Inhibition of Inspiratory Muscle Activity during Sleep: Chemical and Nonchemical Influences

Abstract

The purpose of this study was twofold, namely, to determine (1) if phasic respiratory muscle activity can be inhibited during nocturnal mechanical ventilation, and (2) the mechanism by which this inhibition occurs. Twelve normal subjects were studied during non-rapid eye movement (NREM) sleep (Stages 2 to 4) while receiving negative (NPV, 8 subjects) or positive (PPV, 4 subjects) pressure ventilation and during spontaneous breathing. EMGdia (surface), end-tidal CO₂ pressure (Pet CO₂), esophageal pressure (Pe), and ventilation were measured with a flow-through hood (NPV) or a mask (PPV). The following results were obtained during steady-state (3 to 22 min) mechanical ventilation. (1) A decrease in Pet CO₂ of 2 to 6 mm Hg resulted in elimination of phasic EMGdia in all subjects. Inhibition of respiratory muscle EMG (and a positive shift in Pe) occurred coincident with the breath-by-breath reduction in Pet CO₂, so that EMGdia was usually eliminated after the initial 4 to 6 breaths while using the ventilator. (2) Returning Pet CO₂ to the spontaneous sleeping level by adding CO₂ to the inspired air (isocapnic mechanical ventilation) caused significant increases in EMGdia. During this isocapnic mechanical ventilation, however, EMGdia usually remained less than during eucapnic control. (3) Stopping the ventilator during hypocapnic ventilation caused a prolongation of expiratory time (Te) that was proportional to the degree of hypocapnia during the mechanical ventilation (100 to 1,200% increase over control). During isocapnic ventilation, cessation of mechanical ventilation caused no change in Te. Only 3 of 8 subjects could be successfully hyperventilated with NPV because upper airway resistance often increased, and the subject's respiratory cycle became asynchronous with the imposed ventilator cycle. PPV did not increase resistance and was successful in producing steady-state hyperventilation in all trials. These findings demonstrate that very mild levels of hypocapnia are necessary to completely inhibit the respiratory muscles during NREM sleep and that mechanical factors, independent of chemoreceptor stimulation, can partially inhibit inspiratory muscle activity. PPV is more effective in eliminating phasic respiratory activity than is NPV.