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)

Does nonchemical inhibition of respiratory output occur during mechanical ventilation?

“…In agreement with the data obtained by HENKE et al [12] during mechanical ventilation by CMV, studies in control subjects conducted by SCHEID et al [13] and FAUROUX et al [14] showed that returning PET,CO 2 to the spontaneous level by adding CO 2 to the inspired air during mechanical hyperventilation by PS did not completely restore respiratory activity to the level observed during spontaneous breathing.…”

“…HENKE et al [12] reported that returning PET,CO 2 to the spontaneous level by adding CO 2 to the inspired air during mechanical hyperventilation did not completely restore respiratory activity to the level observed during spontaneous breathing. Some of these studies were performed during sleep [8,10,12], indicating that these nonchemical inhibitory effects are largely of peripheral origin and independent from higher brain centres.…”

The influence of induced hypocapnia and sleep on the endogenous respiratory rhythm in humans.

“…In human subjects however, there is some evidence that inhibition of the diaphragm secondary to activation of pulmonary/chest wall mechanoreceptors may also occur. Henke, Arias, Skatrud & Dempsey (1988) showed that isocapnic or even hypercapnic passive hyperventilation led to a decrease (but not elimination) of diaphragmatic EMG; there is little information on the type of receptor and afferent pathways involved (Simon, Skatrud, Iber, Badr, Griffen & Dempsey, 1990).…”

Effect of Ventilatory Drive on Carbon Dioxide Sensitivity below Eupnea during Sleep

“…First, studies using mechanical ventilation to lower Pa CO 2 reveal that non-rapid eye movement (NREM) sleep unmasks a highly sensitive apneic threshold induced by reductions in arterial carbon dioxide pressure (Pa CO 2 ) that were only 2-4 mm Hg less than eupneic Pa CO 2 (1)(2)(3)(4). Second, the occurrence of central apneas in patients with Cheyne-Stokes respiration (CSR) was shown to be preceded by transient hyperpnea and hypocapnia (5)(6)(7)(8); and in healthy subjects sleeping in hypoxia the apneic periods during periodic breathing coincided with reductions in end-tidal carbon dioxide pressure (P ET CO2 ), which approximated the subjects' independently determined apneic threshold for P CO 2 (1).…”

“…Older studies used an extrapolation of the hypercapnic ventilatory response to zero E intercept to estimate the apneic threshold; but these extrapolations are highly uncertain because of the unknown shape of the CO 2 response near and below eupnea (29,30). Mechanical ventilation may be used to lower Pa CO 2 and provide a direct measure of the hypocapnia-induced apneic threshold (2,4). Using variations of this technique in anesthetized rats, acute CO 2 inhalation was shown to raise both eupneic and apneic threshold P CO 2 and to increase the difference between them (31); and in sleeping healthy humans, mild hypoxia caused a slight hyperventilation and a narrowing of the difference between eupneic P ET CO2 and the apneic threshold P ET CO2 (32).…”