Background: Wood smoke inhalation causes severe ventilation and oxygenation abnormalities. We hypothesized that smoke inhalation would cause lung injury by 2 mechanisms: (1) direct tissue injury by the toxic chemicals in the smoke and (2) a mechanical shear-stress injury caused by alveolar instability (ie, alveolar recruitment/derecruitment). We further postulated that alveolar instability would increase with the size of the cumulative smoke dose.
Methods: Anesthetized pigs were ventilated and instrumented for hemodynamic and blood-gas measurements. After baseline readings, the pigs were exposed to 5 separate doses of wood smoke, each dose lasting 1 min. Factors studied included hemodynamics, pulmonary variables, and in vivo photomicroscopy of alveolar mechanics (ie, the dynamic change in alveolar size with ventilation).
Results: Smoke inhalation significantly increased alveolar instability with 4 min and 5 min of smoke exposure. Significant rises in carboxyhemoglobin levels and in pulmonary shunt were also observed at 4 min and 5 min of smoke exposure. Lung histology demonstrated severe damage characteristic of acute lung injury.
Conclusions: We demonstrated that wood smoke inhalation causes alveolar instability and that instability increases with each dose of smoke. These data suggest that smoke inhalation may cause a "2-hit" insult: the "first hit" being a direct toxic injury and the "second hit" being a shear-stress injury secondary to alveolar instability.