Non-chemical inhibition of respiratory motor output during mechanical ventilation in sleeping humans.
1. To determine the magnitude and time course of changes in respiratory motor output caused by non-chemical influences, six sleeping subjects underwent assist-control mechanical ventilation (ACMV) at increased tidal volume (VT). During ACMV, end-tidal PCO2 (PET,CO2) was either held at normocapnic levels (PET,CO2, 0.6-1.1 mmHg > control) by adding CO2 to the inspirate, or it was allowed to fall (hypocapnia). 2. Each sleeping subject underwent several repeat trials of twenty-five ACMV breaths (VT, 1.3 or 2.1 times control; peak flow rate, 30-40 l min-1; inspiratory time, +/- 0.3 s of control). The end-tidal to arterial PCO2 difference throughout normocapnic ACMV at raised VT was unchanged from eupnoeic levels during studies in wakefulness. 3. Normocapnic ACMV at both the smaller and larger increases in VT decreased the amplitude of respiratory motor output, as judged by decreased maximum rate of rise of mask pressure (Pm) (mean dPm/dtmax, 46-68% of control), reduced diaphragmatic EMG (to 55% of control) and reduced VT on the first spontaneous breath after ACMV (to 70% of control). Expiratory time (TE) was slightly prolonged (13-32% > control). This inhibition of amplitude of respiratory motor output progressed over the first five to seven ventilator cycles, was maintained over the remaining 18-20 cycles and persisted for three to five spontaneous breaths immediately following cessation of ACMV. 4. Hypocapnia did not further inhibit respiratory motor output amplitude beyond the effect of normocapnic ACMV at high VT, but did cause highly variable prolongation of TE when PET,CO2 was reduced by greater than 3 mmHg for at least five ventilator cycles. 5. These data in sleeping humans support the existence of a significant, non-chemical inhibitory influence of ACMV at increased VT and positive pressure upon the amplitude of respiratory motor output; this effect is manifested both during and following normocapnic mechanical ventilation.
Wilson
C R
CR
John Rankin Laboratory of Pulmonary Medicine, Department of Preventive Medicine, University of Wisconsin-Madison, Madison, WI 53705, USA. crwilson@lynx.neu.edu
Satoh
M
M
Skatrud
J B
JB
Dempsey
J A
JA
D000328:Adult; D000399:Air Pressure; D002245:Carbon Dioxide / Q000097:blood / Q000502:physiology; D003964:Diaphragm / Q000502:physiology; D004576:Electromyography; D005260:Female; D006801:Humans; D006863:Hydrogen-Ion Concentration; D016857:Hypocapnia / Q000503:physiopathology; D008297:Male; D011175:Positive-Pressure Respiration; D012121:Respiration, Artificial; D012132:Respiratory Muscles / Q000294:innervation / Q000502:physiology*; D012890:Sleep / Q000502:physiology*; D013990:Tidal Volume / Q000502:physiology
D002245:Carbon Dioxide