Decay of inspiratory muscle pressure during expiration in anesthetized kyphoscoliosis patients.

The decay of pressure developed by the inspiratory muscles during expiration (PmusI) has not been studied in subjects with increased respiratory impedance such as in kyphoscoliosis. PmusI was compared in 11 anesthetized patients with kyphoscoliosis with that in 11 anesthetized normal subjects. PmusI was obtained according to the following equation: PmusI(t) = Ers.V(t) - K1V(t) - K2V2(t), where V is volume and V is airflow at any instant t during spontaneous expiration, Ers is the passive elastance, and K1V + K2V2 is the flow resistance (curvilinear in both groups because of the endotracheal tube and the intrinsic resistance in the kyphoscoliotics) of the total respiratory system. Ers was determined by the relaxation method and resistance from the ensuing V-V relationships during the ensuing relaxed expiration. Changes in impedance due to pliometric work done by the inspiratory muscles during relaxation were neglected. Subjects in both groups showed marked braking of expiratory flow by PmusI. The mean time for PmusI to decrease to 50 and 0% amounted to 17 and 8% less, respectively, in the kyphoscoliosis group. Average values for flow-resistive work in the control and kyphoscoliosis groups both amounted to approximately 40% of the elastic energy stored during inspiration. The remaining portion, used as negative work, amounted to approximately 60% in both groups. Expiratory braking in anesthetized kyphoscoliotic patients appears to be in proportion to their magnitude of elastic recoil and intrinsic flow resistance.