Carbon gas poisoning

Abstract

Carbon monoxide belongs to a group of blood poisons that cause pathological changes in blood pigments. Carbon monoxi­de readily combines with hemoglobin iron to form carboxyhemoglobin. Carboxyhemoglobin is a strong compound and its dissociation is much slower than oxyhemoglobin. There is a violation of the oxygenation of hemoglobin, which causes the development of hemic hypoxia. The pathological process is exacerbated by the fact that the dissociation of oxyhemoglobin in the presence of carboxyhemoglobin in the blood is slowed down. Prolonged hypo­xemia is a leading factor in the mechanism of development of lesions of the nervous system in intoxications caused by carbon mono­xide. Carbon monoxi­de intoxication can be acute or chronic. Acute intoxications are cha­racterized by changes in the blood, nervous, respiratory and cardiovascular systems, trophic skin lesions. There are mild, moderate and severe acute intoxication caused by carbon monoxide. Chronic intoxication develops with prolonged exposure to low concentrations of carbon monoxide, and may be the result of frequent acute carbon monoxide intoxication. The criterion for confirming the diagnosis of acute intoxication is the presence of elevated carboxyhemoglobin in the blood. Diagnostic value in chronic intoxication has an increased content of non-hemoglobin iron in plasma. The complex of therapeutic measures for acute intoxication includes fercoven and acisol. The main measures to prevent the development of carbon monoxide intoxication are sealing the processes associated with its formation, preventing the possible penetration of carbon monoxide into the workplace, providing effective ventilation.

Keywords

• carbon monoxide
• blood poison
• carboxyhemoglobin
• hypoxia
• acute and chronic intoxication