Respiratory load compensation in uremia.

The clinical significance of respiratory-system load-compensation is unknown. We have measured the responses to random presentation of single, elastic inspiratory loads in 36 subjects: 8 normal personnel (N), 9 with obesity (O), 10 with chronic renal failure under hemodialysis (H), 5 with pneumonia (P), and 4 with interstitial lung disease (CILD). We have expressed these responses as: (1) the ratio of elastance (or rigidity) of the system during loaded breathing to the elastance without loading (E'RS/ERS); (2) the ratio of tidal volume (VT) achieved when breathing from an inspiratory load to the VT predicted in the absence of load compensation (VTL/VTP); (3) the ratio of inspiratory flow rates during loaded and unloaded breaths; (4) the ratio of inspiratory time of loaded and unloaded breaths. We found E'RS/ERS in the O, H and P groups less than that of either CILD patients or N controls (F = 6.79; p less than 0.001). Passive elastance (ERS) although greater in groups O and H than in N (F = 3.88; p less than 0.025) did not account for the difference i E'RS in all groups. When expressed as VTL/VTP, the response to a 37-cm H2O/l load for groups H, O and P was less than that for N (F = 5.51; p less than 0.05). Diminished inspiratory time was observed in H, O and P patients when inspiring from this load. In contrast, inspiratory flow did not differ from that of normal subjects. Nerve conduction velocity was slightly reduced or normal in the H patients. Respiratory load compensation is deficient in H, O and P patients. The mechanism, which does not involve peripheral neuropathy, is unclear.