Systemic air embolization from penetrating lung injury.

This study evaluates the role of increased intratracheal pressure in developing systemic air embolization. Twenty healthy mongrel dogs were monitored for air embolization, both by means of an extracorporeal arteriovenous shunt constructed from transparent plastic tubing for visualization of air emboli and by means of a Doppler flow probe implanted at the root of the aorta. Systemic arterial, left atrial, intratracheal, and intrapleural pressures were recorded. In 10 of the dogs, a penetrating wound of the lung 1 cm wide by 4 cm deep was produced; in 5 the chest was left open and in 5 the chest was closed. The remaining 10 dogs served as controls (with no wound of the lung); in 5 the chest was left open and in the other 5 the chest was closed. No air embolization occurred in any animals at intratracheal pressures less than 65 mm Hg. However, systemic air embolization occurred in every dog in all groups upon hyperinflation of the lung above 65 mm Hg. The control groups differed from the groups with penetrating wound only in the quantity of embolized air. This study suggests that hyperinflation of the lung to an intratracheal pressure above 65 mm Hg results in systemic air embolization and that the presence of a penetrating wound of the lung at such intratracheal pressure predisposes to a greater quantity of air embolization.