The basic pathogenesis of obstructive sleep apnea hypoventilation syndrome (OSAHS) is sleep-state-dependent collapse of the upper airway and the resulting intermittent hypoxia with hypercapnia, which eventually leads to fluctuations in oxygen saturation and hemodynamic changes, and its pathophysiological process is closely related to hypertension, coronary heart disease, diabetes mellitus, cerebrovascular disease and other diseases. Noninvasive ventilation therapy is the most effective therapy for OSAHS. Currently, the commonly used clinical ventilation modes are continuous positive pressure ventilation (CPAP) and bi-level positive pressure ventilation (BiPAP). We admitted a patient with severe OSAHS who was treated well with CPAP, but developed central apnea (CSA) and periodic breathing (PB) after being discharged home and switched to BiPAP ventilator. Case report The patient was male, 60 years old. History of snoring for more than 10 years, intermittent nocturnal paroxysmal breath-holding, morning dizziness, and no significant daytime drowsiness. He had a history of hypertension for 15 years, with a maximum of 160/100 mmHg, and was usually treated with oral lorazepam; no diabetes mellitus, etc. He was admitted to the hospital on September 28, 2012 for breath-holding. No other cardiopulmonary disease was found. No other cardiopulmonary disease was found. polysomnography (PSG) on October 8 showed a minimum SpO2 value of 66%; apnea and hypoventilation index of 49.6 breaths/h, of which 43.4 breaths/h for obstructive, 1.7 breaths/h for central, 0.4 breaths/h for mixed, and 4.2 breaths/h for hypoventilation. upper airway examination showed no significant abnormalities. A diagnosis of severe OSAHS and severe hypoxemia was made. Ventilator pressure titration was performed. With the application of CPAP (pressure of 9.5 cmH2O), the patient had a respiratory disturbance index of 4.6 breaths/h and a minimum SpO2 value of 87%, so he was recommended to go home with CPAP ventilator therapy. The patient was discharged home and was followed up by telephone 1 month later. It was found that the patient considered BiPAP to be more comfortable when selecting a ventilator, so the BiPAP-ST ventilator was finally selected for home treatment, with parameters set to 8-12 cmH2O pressure and a backup ventilation frequency of 10 breaths/min. 3 months after treatment, the patient came to the hospital and wore the machine to recheck the PSG, and no apnea The patient’s respiratory rhythm was unstable with fluctuations in blood oxygen and an oxygen decrement index of 9.2 breaths/h. The reason for the patient’s fast and slow respiratory rhythm was considered to be the CSA caused by the application of BiPAP, which triggered backup ventilation and resulted in slower breathing in forced ventilation mode with decreased blood oxygen. Accordingly, the patient was re-titrated to segmental pressure, i.e. BiPAP-ST for 2 h, BiPAP-S for 2 h, and CPAP for 2 h. When BiPAP-ST [inspiratory pressure (IPAP) 12 cmH2O, expiratory pressure (EPAP) 8 cmH2O, and backup ventilation frequency 10 breaths/h)] was given, the patient’s respiratory disturbance index was 1.6 breaths/h, but there was periodic breathing ( PB) with progressively larger and smaller tidal volumes; when BiPAP-S (autonomous ventilation mode with 12 cmH2O for IPAP and 8 cmH2O for EPAP) was given, there was more central apnea (CSA). The total respiratory disturbance index was 5.6 breaths/h and the central apnea index was 4.9 breaths/h. When CPAP was given at 8.5 cmH2O, the respiratory disturbance index was 0.8 breaths/h and the respiratory rhythm was regular, with no periodic breathing or central apnea. Therefore, the patient was recommended to apply CPAP ventilator with a pressure of 8.5 cmH2O. Discussion Noninvasive ventilation therapy is the most effective therapy for OSAHS, and the most clinically used is CPAP, which is stable in efficacy, easy to use, and less expensive. With the development of noninvasive ventilation technology, BiPAP is widely used clinically for its high comfort and can be used for OSAHS, obesity hypoventilation (OHS) [1], neuromuscular disease [2], and overlap syndrome [3] that cannot tolerate CPAP therapy. Compared to CPAP, BiPAP has two pressures (inspiratory and expiratory) and patients are more comfortable when breathing; however, it is also because of the pressure difference between inspiratory and expiratory pressures, superimposed on the patient’s basal tidal volume, which corresponds to a greater ventilatory response with a fixed respiratory drive. Does this have an impact on the patient’s respiratory regulation? Hommura et al [4] reported a 57-year-old patient with severe OSAHS whose CSA did not improve or even worsened when treated with BiPAP; and keeping the expiratory pressure of BiPAP constant, the higher the inspiratory pressure was adjusted, the worse the CSA. Since then, similar reports have been rare. Until 2005, Johnson et al [5] investigated the effects of BiPAP and CPAP, and the authors classified the respiratory forms of central respiratory regulation instability into 3 types of respiration: stale breathing (CSR), periodic breathing (PB), and central apnea (CSA).CSR refers to the repeated cycle of respiratory effort decreasing from strong to weak until the appearance of central apnea.PB refers to the repeated cycle of respiratory The PB is a periodic increase and decrease in respiratory effort without a central apnea, and the CSA is a respiratory apnea without thoracoabdominal movements and without a gradual change in respiratory effort before or after the apnea. This study reported 719 patients with sleep breathing disorders requiring the application of ventilator therapy, of which 95 met the enrollment criteria and entered the process of comparing the efficacy of CPAP and BiPAP, which included 77 patients with obstructive sleep apnea (OSA) and 18 patients with predominantly Chenischian breathing. With the application of BiPAP, the patients had more central respiratory disturbances (including CSR, CSA and PB) after treatment compared with baseline values without ventilator and with CPAP, and the greater the BiPAP pressure difference, the more patients with central respiratory disturbances (CSR, CSA) occurred; while in the improvement of obstructive apnea, hypoventilation and oxygen reduction index, the comparison between BiPAP and CPAP did not There was no statistical difference between BiPAP and CPAP in improving obstructive apnea, hypoventilation and oxygen reduction index. Central respiratory disturbances are associated with respiratory deregulation. CSR is often associated with heart failure, stroke and high altitude, with approximately 50% of heart failure patients having CSR, and heart failure patients with delayed circulatory time, increased respiratory drive secondary to interstitial pulmonary edema and reduced lung volumes predispose to CSR. It was found that BiPAP increases the incidence and severity of central respiratory disturbances through the following mechanisms, namely, for each specific respiratory effort, BiPAP ventilatory support increases the ventilatory response, leading to a hyperventilated state; the greater the BiPAP pressure difference, the heavier the hyperventilation, and the more likely it is that PCO2 will fall below the apnea threshold and thus apnea will occur.Asyali et al [6] proposed Asyali et al [6] proposed the loop gain theory of respiratory regulation to describe the loop mechanism of respiratory regulation. This theory suggests that the greater the loop gain of respiratory regulation, the more unstable the respiratory regulation is. The mechanism by which BiPAP exacerbates respiratory instability can also be explained by this model: BiPAP increases the gain of the effector (plant gain), resulting in a greater ventilatory effect of a specific respiratory drive, leading to an increase in the loop gain of respiratory regulation and causing respiratory instability. In addition to this, large tidal volumes can also lead to apnea through neuro-chemical inhibition mechanisms while maintaining CO2 partial pressure at normal levels. CPAP, on the other hand, can increase respiratory drive and stabilize the pharynx by stimulating upper airway mechanoreceptors, while increasing blood CO2 levels and stabilizing breathing to reduce or eliminate central apnea. Clinically, not all patients with OSAHS develop or exacerbate CSA with BiPAP, and the vast majority show good efficacy with BiPAP pressure titration under PSG, and it is not true that patients with CSR and other central respiratory disturbances cannot use BiPAP. numerous studies have shown that heart failure patients with CSR have significantly reduced CSR and other concomitant respiratory disturbances with BiPAP. This suggests that the effect on respiratory regulation due to increased ventilation by BiPAP is limited to certain patients whose central chemoreceptors are overly sensitive to fluctuations in partial pressure of CO2. However, it is not clear what causes chemoreceptor sensitivity, what population is susceptible to CSA, and what are the characteristics of PSG results that produce CSA. Moreover, is the phenomenon transient? Is it possible to receive BiPAP treatment again after a period of CPAP application and respiratory drive stabilization? Many other questions remain to be further investigated. In conclusion, there is no doubt about the advantages of BiPAP, which is particularly suitable for patients with OHS, neuromuscular disease and CSA due to cerebrovascular disease; however, BiPAP may be one of the factors aggravating central respiratory disturbances in some patients with sensitive central chemoreceptors. Therefore, before applying a ventilator in patients with OSAHS (even without any comorbidities), ventilator pressure titration should be performed under PSG to determine the appropriate therapeutic pressure and ventilation pattern.