Chronic Obstructive Pulmonary Disease (COPD) is a progressive lung disease characterized by airflow limitation and persistent respiratory symptoms. Small airway dysfunction (SAD) plays a crucial role in the progression of COPD, originating in airways less than 2 mm in diameter. Chronic exposure to smoke and toxins leads to inflammatory remodeling and luminal obstruction, which can be detected through micro-CT studies before spirometric airflow limitation becomes apparent. SAD exacerbates COPD by increasing airway resistance and promoting dynamic airway collapse during exhalation. Clinically, SAD manifests as gas trapping, hyperinflation, and exercise intolerance, correlating with accelerated lung function decline. Recent evidence suggests that SAD may represent a potentially modifiable and clinically meaningful trait in COPD, with management strategies including extrafine-particle inhalers, smoking cessation, pulmonary rehabilitation, and emerging biologic approaches. Various measurement methods, including pulmonary function tests and computed tomography (CT) imaging, are used to assess SAD. This review focuses on the role of SAD in COPD pathophysiology and the clinical implications of relevant and easily applicable measurements, such as FEF25-75%, impulse oscillometry, Pi10, and parametric response mapping (PRM) and potential treatment modalities of SAD in COPD.
Jang et al. (2026) studied this question.