Carbon monoxide poisoning
The deadly effect of carbon monoxide was known as long ago as Greek and Roman times, when the gas was ud for executions. In 1857 Claude Bernard postulated that its noxious effect was caud by reversible displacement of oxygen from haemoglobin to form carboxyhaemoglobin. In 1926 it became apparent that hypoxia was caud not only by deficient oxygen transport but also by poor tissue uptake. Warberg ud yeast cultures to show that cellular uptake of oxygen was inhibited by exposure to a large amount of carbon monoxide.
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Carbon monoxide is known as the silent killer since it has no colour or smell. Each year in Britain about 50 people die and 200 are verely injured by carbon monoxide poisoning4. Some poisonings are caud by lf-harm but most are accidental. It is the commonest cau of accidental poisoning and, according to one estimate, as many as 25000 people in the UK have symptoms due to faulty gas appliance. In the 1960s and 1970s the conversion from coal gas to carbon-monoxide-free natural gas caud a dramatic reduction in poisoning. In this review I discuss modern approaches to management and prevention
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Carbon monoxide is produced endogenously in small amounts as a byproduct of haem catabolism. Together with nitric oxide it affects cellular function and acts as a neurotransmitter. Environmental carbon monoxide is produced by incomplete combustion of any carboncontaining fuel (coal, petroleum, peat, natural gas). In Britain most accidents ari through central heating faults. By contrast, in the USA most deaths are caud by inhalation of exhaust fumes. In the United Kingdom car exhaust emissions of carbon monoxide have been reduced by catalytic convertors in all new cars. Surprisingly, when deaths occur in garages there have usually been open doors and windows色环电阻识别9. There are even reports of poisoning occurring from carbon monoxide inhalation in the open air. Methylene chloride (paint stripper) fume inhalation is a rare cau of poisoning. In the liver it is converted to carbon monoxide
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Carbon monoxide has 210 times greater affinity for haemoglobin than oxygen. A small environmental concentration will thus cau toxic levels of carboxyhaemoglobin. After the carbon monoxide has lectively bound to haemoglobin the oxygen-haemoglobin dissociation curve of the remaining oxyhaemoglobin shifts to the left, reducing oxygen relea .The affinity of carbon monoxide for myoglobin is even greater than for haemoglobin. Binding to cardiac myoglobin caus myocardial depression, hypotension and arrhythmias. Cardiac decompensation results in further tissue hypoxia and is ultimately the cau of death.Carbon monoxide shifts the oxygen-haemoglobin saturation curve to the left and changes it to a more hyperbolic shape. Less oxygen is available for the tissues. Shown is the oxygen diffusion gradient difference at 50% saturation.Cellular uptake of oxygen is blocked by binding of carbon monoxide with mitochondrial cytochrome aa3vnn. The hypoxia precipitates endothelial cell and platelet relea of nitric acid, which forms the free radical peroxynitrate. In the brain this caus further mitochondrial dysfunction, capillary leakage, leukocyte questration and apoptosis. The pathological changes occur mainly during the recovery (reperfusion) pha when lipid per
oxidation (degradation of unsaturated fatty acids) occurs. The net result is reversible demyelination in the brain. Such changes are clearly evident on magnetic resonance imaging. Carbon monoxide has a predilection for ‘watershed’ areas of the brain where there is a meagre blood supply. The basal ganglia, with their high oxygen consumption, are most often affected. Other commonly affected areas are the cerebral white matter, hippocampus and cerebellum.
CLINICAL SIGNS AND DIAGNOSIS
The signs of carbon monoxide poisoning vary with concentration and length of exposure. Subtle cardiovascular or neurobehavioural effects occur at low concentrations. Lengthy exposure or acute exposure to high concentrations often caus coma and death. The ont of chronic poisoning is usually insidious and easily mistaken for 'flu, depression, food poisoning or in children gastroenteritis. Other family members may have a similar illness.
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The most common symptoms are headache, naua and vomiting, dizziness, lethargy and a feeling of weakness. Infants may be irritable and feed poorly. Neurological signs include confusion, disorientation, visual disturbance, syncope and izures. In acute poisoning, common abnormalities of posture and tone are cogwheel rigidity, opisthotonus and flaccidity or spasticity. Adults with coronary heart dia may experience angina, arrhythmias and myocardial infarction. Retinal haemorrhages and the classic cherry red skin colour are ldom en. Other organs such as the kidney, liver and pancreas are rarely affected. A ri in creatine phosphokina follows muscle necrosis. Hypoxaemia caus lactic acidaemia.
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britney murphyCarbon monoxide poisoning is diagnod by measuring carboxyhaemoglobin in a heparinized blood sample (arterial or venous. Symptoms usually begin when the concentration ris above 10%. There is a poor correlation between the blood level and the clinical condition. Symptoms reflect the dissolved concentration, which may be low in the face of a high carboxyhaemoglobin. In general, levels below 40% are not associated with coma or death. In a normal non-smoker the average is about 1%, rising to 15% in a
heavy smoker. Levels of 5% are found in haemolytic anaemias and pregnancy. Pul oximeters are not suitable for the diagnosis of carbon monoxide poisoning. The wavelength of most cannot distinguish between oxyhaemoglobin and carboxyhaemoglobin. A carbon monoxide breathalyr is a simple bedside screening test but its practical value is limited by numerous confounders such as smoking and alcohol
