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COVID-19/SARS May Be Due Simply To Serum PUFA And Its Peroxidation

haidut

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During the last podcast with Danny Roddy, Dr. Peat and I discussed the role of elevated free fatty acids (FFA) in the blood as facilitators of viral infection. I opined that the hydrophilic nature of PUFA circulating in the blood increases the permeability of cells and allows for easier viral entry inside the cell and subsequent infection. In yet another example of synchronicity, one of the regular readers of my posts sent me two studies that not only corroborate the discussion with Dr. Peat but suggest that the core of the respiratory illness (COVID-19/SARS) associated with the coronavirus may be driven primarily by elevated PUFA in the blood and its peroxidation products. The virus certainly plays a facilitating role as its presence in the bloodstream triggers the stress response (HPA axis) and thus elevation of FFA. However, whether one will develop COVID-19/SARS or not seems largely determined by the amount of PUFA in the person's blood and its peroxidation levels (mostly determined by vitamin E status). Thus, once again we have a situation where the focus of medicine is on the wrong "enemy". In this case, a virus - a complicated and elusive foe - while in reality it is not the virus itself, but metabolic status and lipid composition of fat stores that are the true determinants if a patient will develop COVID-19/SARS or not. As the study demonstrated, the ARDS (another name for COVID-19/SARS) was successfully treated with lisofylline - a compound that lowers serum PUFA levels. These findings suggest a rather simple and safe way to prevent COVID-SARS development (and potentially treat it) even in vulnerable patients - administration of niacinamide to control excessive lipolysis (and thus keep FFA blood levels low) and vitamin E to keep lipid peroxidation under control. In addition, it just so happens that vitamin E has already been demonstrated to improve immunity in the elderly and prevent/treat pneumonia. Throwing in a bit of aspirin would likely further increase the benefits as aspirin has a direct anti-viral effect, in addition to its anti-lipolytic and FAO blocking effects.

Plasma fatty acid changes and increased lipid peroxidation in patients with adult respiratory distress syndrome. - PubMed - NCBI

"...During intensive care treatment, in patients with ARDS ...there was usually an increase in plasma 4-hydroxy-2-nonenal values, one of its specific peroxidation products, suggestive of severe oxidative stress leading to molecular damage to lipids."

An increase in serum C18 unsaturated free fatty acids as a predictor of the development of acute respiratory distress syndrome. - PubMed - NCBI
"...MEASUREMENTS AND MAIN RESULTS: We measured the serum free fatty acid concentrations in the 39 healthy control subjects, and then we prospectively examined the serum free fatty acid concentrations in 30 age-matched patients in samples obtained within 24 hrs from the onset of sepsis, trauma, or development of ARDS. We then prospectively studied eight septic, at-risk patients who were matched for age, Acute Physiology and Chronic Health Evaluation II scores, Multiple Organ Failure index, and Glasgow Coma Score, in a double-blind, placebo-controlled, pilot study. These patients included four patients who received no treatment and four patients who received lisofylline, a compound that decreases serum unsaturated free fatty acids and diminishes acute lung injury in animals caused by sepsis and/or trauma. The calculated ratios of serum free fatty acids (Le., the ratio of C18 unsaturated fatty acids linoleate and oleate to fully saturated palmitate, C16:0) increased and predicted the development of ARDS in at-risk patients. Serum samples from the 30 patients, obtained within 24 hrs from the onset of sepsis, trauma, or development of ARDS, had significantly increased mean acyl chain ratios (1.42 +/- 0.35 [SD]) compared with healthy control subjects (0.86 +/- 0.25; p < .01). Sera from 13 patients with sepsis or trauma who did not develop ARDS (group A [at-risk, non-pre-ARDS]) also had increased acyl ratios (1.23 +/- 0.27) compared with sera from healthy control subjects (0.86 +/- 0.25; p < .01). Sera from seven patients who subsequently developed ARDS (group B [at-risk, pre-ARDS]) had higher acyl ratios (1.70 +/- 0.21) than group A at-risk patients who did not develop ARDS (1.23 +/- 0.27; p < .01) or healthy control subjects (0.86 +/- 0.25; p < .001). Sera from ten group C patients with ARDS at the time of admission to the study had the highest acyl ratios (1.80 +/- 0.75), which exceeded values for healthy control subjects (p < .001) and group A at-risk patients without ARDS (p = .01), but were not significantly different then group B at-risk, pre-ARDS patients (p = .17). Prospective study of eight septic, at-risk patients demonstrated significantly (p < .05) increased serum acyl ratios in the four untreated patients (findings consistent with the first study) but a significantly (p = .02) reduced ratio in the four at-risk patients treated with lisofyline. CONCLUSIONS: Increases in unsaturated serum acyl chain ratios differentiate between healthy and seriously iII patients, and identify those patients likely to develop ARDS. Thus, the serum acyl ratio may not only prospectively identify and facilitate the assessment of new treatments in patients at highest risk for developing ARDS, but may also lead to new insights about the pathogenesis of ARDS."
 

DatAudioGuy

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Hi! What do you think of the proposed theory of the virus being a "blood disease"? I've seen multiple variants of this theory. One of them going so far as to say that this isn't ARDS in the commonly understood sense, and that treatment with ventilators will only make it worse. If I understand it correctly, they theorize that the virus binds to heme, and in doing so will a) block the ability of hemoglobin to bind to oxygen leading to hypoxia (and thus rendering ventilation a futile treatment), and b) releasing iron from the heme causing substantial oxidative damage.

Early in march I remember reading an article in a mainstream newspaper here in Scandinavia were they interviewed a doctor treating covid-19 patients. He mentioned the much talked about ground glass opacity seen in the lungs, but also said that in his patients they saw a peculiar effect on the blood. They never spelled out what that effect was, but I did find it very interesting because this was at the very onset of pandemic, with only a few 100 confirmed cases nationally, and long before anyone here was talking about any specific mechanics of the disease.

I'm no expert, and not sure if this angle and the one you have postulated are mutually exclusive. I guess having both elevated FFA and free iron roaming around in the blood will cause extensive damage. If free iron is indeed a component of this, then perhaps that explains the effectiveness of high dose vitamin C therapy, as reported from China and some hospitals in NY. I would love to hear your take on this.
 

schultz

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Regarding PUFA and cell permeability: I mentioned this in another thread, but endotoxin seems to do the same thing.

KMUD: Bowel Endotoxin

Ray [approximately 10 minutes in]: "The whole structure of the cell, the cytoplasm, as it takes up water, instead of being fat-like and tending to exclude water and prefer to absorb fats, the introduction of this sugar connected to a fat [endotoxin] acts like a soap and makes the cell tend to admit not only more water but pretty much anything that's in its environment. So the whole substance of the cell becomes kind spongy and leaky. When this starts affecting the whole organism that kind of change occurs all through the body. Once this stuff has passed through the lining of the intestine and crosses across capillaries and gets into the blood stream, then the endotoxin starts doing the same thing to any cell it comes to. And so it will leak out of capillaries, no matter where it is in the blood stream, if the liver hasn't filtered it. So if it happens to reach the brain, it will cause the brain capillaries to leak whatever is in the blood stream. So it can contribute to MS. And the endotoxin leaking into the brain does the same thing. It triggers the release of nitric oxide and a whole chain of chemical reactions. Every organ has its particular way of responding to the endotoxin, but there's a generality, no matter what the organ, there are basic defense reactions that will occur not only to endotoxin but to any radical threat to the survival of the cell so that x-rays and gamma rays will produce essentially the same kind of change in brain cells or bowel cells that endotoxin does."
 

yerrag

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During the last podcast with Danny Roddy, Dr. Peat and I discussed the role of elevated free fatty acids (FFA) in the blood as facilitators of viral infection. I opined that the hydrophilic nature of PUFA circulating in the blood increases the permeability of cells and allows for easier viral entry inside the cell and subsequent infection. In yet another example of synchronicity, one of the regular readers of my posts sent me two studies that not only corroborate the discussion with Dr. Peat but suggest that the core of the respiratory illness (COVID-19/SARS) associated with the coronavirus may be driven primarily by elevated PUFA in the blood and its peroxidation products. The virus certainly plays a facilitating role as its presence in the bloodstream triggers the stress response (HPA axis) and thus elevation of FFA. However, whether one will develop COVID-19/SARS or not seems largely determined by the amount of PUFA in the person's blood and its peroxidation levels (mostly determined by vitamin E status). Thus, once again we have a situation where the focus of medicine is on the wrong "enemy". In this case, a virus - a complicated and elusive foe - while in reality it is not the virus itself, but metabolic status and lipid composition of fat stores that are the true determinants if a patient will develop COVID-19/SARS or not. As the study demonstrated, the ARDS (another name for COVID-19/SARS) was successfully treated with lisofylline - a compound that lowers serum PUFA levels. These findings suggest a rather simple and safe way to prevent COVID-SARS development (and potentially treat it) even in vulnerable patients - administration of niacinamide to control excessive lipolysis (and thus keep FFA blood levels low) and vitamin E to keep lipid peroxidation under control. In addition, it just so happens that vitamin E has already been demonstrated to improve immunity in the elderly and prevent/treat pneumonia. Throwing in a bit of aspirin would likely further increase the benefits as aspirin has a direct anti-viral effect, in addition to its anti-lipolytic and FAO blocking effects.

Plasma fatty acid changes and increased lipid peroxidation in patients with adult respiratory distress syndrome. - PubMed - NCBI

"...During intensive care treatment, in patients with ARDS ...there was usually an increase in plasma 4-hydroxy-2-nonenal values, one of its specific peroxidation products, suggestive of severe oxidative stress leading to molecular damage to lipids."

An increase in serum C18 unsaturated free fatty acids as a predictor of the development of acute respiratory distress syndrome. - PubMed - NCBI
"...MEASUREMENTS AND MAIN RESULTS: We measured the serum free fatty acid concentrations in the 39 healthy control subjects, and then we prospectively examined the serum free fatty acid concentrations in 30 age-matched patients in samples obtained within 24 hrs from the onset of sepsis, trauma, or development of ARDS. We then prospectively studied eight septic, at-risk patients who were matched for age, Acute Physiology and Chronic Health Evaluation II scores, Multiple Organ Failure index, and Glasgow Coma Score, in a double-blind, placebo-controlled, pilot study. These patients included four patients who received no treatment and four patients who received lisofylline, a compound that decreases serum unsaturated free fatty acids and diminishes acute lung injury in animals caused by sepsis and/or trauma. The calculated ratios of serum free fatty acids (Le., the ratio of C18 unsaturated fatty acids linoleate and oleate to fully saturated palmitate, C16:0) increased and predicted the development of ARDS in at-risk patients. Serum samples from the 30 patients, obtained within 24 hrs from the onset of sepsis, trauma, or development of ARDS, had significantly increased mean acyl chain ratios (1.42 +/- 0.35 [SD]) compared with healthy control subjects (0.86 +/- 0.25; p < .01). Sera from 13 patients with sepsis or trauma who did not develop ARDS (group A [at-risk, non-pre-ARDS]) also had increased acyl ratios (1.23 +/- 0.27) compared with sera from healthy control subjects (0.86 +/- 0.25; p < .01). Sera from seven patients who subsequently developed ARDS (group B [at-risk, pre-ARDS]) had higher acyl ratios (1.70 +/- 0.21) than group A at-risk patients who did not develop ARDS (1.23 +/- 0.27; p < .01) or healthy control subjects (0.86 +/- 0.25; p < .001). Sera from ten group C patients with ARDS at the time of admission to the study had the highest acyl ratios (1.80 +/- 0.75), which exceeded values for healthy control subjects (p < .001) and group A at-risk patients without ARDS (p = .01), but were not significantly different then group B at-risk, pre-ARDS patients (p = .17). Prospective study of eight septic, at-risk patients demonstrated significantly (p < .05) increased serum acyl ratios in the four untreated patients (findings consistent with the first study) but a significantly (p = .02) reduced ratio in the four at-risk patients treated with lisofyline. CONCLUSIONS: Increases in unsaturated serum acyl chain ratios differentiate between healthy and seriously iII patients, and identify those patients likely to develop ARDS. Thus, the serum acyl ratio may not only prospectively identify and facilitate the assessment of new treatments in patients at highest risk for developing ARDS, but may also lead to new insights about the pathogenesis of ARDS."
I like this idea more than the idea of receptors. Isn't the idea of receptors a false construct, yet we are not discarding this construct in our conversations just because the available literature is permeated with it that it is hard to ignore mentioning it.

But each time we encounter talk of receptors, we should simply think of it as a fable taught to kindergarten children to make them understand reality. Like the Pied Piper of Hamlin. And the Emperor with No Clothes.
 

nwo2012

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Could 5G be a factor potentially affecting oxygen molecules and compounding the hypoxia? Some doctors were comparing severe cases of corona with altitude sickness.
And also possibly causing electroporation and making cells more permeable to endotoxin, chemical toxins and even bacteria or viruses.
 

haidut

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Regarding PUFA and cell permeability: I mentioned this in another thread, but endotoxin seems to do the same thing.

KMUD: Bowel Endotoxin

Ray [approximately 10 minutes in]: "The whole structure of the cell, the cytoplasm, as it takes up water, instead of being fat-like and tending to exclude water and prefer to absorb fats, the introduction of this sugar connected to a fat [endotoxin] acts like a soap and makes the cell tend to admit not only more water but pretty much anything that's in its environment. So the whole substance of the cell becomes kind spongy and leaky. When this starts affecting the whole organism that kind of change occurs all through the body. Once this stuff has passed through the lining of the intestine and crosses across capillaries and gets into the blood stream, then the endotoxin starts doing the same thing to any cell it comes to. And so it will leak out of capillaries, no matter where it is in the blood stream, if the liver hasn't filtered it. So if it happens to reach the brain, it will cause the brain capillaries to leak whatever is in the blood stream. So it can contribute to MS. And the endotoxin leaking into the brain does the same thing. It triggers the release of nitric oxide and a whole chain of chemical reactions. Every organ has its particular way of responding to the endotoxin, but there's a generality, no matter what the organ, there are basic defense reactions that will occur not only to endotoxin but to any radical threat to the survival of the cell so that x-rays and gamma rays will produce essentially the same kind of change in brain cells or bowel cells that endotoxin does."

Yep, and other mediators of stress have similar effects. Serotonin increases capillary leakiness and promotes viral replication. Hence, the studies on serotonin antagonists helping. Estrogen increases cell affinity for water, so the cell will take up more virus, endotoxin, serotonin, etc. Nitric oxide will inhibit respiration, which also has the immediate effects of causing the water inside the cell to become more bulky which makes the cell more hydrophilic. And so on, and so on.
 

haidut

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I like this idea more than the idea of receptors. Isn't the idea of receptors a false construct, yet we are not discarding this construct in our conversations just because the available literature is permeated with it that it is hard to ignore mentioning it.

But each time we encounter talk of receptors, we should simply think of it as a fable taught to kindergarten children to make them understand reality. Like the Pied Piper of Hamlin. And the Emperor with No Clothes.

I think the talk about receptor can be helpful because some people (especially doctors) will refuse to take a discussion seriously until you mention a substance and its effects on receptors. Also, receptors are helpful when discussing the fact that they can be activated by many substances other than their "key". Namely, hypoxia, inflammation, certain PUFA metabolites, endotoxin, etc can all activate the estrogen "receptor" even in the absence of estrogen. So, when used to demonstrated systemic effects by multitude of substances belonging to a similar class (e.g. metabolism blockers) the talk about receptors helps to both show the generality of their influence as well just how crucial and multifaceted the environment is. But yes, if the discussion is only about the traditional "one key one receptor" idea then it is meaningless.
 

haidut

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Could 5G be a factor potentially affecting oxygen molecules and compounding the hypoxia? Some doctors were comparing severe cases of corona with altitude sickness.
And also possibly causing electroporation and making cells more permeable to endotoxin, chemical toxins and even bacteria or viruses.

Yes, all of these are known effects of EMF, and it is not just 5G but the 5G is probably the most effective at causing them (especially at short-enough distances). There was a discussion on Reddit about this very topic a few years ago. The invited "speaker" was one of the most knowledgeable people on the topic in the entire world and he kept telling the herd on Reddit that EMF inhibits metabolism and it is not at all benign. He still got slaughtered, and his responses got downvoted into oblivion so at some point he just quit the AMA event and cancelled the planned follow-up.
Science AMA Series: I'm Paul Héroux, a Professor of Toxicology and Health Effects of Electromagnetism at McGill University in Montreal, Canada. I do research on health effects of electromagnetic radiation at all frequencies, both in terms of disease risks and therapeutic medical applications. AMA! : science
Science AMA Series: I'm Paul Héroux, a Professor of Toxicology and Health Effects of Electromagnetism at McGill University in Montreal, Canada. I do research on health effects of electromagnetic radiation at all frequencies, both in terms of disease risks and therapeutic medical applications. AMA! : science
"...Very often, effects of EM radiation are detected, and people use what I would call popular assumptions to explain them, in great part because mechanistic work is difficult and time-consuming. In our work, we propose a mechanism in which the presence of ELF magnetic fields inhibits the passage of protons through the water channel of the enzymes ATP Synthase. This reduces the amount of protons produced by the cell. The mitochondrion reacts by releasing calcium, which commands more ATP production, and by stimulating the enzymes AMPK which controls further cell adaptations (as long as a month). Then, glycolysis taken over part of the role of ATP production from redox. The mitochondrial uncoupling stimulates ATPase and electron tranfer, which react directly with oxygen to form free radicals."
 

haidut

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treatment with ventilators will only make it worse.

Don't know about treatment with ventilators but treatment with pure O2 (which is basically the standard) is likely to make the hypoxia and the lactic acidosis much worse. The latter is often lethal if severe enough and from what I saw in medical reports almost all patients admitted to the hospital and became critical (or died) had some stage of lactic acidosis. In such a state, getting pure O2 treatment is basically death sentence.
Hyperoxic Brain Effects Are Normalized by Addition of CO2
Imaging Study Reveals How Pure Oxygen Harms The Brain
"...Yet growing research suggests that inhaling straight oxygen can actually harm the brain. For the first time, a new UCLA brain-imaging study reveals why. Published in the May 22 edition of Public Library of Science (PLoS) Medicine, the findings fly in the face of national guidelines for medical practice and recommend a new approach adding carbon dioxide to the gas mix to preserve brain function in patients..."For decades, the medical community has championed 100 percent oxygen as the gold standard for resuscitation. But no one has reported what happens inside our brains when we inhale pure oxygen," explained Ronald Harper, distinguished professor of neurobiology at the David Geffen School of Medicine at UCLA. "What we discovered adds to a compelling body of evidence for modifying a widely practiced standard of care in the United States...."When the children inhaled pure oxygen, their breathing quickened, resulting in the rapid exhalation of carbon dioxide from their bodies," said coauthor Paul Macey, associate researcher in neurobiology. "The drop in carbon dioxide narrowed their blood vessels, preventing oxygen from reaching tissue in the brain and heart....All this activity awakened the hypothalamus, which regulates heart rate and hormonal outflow. Activation of the hypothalamus triggered a cascade of harmful reactions and released chemicals that can injure the brain and heart.... "Several brain areas responded to 100 percent oxygen by kicking the hypothalamus into overdrive," explained Harper. "The hypothalamus overreacted by dumping a massive flood of hormones and neurotransmitters into the bloodstream. These chemicals interfere with the heart's ability to pump blood and deliver oxygen -- the opposite effect you want when you're trying to resuscitate someone." When the children inhaled the carbon dioxide-oxygen mix, the hypothalamus' hyperactivity vanished from the MRI scan. "Adding carbon dioxide to the oxygen relaxed the blood vessels, allowed oxygen to reach the heart and brain, calmed the hypothalamus and slowed the release of dangerous chemicals," said Macey. "Pure oxygen kindles the match that fuels a forest fire of harm to the body," said Harper. "But a little whiff of carbon dioxide makes it all go away...Based on their findings, the researchers strongly encourage healthcare providers to add carbon dioxide to oxygen dispensation, especially when resuscitating infants or administering oxygen for more than a few minutes. The new direction could hold particular implications for patients of stroke, heart attack, carbon monoxide poisoning and any long-term oxygen therapy."
 

yerrag

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I think the talk about receptor can be helpful because some people (especially doctors) will refuse to take a discussion seriously until you mention a substance and its effects on receptors. Also, receptors are helpful when discussing the fact that they can be activated by many substances other than their "key". Namely, hypoxia, inflammation, certain PUFA metabolites, endotoxin, etc can all activate the estrogen "receptor" even in the absence of estrogen. So, when used to demonstrated systemic effects by multitude of substances belonging to a similar class (e.g. metabolism blockers) the talk about receptors helps to both show the generality of their influence as well just how crucial and multifaceted the environment is. But yes, if the discussion is only about the traditional "one key one receptor" idea then it is meaningless.
I understand the need for that term, if only to encase in a sausage a concept in order to make mental digestion easier. But there really is no physical receptor in reality, as there is no membrane pump in a cell. Just as there has never been an emperor with no clothes in history.
 

Mellow

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And yet..... we should do the opposite!

WHO.png
 

yerrag

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And yet..... we should do the opposite!

WHO.png
This: Coming from WHO. Wrong advice. Polyunsaturated fats (PUFAs) cause lipid perodixation, produce oxidative stress, and damage tissues. Another bad advice from a corrupt political organization that serves multinational pharma companies. The sicker you are, the more you need their maintenance drugs and vaccines, and the more you're likely to die in an ICU, where they rob you of what you can bequeath to your heirs.
Your cells are protected by a phospholipid membrane - this is a fatty membrane. This membrane is more impenetrable when made up of saturated fats and less so when PUFAs take its place. The COVID virus readily penetrates this barrier when PUFAs line it, as PUFAs are more miscible with foreign substances. Do not eat what the AHA (American Heart Association) calls heart-healthy, such as soya oil, corn oil, and canola oil. The AHA is the propaganda arm of US seed oil agribusiness concerns.

When the paint and ink market shifted from using seed oils to synthetic binders such as acrylics, the seed oil makers decided to market these toxic oils for human consumption. They had to fund studies to legitimize false claims that saturated fats such as coconut oil, butter, and beef tallow are bad.

Eating PUFAs cause plaques to form inside your blood vessels as PUFAs turn into oxidized LDL and into cholesteryl esters that line the vascular walls.

Your doctors won't agree with this as their training curriculum is designed by big pharma. Their indoctrination is complete when they graduate.

They don't cure you. They give you maintenance drugs and they like to vaccinate. And because they have a degree, you believe them despite evidence to the contrary (which is out there if you care to look).

Because you believe them, you believe your body is weak and needs drugs and vaccines. But before doctors got mass-produced by big pharma, the human body has evolved and adapted through millenia and has already developed a sophisticated internal immune system.

But feed it garbage, you will get garbage immunity as well. Learn to rely on good sources to know what is actually good for you. And you will not need to die in an ICU. And you will not fear having no health insurance.
 

Giraffe

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Throwing in a bit of aspirin would likely further increase the benefits as aspirin has a direct anti-viral effect, in addition to its anti-lipolytic and FAO blocking effects.
Prof. Püschel a German pathologist who did post-mortem examinations of covid-19 patients mentioned that pulmonary embolism was found in very many.


14 - Expertengespräch Covid-19. Prof. Püschel, Prof Bhakti, Dr. Petersohn, Dr. Völz


wikipedia said:
Pulmonary embolism (PE) is a blockage of an artery in the lungs by a substance that has moved from elsewhere in the body through the bloodstream (embolism).[6] Symptoms of a PE may include shortness of breath, chest pain particularly upon breathing in, and coughing up blood.[1] Symptoms of a blood clot in the leg may also be present, such as a red, warm, swollen, and painful leg.[1] Signs of a PE include low blood oxygen levels, rapid breathing, rapid heart rate, and sometimes a mild fever.[10] Severe cases can lead to passing out, abnormally low blood pressure, and sudden death.[2]
 
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