Throughout the entire process of body metabolism, the acid produced exceeds the base produced, therefore, the buffering acid function often becomes the basic contradiction. The key substance of buffering acid is also NaHCO3/NaCO3, in which NaHCO3 is the key. If the body produces too much acid, the content of NaHCO3 will decrease. Therefore, by mastering the content of NaHCO3 in the blood, one can indirectly understand the condition of strong acid and strong alkali in the body. Since NaHCO3 is not easy to measure directly, in clinical medicine, it is generally used to measure the carbon dioxide with a carbon dioxide measuring instrument, add a certain amount of acid (such as lactic acid bacteria) to the blood for quantitative analysis, and react with the NaHCO3 in the blood to release CO2. The amount of CO2 released is measured and converted into the amount of CO2 released per 100ml of blood, which is called the blood CO2 binding capacity or CO2 fusion amount.

Standard value of carbon dioxide binding

The standard value of carbon dioxide binding: 50-62.7 volume% or 50-70 volume%.

Why does the binding of carbon dioxide decrease during metabolic acidosis of respiratory acidosis, while the binding capacity of carbon dioxide increases during respiratory metabolic acidosis?

Metabolic acidosis caused by the accumulation of non-volatile acidic substances in the body or excessive loss of alkaline substances. At this time, the acidic substances in the body are first converted into H2CO2 in the buffering system and then decomposed, with part of them being exchanged with K and Na, and H2CO3 with Cl- to enter the cell. The HCO3- is then transported to the pulmonary capillaries by the hemoglobin concentration system, converted into CO2, and exhaled from the lungs. Therefore, the CO2-C.p decreases. In cases of respiratory dysfunction, the acidic substances produced by the body’s metabolism remain in the buffering system as CO2, leading to a higher proportion of carbonic acid to sodium bicarbonate than the normal 1:20, resulting in a decrease in blood pH and the development of respiratory metabolic acidosis, with an increase in CO2-C.p.