia.
Now, our main goal at The Nurse Anesthesia is to give you an edge, to give you an advantage in your nurse anesthesia education. We know what it takes to succeed in anesthesia and in school. We want to set you up to be successful. We want to accelerate your nurse anesthesia learning boost your nurse anesthesia clinical experience, and we want to help you become the CRNA that you want to be. So if you’re an ICU nurse and you’re waiting to get into CRNA school or if you are a critical care RN and you just want to learn more about anesthesia and critical care, our courses are for you. If you’re a student in Nurse Anesthesia school, our courses are for you. We provide anesthesia and critical care courses that will help you stay ahead of the curve. We want to provide you with that essential knowledge that will help you succeed on your nurse anesthesia journey, you guys.
And we want to do it together. So check us out. If you want to learn more, check us out on the web at thenurseanesthesia.com. We’re also on social media, especially Instagram @thenurseanesthesia. And I got one more thing for you. We also have a podcast, The Nurse Anesthesia Podcast. That’s right. We like to provide free education as well. We’ve done some podcasting in the past and we’re back at it. The Nurse Anesthesia podcast. Here’s an example of some of the episodes that we’ve already released, and what we do is right here in the caption, we discuss anything anesthesia related. We’ll talk about CRNA school, we talk about clinical practice, we talk about Q and A, crisis management, really anything that pertains to the practice of anesthesia. So with all that being said, this is our favorite motto. Let’s get going because it’s go time. Thanks again to CSPA for this opportunity and I’ll see you next time.
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Thank you future CRNA for tuning in today’s episode. It was chockful of wonderful, dense information. I hope you absorb it like a sponge. And thank you, Dr. Heiner, for sharing your wisdom with us. We appreciate you. We hope to have you back on the show very soon. As always, thank you for tuning in and if you have not left a review yet of our show, I would greatly appreciate that. Until next time, take care.
Important Links
FREE! 8 Steps to Becoming a CRNA: https://www.cspaedu.com/ruxzegbt
Join the Free CSPA Community! Connect with a network of Aspiring CRNAs, Nurse Anesthesia Residents, practicing CRNAs and CRNA Program Faculty Mentors here: https://www.cspaedu.com/community
Get access to application & interview preparation resources plus ICU Educational Workshops that have helped 1,000s of nurses accelerate their CRNA success. Become a member of CRNA School Prep Academy: https://cspaedu.com/join
Get CRNA School insights sent straight to your inbox! Sign up for the CSPA email newsletter: https://www.cspaedu.com/podcast-email
Book a mock interview, resume or personal statement critique, transcript review and more: www.teachrn.com
Learn More about The Nurse Anesthesia: https://thenurseanesthesia.com/
