Ventilator-induced lung injury and the evolution of lung-protective strategies in acute respiratory distress syndrome.

Traditional ventilator management of acute respiratory distress syndrome (ARDS), emphasizing normalization of blood gases, promoted high rates of conventional barotrauma. Research revealed a broader range of ventilator-induced lung injury, physiologically and histopathologically indistinguishable from ARDS itself. It is now known that overdistention and cyclic inflation of injured lung can exacerbate lung injury and probably promote systemic inflammation, effects minimized by low tidal volumes/plateau pressures and by application of positive end-expiratory pressure. No compelling data suggest a safe interval for nonprotective ventilation in humans; historically defined "low" tidal volumes may remain excessive for certain patients. Protective ventilation, however, entails carbon dioxide accumulation ("permissive hypercapnia"). Despite extensive study, debate remains, even over whether consequent respiratory acidosis is harmful, tolerable with physiologic adaptation, or intrinsically adaptive. Its gross systemic effects seem generally tolerated by critically ill patients; however, subsets, including those with ischemic heart disease, left or right heart failure, pulmonary hypertension, or cranial injury, may be at higher risk. In controlled trials demonstrating mortality benefit from lung-protective ventilation, acidosis was more tightly controlled than in negative studies. Decreased acidosis-associated dyspnea probably explains reduced use of sedatives and paralytics noted in those trials. There may thus be disparate goals in ARDS management: rapid institution of a restrictive ventilatory strategy, and avoidance of significant acidosis. We review data pertaining to ARDS physiology, ventilator-induced lung injury, lung-protective ventilatory strategies, and the physiology of respiratory acidosis. Tracheal gas insufflation is considered as a means to reconcile the clinical goals of ventilatory reduction and control of acidosis.