<p>Central sleep apnea (CSA) is a&#xa0;sleep-related breathing disorder characterized by repeated cessation of respiratory drive during sleep. Unlike obstructive sleep apnea, CSA is not caused by upper airway obstruction but by a&#xa0;dysfunction in central respiratory regulation. The prevalence of CSA is low in the general population (0.9–1.5%), but significantly higher in risk groups such as patients with heart failure (up to 50%). Pathophysiologically, CSA is marked by instability of respiratory brainstem drive, prolonged circulation time, and increased CO₂ sensitivity. Cheyne-Stokes respiration, a&#xa0;common manifestation in heart failure patients, is associated with increased mortality. Diagnosis is primarily based on polysomnography, which allows differentiation between central and obstructive apneas, as well as sleep stages. A&#xa0;central apnea-hypopnea index (cAHI) ≥ 5/h is considered pathological. Additional assessments, such as echocardiography and blood gas analysis, are important for evaluating underlying conditions. Treatment focuses on treating the underlying disease, especially in heart failure patients. Device-based treatments such as continuous positive airway pressure (CPAP) and adaptive servo-ventilation (ASV) are available, although ASV is contraindicated in symptomatic heart failure patients with reduced left-ventricular ejection fraction (LV-EF) ≤ 45%. Implantable transvenous phrenic nerve stimulation is a&#xa0;promising new treatment option for CSA, particularly for heart failure patients who cannot receive ASV. In the case of neurological diseases and high-altitude exposure, CSA treatment needs to be individually tailored. Clinically, early identification and treatment of CSA are crucial to improve quality of life. Improvement in prognosis through CSA treatment has not yet been conclusively demonstrated, highlighting the need for further research on this topic. CSA remains a&#xa0;dynamic field in sleep and cardiovascular medicine with high clinical relevance.</p>