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Toxic respiratory failure

Early toxic respiratory failure will usually be type 2 (low PaOa and high PaCOa) and adequate ventilation will reverse this situation quickly. If end-tidal CO2 monitoring is available, this will be a valuable indicator of ventilation effectiveness... [Pg.143]

Manufacture, Shipment, and Analysis. In the United States, sodium and potassium thiocyanates are made by adding caustic soda or potash to ammonium thiocyanate, followed by evaporation of the ammonia and water. The products are sold either as 50—55 wt % aqueous solutions, in the case of sodium thiocyanate, or as the crystalline soHds with one grade containing 5 wt % water and a higher assay grade containing a maximum of 2 wt % water. In Europe, the thiocyanates may be made by direct sulfurization of the corresponding cyanide. The acute LD q (rat, oral) of sodium thiocyanate is 764 mg/kg, accompanied by convulsions and respiratory failure LD q (mouse, oral) is 362 mg/kg. The lowest pubhshed toxic dose for potassium thiocyanate is 80—428 mg/kg, with hallucinations, convulsions, or muscular weakness. The acute LD q (rat, oral) for potassium thiocyanate is 854 mg/kg, with convulsions and respiratory failure. [Pg.152]

The effects of protein deficiency on endosulfan toxicity were studied in Wistar rats (Boyd and Dobos 1969 Boyd et al. 1970). Rats fed a diet totally deficient in protein for 28 days prior to administration of a single oral dose of endosulfan had an LDjq of 5.1 mg/kg of endosulfan. Rats fed a low-protein diet (3.5% protein) for 28 days had an LDjq of 24 mg/kg of endosulfan. Rats fed standard laboratory chow (26% protein) had an LDjq of 102-121 mg/kg. The immediate cause of death in all animals was respiratory failure following tonic-clonic convulsions. This study demonstrated that, while a protein-deficient diet does not affect the nature of the toxic reaction, it may affect the sensitivity of rats to the lethal effects of endosulfan. [Pg.48]

Inhaled nickel is at least 100 times more toxic than ingested nickel because it is more readily absorbed from the lungs than from the gastrointestinal tract, and death is more often the result of respiratory failure than of nervous system effects. For example, oral ingestion of 0.05 mg Ni/kg BW and inhalation at 0.005 Ni/m3 are equally effective threshold doses in rats (USPHS 1977). [Pg.498]

Acute Nicotine is a very toxic drug in acute high doses (Taylor 1996). The lethal dose in adult humans is approximately 60 mg. Symptoms of acute poisoning include headache, dizziness, salivation, cold sweats, abdominal pain, nausea, vomiting, and diarrhea. Sensory disturbances, confusion, and convulsions also occur. Blood pressure drops, the pulse becomes weak and irregular, and respiration becomes difficult. Death usually results from respiratory failure. [Pg.117]

Deaths in rats resulting from single-exposure concentration/duration combinations expected to produce 50%-90% mortality usually occurred within 24 hours. These deaths were attributed to cardiac or respiratory failure and were probably a direct effect of 1,2-dibromoethane toxicity. Deaths resulting from exposure concentration/duration combinations expected to produce 0.01%-50% mortality occurred as long as 12 days after exposure and were due to pneumonia. The authors attributed pneumonia to 1,2-dibromoethane-induced lung injury, but this lesion could also have been due to intercurrent bacterial or mycoplasmal pulmonary infection. Rats free of enzootic respiratory infections were not available in 1952. More contemporary inhalation studies of 1,2-dibromoethane using commercially produced rats (Nitschke et al. 1981 NTP 1982) did not report pneumonic lesions or pneumonia-related mortality. [Pg.15]

The toxic effects of Calabar Bean extract were found to be due to excessive cholinergic stimulation giving rise to symptoms such as increased salivation, nausea, bradycardia, muscle cramps and respiratory failure, as well as CNS effects such as agitation. The cholinergic excess was found to be... [Pg.395]

The compound is highly toxic hy oral and subcutaneous routes. Ingestion can cause convulsion, paralysis, and respiratory failure. [Pg.287]

Hydrogen cyanide is extremely toxic hy ingestion, inhalation, skin absorption, and all routes of exposure. An oral dose of 50 mg could be lethal to humans (Patnaik, P. 1999. A Comprehensive Guide to the Hazardous Properties of Chemical Substances, 2nd ed.. New York John Wiley). Symptoms from acute poisoning include labored breathing, shortness of breath, paralysis, unconsciousness, and respiratory failure. Lower doses can cause headache, nausea and vomiting. Oral LDsoin mice is 3.7 mg/kg. Amyl nitrite is an effective antidote. [Pg.366]


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See also in sourсe #XX -- [ Pg.106 , Pg.109 ]




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