Carbon monoxide poisoning

Carbon monoxide poisoning is a significant cause of illness and death. Its protean symptoms probably lead to a gross underestimation of its true incidence. Low levels of carbon monoxide aggravate chronic cardiopulmonary problems, and high levels are associated with cardiac arrhythmias and cerebral edema. Patients who survive acute poisoning are at risk of delayed neurologic sequelae. The measurement of carboxyhemoglobin levels does not reveal the tissue levels of carbon monoxide but is useful in determining therapy. Treatment includes the monitoring and management of cardiac arrhythmias and oxygenation. Hyperbaric oxygenation is beneficial, but there are currently no definite criteria for its use.     

Carbon monoxide poisoning from Sterno.

A high school student became ill and later unconscious while working over a heating table set over three cans of burning Sterno. Measurements of 1000 to 3000 parts per million of carbon monoxide were obtained around and above the apparatus. Although the room was well ventilated there was incomplete combustion of the canned heating fuel because the apparatus was surrounded by aluminum foil, which resulted in poor oxygenation of the flame area. This case demonstrates the hazards of carbon monoxide poisoning from incompletely burned Sterno.     

Carbon monoxide poisoning and nonoliguric acute renal failure.

Carbon monoxide poisoning in a 37-year-old man was complicated by neurologic damage, skin changes, muscle necrosis and nonoliguric renal failure. The relation between nontraumatic rhabdomyolysis and acute renal failure in carbon monoxide poisoning is reviewed. Recognition of the acute renal failure in such cases is important, for this complication can be fatal; the prognosis is excellent, however, if proper medical management is provided.     

Carbon monoxide poisoning at a lowered myocardial adaptation capacity: animal ECG models

Two animal models for testing foreign substances for the hypoxic type of cardiotoxicity proved to be valid and reproducible: i.e. decreased reserve capacity of the heart in rats recovered from the calciferol cardiopathy and increased heart work provoked by isoproterenol (5 mg/kg i.p.). In both cases obvious hypoxic ECG changes appeared at lower levels of exposure to carbon monoxide (500 ppm, 572 mg.m-3) and carboxyhemoglobin (18%), when compared with nonpretreated animals. The models have shown, that injured or overloaded heart displays a substantially increased sensitivity to CO poisoning.