For Outpatients, Does Regional Anesthesia Truly Shorten the Hospital Stay, and How Should We Define Postanesthesia Care Unit Bypass Eligibility?

IN this issue of ANESTHESIOLOGY, Whitehead et al. 1 bring experimental evidence suggesting that a high tidal volume ventilation can markedly reduce the release of inflammatory cytokines in response to intratracheal lipopolysaccharide.They attribute this paradoxical effect to a reduction of the alveolar macrophage population and hypothesize that injurious ventilation may increase susceptibility to infection, a detrimental effect that may participate in ventilator-induced lung injury.Clinicians have long known some of the risks of mechanical ventilation.The classic and well-known manifestations of gross barotrauma (air leaks) and the adverse hemodynamic effects of high pressure/volume mechanical ventilation were described shortly after the generalization of mechanical ventilators in intensive care units.More recently, severe histologic distension of bronchoalveolar structures, 2 lung overinflation, 3-6 large air cysts, and extended bronchiectasis 7,8 have been reported in acute respiratory distress syndrome (ARDS) patients mechanically ventilated with high tidal volumes and pressures.One of the most important breakthroughs in the ventilatory management of such patients was the recognition of another iatrogenic potential of mechanical ventilation, which has been termed ventilator-induced lung injury (VILI).The concept was derived from animal studies that clearly showed that mechanical ventilation with high airway pressure and tidal volume rapidly caused a permeability-type pulmonary edema with diffuse alveolar damage and was accompanied by severe lung inflammation when protracted. 9 High lung volume rather than pressure was identified as responsible for these abnormalities, hence the term volutrauma.In the 1970s, the recommendation was to deliver generous tidal volumes in the range of 15-20 ml/kg to patients with acute lung injury 10,11 to provide adequate carbon dioxide elimination and counterbalance the formation of atelectasis with ensuing development of lung regions with low ventilation/perfusion ratios. 12 In the following years, practices progressively moved toward a