摘要
Inspiratory duty cycle (IDC), the fraction of inspiratory time relative to total breath duration, serves as an adaptive response to flow-limited ventilation in obstructive sleep apnea (OSA). IDC compensation remains incompletely characterized in the context of OSA pathophysiology. We studied the relationship of IDC and flow-limited breathing in OSA during drug-induced sleep endoscopy (DISE). Eighty-two adults with OSA underwent DISE with continuous positive airway pressure (CPAP) titration. Airflow (VI), tidal volume (TV), and IDC were measured across varying levels of flow-limited breathing. Airway collapsibility was assessed by pharyngeal opening (Popen) and critical closing pressures (Pcrit). IDC compensation was quantified as the slope of IDC versus normalized TV (%PopenTV), representing the degree of IDC increase to declining ventilation. Patients were classified as high versus low IDC compensators based on this slope metric, and differences in Popen and Pcrit were compared between groups. As CPAP increased from flow-limited to non-flow-limited breathing, IDC decreased by 20%, whereas TV and ventilation more than doubled. IDC compensation varied among subjects with stronger compensators exhibiting higher airway collapsibility (Popen = 10.2 vs. 8.2 cmH2O; P = 0.01, Pcrit = 4.2 vs. 3.0 cmH2O; P = 0.03). IDC compensation reflects a physiological response that helps maintain ventilation under flow-limited conditions. Greater airway collapsibility was associated with stronger IDC compensation, reflecting the capacity of the respiratory system to tolerate increased mechanical load. DISE provides a unique experimental platform to quantify ventilatory timing responses, advancing our mechanistic understanding of respiratory compensation in OSA.NEW & NOTEWORTHY This study describes inspiratory duty cycle (IDC) compensation as a measurable physiological mechanism that sustains ventilation during flow-limited breathing in obstructive sleep apnea. Using drug-induced sleep endoscopy with continuous positive airway pressure titration, we show IDC increased with worsening inspiratory flow limitation and that stronger IDC compensation is associated with greater airway collapsibility. These findings introduce IDC compensation as a novel marker of ventilatory adaptability and provide a framework for characterizing compensatory responses in OSA.