Renewable Revolution

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May 6, 2020
Doctors Speak Out, Ventilators Make Death Rates Soar

A number of published papers have noted ventilators make COVID-19 death risks soar. One report suggests the comparison was 76.4% vs. 19.8% (18-65) and 97.2% vs. 26.6% (65+). Should we be doing high-flow nasal cannulas (HFNC) instead? 

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Hyperbaric Oxygen Therapy

Sadly missing from the conventional conversation is the use of hyperbaric oxygen therapy (HBOT) which I believe might be an excellent treatment method . As noted by Dr. Andrew Saul, editor-in-chief of the Orthomolecular Medicine News Service, in “A Review of Helpful Antiviral Strategies”:

“Making the oxygen available in a way that's appropriate to the severity of the patient is the answer. We have to remember that our body is singularly good at taking in oxygen or we wouldn't be here. And our lungs have a huge amount of absorptive space. I mean, that's what they do. It's just an extraordinary system that we have.

Oxygen goes in by diffusion. You don't push it in; the body sucks it in because if you have more oxygen outside than you do inside, it just goes through. All you do is give a lot of absorptive surface. And if you flattened out all the little alveoli in the lungs, you'd have an enormous area …

So, by providing the oxygen and then see if the body will take it up, you've made the first step. That can be done preventively by fresh air and exercise and going out and playing …

If somebody needs more oxygen, and you want to give them a little pressure, if that makes the patient better, then you do it. But the idea that you've got to ram this oxygen like a supercharger on a Mustang is, I think, a little bit, shall we say, industry friendly …

[The alveoli] are tiny, tiny little sacks. They have some of the thinnest little membranes you've ever seen. Look at them under a microscope.

Bronchiole and Alveoli

They're very delicate. So, the last thing you want to do is add injury to insult.”

Agelbert NOTE: For those who haven't been living in a cave without internet for the past three months or so, the fact that COVID-19 causes major damage to the lungs is common knowledge.

However, whether it is from the SARS-CoV-2 virus, and/or some retrovirus latent in us that works with it to cause the lethal cytokine storm (i.e. excessive inflammatory immune response that causes your own immune system to attack healthy cells and kills you if it is not stopped), most people are not aware of an important detail about that lung damaging process that relates to the alveoli.

Yes, the ACE2 receptor on certain lung cells (NOT the alveoli) is attacked to gain entry into said cell and enable the virus to replicate. BUT, something else happens at the same time.

Those ACE2 receptors normally dock with ACE (Angiotensin Converting Enzyme) to lower the blood pressure. With the receptor blocked by the virus, blood pressure does go up, but that ain't all.

When all those ACE proteins routinely dock on the cell ACE2 receptors normally, the lung cell produces surfactant. That is a fancy name for a soaplike substance. NO, it isn't soap. However, the analogy is good because it allows us to think of soap bubbles, which don't burst right away when you blow the bubbles because of surface tension surfactant.

You can blow water with not enough soap all day long through the ring and not get soap bubbles. Any child knows that. Well, when our lung cells are not putting out enough surfactant to adequately coat their alveoli neighbors, the alveoli cannot interchange oxygen well.

WHY?

Because a lot of them collapse like those soap bubbles without enough soap. Then it gets even uglier.

Your body is alive. Your immune system is always checking to see if things are as they should be. Collapsed alveoli release cell chemicals that the immune system detects as a big problem. The immune cell soldiers within the lung (i.e phagocytes) set out to eat them to get them out of the way. So far, so good.

Unfortunately, because the viral infection causes so many alveoli to collapse, the abundance of chemicals from collapsed alveoli floating around confuse the phagocytes into attacking healthy alveoli, that get destroyed along with the collapsed ones. Then it gets even worse!

Lung cell tissue repairs are attempted with a fibrous substance that causes rigidity and even less ability to interchange oxygen. That fibrous substance normally works as a temporary seal which is removed later. Normally, only a small percentage of cells need repairing so their temporary dysfuntion will not threaten the overall lung function. BUT, when so many alveoli cells are being attacked because they are collapsing from not enough surfactant to keep them flexible (flexibility is REQUIRED so they can release CO2 and take up oxygen efficiently 👉 they are constantly either contracting or expanding in size as air pressure increases or decreases from breathing), the immune system, which is now causing all this damage from what is lablelled the cytokine storm, makes things even worse than that!

Large amounts of fluid not normally present in the lungs begins to flood the already partly compromised alveolar sacks. Being effectvely under water, they cannot intake any oxygen. The lungs get waterlogged, requiring MUCH more energy from your diaphragm muscles to expand and contract, which you experience as shortness of breath (dyspnea).

As your diaphragm chest muscles begin to work harder to expand your lungs to get oxygen, your heart beats faster to get any oxygen depleted blood to your lungs and oxygen collected by your lungs to the rest of your body.

To make a virus attack story short, you have got to stop the blocking of the ACE2 receptor, like, yesterday. But, in the meantime, you have got to got to get rid of excess CO2 in all your body tissues AND get sufficient oxygen to them until your lungs are cleared of fluid and your alveoli have sufficient surfactant to oxygenate efficiently without getting hammered by your own immune system soldier lung phagocytes.

Here is where the problem begins in our hospitals in the USA. Doctors have protocols they have developed over the decades that they are required to strictly adhere to or face punishemnt or accusations of malpractice.

The patient that has so much trouble breathing for all the reasons I just went through is experiencing what appears to doctors as ARDS (Acute Respiratory Distress Syndrome). They check your Oxygen Perfusion (i.e. measure the percentage of oxygen in your blood with a clever non-invasive device they put on your finger that measures oxygen level by the color of the blood).

If Oxygen Perfusion is below a certain percentage, they go to their standard ARDS therapy protocol. THAT IS, they put you in ICU on a ventilator. That works well with normal ARDS because, with normal ARDS, a person needs help with their diaphragm musles to breathe. If they don't get that help, they can get heart failure (i.e. the large ventricle in your heart that pumps blood into your body from the lungs gets exhausted, you get a heart attack, and can die).

BUT, putting a person with COVID-19 on a ventilator is a very big mistake because, though COVID-19 patients have ARDS symptoms, they DO NOT actually have ARDS!

WHY? Because there is no ACE2 Blocked Receptor CAUSED REDUCTION IN ALVEOLI SURFACTANT IN NORMAL ARDS! And furthermore, COVID-19 patients DO NOT have "tired" diaphragm muscles or any danger of heart failure (unless they have a pre-existing heart disease co-morbidity, which is not the norm).

That is why doctors, after inadvertently causing the death of tens of thousands of COVID-19 patients, have begun to turn patients face down, so the excess lung fluid does not inhibit oxygenation until the virus can be gotten under control, and, instead of entubing the patient with a ventilator, given them high-flow nasal cannulas (HFNC).

Up until now, when the cytokine storm was destroying lung tissue, the COVID-19 patients were given steroids while on a ventilator. The deal with steroids is that they signal the immune system soldiers that "everything is okay". Thus, the attacks on healthy tissue stop. However, if an effective antiviral like Interferon-alfa-2b is not part of that therapy, the virus will take advantage of the steroidal standing down of the immune system by replicating MORE virus. THAT is most likely the main cause of death of those that that were given steroids in the first week of hospitalization with a serious COVID-19 infection.

I've been reading and listening to lectures on all this. Doctors have figured out how to time the steroids to administer them to patients in the hospital with a serious COVID-19 infection AFTER the first week. If the steroids are given the second week, a greater percentage of patients survive.

They figured all that out before the really smart ones figured out HOW AND WHY a ventilator is a lethally counterproductive COVID-19 therapy. Unfortunately, many hospitals in the USA still haven't figured that out.

As for Interferon-alfa-2b, let us hope that the effectiveness of using this proven antiviral to combat COVID-19 will become the norm. As I posted here recently, there is no question that Interferon-alfa-2b kills the SARS-CoV-2 virus (as well as retroviruses in our system). It has been used for a wide range of indications, including viral infections and cancers.

So far, two non-peer reviewed research articles have been published. One study at the University of Texas Medical Branch, Galveston, showed evidence of a direct anti-viral effect of Interferon alpha against novel Coronavirus in vitro. The study demonstrated around 10,000 fold reduction in the quantity of virus that was pre-treated with Interferon alpha 48 hours earlier. A second study by universities in China, Australia and Canada analysed 77 moderate COVID-19 subjects in Wuhan and observed that those who received Interferon alpha-2b showed a significant reduction in the duration of virus shedding period and even in levels of the inflammatory cytokine, IL-6. [6] [7]

https://en.wikipedia.org/wiki/Interferon_alfa-2b