Mechanisms of pulmonary gas exchange improvement during a protective ventilatory strategy in acute respiratory distress syndrome

To investigate the mechanisms underlying improvement of arterial oxygenation during a protective ventilatory strategy (PVS) in early acute respiratory distress syndrome (ARDS), we studied eight patients during volume-controlled mechanical ventilation, keeping respiratory rate and fraction of inspired oxygen (Fi(O2)) (0.82 +/- 0.20) unchanged: (1) at baseline (tidal volume [VT] 10 to 12 ml (.) kg(-1); positive end-expiratory pressure [PEEP] 8 to 10 cm H2O); (2) during PVS (PEEP 2 cm H2O above the low inflexion point (P-FLEX) and VT of S to 7 ml (.) kg(-1)); and (3) post-PVS, back to baseline conditions. Inert gas measurements were done after 30 min in each ventilatory modality. During PVS, Pa-O2 increased significantly from 93 +/- 27 to 166 +/- 77 mm Hg (p < 0.008) and Pa-CO2 rose from 39 +/- 7 to 57 +/- 11 mm. Hg (p < 0.0002) because of the decrease in minute ventilation (VE) (-3.6 L (.) min) (p < 0.005). Both heart rate (HR, +13 min(-1)) (p < 0.002) and cardiac output (Q, +1.2 L (.) min(-1)) (p < 0.05) increased. Static respiratory system linear compliance increased from 36 +/- 14 to 44 +/- 16 ml (.) cm H2O-1 (p < 0.0002). PVS provoked recruitment of previously collapsed alveoli and redistribution of pulmonary blood flow from nonventilated alveoli to normal lung. Despite the increase in Q, intrapulmonary shunt fell from 39 +/- 15% to 31 +/- 11% (p < 0.04). We conclude that the decrease in intrapulmonary shunt owing to alveolar recruitment remains the pivotal mechanism to explain improvement of arterial oxygenation during this PVS.