Hierdie is slegs opinie, dit gaan nie oor of die virus bestaan of nie. Dit gaan oor die maskers, simptome en verwante siektestoestande. Dit gaan selfs oor kinders wat met maskers moet oefen en dan sterf. Niemand kan met ‘n masker loop en oefen en heelhuids anderkant uitkom sonder newe-effekte van jou eie koolsuurgas ( CO2 ) wat ingeasem word nie. Dis logies en niemand het ‘n graad nodig om te weet wat in ‘n masker broei nie as daar 100 keer of meer daarin koolsuurgas geplaas word wat terugkeer na die longe en bloedstroom.
Toevallig is dit nie net die medici wat “maskers” dra met gevolge nie. Leer tog uit elke omstandighede presies hoekom word maskers op ons met wetgewing, geforseer. In sommige terreine, onder voorbeelde genoem, word alles ingespan om suurstof toevoer te verbeter tot die uitrig om take te verrig. Mediese personeel veral. Die fokus is ook op medici wat soms van een geval tot ‘n ander geval gaan en skaars tyd het om behoorlik nuwe suurstof te kry na maskers verwissel is. Wat ook inmekaar gestort het.
Natuurlik sal dokters en mediese personeel siek word, maar alles is beslis nie die virus se skuld nie, nes die dra van ‘n masker iemand met ‘n hart of hipertensie probleem se toestand vererger. Outomaties ontwikkel ‘n tipe van “stres” en asemnood is die gevolg. Hiperventilasie volg ook.
Die Amerikaanse Lugmag het ook probleme met “Hypoxia” wat ook fataal is waaroor geskryf is. Ander lande sal identies dieselfde probleme ervaar waar maskers betrokke is. Tot die marine lewe is dit al gerapporteer soos in China. Wiegiedood en babasterftes in Suid-Afrika.
Tydens die dra van maskers tydens die “Corona virus”, word die dra van maskers op ons almal afgedwing met behulp van wetgewings en regering . Hulle beheer en elkeen wat nie ‘n masker dra as dit ‘n wit persoon is, word ‘n boete opgelê. Die massas kan maar staan sonder enige masker. Hulle lag al die pad, want hulle asem skoon lug in. Daar word net in sommige gevalle wetgewing toegepas, want min massas is al in hegtenis geneem, het nog nooit dit gesien nie.
Dit word ons geforseer om minder stuurstof in te asem wat fataal opeindig met lelike en erge gesondheidstoestande of gevolge.
Dit is skending van menseregte om skoon suurstof in te asem.
Mens kan nie help om te vra – Wie word aangesteek as ‘n bestuurder alleen is in ‘n voertuig, of die wat saam in een huis bly vir maande onder een dak? ‘n Paartjie mag nie eers saam loop of gesien word nie, maar die massas staan kilometers langs en agtermekaar, sonder ‘n sogenaamde masker. Is hier dan dubbel standaarde wat toegepas word – beslis.
Hoeveel medici en oorsese “gevalle” het nie inmekaar gesak van “uitputting” of “Hypoxia” nie, en dan word die virus die skuld gegee daarvoor. Veral in lande soos Amerika, Italie, ander EU lande, Engeland, ens.
Ouer mense en kinders, oningeligtes wat nie weet dit is beter om masker af te haal as daar “dizzyness” ervaar word moet begin slim raak – gebruik ‘n serp en net as dit nodig is. Haar edele Zuma doen dit dan en Ramaphosa gebruik selde of ooit ‘n digte masker en sit dit net op as hy op kamera verskyn. Het iemand al ooit vir Donald Trump of sy vrou / kabinet of van die ander regeringspartye met maskers gesien in die openbaar?
Bestuurders in SA is baie blootgestel as hul maskers die hele tyd ophet om ongelukke te veroorsaak. Kan net dink hoe voel ‘n taxi of bus bestuurder wat heelwat passasiers in het en hy raak flou as gebrek aan suurstof. Wie gaan van moord aangekla word, of nee, die virus kry die skuld. Dit loop uiteindelik die fatale pad.
Asemnood (longontsteking of “eerder stresverwante” of selfs voorheen behandelde siektestoestande, word dan waarskynlik ook verkeerd behandel, veral oormaat van jou eie (koolsuurgas) SO2. Hoe dokters dit behandel, is ‘n ope vraag, want wie se toerusting word hiervoor aangewend – uit China uit – of eerder, wie vind baat by hierdie hele dilemma?
The Air Force cut the number of hypoxia and similar incidents in the T-6A Texan II by more than half in fiscal 2019 after putting into place a series of changes it hoped would fix the problem.
Air Force pilots still recorded 41 hypoxia-like incidents in the crucial trainer aircraft last year, according to data provided at Air Force Times’ request. That was by far the highest number of individual incidents compared with other aircraft platforms across the fleet, and also meant the T-6 had the Air Force’s second-highest hypoxia rate per-100,000 flying hours.
The Air Force experienced a rash of incidents involving hypoxia — a condition caused by a lack of oxygen in the blood, which can sometimes CAUSE shortness of breath, dizziness or a loss of consciousness, and can be extremely dangerous or fatal for pilots — and similar conditions among pilots flying T-6s during fiscal 2018. That year, T-6 pilots alone experienced 89 hypoxia-like incidents, the vast majority of the 135 such incidents across the Air Force’s fleet in 2018.
The frequency of the incidents set off alarm bells across the Air Force and led to several groundings that year — including a month-long grounding of the entire T-6 fleet at one point. The Air Force spent months searching for the problem’s cause, and ultimately concluded that rapidly fluctuating oxygen concentrations were the culprit.
“The problem’s not solved, clearly,” Leist said. “We think that [fixing] the breathing systems, especially hygiene and maintenance, has resulted in reduced rates, but not entirely eliminated the problem. And that’s why we continue to explore areas” to further improve how the T-6 delivers oxygen to pilots.
The progress made so far, Leist said, has come from a sweeping overhaul of maintenance practices and technical orders, as well as engineering tweaks to the plane’s oxygen system. The Air Force also took several cues from how the Navy maintains its planes’ oxygen systems, and has come to agree with the Navy’s conclusion that not one, but several factors cause hypoxia problems.
For example, the Air Force has drastically increased the frequency it replaces oxygen concentrators in the T-6. The concentrators are the heart of the On-Board Oxygen Generating System, or OBOGS — a “molecular sieve” that concentrates oxygen and flows it into the aircrew’s breathing systems, AFPEAT director and physician Col. William Nelson said at the Pentagon.
The Air Force also increased the frequency at which it purges moisture from the OBOGS system. The Navy’s experience operating aircraft at sea revealed the risk of excessive moisture buildup causing hypoxia problems, and passed that lesson on to the Air Force, Leist said.
Another contributing factor: Throttling down the relatively lower-power engine in the T-6, as compared to fighter such as the F-15E Strike Eagle. Pilots flying the Strike Eagle, which has a lot more power fueling its oxygen system, recorded four hypoxia-like incidents in 2018, and just one last year.
Leist hopes that the new system will further bring down hypoxia rates in the T-6, though he acknowledged it probably will never get down to zero.
“We’re operating humans and machines in a very perilous environment, and there will always be equipment failures, even with the best of maintenance practices,” Leist said. “We believe the current rates are unacceptable, though. That’s why we continue to research and develop remedies toward reducing those rates.”
(rates per 100K flight hours)
F-22A F-15C/D F-15E F-16C/D A-10C F-35A T-38C T-6A Total FY18 10.41 17.91 6.48 8.62 6.52 23.84 4.85 55.83 19.49 FY19 14.57 24.17 1.55 4.17 2.56 15.43 3.98 23.77 10.49 Total 12.14 21.13 3.96 6.43 4.52 19.33 4.42 39.17 14.98
Nelson said the Air Force and Navy are developing sensors that will go in air crew’s breathing masks, that can record exactly how much oxygen and carbon dioxide they’re getting. And if a physiological event happens, that data will help the Air Force accurately diagnose what happened. Those sensors have been in the works for a few years at the Air Force Research Laboratory’s 711th Human Performance Wing and the Naval Medical Research Unit-Dayton, both at Wright-Patterson Air Force Base in Ohio, Nelson said.
“That combination of sensors — knowing what the human is experiencing and what the aircraft is producing to support that human — is really the next step in understanding …. this particular issue,” Leist said.
And the Air Force has multiple ongoing studies involving pulmonary medicine and respiratory physiology to better understand what’s causing physiological episodes and how to lessen their effects or stop them, Nelson said.
This includes studying how best to position rescue gear or looking for ways to make it lighter, so it’s not pushing as hard on pilots’ chests and making it harder to breather.
But the Air Force also has to be careful that as it solves one problem, it doesn’t inadvertently create another, Nelson said. For example, he said, what if moving one piece of gear from the chest to the leg increases the risk of it catching on the cockpit as a pilot ejects?
Other air frames also experienced multiple hypoxia-like events in recent years. Pilots flying the F-15 C and D air frames, for example, recorded 10 physiological episodes in 2019, or about 24 for every 100,000 flight hours.
That’s likely due to the advancing age of the Eagle, Leist said.
Reported 1 August 2018
JB SAN ANTONIO-RANDOLPH, Texas — Since late last year, a rash of unexplained physiological events such as hypoxia has caused dangerous breathing problems for pilots of T-6 Texan II training aircraft, and led to multiple groundings.
But now, the Air Force is finding more clues, and coming closer to solving the problem once and for all, said Lt. Gen. Steven Kwast, head of Air Education and Training Command.
“We’re finding insights that we did not know before, that will help us understand what’s going on and give us a pathway to solving the problem permanently. We’re getting close, and you should see something soon.”
For example, Kwast said the board has discovered that the proportion of oxygen in the air sometimes fluctuates more than intended while T-6s are in flight.
“So the question is, what does that do to the human body, when you have a fluctuation of oxygen?” Kwast said. “That’s the kind of work they’re doing as they discover something that is a little … different than what we thought. Because we’re measuring it with more precision; we do the work, the scientific method [to find out] ‘What does that mean?’ ” and what’s causing it.
He stressed, however, that oxygen fluctuation is only one of several possible issues the board is looking at, and that it’s too soon to say whether it is actually causing or contributing to the problem. It could also be a combination of factors working together to cause the so-called unexplained physiological events, or UPEs.
Pilots suffering these problems report experiencing shortness of breath and disorientation, which can be extremely dangerous and lead to confusion, faintness or even loss of consciousness. These conditions include hypoxia, or too little oxygen in the body, or hypocapnia and hypercapnia, conditions when the bloodstream has either too little or too much carbon dioxide.
He also said that the increased awareness and visibility of the UPE problem could be contributing to the increased reporting of issues like hypoxia, because people now know what to look for.
It’s also led Kwast — a former T-6 instructor pilot — to reconsider some of his own experiences in the air. When Kwast looks back on his 650 hours in the Texan, he now realizes that he may have had some physiological incidents in years past that went unrecognized.
“I just thought that I hadn’t drunk enough water that day and so I was feeling lightheaded, or that I was tired because I hadn’t slept well that night, but I felt good enough to fly,” Kwast said. “But thinking back on it, maybe it was that the system wasn’t quite delivering the way it should have been delivering.”
But it also sometimes leads to confusion over whether a rookie pilot is actually experiencing a problem like hypoxia, or simple nervousness.
“A young kid that’s brand new to this, gets in the aircraft, and it’s their first flight, they’re hyperventilating,” Kwast said. “And they go up, and they’re like, ‘I had an unexplained physiological event.’ And it’s really hard to know whether they did, or whether it’s just the fact that they are so new to this, they don’t know what right looks like, and they were hyperventilating.”
Without systems to precisely measure whether a pilot is actually having a problem like hypoxia, or simply nervous and hyperventilating, such incidents can get buried in the data alongside actual physiological incidents, Kwast said. This makes it even tougher for investigators to find the true root causes, he said.
The first written report about the effect of high-altitude air on human organism dates back to the IV th century BC.
Francis Bacon (1561-1626) citing Titus Livius (59 BC to AD 19), the author of History of Ancient Rome, noted that Aristotle (384-322) knew that those climbing the Olympus had to breath through sponges wetted in water and vinegar, because high altitude air was very dry and not fit for breathing .
Robert Boyle (1627-1691) also referred to Aristotle in 1666 in his book New Experiments Physico-Mechanical Touching the Spring of the Air . However authors of later times could not find relevant note in Aristotle’s works (2, p. 8), as time and wars destroyed the greater part of precious texts. There is indirect evidence that ancient Greek philosopher and physician Empedokles (490-430 BC) climbed Etna (3263 m) on Sicily, the highest volcano in Europe.
Several years later an ancient Greek historian Xenophon (43()355 BC) described how the soldiers of Kyrus Jr. crossed high Armenian mountains on their way to Byzantia; the ten-thousand army lost many soldiers during this crossing. The same happened to one hundred thousand army of celebrated Hannibal in the year 218 BC in the Pyrenees and Alps.
The chronicler writes that the court counselor Too Kin advised Emperor Chung ti who governed in 37-32 BC not to send a Caravan of a hundred people to Afghanistan across Tibetan mountains: “Next, one comes to Big Headache and Little Headache Mountains, as well as Red Earth and Swelter Hills. They make a man so hot that his face turns pale, his head aches, and he begins to vomit. Even the donkeys and swine react this way” [6, p. 316].
Four hundred years later, about the year 403, Chinese monk Fa Hsien described his companion death from mountain sickness when they passed from Kashmir to Afghanistan across the high Karakoram Pass at an altitude of 5690 m . The fellow died with foam on his lips, which might be a characteristic of acute lung edema.
Acute lung edema
Acute pulmonary oedema has a high mortality. It requires emergency management and usually admission to hospital. The goals of therapy are to improve oxygenation, maintain an adequate blood pressure for perfusion of vital organs, and reduce excess extracellular fluid. The underlying cause must be addressed. There is a lack of high-quality evidence to guide the treatment of acute pulmonary oedema. The strongest evidence is for nitrates and non-invasive ventilation.
Diuretics are indicated for patients with fluid overload. Furosemide (frusemide) should be given by slow intravenous injection. Routine use of morphine is not recommended because of its adverse effects. Oxygen should only be administered in cases of hypoxaemia. Inotropic drugs should only be started when there is hypotension and evidence of reduced organ perfusion. In these cases, dobutamine is usually first-line treatment.
Acute pulmonary oedema is a medical emergency which requires immediate management.1 It is characterised by dyspnoea and hypoxia secondary to fluid accumulation in the lungs which impairs gas exchange and lung compliance.2
The one-year mortality rate for patients admitted to hospital with acute pulmonary oedema is up to 40%.3 The most common causes of acute pulmonary oedema include myocardial ischaemia, arrhythmias (e.g. atrial fibrillation), acute valvular dysfunction and fluid overload. Other causes include pulmonary embolus, anaemia and renal artery stenosis.1,4 Non-adherence to treatment and adverse drug effects can also precipitate pulmonary oedema.
There are no current Australian data on the incidence of acute pulmonary oedema or heart failure. However, self-reported data from 2011–12 estimated that 96 700 adults had heart failure, with two-thirds of these being at least 65 years old.5 Most patients with chronic heart failure will have at least one episode of acute pulmonary oedema that requires treatment in hospital.6
There are several different clinical guidelines for the management of acute pulmonary oedema.7–15 However, these are based predominantly on low-quality evidence and expert opinion. The goals of treatment are to provide symptomatic relief, improve oxygenation, maintain cardiac output and perfusion of vital organs, and reduce excess extracellular fluid. Any underlying cause should be identified when starting treatment.
The first step in improving ventilation for patients with acute pulmonary oedema is to ensure that they are positioned sitting up.1 This reduces the ventilation– perfusion mismatch and assists with their work of breathing.
Oxygen is not routinely recommended for patients without hypoxaemia as hyperoxaemia may cause vasoconstriction, reduce cardiac output and increase short-term mortality.21 There is a risk that prescribing oxygen for a breathless patient in the absence of hypoxaemia may mask clinical deterioration and hence delay appropriate treatment.11 Supplemental oxygen and assisted ventilation should only be used if the oxygen saturation is less than 92%.11
If required, oxygen should be administered to achieve a target oxygen saturation of 92–96%. Depending on the clinical scenario, oxygen titration can occur using a number of oxygen delivery devices. These include up to 4 L/minute via nasal cannulae, 5–10 L/minute via mask, 15 L/minute via a non-rebreather reservoir mask or high-flow nasal cannulae with fraction of inspired oxygen greater than 35%. For patients with chronic obstructive pulmonary disease, the target oxygen saturation is 88–92% and the use of a Venturi mask with inspired oxygen set at 28% is recommended.11
If the patient has respiratory distress, acidosis or hypoxia, despite supplemental oxygen, non-invasive ventilation is indicated.2 There is no significant clinical benefit of bi-level positive airway pressure ventilation (BiPAP) over continuous positive airway pressure ventilation (CPAP), so the modality chosen should be guided by local availability.22,23 Non-invasive ventilation should be commenced at 100% oxygen with recommended initial settings of 10 cm of water pressure for CPAP and 10/4 cm water pressure (inspiratory positive airway pressure/expiratory positive airway pressure) for BiPAP.8 Contraindications to non-invasive ventilation include hypotension, possible pneumothorax, vomiting, an altered level of consciousness or non-compliance.7
If, despite non-invasive ventilation, there is persistent hypercapnia, hypoxaemia or acidosis, then intubation should be considered.7 Other indications for intubation include signs of physical exhaustion, a decreasing level of consciousness or cardiogenic shock. Endotracheal intubation is only indicated in a very limited number of cases and carries inherent risks and challenges. The rapid sequence induction needs to be modified to account for the haemodynamic compromise of the patient. After intubation constant suctioning is usually required and ventilation can be very challenging.7,19 Additionally, positive pressure ventilation is likely to potentiate any hypotension.
AFRICA – SOUTH AFRICA
Asphyxia-hypoxia is responsible for about one-third of neonatal deaths. Intrapartum asphyxia is the major primary obstetric cause of deaths from hypoxia. A third of the deaths were judged to be preventable.
Among 4502 neonatal deaths weighing >999 g, 1459 (32.4%) were identified as being related to asphyxia-hypoxia.
Intrapartum asphyxia was the most common diagnosis (72% of deaths). Hypoxic-ischaemic encephalopathy was identified as the main neonatal diagnosis in these deaths. The most common category of probable avoidable factors was health worker-related. Inadequate fetal monitoring was the most common health worker-related probable avoidable factor. Substandard care related to resuscitation was recorded infrequently, most likely because of inability to assess neonatal resuscitation.
Intrapartum asphyxia and hypoxic ischaemic encephalopathy in a public hospital: Incidence and predictors of poor outcome.
Results. There were 21 086 liveborn infants with a birth weight of ≥2 000 g over the study period. The incidence of asphyxia ranged from 8.7 to 15.2/1 000 live births and that of HIE from 8.5 to 13.3/1 000, based on the definition of asphyxia used. In 60% of patients with HIE it was moderate to severe.
The overall mortality rate was 7.8%. The mortality rate in infants with moderate and severe HIE was 7.1% and 62.5%, respectively. The odds of severe HIE and/or death were high if the Apgar score was <5 at 10 minutes (odds ratio (OR) 19.1; 95% confidence interval (CI) 5.7 – 66.9) and if there was no spontaneous respiration at 20 minutes (OR 27.2; 95% CI 6.9 – 117.4), a need for adrenaline (OR 81.2; 95% CI 13.2 – 647.7) and a pH of <7 (OR 5.33; 95% CI 1.31 – 25.16). Predictors of poor outcome were Apgar score at 10 minutes (p=0.004), need for adrenaline (p=0.034) and low serum bicarbonate (p=0.028).
Conclusion. The incidence of asphyxia in term and near-term infants is higher than that reported in developed countries. Apgar score at 10 minutes and need for adrenaline remain important factors in predicting poor outcome in infants with asphyxia.
Hypoxic-ischaemic encephalopathy: Identifying newborns who will benefit from therapeutic hypothermia in developing countries
Hypoxia-reprogrammed tricarboxylic acid cycle promotes the growth of human breast tumorigenic cells.
Clinical applications of antiangiogenic agents profoundly affect tumor cell behaviors via the resultant hypoxia. To date, how the hypoxia regulates tumor cells remains unclear. Here, we show that hypoxia promotes the growth of human breast tumorigenic cells that repopulate tumors [tumor-repopulating cells (TRCs)] in vitro and in vivo.
This stimulating effect is ascribed to hypoxia-induced reactive oxygen species (ROS) that activates Akt and NF-κB, dependent on the attenuated tricarboxylic acid (TCA) cycle. We find that fumarate is accumulated in the TCA cycle of hypoxic TRCs, leading to glutathione succination, NADPH/NADP+ decrease, and an increase in ROS levels.
Mechanistically, hypoxia-increased HIF-1α transcriptionally downregulates the expression of mitochondrial phosphoenolpyruvate carboxykinase (PCK2), leading to TCA cycle attenuation and fumarate accumulation. These findings reveal that hypoxia-reprogrammed TCA cycle promotes human breast TRCs growth via a HIF-1α-downregulated PCK2 pathway, implying a need for a combination of an antiangiogenic therapy with an antioxidant modulator.
MARINE AND ENVIRONMENT
Factors Contributing to Hypoxia in the Minjiang River Estuary, Southeast China
Dissolved oxygen (DO) is not only a fundamental parameter of coastal water quality, but also an indication of organics decomposed in water and their degree of eutrophication. There has been a concern about the deterioration of dissolved oxygen conditions in the Minjiang River Estuary, the longest river in Fujian Province, Southeast China.
In this study, the syntheses effects on DO was analyzed by using a four year time series of DO concentration and ancillary parameters (river discharge, water level, and temperature) from the Fuzhou Research Academy of Environmental Sciences, at three automated stations along the Minjiang River Estuary.
Hypoxia occurred exclusively in the fluvial sections of the estuary during the high temperature and low river discharge period and was remarkably more serious in the river reach near the large urban area of Fuzhou. Enhancement of respiration by temperature and discharge of domestic sewage and industrial wastewater, versus regeneration of waters and dilution of pollutant concentration with increased river discharge, which regarded as the dominant antagonist processes that controlled the appearance of seasonal hypoxia.
An alarming “dead zone” with DO below 2 mg·L−1 has been found in the northern Gulf of Mexico which is the largest zone of oxygen-depleted coastal waters in the United States [14,21]. European estuaries, such as Gironde, Scheldt, Seine, Forth, are also oxygen depleted to different degrees, largely attributable to anthropogenic factors [5,22,23,24,25].
The Minjiang River is the longest river (2959 km) in Fujian Province, Southeast China.
The Minjiang River Estuary is located close to Fuzhou City (Figure 1), which is the capital of Fujian Province . On the Minjiang watershed (59,922 km2 in Fujian Province), rainfall is the highest in summer and the smallest in autumn. The annual average discharge of the Minjiang River is 1760 m3·s−1, which is the seventh highest annual runoff in China . The discharge varies seasonally, reaching a maximum in April–July (average 3200 m3·s−1)  and a minimum in October–March (average 620 m3·s−1). The annual average water temperature is 19.9 °C with a range of 9.8–32.2 °C. Minjiang River Estuary is divided into two branches (the South Channel and the North Channel) in upstream of the Wenshanli, and then merged at the Baiyantan. Minjiang River is approximately 200 m at the Shuikou Dam and gradually broadens to about 2 km at the Baiyantan. The mean depth of the river is −3 m in the upstream with a maximum depth of −30 m near the downstream. The average width of the South Channel is 1 km, wider than the North Channel with the width of 0.5 km.
The occurrence of hypoxia not always occurred in high temperature and low discharge. It also appeared during the floods after a long drought period, when a lot of wastewater and polluted initial rainwater overflows into the river.