So they set a poor precedent that unfortunately got followed in areas where there was healthcare collapse? Italy and New York had so many people in critical condition and on vents. I remember the shock and horror at the lung damage that happened to people who had died of the disease. How much of that was due to ventilators? There's a lot of debate about how government policy fucked up the response, but if vents caused a sizeable number of deaths this part of the response was pretty bad too in hindsight. The New York nurses who spoke out about the shitshow over there brought up medical residents improperly using the vents multiple times.
How many people are going to want this vaccine anyway? The people terrified of this virus aren't going to be all gung-ho about a rush job when Trump's the one who wanted it. A vaccine won't stop the skeptics from being skeptical. The coronahoax crowd thinks TPTB are tracking them. The only people I can think of who will want this are the people who will accept anything fed to them if they think it'll mean things will go back to normal.
I’m not a doctor, but my assessment, based on what I’ve seen, is that COVID-19 leaves one highly susceptible to VILI. Ventilator induced lung injuries. COVID-19 is a form of endotheliitis. It infects the lining of blood vessels and injures them very badly, causing blood clots as the body tries walling off the damage. This endotheliitis could make the blood vessels and small capillaries of the lungs very vulnerable to the mechanical stretching from the ventilator. The ventilators could actually accelerate edema and fill the lungs with blood and fluid. Many patients on ventilators died rather gruesomely, but they were deoxygenating so rapidly and so severely, it was either intubate them or watch them drop below 60% O2 sat, turn blue, and keel over dead. It’s a damned if you do, damned if you don’t kind of scenario.
soundphysicians.com
Treating the vascular pathology of COVID-19 with ARBs, Bradykinin blockers, inhaled nitric oxide, and/or steroids and strong antioxidants might be better than reflexively putting people on vents. In other words, treating it as a vascular disease may restore oxygenation without the need for invasive ventilation, increasing chances of survival in the severe and critical cases.
Dr. Cameron Kyle-Sidell was one of the dissenters. He posted YouTube videos like this:
Actually, a bunch of doctors thought they were treating COVID-19 incorrectly:
I cannot stress this enough; COVID-19 is a vasculotropic illness. It injures blood vessels. It causes the small capillaries of the lungs to leak into the alveoli, resulting in an edematous condition. If you use interventions for pneumonia and ARDS on these patients, it won’t work, because it doesn’t solve the fundamental problem of vascular damage and edema preventing diffusion of oxygen from the alveoli and into the bloodstream.
This is a very good explanation of what could be going on with COVID-19:
This video has an excellent (and very technical) explanation of what the Kinin-Kallikrein system is:
EDIT: Here’s another very interesting paper:
Angiotensin-converting enzyme 2 (ACE2) is a terminal carboxypeptidase with important functions in the renin-angiotensin system and plays a critical role in inflammatory lung diseases. ACE2 cleaves single-terminal residues from several bioactive peptides such as angiotensin II. However, few of its substrates in the respiratory tract have been identified, and the mechanism underlying the role of ACE2 in inflammatory lung disease has not been fully characterized. In an effort to identify biological targets of ACE2 in the lung, we tested its effects on des-Arg9 bradykinin (DABK) in airway epithelial cells on the basis of the hypothesis that DABK is a biological substrate of ACE2 in the lung and ACE2 plays an important role in the pathogenesis of acute lung inflammation partly through modulating DABK/bradykinin receptor B1 (BKB1R) axis signaling. We found that loss of ACE2 function in mouse lung in the setting of endotoxin inhalation led to activation of the DABK/BKB1R axis, release of proinflammatory chemokines such as C-X-C motif chemokine 5 (CXCL5), macrophage inflammatory protein-2 (MIP2), C-X-C motif chemokine 1 (KC), and TNF-α from airway epithelia, increased neutrophil infiltration, and exaggerated lung inflammation and injury. These results indicate that a reduction in pulmonary ACE2 activity contributes to the pathogenesis of lung inflammation, in part because of an impaired ability to inhibit DABK/BKB1R axis-mediated signaling, resulting in more prompt onset of neutrophil infiltration and more severe inflammation in the lung. Our study identifies a biological substrate of ACE2 within the airways, as well as a potential new therapeutic target for inflammatory diseases.
Two years ago, they found that loss of ACE2 function in the lungs of mice led to activation of des-Arg9-bradykinin, increased vascular permeability, neutrophil infiltration in the lungs, and severe inflammation. It’s a similar effect to what happens one someone takes ACE inhibitors. We know that SARS-CoV-2 aggressively down-regulates ACE2, as well.
www.nature.com
COVID-19 had everyone fooled. People were told to expect pneumonia and ARDS, not this sneaky fucker of a virus.
