Broadly, I would suggest that interested people read Corey Hardin's response to the cacophony of voices saying that COVID-19 respiratory failure is not ARDS: https://mailchi.mp/e10a89ac5988/tz4idnzryr-4388986?e=96507de...
Is this a role zinc might play? If there is a zinc deficiency would this not lead to vasodialtion and the dilution of the pneumocytes?
Further evidence for abnormal iron handling was demonstrated by Decker et al. (2011) who showed that zinc protoporphyrin (Zn-pp) levels are high in patients with PAH (mainly iPAH) indicating deficient iron incorporation to form heme suggestive of iron deficiency; levels were closely related to clinical severity (Decker et al., 2011). Zinc competes with iron for binding sites, therefore when iron levels are diminished zinc replaces iron at these sites. PAH patients also had a high red cell distribution width (RDW), again corresponding to markers of clinical severity, such as higher pulmonary arterial pressures and lower 6MWT. Most recently, using proteome analysis in the plasma of patients with PAH, Rhodes et al. (2017) were able to identify a combination of nine circulating proteins associated with a high risk of mortality, two of which, plasminogen and erythropoietin, are associated with abnormal iron metabolism (Rhodes et al., 2017).
What evidence do you have that zinc deficiency, rather than an infection causing a global pandemic, is causing hypoxemic respiratory failure right now?
To me, these seem totally irrelevant to COVID, but can you elaborate a direct connection?
Regarding the zinc deficiency; we see a large variation in outcomes after infection. Part could be viral load, but since we know people with "comorbidities" are more vulnerable to bad outcomes this delta should be an area of interest. Some people are totally asymptomatic!
The comorbidities (let's say heart disease) are caused by environmental or genetic variables. It seems zinc deficiency, to me, might be a common thread to both comorbidity and infection outcomes.
Since ACE2, a zinc metalloprotein which uses zinc as a cofactor, is in the alveoli and is the receptor for the virus, it would make sense to look at this as a serious possibility. ACE2 is a "Therapeutic Target for Heart Failure"
And zinc plays a role in the lung disease as well:
Interleukin-1α (IL-1α) production by alveolar macrophages in patients with acute lung diseases: the influence of zinc supplementation
"These results suggest that zinc can regulate the production of IL-1α from AM in patients with pulmonary tuberculosis or bacterial pneumonia."
Both anecdotally and experimentally there is evidence that zinc inhibits the replication of several virii. So zinc deficiency might make infection more likely and weaken the immune system to make outcome worse.
How can you say vasodialtion is not a vector in COVID19 outcomes? It is vasodialtion that increases capillary permeability leading to fluid in the intercistal space, am I correct? I may be wrong because I am reading that they are showing signs it appears as HAPE initially.
But these patients, from what I have read, also see a dramatic drop in blood pressure at some point as well.
so the connection with zinc is that they also treat HAPE patients with ACE2
ACE2 uses Zinc as a cofactor. So a zinc deficiency could mean less ACE2 and a greater risk of HAPE.
Regarding zinc and heart disease, I am not saying it is THE cause, just a part of the cause. It is demonstrated very well that zinc deficiency is common in people with diabetes and heart disease. The clinical data is there, I just showed you part of it.
Here is a great study, 2017, establishing a clear link beween zinc deficiency and diabetes:
It still shocks me that in 2020 we still have people that think vitamin cofactors play no role in health and should be ignored.
I will share this with you, I do not think hydroxychloroquine is needed, only high dose zinc. It is looking more like lower ACE2 activity is causing the majority of issues. Since ACE2 needs zinc as a cofactor, well...
"Covid-19 enters the lungs via the ACE2 receptor. The virus binds to the receptor, which then pulls it into the lung cell where the virus can multiply. In case of a massive infection, this process makes the ACE2 receptors disappear from the outside of the cell. With that, their function also disappears."
But Zinc does not need to be in the cell to help. It will also increase ACE2 activity, which is more important they are finding. When the ACE2 is destroyed, there is a build up of ANGII, which seems to be causing a majority of the issues. They are in a trial giving ACE2 directly to patients.
ACE inhibitors lower ACE, not ACE2. They actually increase ACE2.
https://www.medrxiv.org/content/10.1101/2020.04.07.20056788v... seems to support your assertion.
But yes, more zinc in meat for sure, and phytic acid will play a role reducing absorption, but deficiency could depend on genetics a lot as well.
Sorry I am old and new to Hacker News but I have a Phd. Am I doing something wrong?
Also, votes are just fake internet points. No need to worry about them too much :)
It takes an open mind to openly entertain a viewpoint that isn’t ones own.
Also takes an open mind to say just because I don’t understand/agree with something, it doesn’t mean there can’t be understanding in it.
Basically we need a mechanism to mitigate the impact of eternal September. There are too many new people with downvote ability changing the culture here for the worse. What’s insane is the number of times I see people downvoted for simply asking for sources/citations/references/ evidence/etc.
People claim that pg said it's not a problem. But he has said that it needed to be addressed: https://news.ycombinator.com/item?id=1057347
The problem isn't just downvoting, it's also that not enough people are upvoting reasonable-but-gray comments.
FWIW this is the majority of my upvoting, and I'd encourage others to do the same.
In terms of the type of behaviour that should be encouraged on YC.. celebrating a diversity of understanding, belief and practice should be OK in a community of individuals wanting to build things that are different.
OP had reflected out loud :)
Wouldn't this process fit with what I was asking about heme involvement and some sort of disruption of the oxygen pathway?
Can anyone else chime in on that idea?
Zinc replacing the iron in heme might help in the lungs.
Both aspects would involve a zinc deficiency.
I did my best to talk about some sort of disruption to the pathway involving oxygen uptake and utilization.
I'm a layman, so I'm maybe not phrasing it the best way. But I'm getting the impression that the reason ventilators are failing so badly is because it's not treating the right problem.
I have this idea that the infection is interfering with the oxygen pathway -- with how red blood cells take on and/or utilize oxygen. If that's the problem, more oxygen won't do much. If the body can't absorb it, extra supplies of oxygen just won't really take.
Can anyone speak to that idea in layman's terms with regards to what is known about the pathology of this class of infection?
Edit: I'm talking about a process similar to anemia or altitude sickness. I'm talking about some barrier to the body adequately using oxygen, in addition to any other challenges like fluid in the lungs blocking oxygen uptake.
Info on dietary sources of zinc:
Vents are not a treatment, they are support. Treatment would either slow replication or lower the inflammation.
But I like your thinking.
So, say, twenty percent of the problem is pneumonia and you can see gains by addressing that, but it's just one piece.
Lowering demand on the system would help accommodate the low oxygen. One way the body does this is by sleeping. People are reporting they are sleeping a lot.
Anyway, zinc makes sense based on stuff I'm aware of. And it's cheap and the body apparently doesn't store it. You need a daily supply.
So if zinc is a critical factor, dietary differences could be a significant detail. People sucking down sufficient zinc keep breathing. People not eating zinc-rich foods suffocate.
Does anyone know what Coronavirus does with regards to zinc usage in the body?
My focus more on nutritional genetics and biochemistry so I am trying to put something I know well with something I can maybe understand. This is why I reached out here.
I was just happy to have a better label than "hypochondriac" and was responding well to treatment and was fighting for my life. I shrugged and thought nothing of it, but that detail undermines my credibility in the CF community. (I mean the fact that I don't know my alleles.)
I was diagnosed nearly 19 years ago and I have been steadily getting better using dietary and lifestyle interventions. I know a lot about things like inflammation in the lungs and how to manage it.
At this point, I most likely have the infection and have had it for a while, though that only recently became clear to me because I'm largely asymptomatic.
The most prominent symptom I do have is that my energy levels are low in a way that suggests a bottleneck in the system on energy supply. Impaired oxygen availability would fit with what I'm experiencing.
I have a history of anemia and it is somewhat similar to that.
My lungs are clearer than they have been in weeks. I had a mold exposure earlier this year and spent weeks coughing up a lot of phlegm multiple times per day.
At the moment and in the last couple of weeks, my lungs aren't all gunked up and my chronic inflammation is currently very well controlled.
But we are all three (me and my sons, one of whom also has atypical CF) sucking down zinc-rich foods. And we feel notably better after eating.
So your remarks hit a nerve for me.
I'm not suggesting it's the entire answer. But CF is, itself, a bottleneck in the system at the cellular level. The mechanism causing the condition is a defective channel that handles traffic of certain molecules into and out of the cell.
That's what is known by medical science and it has been enormously helpful information for me. Beyond that, my mental models for what is going on with my body depart from current medical dogma and I get attacked and dismissed a lot as a loon because I'm a former homemaker, not a doctor.
But I'm extremely familiar with what it feels like to have a bottleneck in the system and this feels to me like a bottleneck in the system somewhere. And it's not lung function per se. I'm not having any breathing difficulties at all.
This is why I think Coronavirus is impairing oxygen uptake somehow in terms of some biochemical pathway.
I work from home, part time and when I feel like it. I'm poor, but I have a lot of control over my schedule.
My sons and I are lazing about a lot and struggling to come up with the energy to take care of what few tasks must be done daily. But with pollution levels down and no pressure to perform, we are managing to not end up in serious crisis. We just aren't pushing ourselves.
With a bottleneck in the system, you can't readily recover from stress events. You don't have the capacity.
For normal people who are used to being able to push themselves to do something when they don't feel well, a bottleneck in the system would create a potentially deadly problem where pushing themselves could be a cataclysmic event from which they cannot recover.
If there is a bottleneck, you have to slow down, take it easy, don't push. You have to take pressure off the system by lowering demand.
You have to max out support of all other areas that might impinge on the system in a way that would further narrow the bottleneck. I'm still doing lung clearance multiple times per day. I'm not bringing up much, but I'm keeping my lungs clear of obstruction because any obstruction further narrows the bottleneck.
So other things, like fluid in the lungs or inflammation, would further narrow the bottleneck. But clearing those additional burdens on the system doesn't, per se, fix the problem. It just lets the body get as much throughput through the bottleneck as possible.
My impression currently is that zinc consumption is easing the bottleneck itself. It's opening up capacity modestly, though it's certainly not a cure. It's just a means to keep energy levels up enough to not be a dire problem.
Please, if you can think of or learn of anything in terms of how Coronavirus impacts cell function that may cast light on interference with oxygen uptake at the biological pathway level (as opposed to mechanically in the lungs, which is what ventilators are trying to address and failing), shoot me an email. My email is in my profile.
There of many people with common disease living on on the nature----nurture spectrum. But the nurture part is largely overlooked in the PRACTICE of medicine. MD's have admitted to me that it is just easier to not focus on it.
Back to Coronavirus, it might be that the zinc is not as available to replace the iron in the Porphyrin ring.
I am not yet ready to see the low blood oxygen as totally bad. We used to think fevers were totally bad. It might be a way the body fights coronavirus. See:
I will send you an email as well.
Ventilators may be the wrong treatment because the low oxygen levels may be largely due to a process more like anemia rather than primarily due to lung issues. You don't treat anemia by putting people on ventilators.
We can't successfully treat people if our mental models of the problem are entirely wrong.
Current thinking is that CF is relatively common in some populations because it is protective against certain conditions and those conditions swept through Europe a lot for a while. CF is predominantly Caucasian and it's homozygous recessive.
So the current belief is that it's sort of like Sickle Cell Anemia. One copy of the gene improves survival against certain infections without being an egregious burden to live with. Two copies are a terrible problem that kill you at an early age.
About 18 years ago, not long after me and my older son were diagnosed with CF, my younger son -- who is only a carrier -- had Winter Vomiting. It was a very deadly stomach flu.
He spent eight days miserable and barely eating. I told him if he got dehydrated, I was taking him to the ER to get an IV. He had an IV once and didn't want it again. So once a day, he drank 32 ounces of water, had a few crackers or ramen and then immediately projectile vomited it all back up. But it kept him from ending up dehydrated.
Me and my oldest son felt kind of meh for like maybe a day and a half. Our gut doesn't work right. This stomach flu didn't thrive in our system.
So I am abundantly familiar with the concept you are talking. What you are saying is like that X Files scene where she says "The cold is the only thing keeping him alive." when they are trying to treat him for hypothermia.
But ventilators are apparently killing people and apparently not primarily due to antibiotic resistant secondary infection. This is a clue. We need to follow the clues and see where they take us.
The lung issues are the obvious explanation for low oxygen, but treating for lung issues isn't getting the expected result. Ergo the low oxygen most likely is due to a different mechanism. Logically, it's a mechanism more akin to anemia, which is basically a bottleneck on how much oxygen the body can absorb at one time.
That's where we need to look, I think.
I am wondering about how NOS enzymes (like NOS2) might play a role since they are expressed at high altitudes and COVID is looking a lot like high altitude sickness by one doctor in NYC.
I am thinking myself that some people with poor NOS genetics or poor nutrition will have this issue. The result of higher need for NOS2 will lead to polycythemia and to improved oxygen delivery to tissue when accompanied by increased blood volume.
This image might explain a lot:
I have such a strong intuition that ACE2 inhibition or destruction is an important issue with COVID.
(Yes, I'm aware the last two are trying to sell you something and are probably skeevy.)
So, some general off-the-cuff thoughts:
Glutathione is a big deal with CF. There is too little on the surface of cells and too much inside the cells.
Some people with CF report good results from inhaling NAC (iirc) tro promote glutathione on the surface of the lungs.
I think people with CF have too much inside their cells because we hoard it, along with calcium, to buffer against high acidity and other chemical derangement. As I have been getting healthier, I periodically experience what I think is glutathione dumping. My armpits and bowel movements smell strongly sour, similar to a skunk, and then my baseline function permanently improves afterwards.
I took milk thistle for a while, maybe a couple of years or something. It's a glutathione precursor. You can't supplement glutathione directly. You have to take precursors so the body can manufacture it.
I did it in part as liver support. Glutathione is important to liver function which is important to cleaning the blood. I spent a whole lot of time worried about my circulatory health as that seems to be the key that pulls everything together.
I read up on altitude sickness at one time and it was hugely eye opening. The mechanism involved provides a clear connection between the lung and gut issues in CF via the bloodstream.
I lived at 3000 feet above sea level for 2.75 years. My rib cage size enlarged and has remained enlarged ever since (as evidence by changes in the band size of my bras). I likely had underdeveloped lungs.
From there, I moved to about 100 feet above sea level and was soon bedridden due to pneumonia and this led to my diagnosis just before I turned to 36. It is known that people who live at altitude and then go down in altitude experience a big boost in energy levels. I likely survived being bedridden from pneumonia in part because of my recent time at altitude.
I'm wondering if you know of any research into long-term effects of NO production for having lived at altitude for a time.
I'm thinking my more normal distribution of glutathione these days may be a factor in why I have been largely asymptomatic, in spite of being in a high risk category.
One of those articles indicates that NO deficiency also inhibits glucose and/or NO enhances glucose uptake. This would also lower energy levels.
My impression of what I am experiencing absolutely fits with the idea that poor vasodilation in the lungs, and thus poor trafficking of oxygen into the blood stream, could explain the low oxygen levels, at least in part.
I don't know how to describe it, but I feel like, yes, my lungs are cut off in some way from my body, in spite of not being full of fluid. I breathe fine, but I sometimes feel like my airways aren't really doing their job in some important way. I feel like the tissues are "closed" in some sense, in spite of not being gunked up and covered over.
Insufficient vasodilation impairing oxygen uptake fits with that impression.
I think that's all I had in mind to say.
Edit: I have just spoken with my son (who also has atypical CF) about this discussion and he says lack of vasodilation -- and oxygen thus failing to cross adequately into the blood stream -- also fits with what he is experiencing. None of us has an active cough. We are mostly just really tired.
And there is a clear link to low NO and CF
It seems the issue with CF is NOS1. (I have an issue with NOS2)
Look at the cofactors that help NOS1 function and that might give you some clues at what may help:
Glutathione will help protect against both BH4 depletion as well as forming peryoxinitires.
You intuitions are excellent.
I have your email. We can continue discussion there.
Just as a pedantic note, I said above:
I lived at 3000 feet above sea level for 2.75 years.
I think that's wrong. I think it was more like 2 years, 5 months.
But as others have said, if you only use the ventilator for the very sickest people, then the more pressed you are the fewer survivors you'll get because people who have a chance without it will be kept off the ventilator if at all possible. My very limited understanding is that ventilation has major issues around bacterial infection.
other sources I've seen recently:
 https://icmanaesthesiacovid-19.org/covid-19-airway-managemen... (good detail on managing risk to staff, and on tracheal intubation)
This is why everybody is locking down so you don't have to make a choice between those that will benefit the most from ventilation and those that have little hope left. For most socialized healthcare systems once a resource is in sort supply guidelines for selecting those that will benefit the most are established. So at the end of the day the 80 y.o won't receive the ventilator but the 50 y.o. will( at least that's how it works here).
The report and data can be found here: https://www.icnarc.org/Our-Audit/Audits/Cmp/Reports
It's a short report but it's crammed full of information.
Critical care unit outcome Patients receiving advanced respiratory support*
(N=1053) (first and second columns)
Patients receiving only basic respiratory support*
(N=444) (third and forth columns)
Outcome at end of critical care, n (%)
Alive 355 (33.7) 358 (80.6)
Dead 698 (66.3) 86 (19.4)
The current protocols became widely agreed upon after clinical trials showed that this approach to mechanical ventilation reduced mortality. It is in physicians' nature to speculate about new approaches to care for sick patients. But it's important (for MDs) to put that speculation into the proper context and understand equipoise.
The author has not convinced me (an amateur) that they should be. They don't address the first primary hypothesis properly, which is that perhaps the pCO2 is actually in acceptable ranges in covid patients for some reason. Clearly the mortality for ventilated patients is higher for covid cases than other sources of past, so it's very intriguing they mix and match findings from 2016 with what we observe in covid.
This is not to question the authority of the authors, clearly they are experts, but personal experience from working with experts in academia is that they can also be very wrong because they're lost in the details, which is my worry here.
We should hope to strive and be great scientists though, so if a doctor or a scientist asks _why_ we should consider that the ARdS is slightly different in covid, they are owed some explanation and some data. Which we should explore together. In the meanwhile though, unless my further reading is going to change my mind, my current working hypothesis is going to be that the ARDS or whatever in covid patients is fundamentally slightly different in some way that means patients should be put on ventilators much later than conventional wisdom would suggest.
What is the counterfactual that you or others are proposing? One could use that counterfactual to set up a clinical trial.
There is a Facebook group with 10 or 20,000 doctors exchanging real-time information. One topic coming up is ventilators may be provided too late.
Or maybe looking at the therapy in countries that show low death rates? Could it be that some countries got lucky with the choice of therapy? For example, Russia seem to show surprisingly low death rate so far - 1 per million, as per today's Worldmeter data. As per Reuters/30 Jan, their health ministry recommended "ribavirin, lopinavir/ritonavir and interferon beta-1b".
Officially low rate. There could be low rates, just like there are no gays in Chechnya, or actually low. But it would be very surprising if any recommendation from January wasn't verified by now in other countries and used worldwide if it's successful.
US doctors are using ventialtors because that's how they've always done it.
But China found out months ago they're not working.
The general recommendation now is to use a cannula until you faint, since almost nobody survives the ventilator after a week - it's like major surgery.
You need the death rates of people that "needed" a ventilator but didn't get one. Maybe 90%-100% of them die?
Good on Medium for refusing to host that.
Edit: They do mention that it’s higher than other diseases relatively speaking, but don’t we expect Covid-19 to be higher than say, the flu, given it seems to primarily target the upper respiratory area?
It may be that for some patients going on a ventilator is more dangerous than not because of community acquired infections and/or some other characteristic we don't have a good handle on.
This could also just be an unfortunately characteristic of COVID-19, but we should critically examine that assumption in case it isn't.
Generally speaking, 40% to 50% of patients with severe respiratory distress die while on ventilators, experts say. But 80% or more of coronavirus patients placed on the machines in New York City have died, state and city officials say.
But another concern is that ventilators are known to cause lung damage (because of the high pressure involved) and are typically only used for a day or two with most conditions. With this, people are being kept on them for a week or two in many cases.
So it's not unreasonable to assume that unusually long-term use of a protocol known to harm the lungs is actively creating problems for patients.
I only know a little from my reading in the last month or so, but ventilators (used with intubated patients) seem very adjustable: you can alter the pressure, the Oxygen percentage, the tidal flow, breathing rate and such. I can see that in order to increase blood Oxygen uptake you might use higher pressures, but surely that's necessary to ensure patients get sufficient oxygen to avoid brain damage or other deleterious effects?
Won't the patients suffer in other ways if the Oxygen delivery is lower pressure?
When multiple patients share a single ventilator I see there are issues of balancing the supply, but I don't think that's what we're considering here.
It explains how they pressurize the lungs to try to keep the alveoli open and why that's very problematic, even when it is only short term. It is so problematic, they sedate people on ventilators so they won't pull the tubing out.
It sounds just really gruesome and like a brute force method that can't help but cause serious problems for delicate tissues if you use it for more than a fairly short period of time, which is the norm but is not how it is being used for Coronavirus cases.
Oxygen delivery is a complicated thing and I think taking a mechanical approach when mechanics may not be the actual problem is likely misguided.
That's a reasonable hypothesis, I think. But yeah, we just don't know. And it may be years before we do. No one has the ability to do a controlled study right now.
(Edit: it's absolutely infuriating to see the comment to which I'm replying here grayed out from downvotes. It's a completely reasonable notion phrased as a question, yet HN... doesn't want to hear the answer?)
You're right and I've given it a corrective upvote. For a time, I had a PSA in my profile indicating that I think downvotes will be weirder and more hair trigger during a global pandemic. I'm trying to be more thick skinned about weirdness happening in votes on my own comments, but, yes, it's just adding sand in the gears at a time when we don't need more noise.
There is a reason why 80 to 90% of doctors would refuse ventilators for themselves.
It could simply be an outlier or maybe defective machines or anything really. We don't know and we'll have to wait until the dust settles and we get more data.
What they are suggesting is to put patients on oxygen or low pressure ventilation first.
* * *
Here’s a preprint from Italian doctors Gattinoni & al. in the journal Intensive Care Medicine https://www.esicm.org/wp-content/uploads/2020/04/684_author-...
^ This article from a few days ago is a more detailed look at what is possibly going on here.
It sounds like forcing air down people's already damaged lungs is what's so dangerous here.
If your doctors are telling you you need to high pressure O2 or ventilation, your sats are in the toilet. You simply can't survive without a breathing aid. High pressure vents can exacerbate damaged lung tissue but it's [probably, citation needed] better than just suffocating.
And no, ECMO has a pile of its own issues, well beside being almost mythically rare.
Listen to your doctors. They're doing their very best.
(ref): Nature, Vol 580, 9 April 2020, page 181, graphics.
I'm not saying that there's not room for manoeuvre here. Positioning and whatever emergent therapies appear will certainly be factored in by doctors (who are desperate for something), but by the time you need ventilation, you are very, very ill.
You simply wouldn't survive without it.
At least to me, it seems like that crisis was created, primarily because of misalignment of the system towards maximizing executive compensation instead of public health.
You are once again pointing at opioids a some unassailable argument that doctors are only in it for the cash and cannot be trusted. If anything, doctors are trying to keep people off ventilation. They have to, they have dramatically more C19 patients than vents. Here, patients over 60 with co-mobidities are actively disqualified.
Beside this global conspiracy amongst physicians to over-prescribe ventilation, you're also suggesting that neither they nor the hundreds of public health bodies are looking at the results of their actions and adapting treatment, despite taking extreme care to collate data. Guidelines here are emergent, but you can't placebo people with resting SpO2s of 80. They die.
Again, "Look, opioids!" is not an argument. It's a harmful comparison.
The parallel seems interesting to me, as just like with opioid epidemic, some doctors were resisting in providing the painkiller therapy. While the mainstream was to use the opioid therapy.
The structure of the health-care system in the United States also contributed to the over-prescription of opioids. Because many doctors are in private practice, they can benefit financially by increasing the volume of patients that they see, as well as by ensuring patient satisfaction, which can incentivize the over-prescription of pain medication. Prescription opioids are also cheap in the short term. Patients’ health-insurance plans often covered pain medication but not pain-management approaches such as physical therapy. “The incentives were there for people to prescribe more and more, particularly when they had already been convinced it was the right thing to do — the compassionate thing to do,” Humphreys says.
This might help to explain why Canada is also experiencing an opioid crisis, with 10,337 opioid-related deaths between January 2016 and September 2018.
Most European countries, however, have so far been insulated from the epidemic. Doctors in Europe are not motivated financially to make prescriptions. - from this article in Nature -.
And by the way, yours "nothing compared" - this is just plain wrong. The level of the prescription-induced crisis, in numbers, was about the same as the current level. And users funneled to non-prescription since the prescription channel is now blocked.
As to the current decision-making. I'm not sure what is a right and efficient solution. Probably it is in the area of developing antivirals as fast as possible. And actively fighting the coefficient in the exponent. Like people wearing masks in Walmart. And allowing doctors to wear masks in hospitals, instead of hospital management making statements like: "THERES NO MORE WUHAN VIRUS IN THE HALLS AT THE HOSPITAL THAN WALMART". See: https://www.nytimes.com/2020/03/31/health/hospitals-coronavi...
But, putting people on ventilators seems like inefficient use of efforts. Yes, if you don't put late-stage patients on ventilators, they'd die. But it looks like, there is 80% chance they'd die, if you'd put on ventilators. And fewer people may die overall, if efforts were not spend on the whole ventilators affair. And instead something else was done.
Where I heard this:
I've also ready some hospitals are using techniques were O2 levels are increased directly in the blood supply? I can't remember what that's called though.
ECMO , it has been used quite a bit in Italy too.
The contaminated air will just be dumped in the room. There are virus filters (HEPA) which you can attach to the tubing so that the virus is caught there.