Peggy M. Simon

Frequency and volume thresholds for inhibition of inspiratory motor output during mechanical ventilation

We quantified volume and frequency thresholds necessary for the inhibition of respiratory motor output during prolonged normocapnic mechanical ventilation in healthy subjects during wakefulness (n = 7) and NREM sleep (n = 5). Subjects were ventilated at eupneic frequency (fR) with 3 min step-wise increases in tidal volume (VT), or at eupneic VT with step-wise increases in fR, or by combinations of these two parameters. Inhibition of respiratory motor output was determined using mask pressure and, when available, esophageal pressure and diaphragmatic EMG. During wakefulness, the volume threshold (at eupneic fR) averaged 969 +/- 94 ml or 1.3-1.4 times the average eupneic tidal volume; the frequency threshold (at eupneic VT was 14.1 +/- 0.7 min-1 or 1.2 times the average eupneic frequency. The volume threshold was reduced when MV was provided at an fR above the eupneic value, and the frequency threshold was decreased when MV was provided at a VT above the eupneic level. During NREM sleep (n = 5) the volume threshold for inhibition was 835 +/- 108 ml or 1.4-1.5 times eupneic VT. The inhibitory thresholds for VT and fR were reproducible upon repeat trials within subjects. We conclude that inhibition of respiratory motor output during prolonged normocapnic mechanical ventilation in wakefulness or NREM sleep is highly sensitive to changes in ventilator VT, fR and their combination.

Inhibition of respiratory activity during passive ventilation: a role for intercostal afferents?

The purpose of this study was to determine whether receptors from the rib cage are primarily responsible for inhibitory feedback of inspiratory muscle activity during mechanical ventilation. Seven quadriplegics with C5-C6 lesions were compared to 6 normals during mechanical ventilation. All subjects were mechanically hyperventilated with a nasal mask to suppress intrinsic inspiratory muscle activity. End-tidal partial pressure of carbon dioxide (PETCO2) was increased by either adding CO2 (FICO2) or decreasing tidal volume (VT) until reoccurrence of inspiratory activity, defined as the recruitment threshold (PCO2RT). The difference between PCO2RT and eupneic PETCO2 indicated the presence and magnitude of volume-related inhibition of inspiratory muscle activity during mechanical ventilation. Substantial inhibition of inspiratory activity was observed in both quadriplegics and normals. We conclude that afferent information from the rib cage is not obligatory for the mediation of volume-related inhibition of inspiratory muscle activity during mechanical ventilation.