BACKGROUND: Wood smoke inhalation (WSI) inhibits pulmonary surfactant function within minutes of exposure, leading to atelectasis, venous admixture, hypoxemia, and pulmonary edema. We hypothesized that addition of positive end-expiratory pressure (PEEP), following WSI, would reinflate the lung and restore oxygenation. The possibility that PEEP may also affect pulmonary edema formation following WSI was also studied. METHODS & MATERIALS: Anesthetized dogs were ventilated with room air and instrumented for blood gas measurements and hemodynamic monitoring. After baseline data were collected, the animals were ventilated with wood smoke for 5 minutes and placed on either 5 or 10 cm H2O PEEP [0.49 or 0.98 kPa], and studied for up to 4 hours. RESULTS: Smoke inhalation resulted in gross atelectasis, a decrease in arterial blood Po2 (from 93 to 48 torr [from 12.4 to 6.4 kPa]), an increase in venous admixture from a mean (SD) of 8 (1) % to 40 (5) % and a decrease in pulmonary compliance (70% of baseline). When 5 cm H2O PEEP [0.49 kPa] was used, these changes persisted for the duration of the experiment (4 hours). Addition of 10 cm H2O PEEP [0.98 kPa] eliminated atelectasis and restored PaO2 (95 torr [12.4 kPa]), venous admixture (5 [2] %), and compliance (95% of baseline) to near-normal values. At 2 hours following WSI, lung water increased but did not increase further over the next 2 hours regardless of PEEP level. CONCLUSIONS: In a canine model of wood smoke inhalation, lung collapse occurs immediately, resulting in hypoxemia. PEEP reinflates the lung and restores oxygenation but does not alter the amount or time course of lung water accumulation.
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