Monoxide Poisoning

Fixation of CO to hemoglobin (Hgb) increases binding of 02 to Hgb and reduces release of 02 to peripheral body tissues [ 1 ] 

Source Many, including propane engines, auto 

Abdomen - pain Arterial press - low Behavior - bizarre or changed Bowel movements, control - loss 

Bowel movements, stool - blood or black (hematochezia) (melena) 

Bowel movements - diarrhea Breathing - diff, rest (rest dyspnea) 

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The Du Pont HaskeU Laboratory for Toxicology and Industrial Medicine has conducted a study to determine the acute inhalation toxicity of fumes evolved from Tefzel fluoropolymers when heated at elevated temperatures. Rats were exposed to decomposition products of Tefzel for 4 h at various temperatures. The approximate lethal temperature (ALT) for Tefzel resins was deterrnined to be 335—350°C. AH rats survived exposure to pyrolysis products from Tefzel heated to 300°C for this time period. At the ALT level, death was from pulmonary edema carbon monoxide poisoning was probably a contributing factor. Hydrolyzable fluoride was present in the pyrolysis products, with concentration dependent on temperature. 

In the past, hyperbaric oxygenation as a medical procedure has received considerable attention. In this treatment the patient is given pure oxygen and may be placed in a pressurized chamber. In effect, the patient may thus receive >400 kPa (>4 atm) of pure oxygen. Beneficial results in cases of carbon monoxide poisoning, gangrene, severe bums, and other difficulties are often achieved as a result of this treatment. 

Occurrence. Carbon monoxide is a product of incomplete combustion and is not likely to result where a flame bums in an abundant air supply, yet may result when a flame touches a cooler surface than the ignition temperature of the gas. Gas or coal heaters in the home and gas space heaters in industry have been frequent sources of carbon monoxide poisoning when not provided with effective vents. Gas heaters, though properly adjusted when installed, may become hazardous sources of carbon monoxide if maintained improperly. Automobile exhaust gas is perhaps the most familiar source of carbon monoxide exposure. The manufacture and use of synthesis gas, calcium carbide manufacture, distillation of coal or wood, combustion operations, heat treatment of metals, fire fighting, mining, and cigarette smoking represent additional sources of carbon monoxide exposure (105—107). 

Prevention of carbon monoxide poisoning is best accompHshed by providing good ventilation where contamination is a problem. If good ventilation is not possible, a self-contained breathing apparatus, such as a Scott Air-Pak, must be used. The use of gas masks containing an adsorbent is generally not recommended since it is difficult to know when the adsorbent is exhausted. 

Kohlen-ozydvergiftung, /. carbon monoxide poisoning, -oxysulfid, n, carbon oxysulfide. -papier, n. carbon paper, -pres (s)stein, m, coal briquet, -puWer, n, coal powder, powdered coal charcoal powder, powdered charcoal, -puppe, /, (Elec.) carbon rod, -riick-stand, m. carbon residue, -sandstein, m. carboniferous sandstone. 

Carbon monoxide poisoning results when carbon monoxide replaces oxygen bound to hemoglobin. The oxygenated form of hemoglobin, Hb 02 carries 02 to the lungs. 

Not only 02 molecules but also other groups can be bound to the iron atom of hemoglobin. Specifically, carbon monoxide molecules can be so attached and, in fact, CO is more firmly bound to hemoglobin than is O2. This is one detail of the carbon monoxide poisoning mechanism. If we breathe a mixture of CO and 02 molecules, the CO molecules are preferentially picked up by the red blood cells. Since the sites... 

This reaction serves for removal of carbon monoxide from gas mixtures and is usually carried out over supported metal catalysts. In reforming techniques, carbon monoxide, poisonous for the catalyst in fuel cells, is removed in such a way. It is also applied in automobiles for reducing the exhaust gas carbon monoxide to an environmentally acceptable level. 

Cardiogenic/distributive/obstructive/hypovolemic shock, carbon monoxide poisoning, severe hypoxemia, severe anemia, and seizures... 

Non-cardiac Anemia, anxiety disorders, carbon monoxide poisoning, cocaine use, esophageal reflux, peptic ulcer, pleuritis, pneumonia, pneumothorax, pulmonary embolus, pulmonary hypertension, thyrotoxicosis... 

Describe the effects of carbon dioxide, pH, temperature, 2,3-bispho-sphoglycerate, anemia, and carbon monoxide poisoning on the transport of oxygen... 

Carbon monoxide poisoning is particularly insidious. An individual exposed to carbon monoxide is usually unaware of it because this gas is odorless, colorless, and tasteless. Furthermore, it does not elicit any irritant reflexes that result in sneezing, coughing, or feelings of dyspnea (difficulty in breathing). Finally, carbon monoxide does not stimulate ventilation. As will be discussed in a subsequent section, the peripheral chemoreceptors are sensitive to decreases in P02, not oxygen content. 

Combined intoxications of carbon monoxide and cyanide should not be treated with the nitrites found in cyanide antidote kits. These nitrites are used to create methemoglobinemia, which will exacerbate carbon monoxide poisoning by further reducing the ability of the blood to deliver oxygen to body tissue. 

In addition, around 10,000 cases of carbon monoxide-related injuries are diagnosed each year. Because the symptoms of prolonged, low-level carbon monoxide poisoning mimic the symptoms of a common flu (headaches, nausea, dizziness, fatigue), many cases are not detected until permanent damage to the brain, heart and other organs has occurred. 

The precise technical name of HCN is Hydrocyanic Acid. The cyanides are true protoplasmic poisons, combining in the tissues with the enzymes associated with cellular oxidation. They thereby render the oxygen unavailable to the tissues, and cause death through asphyxia. Inhaling concentrations of more than 180 ppm of HCN will lead to unconsciousness in a matter of minutes, but the fatal effects would normally be caused by carbon monoxide poisoning after HCN has made the victim unconscious. Exposure to HCN concentrations of 100 to 200 ppm for periods of 30 to 60 minutes can also cause death. 

Methaemoglobin forming compounds should be used cautiously in victims suffering from concurrent carbon monoxide poisoning or hypoxia. The second approach calls for provision of additional sulfur groups to enhance the detoxification of cyanide and thiocyanate by endogenous rhodanese this comes about by giving sodium thiosulphate. 

In addition, other chemicals such as a-adrenergic blocking agents like chlorpromazine (O Flaherty and Thomas 1982 Way and Burrows 1976) or oxygen (Burrows et al. 1973 Sheehy and Way 1968) may be used to enhance the protective action of other antidotes. However, the mechanism of their action is not well understood. Further research for a potent and safe antidote, particularly among smoke inhalation victims who have carbon monoxide poisoning, to mitigate cyanide toxicity is desirable. 

The ideal performance of a fuel cell depends on the electrochemical reactions that occur with different fuels and oxygen as summarized in Table 2-1. Low-temperature fuel cells (PEFC, AFC, and PAFC) require noble metal electrocatalysts to achieve practical reaction rates at the anode and cathode, and H2 is the only acceptable fuel. With high-temperature fuel cells (MCFC, ITSOFC, and SOFC), the requirements for catalysis are relaxed, and the number of potential fuels expands. Carbon monoxide "poisons" a noble metal anode catalyst such as platinum (Pt) in low-temperature... 

One of the most carefully worked out dose-response relationships is that for carbon monoxide poisoning. Based on controlled studies of exposure in humans at low levels and on observations in humans who have suffered high level exposures because of their occupation or because of accidents or suicide attempts, the relationship between blood levels of carboxyhemoglobin (COHb) and toxicity is understood as follows ... 

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