Pressure support ventilation improves oxygenation by redistribution of pulmonary blood flow in experimental lung injury

Introduction

The presence of spontaneous breathing (SB) activity may improve gas exchange during mechanical ventilation. Pressure support ventilation (PSV) is one of the most frequently used modes of assisted mechanical ventilation, but little is known about the mechanisms of improvement of lung function during PSV. To shed light into this issue, we evaluated the regional distribution of aeration and pulmonary blood flow (PBF) during controlled and assisted mechanical ventilation with PSV in experimental acute lung injury.

Methods

In five anesthetized, controlled mechanically ventilated pigs, acute lung injury was induced by surfactant depletion. The ventilatory mode was switched to biphasic intermittent positive airway pressure ventilation and the depth of anesthesia reduced to resume SB. When SB represented 20% of the minute ventilation, animals were ventilated with PSV during 1 hour. Measurements of lung mechanics, gas exchange and hemodynamics, as well as whole lung computed tomography at mean airway pressure, were obtained at baseline, injury and during assisted ventilation with PSV. In addition, PBF was marked with intravenously administered fluorescent microspheres and spatial cluster analysis was used to determine the effects of interventions in the distribution of PBF. Statistical analysis was performed with Wilcoxon's test and P < 0.05 was considered significant.

Results

In injured lungs under controlled mechanical ventilation, impairment of oxygenation was associated with a significant increase of poorly aerated and nonaerated areas in dependent lung regions. Resuming of SB and assisted mechanical ventilation with PSV led to a decrease in mean airway pressures and improvement in oxygenation, but not in total and dependent lung aeration. However, redistribution of PBF toward well aerated nondependent regions was observed.

Conclusion

The improvement of oxygenation during PSV seems not to result from recruitment of dependent lung areas, but rather from redistribution of PBF from dependent, less aerated lung zones toward better aerated, nondependent lung regions.