April 7 Update: some research is emerging since I posted this that COVID related ARDS is not typical ARDS. Here’s the medical reference for providers but it’s very early evidence so far we should keep an eye on: COVID-19 Does Not Lead to a “Typical” ARDS. This was further validated by an article in MedScape that previews some emerging peer-reviewed research. Thus while my explanations of ARDS and ventilators is accurate, the ties to COVID-19 are not and new treatment protocols are emerging.

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 flight 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 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 bit better.

The TL;DR is that COVID-19 damages the lungs, which for some people triggers the body to overreact with too much inflammation. This extra fluid interferes with gas exchange in the lungs, and oxygen can’t as easily get into the bloodstream. You don’t actually stop breathing, so we use the ventilators to change pressure and oxygen levels, in an attempt to diffuse more oxygen through this barrier and into the lungs without, causing more damage by overinflating 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 removing waste products – predominantly CO2. We get oxygen from our environment and release CO2 through ventilation: air moving in and out of our lungs. Those gases are moved around in our blood, and the actual gas exchange occurs in super-small capillaries which basically wrap around our cells. The process of getting blood to tissues is called perfusion.

Theis is all just some technical terminology to say: our lungs take in oxygen and release carbon dioxide, we move the gases around using our circulatory system, and we exchange gases in and out of cells in super-small capillaries. Pure oxygen is a toxin, and CO2 diffused in blood is an acid, so our bodies have 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 are the main ones).

Our lungs have branches and end in leaves called alveoli. Alveoli are pretty wild – they have super-thin walls to allow gases to pass through, and are surrounded by capillaries to transfer gasses into and out of our blood. They look like clumps of bubbles, because they maximize surface area to facilitate the greatest amount of gas exchange in the smallest amount of space. Healthy alveoli are covered in a thin liquid called surfactant, which 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 cell walls, and cause other damage. In smokers a bunch of the alveoli clump together, losing surface area, in a process called atelectasis (remember that word).

Our bodies try to keep things in balance, and have a bunch of tools to nudge things in different directions. The important bit for our discussion today is that ventilation is managed through how much we breathe in for a given breath (tidal volume), and how many times a minute we breathe (respiratory rate). This combination is called our minute ventilation and is normally about 6-8 liters per minute. This is linked to our circulation (cardiac output), which is around 5 liters per minute at rest. The amount of oxygen delivered to our cells is a function 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 they can actually cause ARDS with the wrong settings. This triggers an inflammatory response. A key aspect of inflammation is various chemical mediators altering cell walls, especially those capillaries – and then 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 separates them. This reduces gas exchange.
  • Fluid leaks into the alveoli themselves, further inhibiting gas exchange.
  • The cells are damage by all this inflammation, triggering another 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 stuff up the lungs and reduce gas diffusion even further.
  • The flood of all these inflammatory mediators and other cells/chemicals your body needs for its immune response can cause additional issues and shortages throughout the body.

The net result is that gas exchange becomes much harder and your body fights itself, making things worse. ARDS is very difficult to reverse, because we need to keep gas exchange running while the body chills the hell out. If you do survive you are likely to have lung damage which takes a long time to recover from. And let’s be clear – I am skipping 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 directly because of the infection itself, as with any other respiratory infection. Your gas exchange is still probably decent but you may be exhausted due to less oxygen and your body’s general immune response.

At some point ARDS might kick in. ARDS onset can be super rapid, which explains some people feeling sick but okay, then dying that night. Based on my current reading we don’t know all the risk factors to go from COVID-19 to ARDS, but 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, just to get back to normal healthy breathing. That isn’t enough to treat ARDS.

ARDS is a failure of gas diffusion, not ventilation. We move air normally, but the oxygen doesn’t get into the blood, and the carbon dioxide doesn’t get out. It’s because all that swelling creates a shunt which blocks gas exchange.

We fix this two ways. First we increase expiratory pressure. We call this “PEEP” – basically we keep extra pressure in the lungs so they never fully deflate. This keeps as many alveoli open as possible, maximizing surface area, and adding extra pressure in an attempt to ‘push’ gas into the bloodstream. We still need to carefully manage overall pressure, because we’re risking irritating the lungs more and making the problem worse. See the complexity? We need more pressure to improve gas diffusion (I’m skipping CO2 for now; it’s a factor but O2 is the larger issue). Keeping a bit of constant pressure also reduces 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 – if we hit 100% in the bloodstream, all that extra oxygen is toxic.

For ARDS it’s very 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 avoid further lung injury, while also using higher expiratory pressure to keep the alveoli inflated and gas exchanging. It would be much 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 that just exacerbates 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 these are adjusted in an attempt to involve as many alveoli as possible and diffuse as much gas as possible, without causing further injury.

That’s a lot going on – and at no point did I say “and the patient stops breathing”. We use different sedation and pain management strategies, but unless we paralyze the patient (which we try to avoid) 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 key piece to remember is that when treating ARDS with mechanical ventilation we are really supporting respiration – gas exchange. We use different features of ventilators to diffuse as much oxygen as possible into the bloodstream (and eventually the 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, and also by leaking fluid into the lungs, all of which interferes with oxygen getting into the bloodstream so they can be 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, layperson terms, and explanation, to make this all understandable.