1. The COHb content in the blood of normal people with […]
1. The COHb content in the blood of normal people with acute poisoning can reach 5%~10%. The symptoms of acute CO poisoning are closely related to the COHb% in the blood, as well as the health status of the patient before the poisoning, such as whether there is cardiovascular disease and cerebrovascular disease. disease, and physical activity during poisoning. According to the degree of poisoning can be three.
(1) The blood COHb concentration of mild poisoning can be higher than 10%~20%. The patient has severe headache, dizziness, palpitations, cherry-red mucous membrane of lips, limb weakness, nausea, vomiting, drowsiness, confusion, blurred vision , dysesthesia, delirium, hallucinations, convulsions, etc. Angina pectoris may occur in patients with pre-existing coronary heart disease. Inhale fresh air or oxygen therapy out of the poisoning environment, and the symptoms disappear quickly.
(2) The blood COHb concentration of moderate poisoning can be as high as 30% to 40%. The patient has dyspnea, loss of consciousness, coma, and may respond to painful stimuli. and pulse may change. After oxygen therapy, it can return to normal without obvious complications.
(3) The blood COHb concentration of severe poisoning can be higher than 50%. Deep coma, all reflexes disappeared. The patient can be in a state of de-cerebral cortex: the patient can open his eyes, but is unconscious, does not speak, does not move, does not take the initiative to eat or defecate, does not respond to calls, does not move, and increases muscle tension. There are often cerebral edema, convulsions, respiratory failure, pulmonary edema, upper gastrointestinal bleeding, shock and severe myocardial damage, arrhythmia, myocardial infarction, focal brain damage and signs of pyramidal or extrapyramidal damage. The skin may appear red, swollen and water-marked, and it is more common in areas where the femur is compressed during a coma. Compressive muscle necrosis (rhabdonlyolysis) can occur in compressed muscles. Myosin released from necrotic muscles can cause acute tubular necrosis and renal failure. The mortality rate is high, and many survivors have different degrees of sequelae.