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American Journal of Respiratory and Critical Care Medicine Vol 166. pp. 403-408, (2002)
© 2002 American Thoracic Society

Original Article

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

Scott E. Sinclair, David A. Kregenow, Wayne J. E. Lamm, Ian R. Starr, Emil Y. Chi and Michael P. Hlastala

Departments of Medicine, Physiology and Biophysics, and Pathology, University of Washington, Seattle, Washington

Correspondence and requests for reprints should be addressed to Scott E. Sinclair, M.D., Division of Pulmonary and Critical Care Medicine, University of Washington, BB-1253 HSB Box 356522, Seattle, WA 98195-6522. E-mail: scottes{at}u.washington.edu

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 x 105 ± 0.18 x 105 versus 2.84 x 105 ± 0.28 x 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.

Key Words: respiratory acidosis • hypercapnia • mechanical ventilation • acute lung injury • rabbits




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