Chronic respiratory failure causes

Symptoms of exposure May cause weakness, confusion, depression of central nervous system, dyspnea, weak pulse, and respiratory failure. May irritate eyes and mucous membranes. Contact with skin may cause burns and dermatitis. Chronic effects may include gastrointestinal disorders, nervous disorders, tremor, confusion, skin eruptions, oliguria, jaundice, and liver damage (NIOSH, 1997 Patnaik, 1992). 

In livestock, selenium has been found to be the cause of blind staggers and alkali disease. Blind staggers occurs as a result of acute ingestion of seleniferous plants and is characterized by impaired vision, depressed appetite, a tendency to wander in circles, paralysis, and death from respiratory failure. A more chronic syndrome described in horses and livestock is alkali disease, which also is associated with consumption of grains or plants containing selenium. The disease is characterized by lack of vitality, loss of appetite, emaciation, deformed hoofs, loss of hair, erosion of the joints of long bones, anemia, cirrhosis, and cardiac atrophy ... 

The literature on the toxicity of benzene in humans is extensive. The acute effects of benzene exposure generally differ markedly from the chronic effects. Acute exposure to high doses of benzene in air (at concentrations in excess of 3000 ppm) causes symptoms typical of organic solvent intoxication. Symptoms may progress from excitation, euphoria, headache, and vertigo, in mild cases, to central nervous system depression, confusion, seizures, coma, and death from respiratory failure in severe cases. The rate of recovery depends on the initial exposure time and concentration, but, following severe intoxication, the symptoms may persist for weeks. 

Selenium is an essential element but is toxic when excessive quantities are ingested. Exposure of horses is usually through consumption of seleniferous (accumulator or indicator) plants (e.g.. Astragalus spp.). Exposure to high quantities of selenium over a short time causes diarrhea (which is often foul smelling and contains air bubbles), neurological and cardiovascular effects, and respiratory difficulty. Death in these horses is due to respiratory failure. Chronic exposure to low levels of excessive selenium is characterized by hoof abnormalities at the coronary bands and by discoloration and loss of hair. The hoof deformities are painful and cause lameness. 

The clinical manifestations of serum phosphate depletion depend on the length and degree of the deficiency. Moderate hypophosphatemia of 1.5 to 2,4 mg/dL (0.48 to 0.77 mmol/L) is usually not associated with clinical signs and symptoms (unless chronic, when osteomalacia or rickets develops). Plasma concentrations less than 1.5 mg/dL (0.48 mmol/L) may produce clinical manifestations. Because phosphate is necessary for the formation of ATP, glycolysis and cellular function are impaired by low intracellular phosphate concentrations. Muscle wealmess, acute respiratory failure, and decreased cardiac output may occur in phosphate depletion. At very low serum phosphate (<1 mg/dL or <0.32 mmol/L), rhabdomyolysis may occur. Phosphate depletion in erythrocytes decreases erythrocyte 2,3-diphosphoglycerate, which causes tissue hypoxia because of increased affinity of hemoglobin for oxygen. Severe hypophosphatemia (serum phosphate concentration <0.5 mg/dL [<0.16 mmol/L]) may result in hemolysis of the red blood cells. Mental confusion and frank coma also may be secondary to the low ATP and tissue hypoxia. If hypophosphatemia is chronic, impaired mineralization of bone produces rickets in children and osteomalacia in adults. 

Doxapram is an analeptic that increases the depth of respirations (tidal volume) by stimulating the respiratory center in CNS respiratory rate may increase slightly. It may elevate BP by increasing cardiac output. Respiratory depression from opiates is reversed without affecting pain relief. It is indicated when one requires the stimulation of deep breathing in postoperative patients for reversal of respiratory depression caused by anesthesia (other than muscle relaxants) or drug overdose and as a temporary measure in acute respiratory failure in patients with chronic obstructive pulmonary disease (COPD) who are not undergoing mechanical ventilation. 

HUMAN HEALTH RISKS Acute Risks irritation of mucous membranes, upper respiratory tract, eyes and skin may cause allergic reaction bums colored urine muscle twitch CNS excitement suffocation delirium increased pulse rate without fall in blood pressure respiratory failure Chronic Risks dermatitis anemia skin depigmentation effects on kidney and eyes corneal and conjunctival discoloration cancer. 

Effects As described in Chapter 7, these agents produce increased muscarinic and nicotinic stimulation. The effects include pinpoint pupils, sweating, salivation, bronchoconstric-tion, vomiting and diarrhea, CNS stimulation followed by depression, and muscle fascicula-tions, weakness, and paralysis. The most common cause of death is respiratory failure. Chronic exposure to some organophosphates (not carbamates) has resulted in a delayed neurotoxicity with axonal degeneration. The toxic mechanism appears to involve phosphorylation of a neuropathy target esterase (NTE). 

The toxic effects manifested in humans from inhaling trichloroethylene vapors are headache, dizziness, drowsiness, fatigue, and visual disturbances. A 2-hour exposure to a 1000-ppm concentration affected the visual perception. Higher concentrations can produce narcotic effects. Heavy exposures may cause death due to respiratory failure or cardiac arrest. A 4-hour exposure to 8000 ppm was lethal to rats. Chronic exposure caused increase in kidney and liver weights in test animals. 

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