(Sitaatti:)
Behandlas de sjukaste covid-19-patienterna fel?
Saxat från första länken där John Whyte, MD, intervjuar Cameron Kyle-Sidell, MD
”You’ve been talking a lot about the number of patients, the percentage of patients dying on ventilators.”
”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.”
”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.”
”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.”
”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 you do 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.”
”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.”
”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. ”
”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,”
”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.”
”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 ”
”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. ”
”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.”
https://www.medscape.com/viewarticle/928156 och 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 NOTERA: detta är inte några studier, utan personer som uttrycker tankar och erfarenheter
Mer: http://4health.se/?s=corona
Obelit 120 mg is a lipase inhibitor. It works in the stomach and small digestive system by hindering the ingestion of fat from food by obstructing compounds liable for the breakdown of fat.
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