In my opinion it is exactly ARDS. It fits the criteria and would be included in trials. Indeed, having meta-analysed pressures and tidal volumes in several RCTS of ARDS in the past, I can tell you for certain that a lot of these patients did not require large pressures

especially since the target is 6ml/kg ventilation (which we are bad at policing by the way!). So it is not mind blowing to have ARDS lungs that aren't like trying to open two slices of bread that have frozen together.

As throughout the history of ARDSkind, the causes have always varied. So. Ventilation. We usually ventilate with negative pressure in the pleural cavity, sucking air in, and preferentially sucking air into the alveoli that expand the most

(Law of physics - gas travels from high pressure [atmospheric] to low pressure [expanded alveoli])

These alveoli have a good blood supply, get plenty of oxygen, expansion also helps open up capillaries that supply that area, helping to match V (ventilation) and Q (perfusion).

Ventilation is helpful/NECESSARY in ARDS, for two blanket reasons, and then other reasons that are more pertinent to stiff lungs.

1) patients get exhausted. It is extremely tiring to hyperventilate for hours and days. Both on an oxygen consumption level and in terms of lactate tolerance/endurance of intercostal and diaphragmatic muscles

there is an excellent 70's physiology paper here on the mechanisms of respiratory failure. Suffice it to say, blood flow is not limiting, but the rate of respiration, enhanced rate of inspiration with free expiration essentially caused low lung volumes

leading to VQ mismatch. Work is significantly increased by high intrathoracic resistance. The diaphragm received most of the increased blood flow (up to 14x) https://www.ncbi.nlm.nih.gov/pubmed/830663 

the above is in dogs, much of our cardiorespiratory physiology knowledge comes from dogs, and other than certain pulmonary receptors, consensus is we use respiratory physiology from these experiments to inform human practice.

The second reason ventilation helps is 2) we are now delivering slightly pressurised oxygen into alveoli (positive pressure ventilation) which enhances the alveolar: arterial oxygen difference and improves/hastens gas exchange. More goes across the epithelium basically

It's also the only mechanism that truly allows 100% oxygen delivery, via a sealed airway directly into the trachea.

Positive pressure causes injury for absolutely sure. So we limit them to safer levels and limit tidal volumes. One can paralyse to reduce pressures although this is not proven to reduce mortality. Pressure causes sheer stress, over-distends good alveoli, ruins surfactant

And constant collapse/opening of dodgy alveoli tears their fragile epithelium. Any damage done is exacerbated in the presence of high concentrations of oxygen. Indeed high concentrations of oxygen even inspired by a normal breathing person are bad for the lung

So of course we only want to use the minimum ventilation we can. One does need PEEP in a supine position/or prone because the action of standing normally provides 4-5cmH2O and that is natural physiology.

The other idea behind ventilatory PEEP is that it helps prevent the collapse and re-opening of alveoli (atelectatrauma) by keeping everything a little bit open to start with. That can offset positive pressure damage

Alveoli opening under negative and positive pressure are two totally different dynamics.

So although I can see why we are more used to needing high pressures in classic ARDS diseases like bacterial pneumonia (where pressure aids recruitment of pus filled lung areas or assists the expansion of soggy pulmonary interstitium, allowing excretion of 'lung water')

the idea that covid19 is not ARDS, is not borne out, and nor is the idea that these patients would do better on NIV. When patients fail NIV/tire/remain hypoxic what other strategies do we actually have?

If NIV was the holy grail, why do these patients fail coming off the ventilator and need to be re-intubated? I don't know what global practice IS when it comes to the timing of intubation more broadly

but in my experience it's a last resort anyway. Other advantages to mechanical ventilation are the induction of a coma, reducing oxygen demand, decreased cardiac work due to no longer having to supply increased respiratory work.

the virus DOES attack lung epithelium and capillary endothelium. It DOES cause inflammation. It DOES recruit immune cells which chew through interstitial tissue. It DOES cause IL-6/TNFa cascades

these DO cause lung water via action on endothelium, and effect on sodium channels that usually bail the alveoli out when they start flooding. They also cause a hypercoagulable state, with thrombosis and endothelial sloughing (on lung biopsy) that further wrecks VQ matching

the lack of dyspnoea may represent that normal lung compliance is maintained initially (limit to inspiration is highly dyspnoea-inducing, stretch receptors!),but may also represent neutropic invasion of pulmonary receptors, just like the olfactory nerve can be ruined.

I would like to fast forward 5 years and know all the answers. But for now, we need to use what is proven to work.