About 80% of patients have significant bradycardia, 57%-74% have ventricular ectopic beats, 5%-16% have second-degree AV block, and 2% have third-degree AV block. Ventricular ectopic beats are significantly correlated with arterial SaO2, and Shephard et al. found that the incidence of ventricular prematureness was three times higher in those with SaO2 < 60% than in those with SaO2 > 90%. The vagus nerve is excited during the transition from NREM to REM sleep and during apnea, resulting in slow arrhythmias such as QT interval prolongation, conduction block, and cardiac arrest, while sympathetic excitation at the end of apnea results in tachyarrhythmias due to a lower threshold of myocardial ectopic excitation, which is often the main cause of sudden death in patients with OSAHS. The vagus nerve and sympathetic nerve are periodically excited, and slow and fast arrhythmias alternate. The degree of heart rate slowing is related to the duration of the apnea and the degree of oxygen saturation drop. Increased neurally mediated vagal activity slows the heart rate, while atropine relieves or eliminates bradycardia. The sudden increase in heart rate at the end of apnea may be the result of hypoxemia and a decrease in vagal tone and an increase in sympathetic tone in response to arousal. Decreased oxygen saturation in fast-acting sleep and apnea is an independent causative factor for the development of heart block in patients with OSAHS. The shift from vagal to sympathetic excitation-dominated processes decreases the threshold of myocardial ectopic excitation points and is a major cause of ectopic arrhythmias and sudden death. In upper airway obstruction, the respiratory effort to counteract upper airway occlusion increases negative thoracic pressure, thereby prolonging apnea and directly increasing vagal tone. In addition, indirect stimulation of the vagus nerve through volume changes leads to alterations in heart rate, blood pressure, cardiac output per bo, pressure receptors and intracardiac mechanoreceptor reflexes. Several observations have confirmed that patients with OSAHS complicated by second- or third-degree AV block improved significantly with nCPAP treatment. In contrast, serious complications such as heart failure can occur in untreated cases, despite the presence of a pacemaker? Apnea-related bradycardia leads to decreased myocardial oxygen consumption, increased diastolic time, and improved myocardial oxygen supply. Bradycardia during apnea is therefore considered to be a protective mechanism for the heart to conserve oxygen consumption. However, excessive bradycardia can impair myocardial blood perfusion. It aggravates myocardial ischemia in patients with coronary artery disease, causing ventricular flutter and ventricular fibrillation. Therefore, severe hypoxia during sleep may be an important risk factor for the development of severe arrhythmias in patients with OSAHS or OSAHS combined with coronary artery disease.