Mechanisms of respiratory elastic load compensation in anesthetized humans.

In anesthetized humans the nature of tidal volume (VT) compensation during elastic loading (as reflected in the difference between passive and effective respiratory elastances (Ers) and (Ers), respectively) has not been fully elucidated. We assessed the relative contribution of various mechanisms contributing to VT compensation during linear elastic loading in 10 young anesthetized adults free of cardiorespiratory disease. Ers averaged 22.0 cmH2O X 1(-1), representing 64% of Ers. Most of Ers (84%) was comprised of the active elastance (E'rs), reflecting the major role played by the addition of force-length properties of inspiratory muscles to the internal impedance, and chest wall distortion played in the defense of VT. Of the remaining 16% of Ers, the difference between Ers and isotime Ers, representing the contribution of prolongation of inspiratory time (TI) via the Hering-Breuer reflex, amounted to only 9%. Finally, the remainder of Ers, which reflects the difference between Ers and E'rs in the absence of vagal modulation, and attributed to several factors [shape of driving pressure wave, duration of control TI, and magnitude of E'rs and intrinsic flow resistance plus external resistances (Zin, Rossi, Zocchi, and Milic-Emili. J. Appl. Physiol. 57: 271-277, 1984)], amounted to less than 7%.