Additionally, some studies have found that OSA increases an individual's susceptibility to potentially life-threatening atrial and ventricular arrhythmias. Obstructive sleep apnea has been found to be 18 times more likely to cause cardiac arrhythmias than normal breathing. The mechanism of this adverse effect is not fully understood; however, it has been suggested that OSA creates an imbalance between sympathetic and vagal activity during sleep, which plays a major role in generating or exacerbating cardiac rhythm disturbances. Obstructive events can also lead to hypoxia, which in the case of obstruction can cause reflex bradycardia and increase blood pressure. In addition, hypoxia is associated with increased oxidative stress and the production of reactive oxygen species, which can lead to cell damage, ischemia, and abnormal myocardial excitability. These changes may induce atrial and ventricular arrhythmias. Furthermore, increased intrathoracic negative pressure causes acute stretching of the myocardial wall and intrathoracic vessels, as evidenced by proximal aortic dilation and increased left ventricular volume. These structural changes, along with increased transmural gradients, may create an arrhythmic environment that triggers atrial and ventricular arrhythmias. Finally, nocturnal obstructive events are often terminated by arousal accompanied by a surge in sympathetic nervous system activity, which results in significant increases in blood pressure and heart rate as well as coronary vasoconstriction and microischaemia. Therefore, sympathetic overstimulation can induce various tachyarrhythmias and myocardial repolarization disorders.

Based on the current understanding of the underlying mechanisms of OSA, several treatments for OSA have been promoted. While milder cases of OSA can be managed by losing weight, avoiding muscle relaxants, improving nasal patency, oral appliances, and avoiding sleeping on your back, in more severe cases, continuous positive airway pressure (CPAP) is a good option. This treatment recommends providing positive pressure through a mask to keep the upper airway open during sleep. Early research suggests that although CPAP therapy is effective for OSA, clinicians and researchers face significant problems with patient compliance and compliance. The main reasons for poor compliance with CPAP therapy are thought to be skin irritation due to mask application and difficulty in device handling. However, understanding all aspects of CPAP therapy use, including those of physicians, health care systems, and CPAP distributors, suggests that advocating for its continued use is desirable. Likewise, classifying the benefits of CPAP therapy in the context of several types of arrhythmias may help develop clinical guidelines for patients with arrhythmias to be screened for OSA and receive CPAP therapy to optimize outcomes. Therefore, a comprehensive review of information regarding the use of CPAP therapy in patients with OSA and arrhythmias is necessary to inform more rigorous and ethical clinical decision-making.

Three studies investigated the effects of CPAP therapy on sinus bradycardia in 119 patients. Four studies – 40 in total – evaluated second- and third-degree AV block in 74 patients. Six studies included 194 patients with sinus pause/arrest. Outcome measures included total number of episodes, average number of episodes per 24 hours, and number of episodes per patient. Several studies reported that CPAP therapy significantly reduced or completely prevented the recurrence of nocturnal sinus bradycardia, atrioventricular block, and sinus arrest. In one study, researchers found a positive trend in favor of therapeutic CPAP in reducing nocturnal sinus bradycardia and pauses. However, this result did not reach the level of statistical significance.

Hypoxia caused by obstructive sleep apnea increases carotid chemoreceptor activity, which in the case of obstruction increases vagal stimulation of the heart, triggering bradyarrhythmias. It has been observed that approximately 87% of OSA-related nocturnal bradyarrhythmias occur during the rapid eye movement (REM) phase of sleep due to instability of the autonomic nervous system. Continuous positive airway pressure therapy prevents the development of OSA-induced bradyarrhythmias by restoring normal breathing and eliminating the detrimental effects of hypoxia and autonomic changes during obstructive events. Several studies have reported a reduction in the frequency of nocturnal sinus bradycardia, atrioventricular block, and sinus arrest even after short-term use of CPAP (i.e., 2 nights). Interestingly, 2 studies excluded patients with abnormal electrophysiological studies that would eradicate the presence of sinus node or atrioventricular node dysfunction. In addition to the 48-hour Holter ECG, an insertable loop recorder was applied for long-term heart rhythm monitoring. Importantly, weekly analysis with insertable loop recorders detected arrhythmia in 22% of patients, whereas 48-hour Holter electrocardiography showed arrhythmia in only 13% of patients. Most detected episodes of bradycardia and pauses occur at night and show significant nocturnal variability in individual patients. In patients treated with CPAP, a trend towards a reduction in nocturnal bradycardia and pause frequency was reported, but did not reach a level of statistical significance. Conventional short-term ECG monitoring and lack of assessment of SA/AV node function may have contributed to these nonsignificant results. Likewise, given that previous studies have shown that bradycardia and pauses are more prevalent in patients with severe OSA, concomitant heart failure, longer obstructive events, and greater degrees of oxygen desaturation, demographic characteristics may underlie the nonsignificant results. Confounding factors should be considered in future research on this topic.