Hypercapnic Acidosis Is Protective in an In Vivo Model of Ventilator-induced Lung Injury

To investigate whether hypercapnic acidosis protects against ventilator-induced lung injury (VILI) in vivo, we subjected 12 anesthetized, paralyzed rabbits to high tidal volume ventilation (25 cc/kg) at 32 breaths per minute and zero positive end-expiratory pressure for 4 hours. Each rabbit was randomized to receive either an FiCO2 to achieve eucapnia (PaCO2 ∼ 40 mm Hg; n = 6) or hypercapnic acidosis (PaCO2 80–100 mm Hg; n = 6). Injury was assessed by measuring differences between the two groups' respiratory mechanics, gas exchange, wet:dry weight, bronchoalveolar lavage fluid protein concentration and cell count, and injury score. The eucapnic group showed significantly higher plateau pressures (27.0 ± 2.5 versus 20.9 ± 3.0; p = 0.016), change in PaO2 (165.2 ± 19.4 versus 77.3 ± 87.9 mm Hg; p = 0.02), wet:dry weight (9.7 ± 2.3 versus 6.6 ± 1.8; p = 0.04), bronchoalveolar lavage protein concentration (1,350 ± 228 versus 656 ± 511 μg/ml; p = 0.03), cell count (6.86 × 105 ± 0.18 × 105 versus 2.84 × 105 ± 0.28 × 105 nucleated cells/ml; p = 0.021), and injury score (7.0 ± 3.3 versus 0.7 ± 0.9; p < 0.0001). We conclude that hypercapnic acidosis is protective against VILI in this model.