Nonchemical elimination of inspiratory motor output via mechanical ventilation in sleep.

In six dogs studied in nonrapid eye movement (NREM) sleep, we found that the frequency, volume, and timing of application of mechanical ventilator breaths had marked and sustained inhibitory effects on diaphragm electromyogram (EMG(di)). Single ventilator breaths of tidal volume (VT) 75-200% of control caused apnea (up to three times eupneic expiratory time [TE]) when applied during the initial 25-65% of expiratory time. When continuous controlled mechanical ventilation (CMV) was applied with ventilator frequency increased as little as 1 cycle/min > eupnea and Pa(CO(2)) and VT maintained at near eupneic control levels, EMG(di) was silenced and triangularis sterni EMG (EMG(ts)) became tonic within 2 to 5 ventilator cycles. On cessation of normocapnic CMV, apnea ensued with TE ranging from 1.2 to five times eupneic TE. The spontaneous VT and EMG(di) determined immediately after these prolonged apneas were also markedly reduced in amplitude. The larger the VT applied during the isocapnic CMV (120-200% of eupnea) and the longer the duration of the CMV (3-90 s), the longer the duration of the postventilator apnea. Significant postventilator apneas and postapneic hypoventilation also occurred even when end-tidal CO(2) pressure (PET(CO(2))) was raised 3-5 mm Hg > eupnea (and 7-10 mm Hg > normal apneic threshold) throughout CMV trials at raised frequency and VT. Our findings demonstrate that the increased frequency of CMV was critical to the elimination of inspiratory motor output and the onset of tonic expiratory muscle activity; furthermore, once EMG(di) was silenced, the tidal volume and duration of the passive mechanical ventilation determined the magnitude of the short-term inhibition of inspiratory motor output after cessation of CMV.