Do you know the pathogenesis of CO?

Do you know the pathogenesis of CO?

CO poisoning mainly causes tissue hypoxia. After CO is inhaled into the body, 85% is combined with the hemoglobin (Hb) of red blood cells in the blood to form stable COHb. The affinity of CO and Hb is 240 times greater than that of oxygen and Hb. Inhaling a lower concentration of CO can generate a large amount of COHb. COHb cannot carry oxygen and is not easy to dissociate. It is 1/3600 of the dissociation rate of oxyhemoglobin (O2Hb). The presence of COHb can also shift the oxygen dissociation curve of hemoglobin to the left. Blood oxygen is not easily released to tissues, resulting in cellular hypoxia.

In addition, high concentrations of CO can also bind to myosin containing ferrous iron, affecting the diffusion of oxygen from capillaries to mitochondria in cells, impairing mitochondrial function. Combined with CO and the divalent iron of reduced cytochrome oxidase, it inhibits the activity of cytochrome oxidase, affects the process of cellular respiration and oxidation, and hinders the utilization of oxygen. However, the affinity of oxygen and cytochrome oxidase is greater than that of CO. The degree of tissue hypoxia is proportional to the percentage of COHb in blood. The COHb% in blood is closely related to the CO concentration in the air and the contact time.

In CO poisoning, organs with few vascular anastomotic branches and vigorous metabolism, such as brain and heart, are most vulnerable to damage. The small blood vessels in the brain are rapidly paralyzed and dilated. Adenosine triphosphate (ATP) in the brain is rapidly depleted in the absence of oxygen, the sodium pump does not work well, and sodium ions accumulate in the cells and induce edema in the brain cells. Hypoxia causes vascular endothelial cells to swell and cause brain circulation disorders.

During hypoxia, the accumulation of acidic metabolites in the brain increases vascular permeability and produces interstitial edema of brain cells. Cerebral blood circulation disorders can cause cerebral thrombosis, focal ischemic necrosis of the cerebral cortex and basal ganglia, and extensive demyelinating lesions, resulting in delayed encephalopathy in a small number of patients.

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