Effects of continuous positive airway pressure on upper airway and respiratory muscle activity

To study the effects of continuous positive airway pressure (CPAP) on lung volume, and upper airway and respiratory muscle activity, we quantitated the CPAP-induced changes in diaphragmatic and genioglossal electromyograms, esophageal and transdiaphragmatic pressures (Pes and Pdi), and functional residual capacity (FRC) in six normal awake subjects in the supine position. CPAP resulted in increased FRC, increased peak and rate of rise of diaphragmatic activity (EMGdi and EMGdi/TI), decreased peak genioglossal activity (EMGge), decreased inspiratory time and inspiratory duty cycle (P less than 0.001 for all comparisons). Inspiratory changes in Pes and Pdi, as well as Pes/EMGdi and Pdi/EMGdi also decreased (P less than 0.001 for all comparisons), but mean inspiratory airflow for a given Pes increased (P less than 0.001) on CPAP. The increase in mean inspiratory airflow for a given Pes despite the decrease in upper airway muscle activity suggests that CPAP mechanically splints the upper airway. The changes in EMGge and EMGdi after CPAP application most likely reflect the effects of CPAP and the associated changes in respiratory system mechanics on the afferent input from receptors distributed throughout the intact respiratory system.     

Respiratory timing during NREM sleep in patients with occlusive sleep apnea

To study respiratory timing mechanisms in patients with occlusive apnea, inspiratory and expiratory times (TI and TE) were calculated from the diaphragmatic electromyogram obtained in seven patients during non-rapid-eye-movement (NREM) sleep. Peak diaphragmatic activity (EMGdi) had a curvilinear relationship with TI during the ventilatory and occlusive phases such that TI shortened as EMGdi decreased during the ventilatory phase (r = 0.87, P less than 0.05) and it prolonged as EMGdi increased during the occlusive phase (r = 0.89, P less than 0.02). However, EMGdi vs. TI for the occlusive phase was shifted to the right of that for the ventilatory phase, reflecting the relatively longer TI during upper airway occlusion. TI also had a linear relationship with pleural pressure (r = 0.94, P less than 0.001) that remained unchanged during the ventilatory and occlusive phases such that it prolonged as negative inspiratory pressure increased. These results indicate that respiratory timing is continuously modified in patients with occlusive apnea as inspiratory neural drive fluctuates during NREM sleep and suggest that this modification is due to the net effects of changing inspiratory neural drive and afferent input predominantly from upper airway mechanoreceptors.