Obstructive Sleep Apnea Syndrome (OSAS) is a common and potentially dangerous sleep disorder that has received increasing attention in the last decade or so. Obstructive sleep apnea can affect the function of various systems and organs of the body. In this paper, we will elaborate on the relationship between obstructive sleep apnea and digestive disorders, especially gastroesophageal reflux (GER). The esophagus and the respiratory system are very closely related. There are many commonalities and interactions between the two, from embryogenesis to function. Embryogenesis of the esophagus, tracheobronchus and lungs all originate from the posterior part of the foregut, so they are very close in anatomical location. Dysfunction of one organ can often lead to alterations in the other organ, e.g., pressure changes in the pleural cavity can be transmitted to the esophagus, and similarly, the transport of food masses in the esophagus and its peristaltic waves can affect the function of the lungs. The trachea and esophagus both start in a common lumen, the pharyngeal cavity, and the esophagus is the channel for transporting food (groups or liquids) to the digestive organs, while the trachea is the channel for transporting air to the alveoli. Therefore, a precise and quantitative regulatory mechanism is needed in the central nervous system to coordinate the activities of the trachea and esophagus, and if this protective coordination mechanism fails, it can have various serious consequences for the organism. Because of this special anatomical and physiological relationship between the esophagus and the respiratory system, scholars have been working on the interrelationship between the two systems in recent decades and have reported the presence of various respiratory disorders in patients with GERD, such as apnea and SIDS in children, pulmonary fibrosis and recurrent pharyngitis in adults, recurrent pneumonia, recurrent bronchitis, bronchiectasis and chronic refractory bronchitis in both children and adults. bronchiectasis and chronic refractory asthma in children and adults. The relationship between sleep apnea and nocturnal gastroesophageal reflux has been the subject of interest in recent years. At present, the relationship between apnea and GER in infants and children and its mechanism are widely studied, but relatively little research has been done in adults, whether the relationship is causal or concomitant, or whether the lesion is at a higher level, further research and discussion are needed. I. GER and Apnea in children In recent decades, interest in the relationship between esophageal and respiratory diseases in children has focused on GER, apnea, and sudden infant death syndrome (SIDS). Although there appears to be no clinical doubt that apnea (central or obstructive) is secondary to esophageal reflux, most well-controlled studies have not confirmed a definite causal relationship between the two. As early as 1954, Forshall reported two cases of infants who died from asphyxia caused by vomitus. Since then, it has been extensively studied, but there has been no consensus for a long time. Many authors have claimed that prolonged asphyxia is associated with the development of GER and reported the occurrence of GER in apnea. Ramet et al. demonstrated that balloon dilation and acid injection of the distal esophagus during active sleep in infants can cause apnea. However, the immediate relationship between reflux and apnea could not be confirmed and was denied by other authors. They argue that since both GERD and apnea occur more frequently in infants, it is more likely that they are present together. Benhamon et al. suggested that GER may cause apnea by stimulating the vagus nerve. It has been found that drops of acid in the larynx of anesthetized newborn lambs induce apnea and hypoventilation. Orr et al. also suggested that there is some primary alteration in the ability of children with pathological reflux to awaken from sleep under acid reflux stimulation, which prevents the body from preventing or eliminating the occurrence of sleep reflux. However, Sondheimer et al. studied the changes in EEG of infants with GER during sleep and noted that there was no difference in sleep patterns between the pathological GER group and the control group, and that the amount of awakenings did not decrease in the former group. It was the correlation between GER and obstructive sleep apnea found in children near death (near-miss) that led to further speculation on the existence of a relationship between GER and apnea in adults, first investigated by Tardif et al. Samelson suggested that obstructive sleep apnea should be the cause of GERD, and that the significant negative intrathoracic and intraesophageal pressure in patients with obstructive sleep apnea is a fundamental pathophysiological feature, and that once this pressure exceeds the tone of the gastroesophageal sphincter, gastric contents can be aspirated into the esophagus. Once this negative pressure exceeds the tension of the gastroesophageal sphincter, the stomach contents can be aspirated into the esophagus. If this speculation is valid, gastroesophageal reflux should be very common in obstructive sleep apnea, and Heinemam et al. performed 24-hour esophageal pH monitoring in 30 patients with sleep apnea and confirmed that about 70% of them had pathological reflux. A survey of 150 cases of nocturnal sleep apnea monitored for snoring by Meiyun Ke et al. also showed that 59% of hypoventilated sleep apnea patients had significant GERD symptoms. Repeated reflux can delay or prevent acid removal from the lower esophagus, and prolonged GERD can lead to serious consequences, such as mucosal erosion, damage to the muscular wall resulting in scar stenosis, or in more severe cases, mucosal metaplasia that may lead to tumor formation requiring esophagectomy and gastrectomy, etc. The causal relationship between obstructive sleep apnea and GERD was well demonstrated by Kerr et al. Although they were not able to confirm the immediate relationship between the occurrence of apnea and gastroesophageal reflux, their findings suggest that decreased intraesophageal pH is closely associated with arousal, somatic activity, and decreased intrathoracic pressure, which is secondary to apnea. Since Sullivan et al. introduced nasal continuous positive airway pressure (nCPAP) for the treatment of sleep apnea syndrome in 1981, many patients have benefited from this treatment. A large number of clinical and research studies have demonstrated the effectiveness of nCPAP in the treatment of OSA, and it has become the primary and fundamental non-surgical long-term treatment for OSA patients. The mechanism of nCPAP is to maintain a certain positive pressure in the upper airway during sleep, which is like adding a pressure “splint” to the upper airway to keep the upper airway open, prevent its collapse and avoid the occurrence of apnea. nCPAP treatment is mainly characterized by increasing the pressure in the oropharyngeal airway, thus reversing the pressure gradient through the wall of the pharyngeal cavity. The pressure gradient is reversed. Since there are many important reflexes in the upper airway, nCPAP is also likely to have a reflex pattern that may alter the activity of the upper airway muscles. When the upper airway is subjected to a “sucking” pressure, the reflexes of the upper airway dilators, such as the chin-lingual muscle, are enhanced; however, positive upper airway pressure can suppress the electromyographic activity of the pharyngeal dilators. Studies have shown that the lingual muscle electromyography is suppressed during nCPAP treatment, and therefore the reflexes induced by nCPAP can exacerbate rather than reduce upper airway obstruction. Of course, this inhibition is weak, and nCPAP provides a pressure to open the upper airway, which is its main role in the successful treatment of OSA. In addition to OSA and CSA, nCPAP is also widely used for the treatment of sleep apnea, nocturnal asthma, and severe snoring with chronic lung disorders. In the study of GER in OSAS combined with GER, it was found that general antacid medication did not relieve its symptoms of nocturnal GER. Based on the hypothesis of the mechanism of GER in OSAS, nCPAP was tried to treat nocturnal GER by increasing the negative intraesophageal pressure. nCPAP was found to eliminate apnea and control the symptoms of reflux esophagitis in five patients with severe GER in SAS, and even weaned one patient from antacids. Kerr et al. also showed that nCPAP significantly reduced the mean frequency and duration of nocturnal GER in OSA, which led to the speculation that nCPAP may also have therapeutic effects in other types of nocturnal GER. It is thought that the anti-reflux effect of nCPAP may result from a passive increase in intraesophageal pressure and possible reflex contraction of the LES.