The biology of coronavirus COVID-19 - including research and treatments

These are two new articles.

"What Doctors on the Front Lines Wish They’d Known a Month Ago"

"At Lincoln Hospital in the Bronx, Dr. Nicholas Caputo followed 50 patients who arrived with low oxygen levels between 69 and 85 percent (95 is normal). After five minutes of proning, they had improved to a mean of 94 percent. Over the next 24 hours, nearly three-quarters were able to avoid intubation; 13 needed ventilators. Proning does not seem to work as well in older patients, a number of doctors said.

No one knows yet if this will be a lasting remedy, Dr. Caputo said, but if he could go back to early March, he would advise himself and others: “Don’t jump to intubation.” "

“Intubated patients with Covid lung disease are doing very poorly, and while this may be the disease and not the mechanical ventilation, most of us believe that intubation is to be avoided until unequivocally required,” Dr. Strayer said."

https://www.msn.com/en-us/news/us/w...known-a-month-ago/ar-BB12B6Nw?ocid=spartanntp



"Doctors are finding that placing the sickest coronavirus patients on their stomachs -- called prone positioning - helps increase the amount of oxygen that's getting to their lungs.

"We're saving lives with this, one hundred percent," said Narasimhan, the regional director for critical care at Northwell Health, which owns 23 hospitals in New York. "It's such a simple thing to do, and we've seen remarkable improvement. We can see it for every single patient." "

https://www.msn.com/en-us/health/he...hs-can-save-lives/ar-BB12Bwc2?ocid=spartanntp

 

This is a very interesting observation but a rather puzzling one.

If proning increases oxygen access to alveoli then it is hard to see how, as a direct effect, it can be other than due to opening up collapsed posterobasal alveoli - which is what it is generally thought to do in under ventilated lung.

But this does not seem to fit with the observation that opening up alveoli with positive pressure does not seem help in Covid19.

I wonder whether the stated rise of oxygen saturation to 94% is with pruning plus oxygen supplementation.It is hard to see how opening up alveoli alone would do it if opening up alveoli otherwise does not work.

I just wonder whether in fact the prone position in this particular. case is altering pulmonary vascular flow somehow.

 

was just wondering, if they put them on the belly to not see their faces.
but when googling this "prone positioning" (face down), seems an old thing but only for ppl on ventilators, ppl on artifical respirators - on machines.

above it was said "the sickest patients" were put face down - but this may be misleading. when googling, i only found this recommended for automated respiration.

imo, there seems to be "no evidence" that it indeed helps. studies ? not sure. but hey...

otherwise i can only say - with ace-trouble, respiration trouble and spending years in front of a fan - that lying on the belly was mission impossible. the worst imaginable thing for breathing.
so, i found that puzzling, too...

 

Surely being in the prone position requires people to turn their heads rather a lot, or else they suffocate? And wouldn't that cause immense stress on people's necks? There are various reasons why I wouldn't be able to lie prone, and suffocation is just one of several.

 

I've just found a link on the subject and there are quite a long list of contraindications and complications :

https://litfl.com/prone-position-and-mechanical-ventilation/

 

Pretty good report on how changing assumptions about how to deal with what was originally assumed to be ARDS but doesn't fit the normal patterns, especially of patients showing very low osat levels that are normally only found with severe distress but the patients are lucid, even down to 40-50% oxygen saturation.

Also there appears to be two types of "ARDS", if it can still be called that: heavy (typical) and low. Most COVID cases (~70%) are the low types, which don't present the usual lung tissue stiffness and would not respond well to ventilators.

https://www.youtube.com/watch?v=bp5RMutCNoI

 

80% walk through like a breeze
20% have various troubles... some affecting the heart

im on this angiotensin & the rock and the hard place...

- some ppl may have high angiotensin (II) naturally
- issue: this means opportunities for the virus
- reducing: by hydroxy-chloroquine for example

the problem:
- reducing/inhibiting angiotensin II hits back on the vagus nerve (in stomach, and then heart problems)
- possible fixes: cholinesterase inhibitors + and/or muscarinic agonists/nicotinic agonists ?

is it possible, that angiotensin is going up in the first place, since the virus binds it ?
when its reduced, its good, but something happens with the vagus nerve.
what might lead to (different?) sort of heart dysfunctions, problems.

..but its just a thought...

 

Yes, maybe not so much about how much oxygen is getting into the lungs, but about how much is getting into the red blood cells. Even if the lungs are no less congested, but blood flow improves through the still-healthy parts of the lungs, then the oxygen uptake might also be improved. If I understand you right.

ETA: Also, I imagine that if you are at the borderline level of oxygen update to actually keep you alive, then even a pretty modest increase could significantly improve your survival chances.

 

yes

 

looks as if it were mere a neurological disease, I´d say.

 

Prof Montgomery from UCL says covid 19 is a blood and blood vessel disorder - clotting factors and oxygen changes (3mins30 sec video)

https://www.youtube.com/watch?v=-bOmlF6B4yY

 

https://twitter.com/user/status/1250763181150081024

 

More hints that air pollution may be a crucial factor in lethality.

https://projects.iq.harvard.edu/files/covid-pm/files/pm_and_covid_mortality.pdf

 

on issue of smokers

https://www.qeios.com/read/article/561

 

Finally, some contrast to the "all disease is due to inflammation/damage" school of thought.

 

What is first?

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2141.2005.05753.x

The interactions between inflammation and coagulation

 

Hugh Montgomery has always seemed to me sensible and impressive. He sounds very confident about things that as far as I know are not yet published fact but most of it is just reporting clinical findings and I see n o reason to think he has an axe to grind. What he says also fits with what has been said from the US.

I was interested that he said CO2 levels were high. So this is not problem with harm or with oxygen getting in to red cells specifically. It is a diffusion failure at the interface between vessel and airsac. The suggestion is that this may be a fibrin clot problem. I wonder if shunting might be an alternative. That basically means that diffusion is failing because blood is being sent through vessels that by pass the airsac interface anyway. I am not sure that is feasible though. Shunting in lung disease is usually because blood is going through vessels whose airsacs are blocked off from air.

I think it is useful that he emphasises the fact that Covid19 is nothing to do with flu. It seems more like meningococcal septicaemia if anything.

 

Skin manifestations suggest that

https://www.the-hospitalist.org/hos...ifestations-are-emerging-coronavirus-pandemic

PS: my mom also had a lot of itchy red bumps in random places on her skin in the last weeks and she thinks she's maybe had this virus.

 

Convalescent Plasma - clinical trial

https://www.nhsbt.nhs.uk/how-you-can-help/convalescent-plasma-clinical-trial/