Obstructive Sleep Apnea (OSA): Cerebrovascular risk, respiratory pathophysiology and pulmonary rehabilitation

Obstructive sleep apnea (OSA) is a common chronic sleep-disordered breathing disorder and an independent risk factor for cerebrovascular accidents (CVA) and transient ischemic attacks (TIA). Pre‐existing OSA is found in about 60–75% of stroke survivors, yet up to 80–90% remain undiagnosed before hospitalization. OSA induces physiological stress through intermittent hypoxemia, oxidative injury, severe intrathoracic pressure swings, hypercoagulability, and autonomic instability. These pathways accelerate systemic atherosclerosis, promote atrial fibrillation, worsen acute stroke severity, double the risk of recurrent CVA, and increase all-cause mortality (RR 1.69). Differentiating pre-existing OSA from central apneas due to acute stroke includes patient history, validated screening questionnaires [STOP-BANG, Berlin, ESS], phenotypic markers, and polysomnography.Nonpharmacologic measures have a significant therapeutic effect, although the principal pneumatic treatment is continuous positive airway pressure (CPAP). Complete management, including Oropharyngeal Myofunctional Therapy (OMT), Inspiratory Muscle Training (IMT), breathing retraining, postural modification, and aerobic exercise, results in an average reduction of Apnea-Hypopnea Index (AHI) scores of 50%, an increase in minimum SpO2 nadir (+3.5% to +5.2%), decreases in daytime sleepiness, and an increase in functional exercise capacity. Furthermore, upper airway retraining decreases the therapeutic CPAP pressure settings needed, which improves long-term compliance. These integrated interventions are endorsed by major international societies (ATS, ERS, AACVPR, AASM, CTS, GOLD) to lower vascular risk and improve neurologic recovery.