ABSTRACT
The finding that hypocapnia is injurious to lungs was noted over 30 years
ago with the observations of Edmunds and Holm (1,2). They demonstrated
that hemorrhagic consolidation occurred when alveolar hypocapnia was
produced by unilateral pulmonary artery ligation (1,2). They demonstrated in addition, that correction of alveolar hypocapnia, by addition of inhaled
CO2 to the inspired gas, attenuated such adverse effects. In the clinical con-
text, Trimble et al. (3) documented that hypocapnia was associated with
adverse effects on gas exchange and administered CO2 to patients with what
was then termed ‘‘post-traumatic pulmonary insufficiency,’’ which would
now be called acute respiratory distress syndrome (ARDS). Trimble et al.
recorded that addition of CO2 in the inspired gas improved multiple mar-
kers of systemic oxygenation, including arterial oxygen tension and shunt fraction (3). Because the investigators produced modest hypercapnia by
addition of inspired CO2, and not by reducing tidal volume, this was in
effect the first recorded application of ‘‘therapeutic hypercapnia’’ in the
clinical setting, although it was not recorded as such.
