md_a
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- Aug 31, 2015
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Similar patterns of pulmonary disease between HAPE and COVID-19
Both COVID-19 and HAPE (high altitude pulmonary edema) exhibit a decreased ratio of arterial oxygen partial pressure to fractional inspired oxygen with concomitant hypoxia and tachypnea. There also appears to be a tendency for low carbon dioxide levels in both as well. Radiologic findings of ground glass opacities are present in up to 86% of patients with COVID-19 in addition to patchy infiltrates. Patients with HAPE also exhibit patchy infiltrates throughout the pulmonary fields, often in an asymmetric pattern and CT findings reveal increased lung markings and ground glass-like changes as well. Widespread ground-glass opacities are most commonly a manifestation of hydrostatic pulmonary edema. Similarly, elevated fibrinogen levels in both conditions are likely an epiphenomenon of edema formation rather than coagulation activation. Autopsy results of a COVID-19 fatality revealed bilateral diffuse alveolar damage associated with pulmonary edema, pro-inflammatory concentrates, and indications of early-phase acute respiratory distress syndrome (ARDS). HAPE itself is initially caused by an increase in pulmonary capillary pressure and induces altered alveolar-capillary permeability via high pulmonary artery hydrostatic pressures that lead to a protein-rich and mildly hemorrhagic edema. It appears that COVID-19 and HAPE both discretely converge on ARDS. In light of this, a countermeasure that has been shown to be effective in the analogous condition of HAPE is Acetazolamide. Acetazolamide has a myriad of effects on different organ systems, potently reduces hypoxic pulmonary vasoconstriction, improves minute ventilation and expired vital capacity. Other therapeutics to consider that are also directed towards decreased pulmonary pressure include Nifedipine and Phosphodiesterase inhibitors.
https://www.researchgate.net/public...ine_Phoshpdiesterase_Inhibitors_Acetazolamide
“Kidney disease, diabetes, pregnancy toxemia and retinal degeneration are probably the best known problems involving vascular leakage, but increasingly, cancer and heart disease are being recognized as consequences of prolonged permeability defects. Congestive heart failure and pulmonary hypertension commonly cause leakage of fluid into the lungs, and shock of any sort causes the lung to get "wet," a waterlogged condition called "shock lung." Simply hyperventilating for a couple of minutes will increase leakage from the blood into the lungs; hyperventilation decreases carbon dioxide, and increases serotonin and histamine. Hyperoxia itself contributes to lung injury, and exacerbates emphysema, though it is common to see patients breathing a high concentration of oxygen. Emphysema (which can be caused by hypothyroidism or hyper-estrogenism, and often can be cured by thyroid or progesterone) and many other respiratory problems are associated with capillary leakage. Cells of the lung and intestine are able to synthesize their own fibrin, apparently because of their special problems in preventing leakage. Prolonged systemic inflammation can lead to lung fibrosis, and fibrosis increases the likelihood of lung cancer.
The inflammatory state that causes exaggerated cellular permeability is very closely related to "hyperventilation," the loss of too much carbon dioxide. The release of serotonin during hyperventilation isn't the only cause of vascular leakage; the carbon dioxide itself is an essential factor in regulating the state of cellular electrons and in maintaining cellular integrity. Hyperventilation, like the shift from oxidative to glycolytic energy production that typifies estrogenized or stressed cells or cancer, raises intracellular pH. In the case of mast cells, increasing alkalinity causes them to release histamine (Alfonso, et al., 2005), but similar "alkaline-induced exocytosis" seems to occur in all stressed tissues.
The blood platelets that become incontinent and leak serotonin in the absence of carbon dioxide are undergoing the same structural stresses experience by endothelial cells, smooth muscle cells, mast cells and all other cells when carbon dioxide is depleted. Although it has been about 70 years since Yandell Henderson made it clear that supplemental oxygen should be combined with carbon dioxide, mechanical ventilation in hospitals is still causing lung injury resulting from hyperventilation, i.e., the absence of carbon dioxide. A similar misunderstanding of biology was involved in the use of dialysis to treat kidney disease. Until recently, commercial dialysis fluids contained acetate and/or racemic lactate instead of bicarbonate, because of the difficulty of preparing bicarbonate solutions, and the result was that very prolonged dialysis would damage the brain and other organs. (Veech and Gitomer, 1988, Veech and Fowler, 1987.) Dialysis has been seen to increase lung permeability Bell, et al., 1988).
Amyloidosis produced by chronic dialysis affects all organs, but its effects are best known in the brain, heart, kidneys, and lungs. Serum amyloid-A is one of the acute phase proteins, like C-reactive protein (CRP), that are produced by inflammation. Estrogen, radiation and other stresses increase those pro-inflammatory acute phase proteins, and decrease protective albumin, which is called a "negative acute phase protein," since it decreases when the other acute phase proteins increase. The liver is the major source of the acute phase proteins, and it is constantly burdened by toxins absorbed from the bowel; disinfection of the bowel is known to accelerate recovery from stress.
Seen from the perspective of the stress-leakage syndrome, any serious injury or sickness damages all organs. The exhaled breath is being used to diagnose inflammatory lung disease, since so many of the mediators of inflammation are volatile, but systemic diseases such as cancer and arthritis, and relatively minor stress can be detected by changes in the chemicals found in the breath. Polyunsaturated fats and their breakdown products--aldehydes, prostaglandins, isoprostanes, hydrocarbons, and free radicals--and carbon monoxide, nitric oxide, nitrite, and hydrogen peroxide are increased in the breath by most stresses. Both proline and glycine (which are major amino acids in gelatin) are very protective for the liver, increasing albumin, and stopping oxidative damage.
Saturated fats are protective against free radical damage and can reverse liver fibrosis. Thyroid hormone protects against excess estrogen, and can prevent or reverse fibrosis of the heart. Antiestrogens are widely effective against vascular leakage. Thyroid, progesterone, and testosterone are among the most effective natural antiestrogens, and they are curative in many conditions that involve vascular leakage. Progesterone and pregnenolone have been called the antifibromatic steroids, and it has been used to treat many inflammatory and fibrotic diseases, including cancer.
The antiserotonin drugs are being increasingly used to treat fibrotic diseases, and other problems related to vascular leakage.
Antiinflammatory and anticoagulant things, especially aspirin and vitamin E, protect against the accelerated turnover of fibrinogen/fibrin caused by estrogen and the various inflammatory states.”
Leakiness, aging, and cancer
“Mountain sickness” is a potentially deadly condition that develops in some people when they ascend too rapidly to a high altitude. Edema of the lungs and brain can develop rapidly, leading to convulsions and death. The standard drug for preventing it is acetazolamide, which inhibits carbonic anhydrase and causes carbon dioxide to be retained, creating a slight tendency toward acidosis. This treatment probably mimics the retention of carbon dioxide that occurs naturally in altitude adapted people. The reasons for mountain sickness, and the reasons for the low incidence of heart disease, cancer, cataracts, etc., at high altitude, offer clues to the prevention of death and deterioration from many other causes.”
Altitude and Mortality
“Increasing carbon dioxide lowers the intracellular pH, as well as inhibiting lactic acid formation, and restoring the oxidation of glucose increases CO2. Inhibiting carbonic anhydrase, to allow more CO2 to stay in the cell, contributes to intracellular acidification, and by systemically increasing carbon dioxide this inhibition has a broad range of protective anti-excitatory effects. The drug industry is now looking for chemicals that will specifically inhibit the carbonic anhydrase enzymes that are active in tumors. Existing carbonic anhydrase inhibitors, such as acetazolamide, will inhibit those enzymes, without harming other tissues. Aspirin has some effect as an inhibitor of carbonic anhydrase (Bayram, et al., 2008). Since histamine, serotonin (Vullo, et al., 2007), and estrogen (Barnett, et al., 2008; Garg, 1975) are carbonic anhydrase activators, their antagonists would help to acidify the hypoxic cells. Testosterone (Suzuki, et al., 1996) and progesterone are estrogen antagonists that inhibit carbonic anhydrase.” Ray Peat
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From a doctor: “ We have no idea how many people are infected without sx. There is no way to say 85%
It doesn't look like most people who are sick are old. Corey has all 40-60yos intubated in the ICU
It is IMPOSSIBLE to give someone pure oxygen. No one gets oxygen unless there is pulse oximetry is low (under 95%). If above they are generally discharged. People are at first given nasal oxygen which can only deliver up to 28% oxygen (we normally breath 21%). Even putting on a mask they can only deliver up to 40% because higher flow oxygen spreads the virus to health care workers. The majority of people on ventilators are given 40% oxygen. The goal is always to get patients to breath the lowest % of oxygen they can tolerate cause it is well known to the health care community that oxygen free radicals are bad for the lung, carbon dioxide level is tightly regulated by the body to keep the ph at 7.40. If Ph changes too much the heart stops. This is what is behind co2 levels.”
Ray Peat:
40% and 60% O2 are often used, and the problem is that no CO2 is added; even running the ventilator a little too fast with plain air will provide a harmful amount of O2, decreasing CO2. That statement reflects what too many doctors believe.
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On the other hand, there is no evidence that viral pneumonia from CoV-2 with invasive ventilation takes a better course. Rather, it can be expected that too many patients will be intubated too early in the current phase and especially taking into account established rules of emergency and intensive care medicine. Spontaneous breathing with and without ventilation support should be maintained as long as possible and taking into account known criteria of medical care. The importance of non-invasive ventilation therapy should also be taken into account when the government purchases and distributes ventilation devices in the current crisis.
Only when the saturation falls significantly below 90% should NIV or high-flow therapy be started, especially if the respiratory rate increases, as it indicates that the respiratory pump is beginning to tire. In hypoxemic insufficiency, ventilation is usually given too early on the IS and too much oxygen is given. This accelerates the development of ARDS (lung failure), because high ventilation pressures damage the alveoli and induce inflammation, which is then lacking in the defense against infections. Oxygen concentrations in excess of 50% in the inspiratory air also lead to a considerable radical load in the lungs, which also triggers an inflammatory reaction. However, these values can practically not be achieved with a nasogastric tube or admixture with the NIV.
The transfer to the IS should be made dependent on the individual case. According to clinical experience, many patients outside of IS can be treated with an NIV. This is the primary preferred form of ventilation for viral pneumonia. Experience has shown that a large number of patients with SARS-CoV-2 pneumonia only need temporary breathing support. The ventilation of these patients outside of IS protects valuable resources and thus helps to avoid secondary damage due to lack of space for the typical intensive care patients.
Much of it was published in 2005. At that time, it was recommended to stock up on pandemics with antibiotics, ventilators, protective masks, etc. Unfortunately, not many hospitals implemented this in Germany at the time, so that bottlenecks could now arise. On the other hand, the NIV has now established itself widely in hospitals (especially in the lung clinics), so that more ventilators are available here than before, which simplifies care outside of IS.
Dr. med. Gunter Frank, born in 1963 in Buchen im Odenwald, is a general practitioner in Heidelberg and a lecturer at the St. Gallen Business School.
Sterben Coronapatienten auch an falscher Beatmungstechnik?
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From Ray's newsletter on Gilbert Ling:
"Carbon dioxide had once been seen as a hormone, and it had been used medically for ulcers, arthritis, cancer, and mental problems, and Yandell Henderson’s work had led to its use as “carbogen” (5% CO2, 95% O2) for resuscitation, but by the middle of the century most therapeutic uses had been stopped, and hospitals had been taught to use pure oxygen instead of carbogen, and patients with brain swelling were being hyperventilated with oxygen to lower their blood carbon dioxide."
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BW: Now I remember you once telling me that at one point there was something called "firemen's oxygen" in which they had about 6 - 8 % carbon dioxide in the oxygen.
RP: Yeah, Yandell Henderson was the physiologist who got that popular to the point that fire departments all over the country started using it because the carbon dioxide at that very high concentration is extremely effective for restoring respiration to suffocated people, and for babies too that don't breathe properly.
BW: Is anyone still using carbon dioxide. Isn't it used or was used at some points in operation rooms?
RP: Oh, every now and then there is some person who says that hospitals are killing patients by giving them pure oxygen and say they would wish that hospitals switch, start using 5-8 % carbon dioxide whenever they give oxygen because it's basically stress inducing and toxic to give people oxygen in excess. At sea level we really have an excess of oxygen.
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The Treatment of Pneumonia by Inhalation of Carbon Dioxide (Yandell Henderson)
"Nature has provided the lungs with several protective devices and reactions. The most obvious is the cough reflex by which irritating foreign bodies are removed. Less obvious, but more constantly acting, are the movements of respiration which are probably accompanied by peristaltic contractions and relaxations of the air tubes. The mucosa lining these tubes bears cilia which produce a continual flow of secretion from the depths of the lungs outward."
"Occlusion of an air tube puts all of these mechanisms for the clearing of the lungs out of action. The air in the occluded portion of the lung is soon absorbed, and the alveoli are deflated and collapsed. They are then gradually filled by accumulation of secretion. The conditions resulting are in all respects favorable to the development of microorganisms and, correspondingly, unfavorable both to the general defenses of the body and the special defenses of the lungs. It is a highly significant fact, as revealed by experiment, that in order to induce pneumonia in dogs it is not enough merely to introduce the pathogenic organisms into the lungs ; it is essential also to narcotize the animals so deeply that the cough reflex is abolished and respiration is depressed. In general, depressed or shallow breathing tends to permit the development of pneumonia, and deep breathing with full ventilation of the lungs tends strongly to inhibit it."
"In pneumonia it is the blocking of the lung airways, bronchi or bronchioli, by plugs of thick and sticky secretion which is the critical morbidic factor producing atelectasis [= collapse or closure of a lung resulting in reduced or absent gas exchange] and the conditions characteristic of an undrained infection." Inhalation of carbon dioxide results in opening up of pneumonic lungs."
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https://www.researchgate.net/public...W3oPZKJU8JvpxGul7cTsCITixZu1xGP3cQiX9eTNSaqZE
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