Asphyxia

ASPHYXIA The result of a diminished supply of oxygen to the blood and tissues and interference with the respiratory function. Simple anoxia may be caused by inert gases , e.g. nitrogen, and some flammable gases, e.g. methane. Toxic anoxia may be caused by certain substances, e.g. carbon monoxide and hydrogen cyanide, which interfere with the body s ability to transfer or utilize oxygen in the tissues. Rapid unconsciousness and death can occur in either case. 

Serious coughing, bronchial spasms, <30 min exposure may be fatal Serious oedema, strangulation, asphyxia Fatal almost immediately... 

Serious edema, strangulation, asphyxia rapidly fatal... 

Erstickung,/. suffocation choking asphyxia, erstklassig, a. first-class, first-rate, eistlich, a. adv. first. 

Toxicity. Max allowable concn for an 8 hr exposure is lOOOppm or 2950mgs/cm of air. Higher concns produce a narcotic effect and eventual asphyxia (Refs 16a 22)... 

Toxicity. Injection of aq Na perchlorate into rabbits caused no long term toxic effects. It behaved as a mild muscular poison, and large doses caused liver damage and diarrhea. Goldfish will live indefinitely in a 0.1% soln, but a 1% soln will cause asphyxia (Ref 4)... 

Serious oedema, strangulation, asphyxia Fatal almost immediately... 

Birth asphyxia Hypothermia Meconium or amniotic fluid aspiration Necrotizing enterocolitis Respiratory distress syndrome Shock Obstetrics Abortion... 

Freireich AW. 1946. Hydrogen sulfide poisoning Report of two cases, one with fatal outcome, from associated mechanical asphyxia. Am J Pathol 22 147-155. 

White, granular, or crystalline deliquescent solid that is odorless when dry but has a faint odor like almond when wet. This material is hazardous through inhalation, skin absorption, penetration through broken skin, and ingestion, and produces local skin/eye impacts. It causes irritation of the eyes and skin, asphyxia, lassitude, headache, confusion, nausea, vomiting, increased respiratory rate, slow gasping respiration, thyroid, and blood changes. 

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. 

Relative to body weight, humans have a much lower respiratory rate and cardiac output than rodents. These are the two primary determinants of systemic uptake of volatile chemicals. Therefore, at similar nominal concentrations, rodents absorb substantially more cyanide than primates. From a pharmacokinetic view, lower hepatic rhodanese levels in primates will not be significant at high, acute HCN exposures. It should be noted that Barcroft s subject withstood a 1 min and 31 s exposure at approximately 500 to 625 ppm without immediate effects (Barcroft 1931), whereas mice suffer asphyxia during a 2 min exposure at 500 ppm (Matijak-Schaper and Alarie 1982). Compared with rodents, the respiratory tracts of humans and monkeys are more similar in gross anatomy, the amount and distribution of types of respiratory epithelium, and airflow patterns (Barrow 1986 Jones et al. 1996). 

Asphyxia has been observed in rats exposed to 250 ppm cyanogen (125 ppm cyanide) for 7.5-120 minutes (McNemey and Schrenk 1960), asphyxia and pulmonary edema were observed in dogs exposed to concentrations ranging from 149 to 633 ppm hydrogen cyanide (143-608 ppm cyanide) for 2-10 minutes (Haymaker et al. 1952), while severe dyspnea was observed in monkeys exposed to 100 ppm hydrogen cyanide (96 ppm cyanide) for 30 minutes (Purser et al. 1984). Exposure to 63 ppm hydrogen cyanide (60 ppm cyanide) for 30 minutes resulted in a 50% decrease in respiratory rate of mice due to depression of the respiratory center (Matijak-Schaper and Alarie 1982). 

The respiratory effects of cyanide include dyspnea, asphyxia, and a decrease in respiratory rate (Blanc et al. 1985 Matijak-Schaper and Alarie 1982 McNemey and Schrenk 1960). A recent study (Bhattacharya et al. 1994) demonstrated increased air flow, transthoracic pressure, and tidal volume accompanied by a significant decrease in pulmonary phospholipids following inhalation of hydrogen cyanide in rats. This study also showed that hydrogen cyanide exhibited a direct effect on pulmonary cells in rats. 

Gettler and St. George 1934). Dyspnea, convulsions, and death from asphyxia follow. Dermal exposure to cyanide results in comparable effects. Based on case report studies, LC50 values for humans were estimated for inhalation (McNamara 1976, as cited in Ballantyne 1987), oral (EPA 1987a), and dermal (Rieders 1971) routes as 524 ppm, 1.52 mg/kg, and 100 mg/kg, respectively. 

With higher concentrations than those mentioned above, animals exhibit, in addition to myosis, the following symptoms salivation, muscular weakness, loss of muscular co-ordination, gasping, diarrhoea and finally cessation of respiration. There is intense constriction of the bronchioles and the immediate cause of death is asphyxia. Respiration ceases before the heart stops beating. The L.c. 50 s for rats and for mice for a 10 min. exposure are respectively 0-36 and 0-44 mg./l. Air saturated with D.F.P. at ordinary temperatures contains about 8 mg./l. and this will kill mice within 1 min. During exposures for a limited time (e.g. 5 min.), rabbits appear to be more resistant to the inhaled vapour of D.F.P. than are other animals. It appears that the peculiar nasal structure of the rabbit is responsible for its great resistance. 

Death. No studies were located regarding death in humans after inhalation or dermal exposure to disulfoton. One case report of human death after acute oral exposure to disulfoton was found (Hattori et al. 1982). Because an unknown amount was ingested, the lethal dose was not determined. Autopsy results suggested that death may have been due to asphyxia resulting from respiratory failure. Pulmonary edema is associated with disulfoton-induced overstimulation of secretory glands and bronchial secretions in the respiratory tract. 

Asphyxia means deprivation of oxygen. As you well know, if you are deprived of oxygen for more than a few minutes, you die, and whether that deprivation comes because someone is choking you with a pillow... 

Chen Y, Engidawork E, Loidl F, Dell Anna E, Goiny M, et al. 1997. Short- and long-term effects of perinatal asphyxia on monoamine, amino acid and glycolysis product levels measured in the basal ganglia of the rat. Brain Res Dev Brain Res 104(1-2) 19-30. 

Symptoms of exposure Inhalation may cause nausea, vomiting, asphyxia, and tightness of the chest. Symptoms of ingestion may include gastrointestinal pain, vomiting, nausea, stupor, convulsions, and weakness (Patnaik, 1992). An irritation concentration of 875.00 mg/m in air was reported by Ruth (1986). 

Symptoms of exposure Eye and skin irritant. Inhalation may cause asphyxia and headache. Ingestion and skin absorption may cause headache, lightheadedness, sneezing, weakness, nausea,... 

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