A surge of data has reproducibly identified strong associations of obstructive sleep apnea (OSA) with cardiac arrhythmias. As an extension of epidemiologic and clinic-based findings, experimental investigations have made strides in advancing our understanding of the putative OSA and cardiac arrhythmogenesis mechanistic underpinnings. While most studies have focused on the links between OSA and atrial fibrillation (AF), relationships with ventricular arrhythmias have also been characterized. Key findings implicate OSA-related autonomic nervous system fluctuations typified by enhanced parasympathetic activation during and sympathetic surges subsequent to respiratory events which contribute to augmented arrhythmic propensity. Other more immediate pathophysiologic influences of OSA enhancing arrhythmogenesis include intermittent hypoxia, intrathoracic pressure swings leading to atrial stretch, and hypercapnia. Intermediate pathways by which OSA may trigger arrhythmia include increased systemic inflammation, oxidative stress, enhanced pro-thombotic state, and vascular dysfunction. Long-term OSA sequelae associated such as hypertension, atrial enlargement and fibrosis, ventricular hypertrophy, and coronary artery disease also predispose to cardiac arrhythmia. The above can lead to reduction in atrial effective refractory period, triggered and abnormal automaticity, promote slowed and heterogeneous conduction – mechanisms that increase the persistence of re-entrant arrhythmias and prolong the QT interval. Cardiac electrical and structural remodelling observed in OSA animal models can progress the arrhythmogenic substrate to further enhance arrhythmia generation. Future investigations clarifying specific OSA-related mechanistic pathways contribution to arrhythmia generation may allow targeted preventative therapies to mitigate OSA-induced arrhythmogenicity. Furthermore, interventional studies are needed to clarify the impact of OSA pathophysiology reversal on cardiac arrhythmogenesis and related adverse outcomes.