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<0.01-P<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 (ΔTGV). The ΔTG after LVB-O₂ (180 sec) was significantly greater than that after PVB-air (P<0.001) or FRC-O₂ (P<0.001). There was a significant correlation between the increase of ΔTGV (DTGV) and the increase of PL₂₅ (ΔPL₂₅) (P<). The ΔTGV after FRC-O₂ was 128.6 ± 50.3 ml (1.61 ± 0.63% of (180 sec) averaged 5.4 ± 40.5 m (7.5 ± 0.37% TLC). The significant increase in ΔTGV 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.