top of page

ARDS: The Death You Didn't Know You Were Responsible For




In the field we are often confronted with a sick and dying patient and our only thought is of the short-term resuscitation of the patient. In fact, most of us will say that out-loud, “as long as they’re slightly more alive when I drop them off (as compared to when I picked them up), that’s a win.” I don’t care what happens to the patient after I drop them off, as long as they’re alive when I drop them off. Unfortunately, I think that’s a huge problem in EMS and has been since its inception. We want so badly to be “different” from the in-hospital people that we don’t consider the continuum of care when we’re doing our interventions.

 

One issue that I’m talking about is ARDS. Now, most paramedics have heard of this syndrome, and almost every flight clinician has taken care of an ARDS patient. ARDS is characterized by a slew of issues happening in the lungs. There are both direct pulmonary causes – pneumonia, inhalation injuries, etc.. – and non pulmonary causes – sepsis, pancreatitis. What I would like to focus on is our resuscitative phase of treating these diseases. To date, all studies that looked at septic patients blamed the aberrant immune response for the development of ARDS in almost 27% of septic patients.

 

I wonder if the emergency care was the culprit in many of these patients. Unfortunately, there aren’t any studies that I’ve seen where ventilator-induced lung injury (VILI) was removed as an independent factor in the presence of these patient’s diagnoses. Yes, we know that sepsis carries a high risk for the development of ARDS, but is it the sepsis itself, or is it the fact that we’re overloading these patients with IV fluids and injuring their lungs with our bag-valve masks?

 

Creating hypervolemia in the body secondary to over-resuscitation with IV fluids has been talked about for several years and likely doesn’t need repeating. However, the trauma we cause during bag-valve mask ventilation is something that only a few organizations will even admit to. I can walk into any of my local hospitals and watch a respiratory therapist absolutely obliterate a patient’s lungs during “preoxygenation”. I can respond to ANY 911 call in my county and watch a twenty-two-year-old firefighter commit murder with 1,200mL tidal volumes on a little old lady. Yet, they both go home and tell their spouses how they helped to save a patient today. They are completely unaware of the consequences from their actions and their agencies aren’t providing them with education or resources to change their ways. Why is this? How can we not see the problem? For starters, these patients are generally pretty sick. The fact that they develop ARDS on day five or six in the ICU was inevitable, wasn’t it? Or was it us and we just don’t follow a patient’s course for that length of time? I would argue it’s the latter.

 

When it comes to the risk for developing ARDS due to a lung injury, there are two different causes: volutrauma and atelectrauma. What are the differences between the two and how are each of them caused? First, we’ll look at volutrauma as this is the one everyone is more aware of. Even if you’re new to the world of critical care, you know that consistent tidal volumes of 10mL/kg of IBW is bad for your lungs. If you don’t work in critical care, take note of that volume. If you’re a 5’10” male, you have an ideal body weight of approximately 75kg. Meaning, a tidal volume greater-than-or-equal-to 750mL is injurious for your lungs. If you’re shorter than 5’10”, the volume needed to injure you is even less. That begs the question: how large are our tidal volumes when we’re breathing for patients with a bag-valve mask?

 

Enter stage left “It’s in the Bag: tidal volumes in adult and pediatric bag valve masks.” This study was released in mid 2020 and looked at the average tidal volumes amongst over 150 providers. These were doctors, registered nurses, paramedics, EMT’s, and respiratory therapists. Essentially, everyone who would potentially be ventilating a patient in real life. What did they find? The average tidal volumes delivered from the adult bag valve masks was 807.7mL. The study was set up for a 70kg patient so tidal volumes were supposed to be targeted at 560mL or less. Over 93% of the providers exceeded the 560mL mark on a consistent basis during the study period.

 

What are the ramifications of exceeding our tidal volume targets? When excessive volumes are introduced into the lungs, it accelerates the lungs natural desorption of surfactant. Additionally, the lungs cells are stretched and injured, causing macrophages to secrete inflammatory substances (cytokines). This causes two problems. The reduction in surfactant causes the alveoli to collapse between breaths, making it more challenging to open them up in each subsequent breath. The inflammatory response reduces the usable surface area of the alveoli and causes an overall reduction in the lungs compliance as surface tension increases.

 

The solution to this is that we need to ensure we’re delivering smaller tidal volumes. I’m not convinced that education will be sufficient on this front, as people tend to revert to the old ways when they’re in a stressed environment. To take the “human error” out of this equation, we could remove adult bag valve masks from the resuscitation room and replace them with pediatric bag valve masks. In the study mentioned above, the same providers who delivered around 810mL tidal volumes (with the adult BVM) were only delivering around 630mL tidal volumes when given a pediatric (small adult) bag valve mask. Simply taking the tool out of their hands and giving no feedback was enough to reduce tidal volumes by almost 200mL.

 

What would happen if the entire medical community decided to implement a robust training program to correct our deficiencies with over-volumizing the lungs? Well, at first the difference in patient outcomes would be no different, or even slightly worse. Why? We’ve actually looked at that. In several studies performed in the late 1990’s and early 2000’s, we looked at patient outcomes when low tidal volumes (approximately 6mL/kg, or 420mL in a 70kg patient) were used. The same issues arose that were present in the large tidal volume patients. While there was no volutrauma present in this patient population, the atelectrauma was.

 

What exactly is atelectrauma? We know that surfactant, along with nitrogen being present in the lungs, are the two key factors that prevent alveolar collapse between breaths. Ventilating a patient with consistent tidal volumes (whether they’re high or low) seems to reduce the presence of surfactant in the lungs. Couple this with the fact that many providers have patients on 100% FiO2 for long periods of time, we have a recipe for atelectasis. Keep in mind, if you’re delivering 100% FiO2, the nitrogen in the lungs will be “washed out” so oxygen can take its place. Oxygen is a much smaller molecule and does not provide the same level of “stenting” that nitrogen does. Let’s get back to our question: what is atelectrauma. Imagine that your alveoli are surrounded by rubber bands – what we would call elastin. For sake of simplicity, let’s say that every alveoli is wrapped in 10 of these rubber bands and they are essentially holding the “weight” of the alveoli when it’s being distended - during a breath.

 

When a breath is delivered into the patient, let’s say that each alveoli is exposed to 1kg of weight (this is a gross overestimation, but it makes the math easy). That would mean that each rubber band was responsible for supporting around 100grams of weight. However, due to perpetual closing and forceful opening of the alveoli, four of these rubber bands have broken or become dysfunctional. Now, each rubber band must support 167grams of weight. This forces them to work harder, stretch harder, and squeeze harder. After a short time, cell dysfunction from the immune response makes the entire alveoli incapable of opening and closing. If we do this to enough of them, the patient develops ARDS or possibly dies from severe VQ mismatch.

 

Therefore, if we simply train our folks to reduce their tidal volumes, the outcomes won’t change. We need to consider the fact that with a reduction in tidal volumes, the risk for lung derecruitment and atelectasis is increased, not decreased. Consequently, unless we combat the inevitable atelectasis we may as well keep delivering massive tidal volumes. What’s the simple fix? Any time you have bag valve mask in your hand, there had better be a PEEP valve on it. If you’ve ever attended a conference where I was speaking, or listened to my podcast, you’ve heard me refer to a bag valve mask as a murder weapon. To elaborate, a BVM without a PEEP valve on it is a murder weapon.

 

What would be my overall opinion on the matter? On all patients under 6’2” (which is around 90% of all patients) we should probably be using a pediatric bag valve mask during positive pressure ventilation. Additionally, we should be practicing with these devices to learn how much squeeze is actually needed to achieve various tidal volumes. Building muscle memory is required BEFORE the call, not during the call. Lastly, if we are administering positive pressure ventilation, a PEEP valve is required 100% of the time. The only study that has looked at PEEP for the sole purpose of reducing atelectrauma was a study performed on pigs. Pigs have around half the normal surface tension in their lungs – as compared to humans – and the minimum PEEP required was 4cmH2O. We can infer from that study that the minimum required PEEP in humans would be 8cmH2O, and we have a ton of other data to support to use of 8cmH2O as the minimum. If you would like to read more about the “physiologic” PEEP levels, I encourage you to buy my first book where we spend an entire chapter talking about it.

 

In closing, we spend so much time in the prehospital world and in the emergency department trying to keep our patients from dying. Unfortunately, the bandwidth needed to care for our patients often prevents us from considering the long-term effects of our treatments. With respect to acute lung injuries, we only need to change a few things to reduce the harm we are causing. First, make a conscious effort to reduce your tidal volumes, so your patient doesn’t experience unnecessary volutrauma. Second, make sure you’re using a PEEP valve when ventilating patients to prevent the atelectrauma that WILL occur if you don’t use one. It’s really as simple as that.


Sources:






243 views0 comments
bottom of page