EFFECT OF SLEEP ON RESPIRATORY MUSCLE-ACTIVITY DURING MECHANICAL VENTILATION

The purpose of this study was to determine whether consciousness was critical for the expression of neuromechanical inhibition of breathing during mechanical ventilation. This same mechanical ventilation model also was used to evaluate the relative importance of sleep state in causing CO2 retention during sleep. Positive pressure ventilation was used to suppress respiratory muscle activity; CO2 was then added until a reappearance of inspiratory effort, which defined the recruitment threshold (P(CO2)RT). Keeping the mechanics of the respiratory system constant through the use of passive mechanical ventilation allowed us to measure the output of the respiratory controller, independent of these parameters. Eight normal subjects were mechanically hyperventilated with a nasal mask during wakefulness and sleep with matched flow rates, frequencies, and tidal volumes. When inspiratory muscle activity was undetectable and end-tidal P(CO2) (PET(CO2)) fell below 30 mm Hg, inspired CO2 was added in stepped increments until inspiration reoccurred. The sleeping state increased both eupneic PET(CO2) (42 +/- 4 versus 38 +/- 3 mm Hg) and P(CO2)RT (48 +/- 3 versus 46 +/- 2 mm Hg) compared with that during wakefulness. Neuromechanical inhibition of inspiratory muscle activity during mechanical ventilation was present during both wakefulness and sleep, as evidenced by the mean difference between P(CO2)RT and eupneic PET(CO2) of 8 and 6 mm Hg, respectively. Recruitment thresholds during wakefulness and sleep were compared to evaluate the effect of sleep on respiratory motor output independent of changes in load, i.e., respiratory mechanics held constant. P(CO2)RT was higher during sleep than during wakefulness in every subject, indicating a change in set point associated with the loss of the wakefulness stimulus. The difference in mean eupneic PET(CO2) between wakefulness and sleep (4 mm Hg) also was determined to evaluate the effect of sleep on P(CO2) when respiratory mechanics were no longer held constant. The difference in mean eupneic PET(CO2) (4 mm Hg) was greater than the difference in mean P(CO2)RT (2 mm Hg), suggesting that not all the CO2 retention incurred during sleep was due to changes in set point. We conclude that consciousness is not necessary for the expression of neuromechanical inhibition of breathing during mechanical ventilation. Our findings further support the concept that both changes in set point and respiratory load such as an increase in upper airway resistance are important determinants of sleep-induced CO2 retention.