Lung fuction impairment following cerebral ischemic stroke: Pathophysiology, mechanisms, and clinical challenges

Cerebral ischemic stroke is a leading cause of mortality and morbidity worldwide, with systemic effects extending beyond brain injury to multiple organs, particularly the lungs. Clinical and experimental studies have demonstrated that altered immune function, post-stroke pneumonia, dysphagia and aspiration, pulmonary tissue inflammation, neurogenic pulmonary edema, mucus hypersecretion with impaired debris clearance, abnormal breathing patterns, respiratory muscle weakness, atelectasis and acute lung injury are all potential contributors to post-stroke pulmonary dysfunction development. These complications are associated with measurable changes in lung function, including altered inspiratory and expiratory pressures, impaired spirometry parameters, as well as altered respiratory mechanical parameters, including reduced lung compliance, changes in airway resistance, reduced functional residual capacity in both stroke survivors and animal models of global and focal cerebral ischemia. Mechanical ventilation, frequently required in severe stroke, poses additional short- and long-term challenges. This review integrates evidence from clinical and experimental studies to highlight the mechanisms underlying post-stroke pulmonary dysfunction and underscores the need for optimized ventilation strategies and longitudinal clinical studies to better understand long-term outcomes and reduce respiratory complications in stroke survivors.