Mechanisms of physiological dead space response to PEEP after acute oleic acid lung injury.
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.
D000208:Acute Disease; D000818:Animals; D001696:Biomechanical Phenomena; D004285:Dogs; D009829:Oleic Acids; D011175:Positive-Pressure Respiration; D011654:Pulmonary Edema / Q000139:chemically induced / Q000503:physiopathology*; D012126:Respiratory Dead Space; D014692:Ventilation-Perfusion Ratio
D009829:Oleic Acids