Sigh in acute respiratory failure

Mechanical ventilation, a cornerstone in the management of patients affected by acute respiratory failure, has undergone progressive and profound changes through the last 30 years. In the ’70s, tidal volumes (VT) as high as 10–15 ml/kg and elevated plateau pressures were routinely applied in patients with acute lung injury/acute respiratory distress syndrome (ALI/ARDS); apart from hypocapnia, no other major side effect was recognized at that time [1]. Positive end-expiratory pressure (PEEP) was already in use to enhance alveolar recruitment, targeted to optimize respiratory mechanics, gas exchange, and hemodynamics [2]. High VT could help in providing adequate arterial oxygenation at the lowest PEEP and inspired oxygen fraction (FiO2), considered to be the most important damaging factor for diseased lungs [3]. By the late ’80s, many authors had described animal models of ventilator-induced lung injury (VILI), showing how high airway pressure could induce severe lung injury [4] and histopathological findings strikingly similar to those of patients treated by injurious ventilation (ventilator lung) [5]. Subsequent studies identified the high transalveolar distending pressure (volu-barotrauma) [6] as a possible mechanism for lung rupture, fractures of epithelium and basement membrane [7]. More recent trials suggested that an intense inflammatory response (biotrauma) could be elicited by parenchymal stretching, and that high levels of cytokines could be found both in plasma and bronchoalveolar (BAL) fluid during high volume ventilation [8], though other studies applying similar experimental settings found that a lung injured by high VT ventilation does not cause, per se, a significant release of pro-inflammatory cytokines into the airspaces or the systemic circulation.