Understanding COVID, ARDS, and Mechanical Ventilation

Although this is a security blog, this post has absolutely nothing to do with security. No parallels from medicine, no mindset lessons, just some straight up biology. As many readers know I am a licensed Paramedic. I first certified in the early 1990’s, dropped down to EMT for a while, and bumped back up to full medic two years ago. Recently I became interested in fight and critical care and completed an online critical care and flight medic course from the great team at FlightBridgeED. Paramedics don’t normally work with ventilators; it is an add-on skill specific for flight and critical care (ICU) transports. I’m a neophyte to ventilator management, with online and book training but no practice, but I understand the principles and thanks to studying molecular biology back in college have a decent understanding of cellular processes.

COVID-19 dominates all our lives now, and rightfully so. Ventilators are now a national concern and one the technology community is racing to help with. Because of my background I’ve found myself answering a lot of questions on COVID-19, ARDS, and ventilators. While I’m a neophyte at running vents, I’m pretty decent at translating complex technical subjects for non-experts. Here’s my attempt to help everyone understand things a little better.

The TL;DR is that COVID-19 causes damage to the lungs which, for some people, triggers your body to over-react with too much inflammation. This extra fluid gets in the way of gas exchange in your lungs and oxygen can’t get as easily into your bloodstream. You don’t actually stop breathing, so we use the ventilators to change the pressures and oxygen levels to try and diffuse more oxygen through this barrier and into your lungs without causing more damage by over-inflating them.

We start with respiration

Before we get into COVID and ventilators we need to understand a little anatomy and physiology.

Cells need oxygen to convert fuel into energy . Respiration is the process of getting oxygen into cells and taking waste products, predominantly CO2, out. We get oxygen from our environment and release CO2 through ventilation. Which is just air moving in and out of our lungs. Those gases are moved around in out blood and the actual gas exchange occurs in the super-small capillaries that basically wrap around our cells. The process of getting blood to tissues is called perfusion.

This is just all some technical terms to say our lungs take in oxygen and release carbon dioxide, moves the gases around using our circulatory system, and exchanges the gases in and out of the cells down in those super small capillaries. Oxygen is a toxin and CO2 diffused in blood is an acid so our body has all sorts of mechanisms to keep things running. Everything works thanks to diffusion and a few gas laws (Graham’s, Henry’s, and Dalton’s being big ones).

Our lungs have branches and end in leaves called alveoli. Alveoli are pretty wild; they have super thin walls to allow the gases to pass through and are surrounded by capillaries to transfer the gasses into and out of our blood. They look like clumps of bubbles since they maximize surface area to facilitate the greatest amount of gas exchange in the smallest amount of space. Healthy alveoli are covered with a thin liquid called surfactant that keeps them lubricated so they can open and close and slide around each other as we breathe. Want to know one reason smokers and vapers have bad lungs? All those extra chemicals muck up surfactant, thicken the cell walls, cause other damage and a bunch of the alveoli clump together, losing surface area, in a process called atelectasis (remember that word for a few paragraphs).

Our body always wants to keep things in balance and has a bunch of tools to nudge things in different directions. The important bit for our discussion today is that ventilation is managed using how much we breathe in for a given breathe (tidal volume), and how many times a minute we breathe (respiratory rate). This combination is called our minute ventilation and it’s about 6-8 liters per minute. This matches our circulation (cardiac output), which is around 5 liters per minute at rest. The amount of oxygen delivered to our cells is a combination of our cardiac output and the amount of oxygen in our blood.

We need good gas exchange with our environment, good gas exchange into our bloodstream, and good gas exchange into our cells. COVID-19 screws up the gas exchange in our lungs and everything falls apart from there.

Acute Respiratory Distress Syndrome

ARDS is basically your body’s immune system gone haywire. It starts with lung damage, which can be an infection, trauma, or even metabolic. One of the big issues with ventilators is that we can actually cause ARDS with the wrong settings. This triggers an inflammatory response. A key piece of inflammation is various chemical mediators alter cell walls, especially those capillaries, and they start leaking fluid. In the lungs this causes a nasty cascade:

  • Fluid leaks from the capillaries and forms a barrier/buffer of liquid between the alveoli and the capillaries and separating them. This makes gas exchange harder.
  • Fluid leaks into the alveoli themselves, further inhibiting gas exchange.
  • The cells are damage by all this inflammation, triggering yet a stronger immune response. Your body is now in a negative reinforcement cycle and making things worse by trying to make them better.
  • This liquid and a bunch of the inflammation chemicals dilute the surfactant and damage the alveolar walls, causing atelectasis. In later stages of ARDS your body starts throwing in additional tools which effectively stuffed up the lungs and put even more barriers in place for gas diffusion.
  • The flood of all these inflammatory mediators and other cells/chemicals your body needs for its immune response can cause other issues and shortages throughout the rest of the body.

The net result is gas exchange is MUCH harder and your body is fighting against itself, making it worse. ARDS is REALLY HARD to reverse since we need to try and keep the gas exchange running while the body chills the hell out. If you do survive, you probably have lung damage that will take a long time to recover from. And let’s be clear- I am skipping some major aspects of ARDS to keep things as simple as possible.


SARS-CoV-2 attacks the lungs. This can trigger ARDS, but as you can see from what I described it… might not. It all comes down to your biology, how bad your infection is, and how your body responds.

If you are infected and have shortness of breath that could be because of the direct infection itself, like any other respiratory infection. Your gas exchange is still probably decent but you are exhausted due to less oxygen and your body’s general immune response.

At some point ARDS might kick in. ARDS can be super rapid, which explains some people feeling sick but okay and then dying that night. Based on my current reading we don’t know all the risk factors to go from COVID-19 to ARDS. ARDS is the main killer with COVID-19.

Mechanical Ventilation for ARDS

The primary treatment for ARDS is mechanical ventilation. But a specific way of using ventilators! This is the confusing bit I see lost in a lot of non-medical-professional discussions.

The most basic ventilation settings are tidal volume and respiratory rate- that “minute ventilation” we talked about, and we are just replicating a person breathing. That isn’t enough to treat ARDS.

ARDS is a failure of gas diffusion, not ventilation. We are moving air but the oxygen isn’t getting into the blood, and the carbon dioxide isn’t getting out. It’s because all that swelling creates a shunt that blocks the gas exchange.

We fix this using two things – we first increase expiratory pressure. We call this “PEEP” and basically we keep extra pressure in the lungs so they never fully deflate. This keeps as many alveoli as open as possible, maximizing surface area, and adding extra pressure to try and “push” the gas into the bloodstream. We still need to watch our overall pressure since that just irritates the lungs more and makes the problem worse. See the complexity here? We need more pressure to improve gas diffusion (notice I’m skipping over CO2 for now; it’s a factor but O2 is the bigger issue). Keeping a bit of constant pressure also reduces the movement of the alveolar walls, reducing irritation and injury.

The second thing we do is increase the amount of oxygen in each breath. But not too much, since if we hit 100% in the bloodstream all the extra oxygen is toxic.

For ARDS it’s really important to keep track of a range of pressures beyond PEEP. The idea is to run a lower tidal volume with a higher respiratory rate to reduce further lung injury, but use higher expiratory pressure to keep the alveoli inflated and gas exchanging. It would be a LOT easier if we could just ramp all the pressures up and push the oxygen through all the extra fluid and into the bloodstream more forcefully, but this just exacerbates the problem in ARDS. Instead we balance pressures to keep as much pressure in the lungs as long as possible, WITHOUT stretching the lungs and causing more damage. Aside from PEEP we can control the driving pressure (how hard the push is), the overall Mean Airway Pressure (the pressure average from breath to breath), inspiration and expiration times, inspiratory flow rate, and more. All of these are adjusted to try and recruit as many alveoli as possible and diffuse as much gas as possible, without creating further injury.

Think of everything I just described and at no point did I say “and then the patient stops breathing”. We use different sedation and pain management strategies, but unless we paralyze the patient (which we try to minimize) they will also be breathing spontaneously. Ventilators use sensors to detect this and, depending on the mode, support spontaneous breaths. This is also important to help get the patient off the vent and breathing on their own.

The important piece to remember is that when treating ARDS with mechanical ventilation we are really supporting respiration, which is the gas exchange. We use different features of ventilators to diffuse as much oxygen as possible into the bloodstream (and eventually our cells) while trying to minimize additional damage. COVID-19 sometimes causes ARDS which creates a “shunt” by separating the capillaries from the alveoli with fluid, plus leaking fluid into the lungs, all of which gets in the way of oxygen molecules getting into the bloodstream and then being delivered to cells.

Hit me up if you have any other questions and I’ll do my best to respond. Hopefully I hit the right balance of medical jargon and layperson terms to make this a little bit more understandable.

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