I wonder if anyone has tried ventilating with breathing fluid (perfluorocarbons, PFCs) for Covid-19 yet.
@RaniaLian

@bingst I couldn't find any info in regards to that and COVID-19 so propably not. In general, liquid ventilation has shown promising results in animal models, however it does not seem to improve the outcome in adult patients with acute respiratory distress syndrome (ARDS) when compared with conventional mechanical ventilation.

Meanwhile, the use of conventional mechanical ventilation is being re-evaluated in the treatment of COVID-19, depending on whether a patient presents with ARDS (thus requiring the support of high-pressure ventilation) or atypically (in atypical cases, non-invasive options such as high flow nasal cannula, CPAP etc might suffice).

In ARDS, areas of the lung are “closed” due to:

• an accumulation of fluid. Unlike what happens with PFCs, this fluid is poor in oxygen and leaves nothing to be picked up by the blood. The lungs try to mitigate this by constricting the blood vessels in those poorly-oxygenated areas, diverting the blood flow to other areas of the lungs that are better oxygenated (this phenomenon is called hypoxic pulmonary vasoconstriction). In contrast, COVID-19 usually involves a dry lung and disrupted hypoxic vasoconstriction. This lack of regulation via vasoconstriction might explain a low oxygen saturation in the setting of fluid-free lungs.
• reduced compliance (think of compliance as the capacity of the lungs to expand). This leads to a decreased amount of gass inside the lungs: mechanical ventilation can help recruit (open up) parts of the lung. In many COVID-19 cases, however, there seems to be normal compliance (hence a normal amount of gass inside the lungs), minimizing the need for recruitment and rendering mechanical ventilation less effective.

Accroding to an editorial authored by prof. L. Gattinoni, the majority of covid-19 cases with lung involvement start out atypically. It should be noted, though, that some COVID-19 patients might transition from atypical presentations to text-book ARDS (in fact, 20-30% of patients in this citation developed ARDS), further emphasizing the need for a personalized approach to ventilation. [esicm.org]

Hopefully I didn't go too much on a tangent ^^

@RaniaLian What do you think about PFCs doped with a vasodilator? Or some other medicine that would help with gas exchange? It just seems to me that PFCs would be much better at delivering medicines to the tissues in a more consistent manner. I also wonder about any clearing out effect it might have, given its viscosity.

And I appreciate the level of detail. It's why I tagged you.

@bingst
“It just seems to me that PFCs would be much better at delivering medicines to the tissues in a more consistent manner.”

I think that’s a reasonable assumption. About 20% of a medicine’s concentration can be lost during inhalation and further reduced in areas of the lungs where there’s mucus, inflammation or collapse. In addition, data from preliminary animal studies suggest that the uptake of antibiotics by the lungs and the efficacy of vasoactive drugs is increased during liquid ventilation as compared to intravenous administration.

Even on their own, PFCs open up collapsed alveoli and have anti-inflammatory effects (removal of inflammatory cells and their mediators). As you mentioned, they can indeed drive the removal of infectious and inflammatory debris from the lungs. Unlike saline, PFCs do so without interfering substantially with the function of surfactant, the substance produced by the lungs to reduce surface tension. However, their high viscosity can be problematic (e.g. difficulties in flow).
Despite these theoretical advantages, studies so far have been disappointing and more research is required to figure out the optimal use of liquid ventilation. So far, liquid ventilation has been tried clinically without additional drugs inside the medium. Even though PFCs are poor solvents for most biological compounds, gasses such as nitric oxide, a vasodialator, are soluble in PFCs and could be administered as you have suggested. As a side note, the impaired hypoxic vasoconstriction observed in some COVID-19 patients with dry lungs could be exacerbated by drug-induced vasodialation, which would lead to even more blood flowing through poorly oxygenated areas.

Less soluble compounds can also be "loaded" into PFCs using different processes which depend on the properties of each indivitual drug. For example, water soluble drugs can be incorporated in PFCs through a process of emulcification. PFCs are hydrophobic (they don’t mix well with water) so the drug would first have to be dissolved in water, then added to the PFCs and dispersed via the application of sound waves. If you want to read more, here’s an interesting article that I found on the subject [engineering.cmu.edu]
Other systems (drug-in-fluorocarbon suspensions, oil-in-fluorocarbon emulsions etc) are being investigated as well.

@RaniaLian You are super! I've been interested in treating pulmonary ailments with PFCs since 1996, when I first thought of it. I check from time to time to see if much has been done with them, but it seems not much has.

@bingst It truly is an interesting subject which I knew next to nothing about (so naturally I fell down a rabbit hole ). I had fun looking into different sources, thanks for the tag!

I don't think that's whole virus though, is it? But just enough of it to prompt an immune response?

@bingst No, it is an attentuated form of the living virus, i.e. a dead virus.
The body's Immune system then recognise the genetic material from the attentuated virus and goes about creating the necessary Anti-bodiesin response.

You are saying it would be as bad a big syringe of potassium chloride that stops your heart immediately?

You are saying it would as bad as a large syringe of concentrated potassium chloride which stops your heart almost immediately?

@OleBlueEyes No not quite as quick and lethal but using a 100% a live virus in any vaccine would be counter-productive and potentially fatal at the very least.

You think the virus knows to go to lungs?

And kill 1-3 percent ?

@OleBlueEyes As I understand it, the virus attaches to receptors, in the lung tissues. I'm assuming that once in the bloodstream, it will be carried eventually to the lungs, but on the blood side of the alveoli, as opposed to the air side. Although, I'm not entirely sure the receptors are on both sides of the alveoli.

@OleBlueEyes Since the virus is mostly passed on from host to host via airborne droplets from coughing and sneezing and the next host usually breathes them in, then it goes directly to the lungs via the trachea, the Bronchi and into the alveloi.

@OleBlueEyes I don't think any virus actually thinks as we would see it, it is merely is driven by the need/urge to find host cells so it can use the DNA and nutrients in those host cells to replicate itself, usually in the range of thousands of times in one single host cell.

@bingst are these receptors specific to lung cells only?

@OleBlueEyes Good question. I don't know. I am however assuming that the receptors are absent in any other part of the respiratory tract, which indicates that they could be unique to the lungs.

@OleBlueEyes No, the 'receptors' are specific, for want of a better term, to finding ANY non infected host cells in the body the virus infects.
But being an air-borne virus it IS drawn into the airways of the victim as it breathes, it can ALSO enter the body by tranferance from the skin into the mucosal layers around the eyes, mouth and nosal passages.

When you can`t breath, you got 3 minutes, to gain immunity without dying as often as respiratory infection of covid19.