Marcus Aurelius said:

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My opinion. The vents are not killing pts. Rather, this is raging ARDS with cytokine storm +/- a vasculopathy or a thrombotic diasthesis. Lower inflating pressures, higher PEEPs for traditional ARDS are the only traditional treatments that effect outcomes. I have zero clue what other therapy he is recommending for severe respiratory failure other than a ventilator. The imaging, etc all support ARDS. IMO this is an emotional rant, understandably. But he's abandoning basic pulmonary physiologic tenets.

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Please entertain a layman's thought
Assuming lung scarring is primarily due to cytokine storm. And assuming why the body responds with cytokine storm response is unknown...

Possible a 'counter storm' of HSPs would put the body back in check?


Nope, put'em in a hot tub treatment too simple...

Googled and looks like China researched some appetizers with the thought...

Our data showed that short-term heat shock ameliorated the pulmonary immunopathology and increased the survival rate of H5N1-infected mice.

https://www.frontiersin.org/articles/10.3389/fmicb.2016.00924/full

Infection_Ag11 said:

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While it's worth discussing, it should be noted he is an ER physician and his thoughts are in direct opposition to essentially every pulm/crit physician (the vent experts) I've personally discussed this with and heard speak on the matter.

His thoughts also would not explain why these people have such high PEEP requirements, a defining feature of ARDS.

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For us laypeople, what is PEEP?

Positive end expiratory pressure. PEEP settings control the amount of air left in your lungs after exhalation. Here's an article about it:

https://www.ncbi.nlm.nih.gov/books/NBK441904/

Edit to link a more detailed article.

Also a layperson, would a CPAP machine act like a "bootleg" HFNC?

The company I work for has a site in Germany that has been contracted by a biotechnology customer to supply silica. They are using it for a tankless inhaled nitric oxide system. The system previously used to treat pulmonary hypertension in neonates was granted emergency expanded use by the FDA for treatment of cardiopulmonary symptoms associated with Covid-19.

Another biotechnology company is using our California site for another grade of silica to create Covid-19 test kits. The company was making RNA and DNA kits before this (also using the sane grade of silica).

ABATTBQ11 said:

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Infection_Ag11 said:

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While it's worth discussing, it should be noted he is an ER physician and his thoughts are in direct opposition to essentially every pulm/crit physician (the vent experts) I've personally discussed this with and heard speak on the matter.

His thoughts also would not explain why these people have such high PEEP requirements, a defining feature of ARDS.

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For us laypeople, what is PEEP?

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Positive end expiratory pressure, the pressure supplied by the vent at the end of the expiration. Think of it as the means of artificially propping the airway and alveoli open so they don't collapse when you breath out. It's essentially the same concept as CPAP.

Anyone remember the rook that posted something a few weeks ago about venting being unnecessary and the wrong treatment in most cases? He was with some research group and not actually practicing with patents? Most folks here completely disagreed with him. I wish I could find that post again. I'm not saying he was right or wrong and I don't understand the science of this, but it was an interesting comment.

In general terms, ARDS causes your lungs to be stiff. Those pts need a higher PEEP setting on the vent.

Thanks for all of the explanations. That makes more sense now.

Also, any thoughts on the paper from the posted tweet?

Thinking fear could be a factor inducing a raging cytokine storm. Power of positive thinking is handicapped with the awful experience being intubated - awful pain of intubation. I'm gonna die, I'm gonna die, thoughts inescapable especially now that the MSM set in stone YOUR GONNA DIE.

My medical advice is to LIE BIG TIME to the patients, tell'em everyone in your EXACT condition has SURVIVED. Get the mind in on the team and go for the BIG WIN.

eventually not gonna be lying...

law-apt-3g said:

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Thinking fear could be a factor inducing a raging cytokine storm. Power of positive thinking is handicapped with the awful experience being intubated - awful pain of intubation. I'm gonna die, I'm gonna die, thoughts inescapable especially now that the MSM set in stone YOUR GONNA DIE.

My medical advice is to LIE BIG TIME to the patients, tell'em everyone in your EXACT condition has SURVIVED. Get the mind in on the team and go for the BIG WIN.

eventually not gonna be lying...

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the ultimate fake it till you make it

http://web.archive.org/web/20200405061401/https://medium.com/@agaiziunas/covid-19-had-us-all-fooled-but-now-we-might-have-finally-found-its-secret-91182386efcb

not much on who wrote this article, so I am not claiming it's credible or not...just more discussion. If this disease truly is more "blood gas" than "pneumonia"...could that partially explain why type O blood people do better than others?

Im slowly coming around to this idea, but one main question I have is why haven't we confirmed this by measuring erythropoietin levels? Shouldn't that be a pretty routine test that we commonly use to find EPO abusers? That would at least be a pretty compelling argument for this idea.

Also why aren't these patients clotting ? I would imagine that to be another giveaway that I haven't heard mentioned.

Thinking now Daniel Griffin mentioned on TWiV they were starting to use heparin on some of their patients at Columbia.

This hypothesis from Jennifer Herman on Twitter, A&M faculty, I thought was pretty interesting

How is this not ARDS? by definition - Diffuse pulmonary infiltrates, with a P/F <300, and presumably a PCW of <12, i.e. not cardiogenic pulmonary edema. Nothing else is needed to label the disease "ARDS." BNPs initially low, unless they develop myocarditis. I don't think we are at the stage to label this as "SARS COV2 respiratory failure syndrome" now and presume we know how to treat it differently. And unknown disease mechanisms.

I am growing to be a believer in the prothombotic angiopathic phenomenon however. NEJM case today about a Wuhan ARDS pt with antiphospholipid antibody and severe pulmonary and peripheral arterial ischemia. Plus other reports of hypercoaguability. I am putting these pts on heparin GTTs, especially elevated d-dimer, and terribly sick, if no contraindications.

In the Wuhan study more severe cases were smoker and had COPD statistically.

We are trying to avoid intubation at all cost. HFNC plus surgical masks. CPAP 15cm +. Steroids earlier.

Actemra if you can. Remdisivir if you can. NO inhaled if you can get it?

Otherwise. ARDS mgmt is core.

AgStuckinLBK said:

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The guy is EM AND CC boarded. He's not "just an ER doctor" give me a break with your sub specialist pretentiousness. He's running an ICU in the ED like Scott Weingart does.

This thing is not acting like a typical viral pneumonia, leading to ARDS. He's right about that. It's not. There's no debating that. It's doing something to screw with how people oxygenate.

I've had people satting 54, with good pleths, speaking in full sentences and texting on their phone. I've had people in the 70s, having conversations. These are not things that happen with typical pneumonia -> ARDS.

Are some of these patients having typical ARDS? Yes. Is there something else going on? Yes.

If this was a primary lung problem causing disease organisms then people with primary chronic lung problems (asthmatics, copd'er) should be the highest risk to do die. They're not. CAD, HTN, DM are all higher risk factors suggesting something else going on that screws with your oxygenation is happening versus a primary lung problem. Kid and you adult asthmatics should be dying at a higher rate if this things primary damage was happening in the lungs.

Physiologically things are not checking out, epidemiologically things are not checking out, so doctors should be checking it out as to why and that's all this guy is doing. He may end up being wrong, but we should all be on the lookout for further explaining why this disease is acting the way that it is.

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I honestly did not know it was possible to have oxygen saturation that low

I have a had a big problem with doctors in the area not listening to Me describing symptoms and just treating it like typical respiratory disease.

I told doctors over and over that my lungs felt fine but I was not getting enough oxygen. Pneumonia like symptoms came on after nearly a week and weren't the initial symptoms. Just felt like hypoxia and being on a mountain.

anemia condition iron level
Melatonin inhibits cytokines production
estrogen modulate pro-inflammatory cytokine release

COVID-19: Attacks the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism
chloroquine could prevent orf1ab, ORF3a, and ORF10 to attack the heme to form the porphyrin, and inhibit the binding of ORF8 and surface glycoproteins to porphyrins to a certain extent, effectively relieve the symptoms of respiratory distress. Favipiravir could inhibit the envelope protein and ORF7a protein bind to porphyrin, prevent the virus from entering host cells, and catching free porphyrins. Because the novel coronavirus is dependent on porphyrins, it may originate from an ancient virus.

The predominance of evidence indicates that the pulmonary disease associated with SARS COV2 virus is due to direct viral cytopathic effects and resultant innate immune system responses that are then later amplified by cognate immure responses, particularly via anti-SARS CoV2 antibody production and resultant "disease enhancement" mediated by these antibodies.

The pathogenesis of coronavirus infections and pulmonary lesions has been an area of intense study since the first two coronavirus outbreaks - MERS and SARS. SARS COV2 shares substantial genetic sequence homology with SARS (79.6% homology) and other coronaviruses. Thus, lessons from these two diseases have direct implications for understanding of SARS Cov2 infections (ie, COVID). The strongest evidence to date explaining the pulmonary pathology associated with coronaviruses comes from Liu et al JCI Insight 2019 (fulll citation given below) and is summarized by the following:
1) the SARS COV2 virus binds to ACE2 receptors in pulmonary epithelia and the initial viral cytopathologic effects occur in pulmonary epithelium and endothelium (which also richly expresses ACE2- the SARS COV2 viral receptor)
2) initial pulmonary inflammation is mediated by an innate immune response to the virus which can be intense and obliterate small airways and alveoli.
3)the outcome- either recovery or severe pulmonary deterioration and cytokine storm result from the appearance of anti-SARS Cov2 antibodies in the serum of patients between 7 and 14 days of infection. If these antibodies are neutralizing (ie, the bind to the RBD (receptor binding domain) component of the SARS COV2 spike protein, the patient will improve. However, if the antibodies are not neutralizing (ie, the bind to other areas of the spike protein or other viral surface proteins, they may mediate a phenomenon termed "disease enhancement" where the antibodies bind to viral particles, opsonizing them, and then bind to monocytes and macro****es in the lungs that have been previously activated and trafficked to the lung. Binding of these antibodies binds to the high affinity Fc receptor (CD64) on monocytes and macro****es, resulting in intense activation and cytokine production (IL-1, IL-6, TNF, IL-10, MCP1 amongst others).

Thus the pneumonitis of COVID is an intense combination of viral cytopathic effects and inflammation. These same mechanisms occur with SARS, MERS, and severe influenza, and RSV. Disease enhancement is why there are no successful RSV vaccines to date. Disease enhancement will be the major risk associated with vaccine development for COVID. Currently, vaccine leaders in big pharma are actively designing vaccines so that neutralizing antibodies are the consistent and primary result rather than non-neutralizing antibodies.

The reason that RSV vaccines failed in the late 1960s is that they produced primarily disease enhancing antibodies rather than neutralizing antibodies.

one explanation for why diabetes is associated with increased risks is that diabetes markedly increases expression of ACE2, the SARS COV2 receptor.....

Those interested in the scientific literature supporting these observations should start with the reference list in Anti-spike IgG causes severe acute lung injury by skewing macro****e responses during acute SARS-CoV infection.
Liu L, Wei Q, Lin Q, Fang J, Wang H, Kwok H, Tang H, Nishiura K, Peng J, Tan Z, Wu T, Cheung KW, Chan KH, Alvarez X, Qin C, Lackner A, Perlman S, Yuen KY, Chen Z.
JCI Insight. 2019 Feb 21;4(4). pii: 123158. doi: 10.1172/jci.insight.123158. eCollection 2019 Feb 21.
PMID: 30830861

Thanks for that summary.

I'm certainly curious about the "Disease Enhancement" angle in that it seems key to potential treatments and the success of vaccines. Is the thinking that people mount a proper production of neutralizing and non-neutralizing antibodies but in some subset of people (particularly those with co-morbidities) the non-neutralizing antibodies don't get properly regulated?

AgStuckinLBK said:

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The guy is EM AND CC boarded. He's not "just an ER doctor" give me a break with your sub specialist pretentiousness. He's running an ICU in the ED like Scott Weingart does.

This thing is not acting like a typical viral pneumonia, leading to ARDS. He's right about that. It's not. There's no debating that. It's doing something to screw with how people oxygenate.

I've had people satting 54, with good pleths, speaking in full sentences and texting on their phone. I've had people in the 70s, having conversations. These are not things that happen with typical pneumonia -> ARDS.

Are some of these patients having typical ARDS? Yes. Is there something else going on? Yes.

If this was a primary lung problem causing disease organisms then people with primary chronic lung problems (asthmatics, copd'er) should be the highest risk to do die. They're not. CAD, HTN, DM are all higher risk factors suggesting something else going on that screws with your oxygenation is happening versus a primary lung problem. Kid and you adult asthmatics should be dying at a higher rate if this things primary damage was happening in the lungs.

Physiologically things are not checking out, epidemiologically things are not checking out, so doctors should be checking it out as to why and that's all this guy is doing. He may end up being wrong, but we should all be on the lookout for further explaining why this disease is acting the way that it is.

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I didn't mean to imply anything other than I'm not going to take the anecdotal words of other specialities over experienced pulm/crit physicians when it comes to pulmonary and respiratory failure physiology without really good data to back it up. I also didn't realize he was dual board certified in CC as well though.

Everyone has their thing was all I meant. I wouldn't trust the trauma triage of medicine specialties over those of an ED physician for instance. Apologies if anyone was offended.

That being said, to my eye and the eyes of most of the CC docs I respect highly, the physiology behaves more or less like severe ARDS in the patients getting tubed. Very high PEEP requirements to maintain oxygenation, require lower TV to avoid very high plateau pressures, proning at least transiently improving oxygenation (though not seemingly impacting mortality), etc. Their sats seem to correlate well with their pO2 on ABG throughout the disease course from what I've seen as well.

Posted this in another thread... Watch the video in the page below....skip to the 1 hour mark (1:00:49 to be exact) to hear a doctor talk about much of the same things...

https://www.acmt.net/ARBs_NSAIDS_Remdesivir_Updates_from_the_Front_Lines.html

Twitter account for this particular Doc - https://twitter.com/cameronks

Dang - I just realized it the the same Doc from the OP. My bad. Anyway...

Exsurge Domine said:

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AgStuckinLBK said:

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The guy is EM AND CC boarded. He's not "just an ER doctor" give me a break with your sub specialist pretentiousness. He's running an ICU in the ED like Scott Weingart does.

This thing is not acting like a typical viral pneumonia, leading to ARDS. He's right about that. It's not. There's no debating that. It's doing something to screw with how people oxygenate.

I've had people satting 54, with good pleths, speaking in full sentences and texting on their phone. I've had people in the 70s, having conversations. These are not things that happen with typical pneumonia -> ARDS.

Are some of these patients having typical ARDS? Yes. Is there something else going on? Yes.

If this was a primary lung problem causing disease organisms then people with primary chronic lung problems (asthmatics, copd'er) should be the highest risk to do die. They're not. CAD, HTN, DM are all higher risk factors suggesting something else going on that screws with your oxygenation is happening versus a primary lung problem. Kid and you adult asthmatics should be dying at a higher rate if this things primary damage was happening in the lungs.

Physiologically things are not checking out, epidemiologically things are not checking out, so doctors should be checking it out as to why and that's all this guy is doing. He may end up being wrong, but we should all be on the lookout for further explaining why this disease is acting the way that it is.

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I honestly did not know it was possible to have oxygen saturation that low

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After my heart attack/near drowning the nurse woke me up once and told me my O2 saturation was at 35. She was calm and just told me, "I need you to breathe." I responded, Whoa, that's like someone on Everest" and started taking some deep breaths. Used the spriometer and pulled out a bunch of blood from my lungs. She told me that if I got low again they were putting me on O2. Got better after that.