Long-term oxygen therapy is beneficial in increasing patient survival, improving quality of life and neuropsychiatric status, reducing erythrocytosis, preventing nocturnal hypoxemia, improving sleep quality, preventing the development of pulmonary heart disease and right heart failure as well as reducing medical costs including the number of hospitalizations and hospital days. (i) Correction of hypoxemia and slowing down the deterioration of pulmonary function Long-term oxygen therapy can correct hypoxemia in patients with chronic hypoxia without significantly aggravating carbon dioxide retention and can also have a beneficial effect on pulmonary function. goldstein et al. observed the effect of nocturnal oxygen therapy on blood gases in eight patients with stable pulmonary heart disease and compared it with the non-oxygenated group. The results found that nocturnal oxygen therapy could maintain SaO2 above 0.90 and that arterial partial pressure of carbon dioxide (PaCO2) increased only mildly during sleep, usually <0.8 kPa (6 mmHg), mostly occurring in the first half of the night and not progressively. The mild increase in PaCO2 during nocturnal oxygen therapy in steady-state patients with chronic obstructive pulmonary disease is not considered clinically important. In normal adults the decrease in exertional expiratory volume in one second averages 30-40 ml/year, and in patients with COPD the decrease is even greater, about 50-100 ml/year, and the continued deterioration of pulmonary function is delayed after the implementation of oxygen therapy. (b) Lowering pulmonary artery pressure and delaying the progression of COPD Long-term oxygen therapy can lower pulmonary artery pressure and reduce or reverse the deterioration of pulmonary hypertension. desaturation). The patients were randomized into two groups using a double-blind method. In the first group, 19 cases were administered with an oxygen concentrator with an oxygen flow rate of 3 L/min; in the second group, 19 cases actually inhaled room air with a disguised oxygen concentrator; and in the third group, 13 cases inhaled room air directly. Both the first group and the second group were patients with sleep hypoxemia. The results showed that the mean reduction in pulmonary artery pressure in the first group was 0.49 kPa (3.7 mmHg), while the mean increase in pulmonary artery pressure in the second group was 0.52 kPa (3.9 mmHg). The effect of long-term oxygen therapy on pulmonary artery pressure is influenced by the following factors: ① time of oxygen therapy: the longer the duration of oxygen therapy per day, the more significant the improvement in pulmonary artery pressure; ② level of pulmonary artery pressure: long-term oxygen therapy is more effective for mild to moderate pulmonary hypertension; ③ individual variability: there is individual variability in the response of patients with COPD to hypoxia and oxygen therapy. Daily oxygenation for 15h or more can correct the deterioration of pulmonary hypertension in most patients with severe COPD. In fact, however, it is not entirely clear whether there are potentially reversible factors in the structural alterations of the small blood vessels of the lungs in COPD or whether such vascular structural alterations are exclusively the result of chronic hypoxia. It has been observed that pulmonary artery pressure increases progressively year by year before the start of long-term oxygen therapy, and gradually returns to the initially observed level during the years after the start of long-term oxygen therapy, but still does not drop to normal. Therefore, it is safe to say that long-term oxygen therapy stabilizes or interrupts the development of pulmonary hypertension and may relieve it in some patients. In addition, long-term oxygen therapy may also reduce red blood cell pressure and blood viscosity, as well as increase cardiopulmonary oxygen supply, further improving cardiac functional status and consequently delaying the progression of COPD. The effect of long-term oxygen therapy in reducing erythrocyte pressure in patients with COPD often appears 4-6 weeks after oxygen therapy, and the higher the erythrocyte pressure before oxygen therapy (≥0.55) (iii) Improved survival In 1980, the North American Nocturnal Oxygen Therapy Trial Group (NOTT) reported the results of 203 patients with COPD hypoxemia in 6 centers who underwent continuous nocturnal oxygen therapy with a mean follow-up of 19.3 months. The results found that the 1-year morbidity and mortality rate was 20.6% and 40.8% at 2 years in the nocturnal oxygen therapy group (12 h of daily nocturnal oxygen administration), while the 1-year morbidity and mortality rate was 11.9% and 22.4% at 2 years in the continuous oxygen therapy group (at least 19 h of continuous daily oxygen administration). The relative risk factor for death was 1.94 times higher in the nocturnal oxygen therapy group than in the continuous oxygen therapy group. The mechanism by which long-term oxygen therapy improves prognosis is not well understood and may be related to the following factors: ① Improved pulmonary hemodynamics: reduced pulmonary vascular resistance and stabilization of pulmonary artery pressure, which avoids continuous and continued deterioration of pulmonary artery pressure. After long-term oxygen therapy most patients have reduced pulmonary vascular resistance and pulmonary artery pressure, increased cardiac output and cardiac index, and reduced right heart failure. ② Correction of hypoxemia: In severe hypoxia, the relationship between PaO2 and SaO2 is in the part of the slope of the oxygenated hemoglobin dissociation curve that has the greatest slope, and a slight decrease in PaO2 can cause a large decrease in SaO2. Any cause such as sleep, aggravation of ventilatory dysfunction and ventilation/blood flow ratio disorders can cause a rapid drop in SaO2 and lead to cardiac arrhythmia and myocardial infarction, which can be fatal. Long-term oxygen therapy can maintain PaO2 above 8.0kPa (60mmHg), which can avoid or reduce the occurrence of the above conditions. (iv) Improve the quality of life Long-term oxygen therapy can not only reduce dyspnea at rest, but also reduce shortness of breath after activity, increase the range of daytime activities and improve exercise endurance. Long-term oxygen therapy patients have a decreased incidence of respiratory failure, fewer hospitalizations, reduced symptoms, improved sleep, and improved psychological and mental status, resulting in improved quality of life. (E) Improvement of neuropsychiatric symptoms Long-term chronic hypoxia patients may show inattention, memory and intellectual impairment, disorientation, headache, drowsiness, irritability and other manifestations. The severity of neuropsychiatric symptoms is related to the degree of chronic hypoxemia. Long-term oxygen therapy can improve the hypoxic state of the brain and reduce neuropsychiatric symptoms. In conclusion, the goal of long-term oxygen therapy is to prevent or reduce the adverse effects of chronic hypoxia, to restore normal activity levels, and to achieve the goal of applying portable oxygen devices for walking or traveling away from home.