Biologic Impact of Mechanical Power at High and Low Tidal Volumes in Experimental Mild Acute Respiratory Distress Syndrome.

Background: The authors hypothesized that low tidal volume (V-T) would minimize ventilator-induced lung injury regardless of the degree of mechanical power. The authors investigated the impact of power, obtained by different combinations of V-T and respiratory rate (RR), on ventilator-induced lung injury in experimental mild acute respiratory distress syndrome (ARDS). Methods: Forty Wistar rats received Escherichia coli lipopolysaccharide intratracheally. After 24h, 32 rats were randomly assigned to be mechanically ventilated (2 h) with a combination of different V-T (6 ml/kg and 11 ml/kg) and RR that resulted in low and high power. Power was calculated as energy (Delta P,(2)(L)/E,(L)) x RR (Delta P,(L) = transpulmonary driving pressure; E,(L) = lung elastance), and was three-fold higher in high than in low power groups. Eight rats were not mechanically ventilated and used for molecular biology analysis. Results: Diffuse alveolar damage score, which represents the severity of edema, atelectasis, and overdistension, was increased in high V-T compared to low V-T, in both low (low V-T: 11 [9 to 14], high V-T: 18 [15 to 20]) and high (low V-T: 19 [16 to 25], high V-T: 29 [27 to 30]) power groups. At high V-T, interleukin-6 and amphiregulin expressions were higher in high-power than in low-power groups. At high power, amphiregulin and club cell protein 16 expressions were higher in high V-T than in low V-T. Mechanical energy and power correlated well with diffuse alveolar damage score and interleukin-6, amphiregulin, and club cell protein 16 expression. Conclusions: In experimental mild ARDS, even at low V-T, high mechanical power promoted ventilator-induced lung injury. To minimize ventilator-induced lung injury, low V-T should be combined with low power.