Chest flow during the initial inspiratory phase (V0.1) in pulmonary diseased patients.

We measured the chest flow 0.1 s after the onset of the inspiratory phase (V0.1) in patients with chronic pulmonary emphysema (CPE: n = 5), interstitial pneumonitis (IP: n = 5) and normal subjects (Nor: n = 5). The subjects sat in a body box and breathed air from outside of the body box. V0.1 was measured during rest and during maximal breathing (V0.1-rest, V0.1-max) and then these results were compared with P0.1 (P0.1 rest, P0.1-max) values. V0.1-rest was not significantly different between the three groups (Nor: 0.25 +/- 0.10, CPE: 0.27 +/- 0.06, IP: 0.26 +/- 0.06, l/s), whereas the P0.1-rest in IP patients was significantly greater than in normal subjects (Nor: 1.98 +/- 0.61, CPE: 3.00 +/- 0.80, IP: 3.60 +/- 0.68 hPa; P < 0.05 compared with normal). The V0.1-max in CPE and IP patients was significantly lower than in normal subjects (Nor: 3.66 +/- 1.16, CPE: 0.82 +/- 0.25, IP: 1.02 +/- 0.21 l/s, P < 0.05 compared with normal subjects (Nor: 3.66 +/- 1.16, CPE: 0.82 +/- 0.25, IP: 1.02 +/- 0.21 l/s, P < 0.05 compared with normal), whereas P0.1-max in IP patients was not significantly different with in normal subjects (Nor: 33.2 +/- 10.2, CPE: 9.8 +/- 3.7, IP: 19.5 +/- 3.4 hPa, P < 0.05 compared with normal, P < 0.05 compared with CPE). A simulation of the influence of the mechanical properties of the respiratory system on V0.1 and P0.1 using the Runge-Kutta method suggested that V0.1 was negatively affected by airway resistance but positively affected by chest wall and lung compliance. In contrast, the influence of respiratory mechanics on P0.1 was much less than on the V0.1, except for highly decreased lung compliance. In CPE patients, it was suspected that mechanical disorders might not simply be the determining factors of V0.1-max, but that limitations of the neuro-muscular drive due to chest wall deformity may also play a definitive role in the smaller V0.1-max. In contrast, it may be inferred that IP patients had to exert greater inspiratory effort as compared with the other two groups in order to maintain a similar V0.1-rest because of the increased airway resistance and decreased tissue compliance; thus these abnormal mechanical properties suppress the increase in the V0.1-max. It may be concluded that V0.1 is a good index of chest wall acceleration, which is determined by both the neuro-muscular drive and the mechanics of the respiratory system.