Editorial Views  |   January 2019
Mechanical Power: A Biomarker for the Lung?
Author Notes
  • From the Keenan Research Centre, Li Ka Shing Knowledge Institute, St. Michael’s Hospital, Toronto, Ontario, Canada (L.B.); the Interdepartmental Division of Critical Care Medicine, University of Toronto, Toronto, Ontario, Canada (L.B.); and the Intensive and Critical Care Unit, Flinders Medical Centre, Department of Critical Care Medicine, Flinders University, Bedford Park, Australia (A.B.).
  • Accepted for publication September 24, 2018.
    Accepted for publication September 24, 2018.×
  • Corresponding article on page 119.
    Corresponding article on page 119.×
  • Address correspondence to Dr. Brochard: brochardl@smh.ca
Article Information
Editorial Views / Respiratory System
Editorial Views   |   January 2019
Mechanical Power: A Biomarker for the Lung?
Anesthesiology 1 2019, Vol.130, 9-11. doi:10.1097/ALN.0000000000002505
Anesthesiology 1 2019, Vol.130, 9-11. doi:10.1097/ALN.0000000000002505
Ventilator-induced lung injury is a multifaceted problem that has progressively become a preoccupation for intensivists and anesthesiologists. It has taken many years to realize that mechanical ventilation, a life-saving technique, could also induce harm. The first randomized controlled trial in critical care compared extracorporeal membrane oxygenation to mechanical ventilation in patients with severe acute respiratory distress syndrome, with the premise that this technique could improve gas exchange and save lives.1  Because, at the end of the 1970s, the mechanical insult to the lungs caused by mechanical ventilation was not considered as a relevant or important problem (oxygen toxicity was much more of a concern), the two arms in the trials received the same “injurious” mechanical ventilation and had the same dismal outcome. Pioneer experimental work from Webb and Tierney2  and later from Dreyfuss and Saumon3  progressively demonstrated the potential of large volumes and pressures to cause injury either in previously healthy or already injured lungs. The concepts of atelectrauma and biotrauma were later proposed by Tremblay et al.4  in Slutsky’s group to explain the observed protective effects of positive end-expiratory pressure (PEEP) and to show the link between local mechanically induced inflammatory effects with both the systemic multiorgan failure observed in these patients and their high mortality. Pressure limitation in the alveoli, assessed by the plateau pressure, was introduced in clinical practice by recommendations in the early 1990s5  and was based on the baby lung concept6  and an early clinical report by Hickling et al.7  suggesting, in 1990, a marked improvement in survival resulting from deliberately limiting pressures and volumes. The proof of concept was brought by the 12 versus 6 ml/kg positive pressure ventilation trial in 2000,8  which showed that 25% of the actual mortality observed using 12 ml/kg of predicted body weight could be avoided by limiting tidal volume to around 6 ml/kg and plateau pressure to 30 cm H2O. Numerous studies then discussed how far tidal volume should be reduced to remain protective in acute respiratory distress syndrome, whereas other studies have shown that lung protection needed to be extended beyond the field of acute respiratory distress syndrome, including data suggesting that this concept of lung protection could also apply to the field of intraoperative ventilation.9