Covid-19 had us all fooled, but now we might have finally found its secret

medium ^ | 5 April 2020 | libertymavenstock

[grey_whiskers]

Lay people filling in details.

[MortMan]

I assume you are asking the medical community, as opposed to the news. The news readers wouldn’t report good news on this front if they were to die from it themselves.

[Norseman]

>>why is every nation striving to preserve and expand their supply?<<

I certainly hope it’s because it’s working, but feel there’s still the possibility that people are jumping on the bandwagon before convincing evidence is available. That’s why I asked how many you’ve seen turned around and what the timing is. It’s also why the NBC host should have asked the same question. Big difference between three and three hundred.

If we had a functional media today (we don’t) they would be interviewing people like yourself all over the country and the world and a pattern would quickly evolve. For example, there was the New Orleans doctor who dismissed both HCQ and the Z-Pack, separately or together, as I recall) saying simply that he wasn’t seeing them making a difference.

Decent reporting would get at the discrepancy: why is one doctor seeing results and another not? What are they doing differently, or what is the difference in their patients, or is one of them outright lying due to a severe case of TDS, etc.?

[grey_whiskers]

Problem with intubation (paraphrasing from memory as I type) is that some of the alveoli are full of mucus/fluid, some are ruptured, some are intact. But the damage is diffuses, so not limited to just the lowest lobes or just one lung.

So the initial thought is, the people are hypoxic, crank up the O₂ pressure. But that causes further damage to the non-intact alveoli.

This paper is consistent with the clinical findings, that the malaria drugs don't work if the disease has progressed too far: it doesn't combat cytokine storm, but the hydroxychloroquine acts as an ionophore to get the zinc into the cell, where it inhibits viral replication: so if the disease is too far gone, cutting the viral count is a fool's errand.

The idea of red blood infusion *with* hydroxychloroquine /zinc (to prevent the new blood cells from getting infected) is a novel treatment. Won't necessarily repair the lungs though.

[gas_dr]

1. I am using the combination of HCQ and Azithromycin, no zinc because its a routing issue

2. I have seen all my patient turn around (>20)

3. I see an improvement in ABG PaO@ as soon as 12 hours.

[StolarStorm]

Thanks for the info

[grey_whiskers]

If the hypoxia were a defect in blood cells proning would not help nor would increasing O2 delivery but both help in this disease.

Multiple mechanisms of action, many things going on. I read a couple of months ago, or saw on a YouTube, clinical studies on early cases that having the patient prone on a bed with the head slightly downhill, improved survival by helping the junk to drain out of the alveoli. As far as increasing O2 delivery, if you have both the air sacs filled with mucus, and some % of the blood cells out of commission, then a higher O2 % would help the few remaining blood cells, when they *do* make it to somewhere they can pick up O2, load up with more oxygen. Osmosis, diffusion, mole fraction, yada yada.

[grey_whiskers]

Precisely. Truth filtered through a layperson.

[gas_dr]

Blood transfusions are universally a horrid idea. Blood transfusions modulate and key up the immune system (Gives a SIRS response) which is exactly what we are trying to avoid. All gold standard studies in critical care point that a restrictive transfusion practice has a higher survivability at 30 days and one year.

Its not that the alveoli are filled they are not, its that there is increased thickening of the tissues (inflammation) causing diffusion gradient related hypoxemia and additionally probably a surfactant loss from type II pneumocytes. It is ARDS pure and simple from what I am seeing.

Finally all viral PNA are bilateral — there is the subtext coming that most PNA is limited to a lobe — bacterial tends to be lobar, but viral PNA tends to be bilateral.

[gas_dr]

Higher O2 is not always a good thing. >60% is hyperoxemic tx and promotes fibrosis via free radical injury. Proning does not improve 30 day survivability, although it does transiently improve oxygenation, so maybe its just enough to get someone on the fence through. Head down is a bad idea in prone or supine ventilation as it causes an increase in WEST Zone three via a restrictive mechanism (abdominal contents reducing thoracic volume). So the notion of draining is not founded.

[grey_whiskers]

What are the normal modes of hemoglobin? Do they change when it is carrying oxygen?

[Mom MD]

I said the same thing and was told i had the comprehension of a first grader.... i’m glad you picked up on as well

[2nd amendment mama]

1st time I’ve seen it too! You know, some of us don’t live on FR all day because we work, have lives, etc so we don’t see every article that is posted, when it’s posted!

[Mom MD]

I didn’t say nothing seems to work just be someone else. I did say there is no one magic bullet. We are also not seeing an 80% death rate on vents. people are coming off, but some rather slowly

[Mom MD]

I posted the part right below about the bacteria. Who has reading comprehension problems?

[grey_whiskers]

(Digesting.)

1) thank you for the correction on all viral PNAs being bilateral, vs. bacterial being lobar. Is that due to the smaller size of the virions affecting how they are transported through the body?

2) The alveoli being filled, is from an MD-sponsored YouTube presentation early in the epidemic: they found a higher survival rate on severe cases, when the patient was prone, and with the head lower than the feet. Somewhere along the way (maybe not that same video) was a clinician saying they saw improved results from pounding / massaging on the back of the lungs to keep things loosened up.

3) Any proposed mechanism for follow-on cardiac injury? I've seen but didn't bookmark a medical journal article in the last 36 hours detailing this as a delayed result of Sars2-2019 (or whatever they're calling it *this* afternoon) infection.

4) All gold standard studies in critical care point that a restrictive transfusion practice has a higher survivability at 30 days and one year.

Can't be talking about this virus then, there haven't been any patients around for a year yet.

Therefore, in that particular instance, you're the one talking through your hat based on approximate data. Not anecdotal, but of the kind "why are you looking for your wallet over here if you lost it down the street?" / "Well, there's a streetlight over here" sense.

[Mom MD]

i realize that but it was the first part of the article i saw. I also posted several other problems with the article right after

[gas_dr]

The oxygen dissociation curve is unbelievably complex. Its been a while, but there are a few things that influence it...

1. Acidemia tends to promote oxygen dissociation from the HGB molecule (thats why you would rather be a little academic when there is tissue level hypoperfusion in the shock state than alkalemic)

2. The amount of 2,3 DPG available (an enzyme that promotes dissociation). Banked blood is bad (transfusion practices) for a lot of reason, one of the reasons is there is a significant depletion of 2,3 DPG, so oxygen remains bound to the HGB in transfused blood

3. There are other factors, but the main story is that when saturation drops 92% of less there is a very steep decrease in oxygen saturation over a small range of O2 partial pressures.

There are a lot of graphs and I am pretty technically poor at copying graphs in HTML, so I am sure you can find them somewhere on line

As for the conformation of the molecule, If memory serves the reduced state of Iron (Fe2+) is the state of the iron molecule in normal Hgb, and this is what unloads and attracts O2 in normal physiology. If the oxygen reads with the iron itself and oxidizes it to the 3+ state, you get free radical injury with the creation of O2- ion.

If Fe becomes carboxylated or methylated (Carboxyhgb and methemoglobin) it irreversibly binds oxygen and does not permit it to be released at the normal oxygen tension of the proximal and distal capillary.

Ok, I have promises to only say what I know and what I dont know...the above biochemistry is off the top of my head and there may be errors, but the principles are correct. As for CoVID causing a conformation or electrochemical chage in the reduction state of Fe ions on Hgb, we have ways to measure it — it is part of the normal ABG. I am NOT seeing it. I know there has been a question of measuring ferritin in these patients — so then my next question would be has a patient with hemochromatosis ever had CoVID.

There is a lot of conjecture, and it is scientifically interesting, but what this article suggests are practices at the bench that we know at bedside would be dangerous, and I am not seeing these lab results in patients I am treating.

I am enjoying the scientific discussion with you despite some of our differences FWIW.

I will certainly accept any corrections to my biochemistry recall...

[Mom MD]

If you like a lot of fairy tales misinformation and unsourced statements

[grey_whiskers]

Concur. In particular, look at the predictions for fatalities from the top experts at University College London and Johns Hopkins, before the virus left China; and the predictions by CDC / Fauci / etc., for deaths and/or hospitalizations, based on "models".

Experts are often too enamoured of their own chosen paradigm. And the medical field is especially bad, eh, Dr. Semmelweis? See also the Nobel in medicine for ulcers...