Response of respiratory motor output to varying pressure in mechanically ventilated patients

It has been shown in mechanically ventilated patients that pressure support (PS) unloads the respiratory muscles in a graded fashion depending on the PS level. The downregulation of respiratory muscles could be mediated throu gh chemical or load-related reflex feedback. To test this hypothesis, 8 patients with acute lung injury mechanically ven tilated on PS mode (baseline PS) were studied. In Protocol A, PS was random ly decreased or increased by at least 5 cmH(2)O for two breaths. During thi s time, which is shorter than circulation delay, only changes in load-relat ed reflex feedback were operating. Sixty trials where PS increased (high PS ) for two breaths and 62 trials where PS decreased (low PS), also for two b reaths were analysed. Thereafter, the patients were assigned randomly to ba seline, low or high PS and ventilated in each level for 30 min (Protocol B) . The last 2 min of each period were analysed. Respiratory motor output was assessed by total pressure generated by the respiratory muscles (Pmus), co mputed from oesophageal pressure (Poes). In Protocol A, alteration in PS caused significant changes in tidal volume (VT) without any effect on Pmus waveform except for neural expiratory time (ntE). ntE increased significantly with increasing PS. In Protocol B, Pmus was significantly down-regulated with increasing PS. Carbon dioxide tension in arterial blood (Pa,CO2) measured at the end of each period increased wi th decreasing PS. There was not any further alteration in ntE beyond that o bserved in Protocol A. These results indicate that the effect of load-related reflex on respirator y motor output is limited to timing. The downregulation of pressure generat ed by the respiratory muscles with steady-state increase in pressure suppor t is due to a slow feedback system, which is probably chemical in nature.