Continuous versus pulsatile pulmonary hemodynamics in canine oleic acid lung injury

Pulmonary hypertension occurs commonly in the acute respiratory distress sy ndrome (ARDS), but associated right ventricular failure is relatively rare. We tested the hypothesis that this apparent contradiction is explained by a peripheral location of the increased pulmonary vascular resistance (Rpva) . Experimental ARDS was induced in eight dogs by injection of oleic acid (0 .07 ml/kg). Changes in Rpva were evaluated by measurements of pulmonary art ery pressure (Ppa) at several levels of flow ((Q) over dot), which was alte red by manipulation of venous return. The analysis of Ppa decay curves afte r arterial balloon occlusion was used to partition Rpva into arterial and v enous segments. Right ventricular afterload was evaluated by determination of pulmonary vascular impedance (Zpva), which was calculated from spectral analysis of Ppa and (Q) over dot waves. Oleic acid lung injury was associat ed with an increase in both the slope and the extrapolated pressure interce pt of Ppa/(Q) over dot plots, no change in the partitioning of Rpva, no cha nge in time-domain indices in wave reflection or in pulmonary arterial comp liance, and a decrease in both the characteristic impedance and pulsatile c omponent of total right ventricular hydraulic load. We conclude that the si te of increased Rpva in oleic acid lung injury is the smallest pulmonary ar terioles, which, together with a decreased characteristic impedance, contri butes to minimize right ventricular afterload.