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Serious The Secret of COVID-19 Virus Revealed and Why Hydroxychloroquine Works.

kryonlight

Alfrescian (Inf)
Asset
Do COVID-19 Vent Protocols Need a Second Look?

After treating patients with COVID-19, a New York city physician suggests ventilator protocols may need revisiting
John Whyte, MD, MPH; Cameron Kyle-Sidell, MD

This transcript has been edited for clarity.

John Whyte, MD, MPH: Hello. I'm Dr John Whyte, chief medical officer at WebMD. Welcome to "Coronavirus in Context." Today we're going to talk about whether we're managing coronavirus correctly; do we need to think about a change in our treatment regiments? My guest is Dr Cameron Kyle-Sidell. He's a physician trained in emergency medicine and critical care, and he practices at Maimonides in Brooklyn, New York. Welcome, Dr Sidell.

Cameron Kyle-Sidell, MD: Thank you very much. Thank you for inviting me.


Whyte: You've been talking a lot about the number of patients, the percentage of patients dying on ventilators. When did you first notice this trend?

Kyle-Sidell: In preparation of opening what became a full COVID-positive intensive care unit, we scoured the data just to see what was out there—those who have experienced it before us, primarily the Chinese and the Italians; it was hard to find exactly, like the rate of what we call successful extubation—meaning, someone was put on a ventilator and taken off. And that data are still hard to find. I imagine there are a lot of people still on ventilators. But from the data we have available, it appears to be somewhere between 50% and 90%. Most published data puts it around 70%. So, that's a very, very high percentage in general, when one thinks of a medical disease.

Whyte: You've been talking on social media; you say you've seen things that you've never seen before. What are some of those things that you're seeing?

Kyle-Sidell: When I initially started treating patients, I was under the impression, as most people were, that I was going to be treating acute respiratory distress syndrome (ARDS), similar in substance to AIDS, which I saw as a fellow. And as I start to treat these patients, I witnessed things that are just unusual. And I'm sure doctors around the country are experiencing this. In the past, we haven't seen patients who are talking in full sentences and not complaining of overt shortness of breath, with saturations in the high 70s. It's just not something we typically see when we're intubating some of these patients. That is to say, when we're putting a breathing tube in, they tend to drop their saturations very quickly; we see saturations going down to 20 to 30. Typically, one would expect some kind of reflexive response from the heart rate, which is to say that usually we see tachycardia, and if patients go too low, then we see bradycardia. These are things that we just weren't seeing. I've seen literally a saturation of zero on a monitor, which is not something we ever want and something we actively try to avoid. And yet we saw it, and many of my colleagues have similarly seen saturations of 10 and 20. We try to put breathing tubes in to avoid this very situation. Now, these patients tend to desaturate extremely quickly, so these situations have occurred. Still, what we're seeing—that there was no change in the heart rate—is just unusual. It's just something that we are not used to seeing.

Whyte: This is more like a high-altitude sickness. Is that right?

Kyle-Sidell: Yes. The patients in front of me are unlike any patients I've ever seen., and I've seen a great many patients and have treated many diseases. You get used to seeing certain patterns, and the patterns I was seeing did not make sense. This originally came to me when we had a patient who had hit what we call our trigger to put in a breathing tube, meaning she had displayed a level of hypoxia of low oxygen levels where we thought she would need a breathing tube. Most of the time, when patients hit that level of hypoxia, they're in distress and they can barely talk; they can't say complete sentences. She could do all of those and she did not want a breathing tube. So she asked that we put it in at the last minute possible. It was this perplexing clinical condition: When was I supposed to put the breathing tube in? When was the last minute possible? All the instincts as a physician—like looking to see if she tires out —none of those things occurred. It's extremely perplexing. But I came to realize that this condition is nothing I've ever seen before. And so I started to read to try to figure it out, leaving aside the exact mechanism of how this disease is causing havoc on the body, but instead trying to figure out what the clinical syndrome looked like.

Whyte: You talked a little about the data from Italy.

Kyle-Sidell: Yes.


Whyte: [From Luciano] Gattinoni. Were you aware of what was going on in Italy before you noticed these observations or did that come after the fact?


Kyle-Sidell: That came a little bit after. And I wasn't aware. I can't even remember the exact timeline. But in my reading, I came upon decompression, pulmonary sickness, which is essentially the bends—when divers dive and come up too quickly—which seemed to mirror the clinical picture of these patients. And in discussions of other people, it came up that they do appear similar clinically. This is not to say that the pathophysiology underlying it is similar, but clinically they look a lot more like high-altitude sickness than they do pneumonia. Regarding, Gattinoni, he published something on March 20th, which was about 2 days before I opened the ICU. I don't know that I read it then, but somehow it got passed around. In my mind, by the time I read what he was saying, I'd come under the impression that this just wasn't what we were used to seeing. It was a high-compliance disease, which every pulmonologist had. Anyone managing a ventilator can see. That's not a question. So when I read his stuff, where he is suggesting that the management strategy that we use is essentially somewhat flipped, at least in these high-compliant patients, it just became more clear that that if we operate under a paradigm whereby we are treating ARDS in these high-compliant patients, we may not be operating under the right paradigm.


Whyte: Have you changed your protocols, then?


Kyle-Sidell: To be honest, I've run into a great deal of resistance within my institution, which is not to say that anyone is trying to stymie the progress at all. These are the protocols that are in every major (and minor) hospital.


Whyte: You talked about in your videos.


Kyle-Sidell: Yeah.


Whyte: Against a long-standing dogma. So what's been the response from your clinical colleagues as well as hospital administrators?


Kyle-Sidell: I started to try to not my own protocols, but to treat patients as I would have treated my family, with different goals—which is to say, ventilation. However, these didn't fit the protocol, and the protocol is what the hospital runs on with the respiratory therapist, with the nurses; everyone is part of the team. We ran into an impasse where I could not morally, in a patient-doctor relationship, continue the current protocols which, again, are the protocols of the top hospitals in the country. I could not continue those. You can't have one doctor just doing their own protocol. So I had to step down from my position in the ICU, and now I'm back in the ER where we are setting up slightly different ventilation strategies. Fortunately, we've been boosted by recent work by Gattinoni, which was formally published today and which does outline the best evidence, based on at least expert recommendations, for changes in our overall protocols. [Editor's note: Dr Kyle-Sidell is referring to an unedited proof, soon to be published formally in Intensive Care Medicine.]

Whyte: Can you tell us what some of those changes are that you're going to make?


Kyle-Sidell: First, I'll describe what Gattinoni was saying, which is that really what we're seeing in ARDS are two different phenotypes: one in which the lungs display what you call high compliance, low elastance; and one in which they have low compliance and high elastance. To say it simply for people who are not pulmonologists, if you think of the lungs as a balloon, typically when people have ARDS or pneumonia, the balloon gets thicker. So not only do you lack oxygen, but the pressure and the work to blow up the balloon becomes greater. So one's respiratory muscles become tired as they struggle to breathe. And patients need pressure. What Gattinoni is saying is that there are essentially two different phenotypes, one in which the balloon is thicker, which is a low-compliance disease. But in the beginning they display high compliance. Imagine if the balloon is not actually thicker but thinner, so they'd suffer from a lack of oxygen. But it is not that they suffer from too much work to blow up the balloon. As far as how we're going to switch, we're going to take our approach differently from the traditional ARDSnet protocol in that we are going to do an oxygen-first strategy: We're going to leave the oxygen levels as high as possible and we're going to try to use the lowest pressures possible to try to keep the oxygen levels high. That's the approach we're going to do, so long as the patients continue to display the physiology of a low elastance, high-compliance disease.


Whyte: Do you feel that somewhere the world made a wrong turn in treating COVID-19?


Kyle-Sidell: I don't know that they made a wrong turn. I mean, it came so fast. I think that one thing we benefit from is that the Chinese and the Italians were hit first and they were hit hard. New York is being hit so hard. It's hard to switch tracks when the train is going a million miles an hour. In that sense, we'd benefit from their shared experience. And I think it's important that we listen to that experience. But I do think that it starts out with knowing, or at least accepting the idea, that this may be an entirely new disease. Because once you do that, then you can accept the idea that perhaps all the studies on ARDS in the 2000s and 2010s, which were large, randomized, well-performed, well-funded studies, perhaps none of those patients in those studies had COVID-19 or something resembling it. It allows you to move away from a paradigm in which this disease may fit and, unfortunately, walk somewhat into the unknown.


Whyte: You're advocating something a little different. What are the consequences of you being wrong, albeit well intentioned?


Kyle-Sidell: Right now we have some of the greatest experts in the world giving their opinions. By that, I mean the Italians and Dr Gattinoni. I certainly could be wrong. What I'm asking for is not even not an immediate change in the ventilation strategy, because I'm critical care trained, I'm not pulmonary trained and I'm not as experienced as many around the country and many in my own hospital. But what I would like to see is all of these great minds get together. If they can accept this notion that perhaps we need to switch paradigms, and they're able to better create a path forward that fits the disease. I would gladly follow them. Really, what I'm asking and what I'm requesting is that all of the experts in the field get together and perhaps come up with some fresh recommendations.


Whyte: You've been active on social media, as I mentioned. Are you a whistleblower?


Kyle-Sidell: This is sort of my first foray into social media. I don't know that I'm a whistleblower. I don't know that anyone was trying to purposely do any harm. I think that, all of the physicians involved and all of the nurses and everyone writing protocols—everyone is working as fast and as hard as they can with good faith and pure intention. For me, I saw something clinically that didn't make sense. And seeing that New York is about 10 days ahead of the rest of country, I just felt compelled to get that information out.


Whyte: Has speaking up impacted your professional career?


Kyle-Sidell: I don't know yet. In one sense, I have not felt qualms about it. For whatever reason, I trained in critical care and I was an ER doctor, and I think part of that allowed me to see it a little bit better. Because if you just received these patients in the ICU on breathing tubes, it's very hard to see this physiology. I was running around the hospital from the ER to the floors to the ICU, and I saw them in all stages of this disease. When you see them in all those different stages, you're able to see that something physiologically doesn't make sense. So, in a way, I do feel that somehow my training and my position, being in New York City, allowed me to see this. I have not felt any conflict about coming forward, per se. And I don't know what it will do for my career, but I hope that people know that I'm not doing this with any kind of— I'm not trying to stymie anything. It's really that I'm doing what I think is right.


Whyte: What are the two things that we need to be doing right now to really address the mortality?


Kyle-Sidell: That goes back to your question of "if I am wrong." We are desperate now in the sense that everything we are doing does not seem to be working. So we've reached a point that most other diseases have not reached, where many physicians are willing to try anything that may help because so little seems to be helping. One of the reasons I speak up, and I hope people at the bedside speak up, is that I think there may be a disconnect between those who are seeing these patients directly, who are sensing that something is not quite right, and those brilliant people and researchers and administrators who are writing the protocols and working on finding answers. The first thing to do is see if we can admit that this is something new. I think it all starts from there. I think we have the kind of scientific technology and the human capital in this country to solve this or at least have a very good shot at it. I think the second thing is that whatever collaboration we can do with those who came before us—and by that, I mean the Chinese and the Italians and the Egyptians and whoever else has experienced this—if there's anything we can learn from them, I think we need to open up and be ready to receive their help.


Whyte: Dr Kyle-Sidell, I want to thank you for speaking up and sharing your story with us.


Kyle-Sidell: Thank you very much. I appreciate you allowing me to speak.


Whyte: I want to thank you for watching "Coronavirus in Context." I'm Dr John Whyte.
 

kryonlight

Alfrescian (Inf)
Asset
Covid-19 had us all fooled, but now we might have finally found its secret.

In the last 3–5 days, a mountain of anecdotal evidence has come out of NYC, Italy, Spain, etc. about COVID-19 and characteristics of patients who get seriously ill. It’s not only piling up but now leading to a general field-level consensus backed up by a few previously little-known studies that we’ve had it all wrong the whole time. Well, a few had some things eerily correct (cough Trump cough), especially with Hydroxychloroquine with Azithromicin, but we’ll get to that in a minute.

There is no ‘pneumonia’ nor ARDS. At least not the ARDS with established treatment protocols and procedures we’re familiar with. Ventilators are not only the wrong solution, but high pressure intubation can actually wind up causing more damage than without, not to mention complications from tracheal scarring and ulcers given the duration of intubation often required… They may still have a use in the immediate future for patients too far to bring back with this newfound knowledge, but moving forward a new treatment protocol needs to be established so we stop treating patients for the wrong disease.

The past 48 hours or so have seen a huge revelation: COVID-19 causes prolonged and progressive hypoxia (starving your body of oxygen) by binding to the heme groups in hemoglobin in your red blood cells. People are simply desaturating (losing o2 in their blood), and that’s what eventually leads to organ failures that kill them, not any form of ARDS or pneumonia. All the damage to the lungs you see in CT scans are from the release of oxidative iron from the hemes, this overwhelms the natural defenses against pulmonary oxidative stress and causes that nice, always-bilateral ground glass opacity in the lungs. Patients returning for re-hospitalization days or weeks after recovery suffering from apparent delayed post-hypoxic leukoencephalopathy strengthen the notion COVID-19 patients are suffering from hypoxia despite no signs of respiratory ‘tire out’ or fatigue.
Here’s the breakdown of the whole process, including some ELI5-level cliff notes. Much has been simplified just to keep it digestible and layman-friendly.

Your red blood cells carry oxygen from your lungs to all your organs and the rest of your body. Red blood cells can do this thanks to hemoglobin, which is a protein consisting of four “hemes”. Hemes have a special kind of iron ion, which is normally quite toxic in its free form, locked away in its center with a porphyrin acting as it’s ‘container’. In this way, the iron ion can be ‘caged’ and carried around safely by the hemoglobin, but used to bind to oxygen when it gets to your lungs.

When the red blood cell gets to the alveoli, or the little sacs in your lungs where all the gas exchange happens, that special little iron ion can flip between FE2+ and FE3+ states with electron exchange and bond to some oxygen, then it goes off on its little merry way to deliver o2 elsewhere.

Here’s where COVID-19 comes in. Its glycoproteins bond to the heme, and in doing so that special and toxic oxidative iron ion is “disassociated” (released). It’s basically let out of the cage and now freely roaming around on its own. This is bad for two reasons:

1) Without the iron ion, hemoglobin can no longer bind to oxygen. Once all the hemoglobin is impaired, the red blood cell is essentially turned into a Freightliner truck cab with no trailer and no ability to store its cargo.. it is useless and just running around with COVID-19 virus attached to its porphyrin. All these useless trucks running around not delivering oxygen is what starts to lead to desaturation, or watching the patient’s spo2 levels drop. It is INCORRECT to assume traditional ARDS and in doing so, you’re treating the WRONG DISEASE. Think of it a lot like carbon monoxide poisoning, in which CO is bound to the hemoglobin, making it unable to carry oxygen. In those cases, ventilators aren’t treating the root cause; the patient’s lungs aren’t ‘tiring out’, they’re pumping just fine. The red blood cells just can’t carry o2, end of story. Only in this case, unlike CO poisoning in which eventually the CO can break off, the affected hemoglobin is permanently stripped of its ability to carry o2 because it has lost its iron ion. The body compensates for this lack of o2 carrying capacity and deliveries by having your kidneys release hormones like erythropoietin, which tell your bone marrow factories to ramp up production on new red blood cells with freshly made and fully functioning hemoglobin. This is the reason you find elevated hemoglobin and decreased blood oxygen saturation as one of the 3 primary indicators of whether the shit is about to hit the fan for a particular patient or not.

2) That little iron ion, along with millions of its friends released from other hemes, are now floating through your blood freely. As I mentioned before, this type of iron ion is highly reactive and causes oxidative damage. It turns out that this happens to a limited extent naturally in our bodies and we have cleanup & defense mechanisms to keep the balance. The lungs, in particular, have 3 primary defenses to maintain “iron homeostasis”, 2 of which are in the alveoli, those little sacs in your lungs we talked about earlier. The first of the two are little macrophages that roam around and scavenge up any free radicals like this oxidative iron. The second is a lining on the walls (called the epithelial surface) which has a thin layer of fluid packed with high levels of antioxidant molecules.. things like abscorbic acid (AKA Vitamin C) among others. Well, this is usually good enough for naturally occurring rogue iron ions but with COVID-19 running rampant your body is now basically like a progressive state letting out all the prisoners out of the prisons… it’s just too much iron and it begins to overwhelm your lungs’ countermeasures, and thus begins the process of pulmonary oxidative stress. This leads to damage and inflammation, which leads to all that nasty stuff and damage you see in CT scans of COVID-19 patient lungs. Ever noticed how it’s always bilateral? (both lungs at the same time) Pneumonia rarely ever does that, but COVID-19 does… EVERY. SINGLE. TIME.

— — — — — — — — — — — — -

Once your body is now running out of control, with all your oxygen trucks running around without any freight, and tons of this toxic form of iron floating around in your bloodstream, other defenses kick in. While your lungs are busy with all this oxidative stress they can’t handle, and your organs are being starved of o2 without their constant stream of deliveries from red blood cell’s hemoglobin, and your liver is attempting to do its best to remove the iron and store it in its ‘iron vault’. Only its getting overwhelmed too. It’s starved for oxygen and fighting a losing battle from all your hemoglobin letting its iron free, and starts crying out “help, I’m taking damage!” by releasing an enzyme called alanine aminotransferase (ALT). BOOM, there is your second of 3 primary indicators of whether the shit is about to hit the fan for a particular patient or not.

Eventually, if the patient’s immune system doesn’t fight off the virus in time before their blood oxygen saturation drops too low, ventilator or no ventilator, organs start shutting down. No fuel, no work. The only way to even try to keep them going is max oxygen, even a hyperbaric chamber if one is available on 100% oxygen at multiple atmospheres of pressure, just to give what’s left of their functioning hemoglobin a chance to carry enough o2 to the organs and keep them alive. Yeah we don’t have nearly enough of those chambers, so some fresh red blood cells with normal hemoglobin in the form of a transfusion will have to do.

The core point being, treating patients with the iron ions stripped from their hemoglobin (rendering it abnormally nonfunctional) with ventilator intubation is futile, unless you’re just hoping the patient’s immune system will work its magic in time. The root of the illness needs to be addressed.

Best case scenario? Treatment regimen early, before symptoms progress too far. Hydroxychloroquine (more on that in a minute, I promise) with Azithromicin has shown fantastic, albeit critics keep mentioning ‘anecdotal’ to describe the mountain, promise and I’ll explain why it does so well next. But forget straight-up plasma with antibodies, that might work early but if the patient is too far gone they’ll need more. They’ll need all the blood: antibodies and red blood cells. No help in sending over a detachment of ammunition to a soldier already unconscious and bleeding out on the battlefield, you need to send that ammo along with some hemoglobin-stimulant-magic so that he can wake up and fire those shots at the enemy.

The story with Hydroxychloroquine
All that hilariously misguided and counterproductive criticism the media piled on chloroquine (purely for political reasons) as a viable treatment will now go down as the biggest Fake News blunder to rule them all. The media actively engaged their activism to fight ‘bad orange man’ at the cost of thousands of lives. Shame on them.

How does chloroquine work? Same way as it does for malaria. You see, malaria is this little parasite that enters the red blood cells and starts eating hemoglobin as its food source. The reason chloroquine works for malaria is the same reason it works for COVID-19 — while not fully understood, it is suspected to bind to DNA and interfere with the ability to work magic on hemoglobin. The same mechanism that stops malaria from getting its hands on hemoglobin and gobbling it up seems to do the same to COVID-19 (essentially little snippets of DNA in an envelope) from binding to it. On top of that, Hydroxychloroquine (an advanced descendant of regular old chloroquine) lowers the pH which can interfere with the replication of the virus. Again, while the full details are not known, the entire premise of this potentially ‘game changing’ treatment is to prevent hemoglobin from being interfered with, whether due to malaria or COVID-19.

No longer can the media and armchair pseudo-physicians sit in their little ivory towers, proclaiming “DUR so stoopid, malaria is bacteria, COVID-19 is virus, anti-bacteria drug no work on virus!”. They never got the memo that a drug doesn’t need to directly act on the pathogen to be effective. Sometimes it’s enough just to stop it from doing what it does to hemoglobin, regardless of the means it uses to do so.

Anyway, enough of the rant. What’s the end result here? First, the ventilator emergency needs to be re-examined. If you’re putting a patient on a ventilator because they’re going into a coma and need mechanical breathing to stay alive, okay we get it. Give ’em time for their immune systems to pull through. But if they’re conscious, alert, compliant — keep them on O2. Max it if you have to. If you HAVE to inevitably ventilate, do it at low pressure but max O2. Don’t tear up their lungs with max PEEP, you’re doing more harm to the patient because you’re treating the wrong disease.

Ideally, some form of treatment needs to happen to:

  1. Inhibit viral growth and replication. Here plays CHQ+ZPAK+ZINC or other retroviral therapies being studies. Less virus, less hemoglobin losing its iron, less severity and damage.
  2. Therapies used for anyone with abnormal hemoglobin or malfunctioning red blood cells. Blood transfusions. Whatever, I don’t know the full breadth and scope because I’m not a physician. But think along those lines, and treat the real disease. If you’re thinking about giving them plasma with antibodies, maybe if they’re already in bad shape think again and give them BLOOD with antibodies, or at least blood followed by plasma with antibodies.
  3. Now that we know more about how this virus works and affects our bodies, a whole range of options should open up.
  4. Don’t trust China. China is ASSHOE. (disclaimer: not talking about the people, just talking about the regime). They covered this up and have caused all kinds of death and carnage, both literal and economic. The ripples of this pandemic will be felt for decades.
Fini.
 

Leongsam

High Order Twit / Low SES subject
Admin
Asset
Covid-19 had us all fooled, but now we might have finally found its secret.

In the last 3–5 days, a mountain of anecdotal evidence has come out of NYC, Italy, Spain, etc. about COVID-19 and characteristics of patients who get seriously ill. It’s not only piling up but now leading to a general field-level consensus backed up by a few previously little-known studies that we’ve had it all wrong the whole time. Well, a few had some things eerily correct (cough Trump cough), especially with Hydroxychloroquine with Azithromicin, but we’ll get to that in a minute.

There is no ‘pneumonia’ nor ARDS. At least not the ARDS with established treatment protocols and procedures we’re familiar with. Ventilators are not only the wrong solution, but high pressure intubation can actually wind up causing more damage than without, not to mention complications from tracheal scarring and ulcers given the duration of intubation often required… They may still have a use in the immediate future for patients too far to bring back with this newfound knowledge, but moving forward a new treatment protocol needs to be established so we stop treating patients for the wrong disease.


Here’s the breakdown of the whole process, including some ELI5-level cliff notes. Much has been simplified just to keep it digestible and layman-friendly.

Your red blood cells carry oxygen from your lungs to all your organs and the rest of your body. Red blood cells can do this thanks to hemoglobin, which is a protein consisting of four “hemes”. Hemes have a special kind of iron ion, which is normally quite toxic in its free form, locked away in its center with a porphyrin acting as it’s ‘container’. In this way, the iron ion can be ‘caged’ and carried around safely by the hemoglobin, but used to bind to oxygen when it gets to your lungs.

When the red blood cell gets to the alveoli, or the little sacs in your lungs where all the gas exchange happens, that special little iron ion can flip between FE2+ and FE3+ states with electron exchange and bond to some oxygen, then it goes off on its little merry way to deliver o2 elsewhere.

Here’s where COVID-19 comes in. Its glycoproteins bond to the heme, and in doing so that special and toxic oxidative iron ion is “disassociated” (released). It’s basically let out of the cage and now freely roaming around on its own. This is bad for two reasons:

1) Without the iron ion, hemoglobin can no longer bind to oxygen. Once all the hemoglobin is impaired, the red blood cell is essentially turned into a Freightliner truck cab with no trailer and no ability to store its cargo.. it is useless and just running around with COVID-19 virus attached to its porphyrin. All these useless trucks running around not delivering oxygen is what starts to lead to desaturation, or watching the patient’s spo2 levels drop. It is INCORRECT to assume traditional ARDS and in doing so, you’re treating the WRONG DISEASE. Think of it a lot like carbon monoxide poisoning, in which CO is bound to the hemoglobin, making it unable to carry oxygen. In those cases, ventilators aren’t treating the root cause; the patient’s lungs aren’t ‘tiring out’, they’re pumping just fine. The red blood cells just can’t carry o2, end of story. Only in this case, unlike CO poisoning in which eventually the CO can break off, the affected hemoglobin is permanently stripped of its ability to carry o2 because it has lost its iron ion. The body compensates for this lack of o2 carrying capacity and deliveries by having your kidneys release hormones like erythropoietin, which tell your bone marrow factories to ramp up production on new red blood cells with freshly made and fully functioning hemoglobin. This is the reason you find elevated hemoglobin and decreased blood oxygen saturation as one of the 3 primary indicators of whether the shit is about to hit the fan for a particular patient or not.

2) That little iron ion, along with millions of its friends released from other hemes, are now floating through your blood freely. As I mentioned before, this type of iron ion is highly reactive and causes oxidative damage. It turns out that this happens to a limited extent naturally in our bodies and we have cleanup & defense mechanisms to keep the balance. The lungs, in particular, have 3 primary defenses to maintain “iron homeostasis”, 2 of which are in the alveoli, those little sacs in your lungs we talked about earlier. The first of the two are little macrophages that roam around and scavenge up any free radicals like this oxidative iron. The second is a lining on the walls (called the epithelial surface) which has a thin layer of fluid packed with high levels of antioxidant molecules.. things like abscorbic acid (AKA Vitamin C) among others. Well, this is usually good enough for naturally occurring rogue iron ions but with COVID-19 running rampant your body is now basically like a progressive state letting out all the prisoners out of the prisons… it’s just too much iron and it begins to overwhelm your lungs’ countermeasures, and thus begins the process of pulmonary oxidative stress. This leads to damage and inflammation, which leads to all that nasty stuff and damage you see in CT scans of COVID-19 patient lungs. Ever noticed how it’s always bilateral? (both lungs at the same time) Pneumonia rarely ever does that, but COVID-19 does… EVERY. SINGLE. TIME.

— — — — — — — — — — — — -

Once your body is now running out of control, with all your oxygen trucks running around without any freight, and tons of this toxic form of iron floating around in your bloodstream, other defenses kick in. While your lungs are busy with all this oxidative stress they can’t handle, and your organs are being starved of o2 without their constant stream of deliveries from red blood cell’s hemoglobin, and your liver is attempting to do its best to remove the iron and store it in its ‘iron vault’. Only its getting overwhelmed too. It’s starved for oxygen and fighting a losing battle from all your hemoglobin letting its iron free, and starts crying out “help, I’m taking damage!” by releasing an enzyme called alanine aminotransferase (ALT). BOOM, there is your second of 3 primary indicators of whether the shit is about to hit the fan for a particular patient or not.

Eventually, if the patient’s immune system doesn’t fight off the virus in time before their blood oxygen saturation drops too low, ventilator or no ventilator, organs start shutting down. No fuel, no work. The only way to even try to keep them going is max oxygen, even a hyperbaric chamber if one is available on 100% oxygen at multiple atmospheres of pressure, just to give what’s left of their functioning hemoglobin a chance to carry enough o2 to the organs and keep them alive. Yeah we don’t have nearly enough of those chambers, so some fresh red blood cells with normal hemoglobin in the form of a transfusion will have to do.

The core point being, treating patients with the iron ions stripped from their hemoglobin (rendering it abnormally nonfunctional) with ventilator intubation is futile, unless you’re just hoping the patient’s immune system will work its magic in time. The root of the illness needs to be addressed.

Best case scenario? Treatment regimen early, before symptoms progress too far. Hydroxychloroquine (more on that in a minute, I promise) with Azithromicin has shown fantastic, albeit critics keep mentioning ‘anecdotal’ to describe the mountain, promise and I’ll explain why it does so well next. But forget straight-up plasma with antibodies, that might work early but if the patient is too far gone they’ll need more. They’ll need all the blood: antibodies and red blood cells. No help in sending over a detachment of ammunition to a soldier already unconscious and bleeding out on the battlefield, you need to send that ammo along with some hemoglobin-stimulant-magic so that he can wake up and fire those shots at the enemy.

The story with Hydroxychloroquine
All that hilariously misguided and counterproductive criticism the media piled on chloroquine (purely for political reasons) as a viable treatment will now go down as the biggest Fake News blunder to rule them all. The media actively engaged their activism to fight ‘bad orange man’ at the cost of thousands of lives. Shame on them.

How does chloroquine work? Same way as it does for malaria. You see, malaria is this little parasite that enters the red blood cells and starts eating hemoglobin as its food source. The reason chloroquine works for malaria is the same reason it works for COVID-19 — while not fully understood, it is suspected to bind to DNA and interfere with the ability to work magic on hemoglobin. The same mechanism that stops malaria from getting its hands on hemoglobin and gobbling it up seems to do the same to COVID-19 (essentially little snippets of DNA in an envelope) from binding to it. On top of that, Hydroxychloroquine (an advanced descendant of regular old chloroquine) lowers the pH which can interfere with the replication of the virus. Again, while the full details are not known, the entire premise of this potentially ‘game changing’ treatment is to prevent hemoglobin from being interfered with, whether due to malaria or COVID-19.

No longer can the media and armchair pseudo-physicians sit in their little ivory towers, proclaiming “DUR so stoopid, malaria is bacteria, COVID-19 is virus, anti-bacteria drug no work on virus!”. They never got the memo that a drug doesn’t need to directly act on the pathogen to be effective. Sometimes it’s enough just to stop it from doing what it does to hemoglobin, regardless of the means it uses to do so.

Anyway, enough of the rant. What’s the end result here? First, the ventilator emergency needs to be re-examined. If you’re putting a patient on a ventilator because they’re going into a coma and need mechanical breathing to stay alive, okay we get it. Give ’em time for their immune systems to pull through. But if they’re conscious, alert, compliant — keep them on O2. Max it if you have to. If you HAVE to inevitably ventilate, do it at low pressure but max O2. Don’t tear up their lungs with max PEEP, you’re doing more harm to the patient because you’re treating the wrong disease.

Ideally, some form of treatment needs to happen to:

  1. Inhibit viral growth and replication. Here plays CHQ+ZPAK+ZINC or other retroviral therapies being studies. Less virus, less hemoglobin losing its iron, less severity and damage.
  2. Therapies used for anyone with abnormal hemoglobin or malfunctioning red blood cells. Blood transfusions. Whatever, I don’t know the full breadth and scope because I’m not a physician. But think along those lines, and treat the real disease. If you’re thinking about giving them plasma with antibodies, maybe if they’re already in bad shape think again and give them BLOOD with antibodies, or at least blood followed by plasma with antibodies.
  3. Now that we know more about how this virus works and affects our bodies, a whole range of options should open up.
  4. Don’t trust China. China is ASSHOE. (disclaimer: not talking about the people, just talking about the regime). They covered this up and have caused all kinds of death and carnage, both literal and economic. The ripples of this pandemic will be felt for decades.
Fini.

Why has medium.com removed the original post? Any idea why it has to be retrieved from web archives?
 

saynotomsm

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Reaper

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Covid19 hoax and sh*tshow.

When the truth comes out about covid19, Fauci will be elevated multiple levels above Dr. Mengele.

Fauci prevented the use of IVM and HCQ, and put in place the intubation and Remdesivir protocols.

Nuremburg code has been violated. Time for accountability.
 
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