The mechanism limiting forced expiratory flow is explained on the basis that a local flow velocity reaches the local speed of wave propagation at a point, called the choke point, in intrathoracic airways. This theoretical approach to the "waterfall effect" leads to selection of the analogy of constricted open-channel flow to apply to the elastic network of airway tubes. Quantitative results are derived for the case of negligible friction by use of the Bernoulli principle. Shapes predicted for the maximum-flow static recoil curves depend only upon the nature of the pressure-area curve at the choke point in the case of negligible friction; and the magnitude of the critical rate of flow depends on reference values of cross-sectional area and elastic modulus at the choke point, on gas density, and on the static recoil pressure. The present theoretical results are used to interpret previous experiments, but quantitative applicability is limited because of frictional effects and lack of knowledge of choke point conditions.

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With a computer technique variability of the configuration of maximum expiratory flow-volume (MEFV) curves was studied in terms of slope ratio, SR. SR = dV/dV divided by V/V, where V is the instantaneous flow and V is the volume increment above residual volume.) Approximately four SR-V curves, each based on three to five smoothed and averaged MEFV curves, were derived for each of 20 normal subjects (aged 23-55 yr) on a single occasion, and again at least 1 wk later. Individual curves were largely reproducible, the maximum difference in SR at most volumes being 0.3-1 U, but frequently showed substantial yet reproducible fluctuations with volume. These corresponeded to hitherto unrecognized irregularities of maximum expiratory flow that may reflect sudden changes in the location of flow limitation.

We measured transdiaphragmatic pressure (Pdi) during forced expiratory vital capacity (FVC) maneuvers in 13 normal subjects and electromyographic activity of the diaphragm (edi) in 8 of these subjects. In all subjects, Pdi increased at the initiation of the FVC. In most, this increase lasted 30--50 ms and reached levels well above the Pdi observed at total lung capacity (TLC). After the initial transient increase, approximately half of the subjects demonstrated a substantial fall in Pdi to values near the relaxation level in the mid-vital capacity (VC) volume range, while half showed a second large increase in Pdi in this volume range. Seven of eight subjects tested showed a rapid decrease in Edi at the onset of the FVC, reaching a minimum in 30--50 ms. After this initial transient decrease, Edi increased in six subjects in the mid-VC volume range, in association with secondary rises in Pdi. In two subjects, Edi remained low throughout the remainder of the FVC, and Pdi in the mid VC range was generally lower. These results are consistent with the conclusion that the diaphragm is neither electromyographically silent nor mechanically unimportant during the FVC. Changes in abdominothoracic configuration, superimposed upon "antagonistic" activity of the diaphragm, result in substantial reductions in pleural (esophageal) pressure that may influence regional lung emptying during the FVC.