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 (PETCO2), 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 PETCO2 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 PETCO2, so that EMGdia was usually eliminated after the initial 4 to 6 breaths while using the ventilator. (2) Returning PETCO2 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.(ABSTRACT TRUNCATED AT 250 WORDS)