The principle of carbon monoxide poisoning turns out to be like this

The cold winter is the season for heating in the north, and it is also the season when carbon monoxide poisoning is most prevalent. So what exactly causes carbon monoxide poisoning? Most northerners don't understand this. In fact, the principle of carbon monoxide poisoning is that carbon monoxide enters the human body and combines with hemoglobin, reducing the blood's oxygen-carrying capacity.

1. Principle of carbon monoxide poisoning

Carbon monoxide (CO) enters the body through the respiratory tract and can quickly combine with hemoglobin (Hb) in the blood to form carboxyhemoglobin (HbCO). Because the affinity of CO to Hb is about 300 times greater than that of oxygen to Hb, a small amount of CO can compete with oxygen to fully form HbCO, thereby reducing the oxygen-carrying capacity of the blood. The dissociation rate of HbCO is 3600 times slower than that of oxyhemoglobin (HbO2). Therefore, after HbCO is formed, it can persist in the blood for a long time and can prevent HbO2 from releasing oxygen, further aggravating the body's hypoxia.

2. Clinical manifestations

(1) Acute poisoning: The severity of acute carbon monoxide poisoning is closely related to the CO inhalation concentration and time. Clinically, the degree of CO poisoning is often judged by the real-time measured HbCO concentration.

1) Mild poisoning: The main clinical symptoms are brain hypoxia, such as severe headache, dizziness, limb weakness, nausea, vomiting, or mild to moderate disturbance of consciousness. Blood HbCO concentration may be higher than 10%.

2) Moderate poisoning: In addition to the above symptoms, there is a slight to moderate coma, and no obvious complications after rescue and recovery. Blood HbCO concentration can be higher than 30%.

3) Severe poisoning: deep coma or decerebrate state occurs. It may be complicated by cerebral edema, shock or severe myocardial damage, pulmonary edema, respiratory failure, upper gastrointestinal bleeding, and focal brain damage such as pyramidal or extrapyramidal damage. Blood HbCO concentration may be higher than 50%.

4) Delayed encephalopathy caused by acute carbon monoxide poisoning: Some patients with acute carbon monoxide poisoning may develop mental abnormalities (such as apathy, slow reaction, memory impairment, abnormal behavior, loss of orientation, etc.), extrapyramidal damage, cortical blindness, diencephalic syndrome and other neurological changes after the recovery of consciousness disturbance during a "false recovery period" of 2 to 60 days. The occurrence of delayed encephalopathy may be related to the severity of the acute phase of CO poisoning, insufficient rest after waking up, or improper treatment.

(2) Chronic effects: It is still unclear whether long-term exposure to low concentrations of CO can cause chronic poisoning, but some scholars believe that neurological symptoms may occur, such as headache, dizziness, tinnitus, weakness, memory loss, sleep disorders, etc.

3. Principles of prevention and treatment

(1) Treatment: The focus is on correcting brain hypoxia. Move the patient away from the scene quickly, adopt appropriate oxygen administration methods (such as hyperbaric oxygen therapy) according to the degree of poisoning, and actively prevent and treat complications and delayed encephalopathy. For patients with delayed encephalopathy, hyperbaric oxygen, glucocorticoids, vasodilators, etc. can be given, and corresponding symptomatic treatment can be taken.

(2) Prevention: Install a CO alarm to prevent gas leakage in pipelines; improve ventilation in production areas; strengthen individual protection and popularize self-rescue and mutual rescue knowledge; wear a gas mask when entering a dangerous area.