Mechanisms of physiological dead space response to PEEP after acute oleic acid lung injury

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Abstract
In acute increased-permeability edema, the Bohr physiological dead space (VD/VTCC2) can be influenced by changes in anatomic dead space, ventilation-perfusion (.ovrhdot.VA/.ovrhdot.Q) heterogeneity, shunt and the Haldane effect. The multiple inert gas elimination technique was used to assess the effect of positive end-expiratory pressure (PEEP) on each of these components of VD/VTCO2 in 14 pentobarbital-anesthetized dogs with increased-permeability edema induced by infused oleic acid. PEEP of 5, 10, 15 and 20 cm H2O was applied in random sequence. Following injury, VD/VTCO2 increased. It decreased with 5 or 10 cm H2O PEEP but increased progressively at higher PEEP levels. The decrease in VD/VTCO2 at 5 or 10 cm H2O PEEP was due to reductions in shunt and midrange .ovrhdot.VA/.ovrhdot.Q heterogeneity. The increase in VD/VTCO2 that occurred with higher PEEP levels was due to increased ventilation to high .ovrhdot.VA/.ovrhdot.Q regions and a larger anatomic dead space. Haldane effect magnified the shunt component of VD/VTCO2 but reduced the influence of midrange .ovrhdot.VA/.ovrhdot.Q heterogeneity.

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