In the decompensated stage of chronic respiratory failure, the diagnosis is not difficult based on the patient’s history of chronic diseases of the respiratory system or other medical conditions causing respiratory dysfunction, clinical manifestations of O2 deficiency and/or CO2 retention, combined with relevant physical signs. Arterial blood gas analysis can objectively reflect the nature and degree of expiratory failure, and is of great value in guiding oxygen therapy, regulation of various parameters of mechanical ventilation, and correction of acid-base balance and electrolytes. I. Arterial partial pressure of oxygen (PaO2) refers to the pressure generated by the oxygen molecules physically dissolved in the blood. PaO2 in healthy individuals decreases gradually with age and is subject to physiological influences such as body position. According to the relationship between partial pressure of oxygen and oxygen saturation, oxygenated hemoglobin dissociation curve is in S shape, when PaO2>8kPa(60mmHg) or more, the curve is in flat section, oxygen saturation is above 90%, PaO2 changes 5.3kPa(40mmHg), while oxygen saturation changes very little, indicating that partial pressure of oxygen is far more sensitive than oxygen saturation; but when PaO26.6kPa( 50 mmHg), the pH is already below 7.20 according to Henderson-Hassellbalch formula, which will affect the circulation and cellular metabolism. Chronic respiratory failure due to the compensatory mechanism of the body, PaCO2>6.65kPa(50mmHg) as a diagnostic indicator of respiratory failure. Second, pH is the negative logarithmic value of hydrogen ion concentration in the blood. The normal range is 7.35-7.45, with an average of 7.40. Below 7.35 is decompensated acidosis, above 7.45 is decompensated alkalosis, but it does not indicate the nature of acid-base toxicity. Clinical symptoms are closely related to the pH excursion. C. Base excess (BE) The amount of acid-base required to titrate blood to pH 7.4 at 38℃, partial pressure of CO2 5.32kPa (40mmHg), and oxygen saturation amount of 100%. It is a quantitative indicator of metabolic acid-base imbalance in human body. A positive value of BE with acid addition is metabolic alkalosis; a negative value of EB with base addition is metabolic acidosis. The normal range is 0±2.3 mmol/L. It can be used as a reference for estimating the dose of antacid or anti-base drugs when correcting metabolic acid-base imbalance. Buffer base (BB) is the total content of various buffer bases in blood, including bicarbonate, phosphate, plasma protein salts, hemoglobin salts and so on. It reflects the buffering capacity of the body against acid-base interference and the specific situation of the body’s compensation for acid-base imbalance. The normal value is 45mmol/L. V. Actual bicarbonate (AB) AB is the amount of bicarbonate contained in human plasma under the actual partial pressure of carbon dioxide and blood oxygen saturation. The normal value is 22-27mmol/L, with a mean value of 24mmol/L. HCO3-content is related to PaCO2, and as PCO2 increases, plasma HCO3-content also increases. On the other hand, HCO3 is one of the plasma buffer bases. When there is too much fixed acid in the body, the pH can be stabilized by HCO3-buffering and the HCO3-content is reduced. Therefore, AB is affected by both respiration and metabolism. Standard bicarbonate (SB) refers to the plasma bicarbonate (HCO3-) content measured in whole blood specimens isolated from air, at 38℃, with PaCO2 of 5.3kPa and hemoglobin 100% oxygenated, with a normal value of 22-27mmol/L and an average of 24mmol/L. SB is not affected by respiratory factors, and the increase or decrease of its value reflects the amount of HCO3- reserves in the body, thus indicating the tendency and extent of metabolic factors. The SB decreases in metabolic acidosis and increases in metabolic alkalosis, and when AB > SB, it indicates CO2 retention. Carbon dioxide binding capacity (CO2CP) The normal value is 22-29mmol/L, which reflects the main alkali reserve in the body. CO2CP decreases in metabolic acidosis or respiratory alkalosis, and increases in metabolic alkalosis or respiratory acidosis. However, when respiratory acidosis is accompanied by metabolic acidosis, CO2CP does not necessarily increase, because in respiratory acidosis, the kidney excretes H+ in the form of NH4+ or H+ and absorbs back HCO3- for compensation, and the base reserve increases, so the increase of CO2CP reflects the severity of respiratory acidosis to some extent, but it cannot reflect the rapid change of CO2 in blood in time. It is also affected by metabolic alkali or acidosis, so CO2CP has its one-sidedness and must be considered comprehensively in conjunction with clinical and electrolytes. Among these indicators, PaO2, PaCO2 and pH are the most important, reflecting the lack of O2 and CO2 retention in respiratory failure, and the acid-base imbalance, and if BE is added, it can reflect the body’s compensation, the presence of combined metabolic acid or alkaline toxicity, and electrolyte disorders.