Where We Fall With ARDS (Part 1): The Rabbit Hole
By George Barnes, Dr. James Coyle, and Kelsey Day
The pronoun “I” and “me” will often be used during this series, but the words represent the work and knowledge of all three authors.
Pulling the thread
Why did I decide to spend my Sunday mornings researching pulmonary pathophysiology you ask? Well, it started with COVID-19. Which led to two questions: 1. Why is this happening to our patients? 2. What can we do to help? COVID-19 was the big driver that urged me to pull at a small string of information related to pulmonary disease. What I am now left with are three blogs and a heap of thread in my lap.
Learning how to learn
Research isn’t something that has come easily to me. I’ve always struggled with figuring out which articles are relevant, which should be ignored, and which are the golden eggs that I need to use as my bible. After many a weekend morning reading through COVID-19 research, I realized that it’s not about cherry-picking articles. No, it’s about consuming as much of it as possible in order to understand the basic concepts that can be applied to a wide variety of clinical cases. One article would introduce a concept I didn’t know so I would read three more to understand that concept. In those three I was introduced to three more concepts and so nine articles would ensue (down the rabbit hole I go). This happened until my eyes turned red and I finally realized I had to take a step back and start at the very beginning. The result? The genesis of what would become an exploration into the pathophysiology of acute respiratory distress syndrome (ARDS).
COVID-19 and ARDS: A family affair
COVID in its most severe form leads to ARDS. COVID-19 is brand spanking new. ARDS is not. ARDS is the inability of the pulmonary system to sufficiently inhale adequate volumes of air and perform gas exchange, which deprives the lungs and arterial blood of oxygen and, in severe cases, can lead to respiratory failure and death (Rawal et al., 2018). By understanding ARDS, we are not only able to manage COVID-19 better, but we are also able to manage the many other conditions that lead to ARDS (e.g., COPD, pulmonary fibrosis, traumatic injury, severe aspiration, etc.). This three-part blog series is about getting a foundation of knowledge in ARDS to work up from instead of memorizing bits and pieces of information here and there. It’ll be like learning to cook vs memorizing recipes (and then feeding it to our patients).
Most SLPs had limited exposure to ARDS before COVID-19. Then all of a sudden, it was everywhere. We were forced to learn how to swim after being dropped headfirst into the deep end. But once you can swim in the deep end, you can swim anywhere. Even in the deepest of oceans. So instead of getting stuck on how COVID-19 is unique, let’s dive into ARDS so we can understand COVID’s ancient ancestor. But to understand diseased lungs, we must first understand healthy lungs.
The Respiratory System: Where aspiration goes
Speaking of rabbit holes, where does aspiration even go when we aspirate? We get so caught up in preventing aspiration, we forget to determine how a specific aspirate might impact the lungs of an individual patient. We spend our entire careers protecting these two spongy, air-filled organs, but how much do we actually know about what goes on beyond the vocal folds? The more we understand the lungs, the better we will understand what happens when our patients aspirate. And the more we understand that, the better we can manage dysphagia.
An upside-down tree
Think of the respiratory system as an upside-down tree. The tree starts with the trunk (trachea) which splits into two branches (mainstem bronchi). These branches split even further into smaller and smaller stems (bronchioles). At the end of those bronchioles are tiny clusters of microscopic leaves (alveoli). This is where the magic happens. The alveoli are air sacs covered by blood vessels so the O2 can be easily transferred to the bloodstream and CO2 can be easily released out of the blood and out of the body (West, 2012).
A complex system
Sounds straightforward, but it’s actually an intricate array of structures and systems (see these videos if you are interested in learning more). We often focus solely on dysphagia and aspiration pneumonia, but this kind of tunnel vision can be a slippery slope. Our lungs are not simply two balloons that defenselessly fill up with aspirate. When a foreign material is introduced to the lungs it actually has 3 choices: it can go up, in, or nowhere. Let me explain...
Going up
Most of our respiratory system is lined with cilia (other than the alveoli) (West, 2012). These are tiny hairs that mobilize foreign materials out of the lungs (i.e., food, liquid, bacteria, dust, etc.) The act of moving these materials up and out is called the mucociliary escalator (Make way for incoming analogy...). Imagine cilia are an actual escalator (not too far-fetched) and you’ve become small enough to ride that escalator (a little more far-fetched, but ok). There is a thin lining of mucus covering the cilia which sort of acts like oil for its gears (gross, but ok I’m still with you). You ride this escalator along with the foreign materials until you make it all the way up to the trachea where you are coughed out of the body or swallowed into the acidic environment of the stomach (Thornton & Sheehan, 2003; Zheng and Clements, 2018). Sounds like a scary ride, but that’s what we should expect to happen to foreign materials trying to invade our lungs.
Going in
Now think of the respiratory system as a big sponge. Absorption of inhaled particles can occur at any area of the system, but the alveoli are particularly permeable due to their role in allowing oxygen into the bloodstream. The ease at which particles and microbes enter the bloodstream is based on the size and solubility of the material (NIH, 2018). This is why small amounts of water are more easily absorbed and thus less harmful to the lungs due to its viscosity/contents (Carlaw et al., 2012; Olson, 1970; Panther, 2005); while aspiration of thicker, more dense consistencies is more harmful (Feinberg et al., 1996; Holas et al., 1994; Robbins et al., 2008; Schmidt et al., 1994; Zeltzer et al., 2020).
Going nowhere
In the next blog I am going to address what happens when things go wrong with our respiratory defenses, but here is a little intro. Back to our escalator analogy (I know, you were hoping for this): Now you are moving smoothly until you start to notice that at some point during your trip the escalator starts to slow down. The cilia may have become damaged from lung disease and now some of their gears aren’t turning anymore. The oil (mucus) whose purpose is to lubricate the gears (cilia) and filter foreign intruders is now building up and gets thicker and thicker until the escalator comes to a halt. The same oil that once served as a protector and lubricant is now switching teams and serving as a breeding ground for bacteria. This creates a vicious cycle of more damage to the cilia, more mucus, and more bacteria (get me off this ride!) (Thornton & Sheehan, 2003; Zheng and Clements, 2018). BUT our alveoli have one last line of defense...
Lung Lunch
Being that the cilia do not extend to the alveoli, particles that make their way this far either need to be coughed out or absorbed (West, 2012). When this doesn’t happen and inhaled particles stick around, the last line of defense is the macrophages, which are responsible for gobbling up the foreign particles that have avoided the mucociliary escalator and have been deemed a threat (Yum!) (Harwood, 2002).
Following the path to pathophysiology
All this is to say that the complex systems of our lungs are well-equipped to fight off germs, aspiration, and other foreign particles. But with complex systems comes the potential for complex problems (Or as Notorious BIG may have said during anatomy class, “mo’ complexity, mo’ problems”). So what happens when they do fail? And how might unhealthy lungs respond to such invasions? In the next two blogs, you’ll read about the pathophysiology of ARDS and where the SLP fits into the picture. After our research and discussions, I’m still left with many questions, leading me to believe my journey has only just begun. I hope this overview encourages you to keep pulling the thread with me so we can get a little bit closer to unraveling our place in managing this complex, but extremely rewarding patient population.
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Bios:
Dr. Coyle PhD, CCC-SLP, BCS-S is a Professor of Communication Science and Disorders and Otolaryngology at the University of Pittsburgh where he teaches undergraduate, Master’s and doctoral SLP students both in the classrooms and clinics and has an active clinical caseload in the University of Pittsburgh Medical Center. His current research focuses on development of noninvasive sensor-based dysphagia screening and diagnostic systems for dysphagia screening and automated diagnostic annotations. He teaches nationally and internationally about the medical aspects of our profession. He is a Board Certified Specialist in Swallowing Disorders, and an ASHA Fellow.
Affiliations: Department of Communication Science and Disorders, Department of Otolaryngology, University of Pittsburgh.
Kelsey Day, M.S., CCC-SLP is an acute care Speech-Language Pathologist (SLP) who specializes in dysphagia management for the medically complex, critically ill, and tracheostomy dependent populations. She now serves as the Lead SLP at California Hospital Medical Center, a trauma and stroke center in downtown Los Angeles, where she supervises a team of nine SLPs. Kelsey demonstrates her commitment to the education of new medical SLPs through her mentorship for the Medical SLP Collective and supervision of graduate student clinicians and Clinical Fellows in the acute care setting. She is a guest lecturer at several graduate level SLP programs, invited keynote speaker at national and international conferences, course creator and presenter of “Clinical Writing for Dysphagia Diagnostics”, and special guest on the “Swallow Your Pride” and “Speech Uncensored” podcasts.
Affiliations: Department of Rehabilitation, California Hospital Medical Center
