Relative roles of vascular and airspace pressures in ventilator-induced lung injury

Objective. To determine whether elevations in pulmonary vascular pressure i nduced by mechanical ventilation are more injurious than elevations of pulm onary vascular pressure of similar magnitude occurring in the absence of me chanical ventilation. Design: Prospective comparative laboratory investigation. Setting. University research laboratory. Subjects: Male New Zealand white rabbits. Interventions: Three groups of isolated, perfused rabbit lungs were exposed to cyclic elevation of pulmonary artery pressures arising from either inte rmittent positive pressure mechanical ventilation or from pulsatile perfusi on of lungs held motionless by continuous positive airway pressure. Peak, m ean, and nadir pulmonary artery pressures and mean airway pressure were mat ched between groups (35, 27.4 +/- 0.74, and 20.8 +/- 1.5 mm Hg, and 17.7 +/ - 0.22 cm H2O, respectively). Measurements and Main Results: Lungs exposed to elevated pulmonary artery p ressures attributable to intermittent positive Pressure mechanical ventilat ion formed more edema (6.8 +/- 1.3 vs. 1.1 +/- 0.9 g/g of lung), displayed more perivascular (61 +/- 26 vs. 15 +/- 13 vessels) and alveolar hemorrhage (76 +/- 11 % vs. 26 +/- 18% of alveoli), and underwent larger fractional d eclines in static compliance (88 +/- 4.4% vs. 48 +/- 25.1% decline) than lu ngs exposed to similar peak and mean pulmonary artery pressures in the abse nce of tidal positive pressure ventilation. Conclusions: Isolated phasic elevations of pulmonary artery pressure may ca use less damage than those occurring during intermittent positive pressure mechanical ventilation, suggesting that cyclic changes in perivascular pres sure surrounding extra-alveolar vessels may be important in the genesis of ventilator-induced lung injury.