Airway closure and trapped gas during low volume breathing.

We used a plethysmographic technique to estimate the trapped gas volume (TGV) in seven normal subjects after breathing air or O2 normally at functional residual capacity (FRC-air, FRC-O2) and near residual volume (RV) with small breaths (LVB-air, LVB-O2). If airway closure occurs, lung units subtended by closed airways would tend to collapse as TGV is absorbed; rapidly if the gas is O2 and slowly if it is air. Both inspiratory and expiratory quasi-static and static pressure-volume curves after LVB-O2 for 180 sec demonstrated a shift to the right and increased hysteresis, reduced vital capacity (VC) and significantly increased transpulmonary pressures at 25% and 50% control VC (PL25, PL50) as compared with those of FRC-O2 controls (P less than 0.01-P less than 0.001). Three VC breaths reversed these changes which suggested that they were related to atelectasis. The absolute plethysmographic RV level decreased and was also restored after three VC breaths. We used this reproducible decrease in RV level to represent the absorbed TGV (delta TGV). The delta TGV after LVB-O2 (180 sec) was significantly greater than that after LVB-air (P less than 0.001) or FRC-O2 (P less than 0.001). There was a significant correlation between the increase of delta TGV (DTGV) and the increase of PL25 (delta PL25) (P less than 0.01). The delta TGV after FRC-O2 was 128.6 +/- 50.3 ml (1.61 +/- 0.63% of TLC) and the maximal delta TGV after LVB-O2 (180 sec) averaged 504.3 +/- 40.5 m (7.5 +/- 0.37% TLC). The significant increase in delta TGV near RV during O2 as compared to air breathing is best explained by reversible atelectasis and further supports the concept of dependent airway closure at low lung volumes.