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The Annals of Thoracic Surgery, Vol 27, 161-168, Copyright © 1979 by The Society of Thoracic Surgeons
GH Meier, WJ Wood and PN Symbas
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.
ARTICLES
Systemic air embolization from penetrating lung injury
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