Oxygen debt (also known as exercise excess oxygen consumption) is the difference between oxygen demand and actual oxygen supply, and is commonly used in sports medicine [5]. The fever and strong immune response caused by virus infection will inevitably lead to the increase of metabolic rate and oxygen demand. At the same time, however, the persistent hypoxemia caused by lung histopathology of NCP reduces the oxygen supply of the lungs and lungs to the tissues and organs of the whole body. Therefore, when the NCP disease develops to a certain extent, there must be a gap between oxygen demand and oxygen supply, which can also be understood as a special “oxygen debt”. Studies have found that under certain intensity of exercise load, preexisting lung diseases can lead to hypoxemia [6]. In this case, the SO2 before HBOT entered the cabin was significantly lower than that before under the condition of oxygen inhalation in the ward mask (at 08:00), which was caused by the fact that the patient could not absorb oxygen and increased a certain amount of activity during the process from the ward to the HBOT department. As a result, the oxygen intake decreased and the consumption increased, SO2 decreased. This phenomenon suggested that pathological changes in the lungs resulted in a serious imbalance between oxygen demand and oxygen supply in the patient. Arterial blood gas analysis before the first entry of HBOT on February 11 suggested that the blood lactic acid content was significantly increased (3.03mmol/L), suggesting that the patient was in a state of severe anaerobic metabolism.

HBOT based on gas physics characteristic, through the great increase in oxygen partial pressure, reach the cardiopulmonary function in the same condition, the increase of alveolar oxygen partial pressure, increase the blood oxygen tension, increase effective diffusion radius of tissue oxygen, increase oxygen transport capacity, so as to achieve correct hypoxia (1) valid thoroughly at the same time, improve the acidosis, and organize the cell vitality, enhance (2) after the reoxygenation of capillary endothelial cells, the capillary function can be restored and the exudation and edema caused by hypoxia can be blocked. (3) increase the effective diffusion radius of tissue oxygen, correct tissue hypoxia and increase tissue oxygen reserve [2]. The blood gas analysis results of this patient after the first time HBOT went out of the cabin showed that PO2 increased from 37.0mmHg before entering the cabin to 69.0mmHg, showing a good effect of HBOT correction, but there was an obvious gap with the normal value, and SO2 only increased to 90%. This state before entering the cabin can best reflect the degree of hypoxia of the patient’s systemic tissues and organs. The ultimate goal of clinical oxygen therapy is to solve the hypoxia state of the body. This result suggested that the accumulation of “oxygen debt” in the early stage of the patient exceeded the ability of one HBOT to correct, which further reflected the imbalance of oxygen demand and oxygen supply in the patient’s body.

After the patient left the capsule for 90 minutes (at 12:00), the oxygen saturation of the patient significantly decreased, indicating that the tissue oxygen reserve increased by the physical dissolution of HBOT was exhausted in a very short time. On the whole, however, the daily mean SO2 of HBOT patients increased steadily. Can’t use HBOT residual oxygen explanation, the possible mechanism on the one hand is to provide the body’s aerobic HBOT intermittent (before metabolism of anaerobic – aerobic metabolism in the treatment after – treatment of anaerobic metabolism), greatly improved the body tissue tolerance ability of anaerobic metabolism, mechanism of similar HBOT intermittent oxygen oxygen toxicity tolerance of [2]. In addition, for example, the significant increase of d-dimer, plasminogen and TDP in the hematological indicators of this patient suggested that the patient had existed a certain degree of disseminated intravascular coagulation (DIC) prior to HBOT, which can be secondary to viral infection. There were peripheral hemodynamic changes and perfusion disorders. The change of coagulation index in this patient also suggested the obvious role of HBOT in improving terminal circulation and improving oxygen supply to tissues. Whether DIC combined with persistent hypoxemia leads to ischemic loss and tissue edema of capillary endothelial cells in the peripheral circulation and whether it is a common phenomenon in patients with severe NCP requires more clinical studies and observations.

In this case, due to the lack of medical care in the cabin, oxygen was inhaled for 95min from the beginning of pressurization to the end of decompression. Oxygen poisoning has always been an important problem for many hyperbaric oxygen clinicians in the application of HBOT. The human body is adapted to the environment of 20kPa oxygen partial pressure under atmospheric air, and it will inevitably have an impact when exposed to HBOT’s high pressure oxygen. Due to the necessity of breathing the mixed gas or oxygen with high pressure oxygen during diving, the diving program was designed by limiting the exposure dose of high pressure oxygen to avoid large lung type oxygen poisoning injury [2]. The high oxygen exposure dose of conventional HBOT is about 150 UPTD. In this case, the exposure dose was 216 UPTD, but still much less than 615 UPTD. This dose represents a reduction in lung capacity of approximately 1%, the safe limit for conventional high pressure oxygen exposure. Therefore, the patient’s HBOT did not have to worry about the risk of pulmonary oxygen poisoning.

In this case, CT reexamination after 8 HBOT showed that although the pulmonary lesions of the patient were significantly improved, the lesions were still obvious. However, the patient’s SO2 remained in the normal range under the condition of oxygen inhalation by nasal catheter. Separation phenomenon in this lung pathological changes and SO2, prompt HBOT although not directly to clear effect to the disease (virus), but it provides powerful oxygen cure, as the direct cause of lung tissue pathology may lead to continuous hypoxemia, especially the state of the oxygen to body tissues and organs of oxygen debt continues to accumulate, and its important oxygen consumption of tissues and organs of the secondary injury, keep the function of the body is relatively good state, for the body against infection systemic function provides a good foundation.

To sum up, according to the pathological characteristics of NCP, HBOT has a clear mechanism of excellent action different from atmospheric oxygen therapy. Conventional HBOT has been widely used in clinical practice for decades and has a strong therapeutic capacity. On the premise of solving the transfer process sensing control, large-scale treatment of NCP patients can fundamentally solve the problem of supporting treatment of progressive hypoxia that cannot be contained by current atmospheric pressure oxygen therapy, so as to achieve the expected effect of reducing the critical disease rate and mortality. From the changes in the clinical manifestations and examination results of this patient, it can be seen that 1 HBOT can significantly improve the severe and critical NCP patients whose daily average SO2 is still lower than 80% under the condition of atmospheric pressure oronasal mask and high flow oxygen absorption, and 4 HBOT can basically correct the persistent hypoxemia in critically critical patients. According to the existing critical disease NCP stock in wuhan, in the use of clinical HBOT, measures and practices of combining HBOT with atmospheric oxygen therapy can be further explored to comprehensively improve the treatment efficiency of large Numbers of patients.