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J Appl Physiol 55: 1550-1557, 1983;
8750-7587/83 $5.00
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Journal of Applied Physiology, Vol 55, Issue 5 1550-1557, Copyright © 1983 by American Physiological Society

ARTICLES

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

R. L. Coffey, R. K. Albert and H. T. Robertson

In acute increased-permeability edema, the Bohr physiological dead space (VD/VTCO2) can be influenced by changes in anatomic dead space, ventilation-perfusion (VA/Q) heterogeneity, shunt, and the Haldane effect. We used the multiple inert gas elimination technique 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 cmH2O was applied in random sequence. Following injury VD/VTCO2 increased. It decreased with 5 or 10 cmH2O PEEP but increased progressively at higher PEEP levels. The decrease in VD/VTCO2 at 5 or 10 cmH2O PEEP was due to reductions in shunt and midrange VA/Q heterogeneity. The increase in VD/VTCO2 that occurred with higher PEEP levels was due to increased ventilation to high VA/Q regions and a larger anatomic dead space. Haldane effect magnified the shunt component of VD/VTCO2 but reduced the influence of midrange VA/Q heterogeneity.


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