re: DR FAUCI AND THE NIH KNEW IN 2005 CHLOROQUINE STOPS SARS

I used it as kind of a tertiary resource early on (first week of march) to find out which rabbit holes to go down

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Except it didn’t stop SARS.

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It’s not a vaccine

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And a particularly nerdy one at that.

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As I enjoy nerdy questions allow a question. In another thread I read that aspects of this virus mimic HAPE compared to ARDS. It went into vent setting which led me out of my depth. Do you have anything on this?

Understand if you prefer not to derail this thread.

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Guaranteed that Fauci would never have suspended those early flights from Wuhan...on "anecdotal" evidence and WHO's sorry-assed- cover for the Chi-Coms.

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Azar has said that Trump "followed the uniform recommendation of the career public health officials here at HHS" in deciding on the China travel ban.

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virus mimic HAPE compared to ARDS. It went into vent setting which led me out of my depth. Do you have anything on this?

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In terms of how to treat them from a vent standpoint, they're more alike than different.


What exactly are you asking here? A simple overview on how a ventilator works (I can do that) vs the difference between rarely used things that someone in a high-altitude environment may use to tx pulmonary edema vs pulmonary edema from ARDS? I never learned a whole lot about actually treating HAPE first-hand, as I've never been in that environment, and the latter topic would be pretty dull with, again, many more things alike than different.

The post included an article from CHEST which I have not found. It dealt with FiO2 and PEEP settings in vented patients. From what I read they are treated differently in that regard and treating COVID patients as HAPE had more benefits. I will go to PubMed and try to find the referenced article.

ETA: the nerd part had to due with pressures and ariflow with respect to alveoli and blood distribution. Cannot find the article so maybe it was not of clinical significance.

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If you read the IDSA data, they actually encourage enrollment in various clinical trials, and that it is also available outside of trials if enrollment isn't feasible.

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What bugs me is the obvious.
Clinical trials include placebo.

Who in the hell wants to sign up for a clinical trial and receive placebo?

Who wants their loved one in a clinical trial and instead of medicine, they get placebo?

There is a problem with clinical trials when the environment is so dire that hospitals are running out of ventilators.
There is a problem with clinical trials when patients on a ventilator are dying about 50% of the time.

How come people defend clinical trials without defining what a clinical trial means?

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It dealt with FiO2 and PEEP settings in vented patients. From what I read they are treated differently in that regard and treating COVID patients as HAPE had more benefits

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pressures and ariflow with respect to alveoli and blood distribution

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This is pretty complicated to explain, but I'll try to do so in a way that's 1) generally right 2) high enough of a level to be interesting. There will probably be a mis-explained concept or two along the way, and anyone wanting to jump in and explain, feel free. I'm not an academic pulm/crit or anesthesia guy, so I don't explain this twice a week like they do. And I did have a few posts trying to explain this in the thread about multiple vents per patient (I posted a CHEST statement about why not to do that...is this what you're referencing?)
The lungs breath with what is referred to as negative-pressure ventilation. The lungs want to recoil inward. The chest wall wants to recoil outward. This is part of the reason that the lungs stay expanded. You expand your chest cavity (ribs and diaphragm) causing an even lower (negative) pressure in the lungs. Air rushes in. This is negative pressure ventillation, and it's what you do when you don't think about it. At the end of exhalation, your alveoli pressure are approximately 1 atmosphere (obviously lower if you're in a higher elevation where there is lower pressure and higher if you're at the bottom of the ocean).

Now when it comes to alveoli, some essentially close themselves all the way off and need to be "reopened" prior to air rushing in. Think of two balloons tied to a single hose that splits, delivering air to both balloons. If the balloons are the same size and equally empty, they fill equally. If one is partially inflated and the other is empty, you actually fill the already-inflated balloon preferentially to the "unopened" or "uninflated" balloon (alveolus), because the inward elastic recoil of the balloon that isn't inflated is a force that has to be overcome. Now, if one is maximally distended and another one is uninflated, you'll likely get the uninflated one to open preferential to "popping" the distended one. So you get some that stay open and full. Some that are hard to open. And some that are essentially responsible for most of the ventilation that occurs

Here's the "God is somewhere between smart and magical" part:
Poorly ventilated alveoli get less o2 moving in and out (by definition). Less o2 in the alveoli leads to vasoconstriction which "shunts" blood toward the better-ventilated alveoli.


In HAPE, this vasoconstriction occurs not because of ventillation but due to lack of o2 in the air. Therefor, it's happening basically uniformly. So you can't "shunt" the entire lung. You just wind up with higher than normal pressures in the capillaries. If they get too high, they leak into the alveoli. Once you've gotten to this point, re-applying o2 to decrease the pulmonary hypertension works, but adding PEEP (peak end-expiratory pressure...so back up high where the pressure at the end of exhalation was 1 or less atmospheres, you want to give a POSITIVE pressure to keep more alveoli open (recruited and 'actively participating' in the breath as I sort of tried to explain above)) gets more alveoli involved. When you're talking about ventilating an intubated patient, you're going to be referencing PEEP. In some patients, o2 may be enough.

ARDS is quite a bit different. It's an inflammatory process. They both cause pulmonary edema, but inflammation isn't improved by oxygen. It actually tends to make it worse (when you add o2, you can cause some poorly-ventilated alveoli to become more-perfused which is referred to as ventilation-perfusion mismatch, so co2 can build up in those patients).


Physiologically, I don't think there is any difference between "plain, old" ARDS and COVID-19's lung phenomena which appears clinically very much like ARDS with an essentially perfect explanation for why it's the same (and no real explanation for why it would behave like HAPE). It tends to respond better to a lower FiO2 and higher PEEP. o2 seems to be toxic to the alveolar/vascular interface and actually can worsen the patient's condition as well. Now, it's possible there's more to what you were referencing than "HAPE = high Fio2 with modest PEEP; ARDS = high PEEP with modest fio2," but I am not certain that I'm able to clarify what about the HAPE strategy you're referring to would improve



Any of that make any sense?

Am I assuming correctly that this drug is already approved by the FDA to treat arthritis and lupus?

I thought so. Wolf on CNN said it was not FDA approved.