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KEY POINTS

KEY POINTS

  1. The pathophysiologic changes in the acute respiratory distress syndrome (ARDS) produce low-compliant lungs containing areas of atelectasis and reduced lung volumes.

  2. Positive pressure ventilation in this heterogenous syndrome can lead to overdistension of normally aerated lung regions and stress injury in atelectatic alveoli due to cyclic recruitment and derecruitment.

  3. Use of low-tidal-volume ventilation as lung-protection strategy has been studied since 1960s. Despite suggested benefits, concerns regarding additional metabolic abnormalities and hypoxemia in critically ill patients have existed.

  4. Results of the landmark ARDS in a large multicentre randomized trial found that the use of low tidal volume (6 mL/kg ideal body weight [IBW]) rather than “standard” tidal volume (12 mL/kg IBW) significantly reduced mortality. Although the trial was criticized for using excessively large tidal volumes in controls, the trial investigators subsequently published trial data detailing the clinical benefits of tidal volume and plateau pressure reduction across the range of disease severity and plateau pressures.

  5. Recent data suggest that many mechanically ventilated patients with ARDS have stress index that indicates alveolar hyperventilation while receiving positive end-expiratory pressure (PEEP) according to the ARDS Network recommendation, advocating even lower tidal volumes.

  6. Use of adjunct therapies such as extracorporeal membrane oxygenation may be useful in select patients where lowering tidal volume can lead to serious metabolic abnormalities.

INTRODUCTION

The pathophysiologic changes in the acute respiratory distress syndrome (ARDS) produce low-compliant lungs with atelectasis and reduced lung volumes. Such stiff lungs frequently lead to respiratory failure from severe hypoxemia requiring mechanical ventilation for life support. Computed tomography shows a heterogeneous involvement of lung injury in ARDS and that approximately only a third of the lung is normally aerated (“baby lung”).1 Positive pressure ventilation can worsen lung injury due to differential distribution of each ventilator-delivered breath. The normally aerated lung regions with the highest compliance receive the largest part of the tidal volume (TV) and are exposed to overdistention from high alveolar wall tension and stress. Conversely, atelectatic nonaerated alveoli are exposed to further damage from shear stress due to cyclic recruitment and derecruitment. Therefore, ventilation strategies in ARDS need to simultaneously reverse life-threatening hypoxemia while protecting the lungs from further injury. Since the first description of ARDS by Ashbaugh in 1967, several decades of experimental and clinical research have shifted the primary goal of mechanical ventilation from a normalization of the arterial-blood gas to a more “lung-protective” ventilation strategy. What follows is a description of the history of mechanical ventilation in ARDS, data on published clinical trials, the debate on low-TV ventilation, barriers for implementation of this approach, and our conclusions and suggestions to the readers.

HISTORY OF VENTILATORY STRATEGIES IN ARDS

In the 1960s, the use of high TVs in all mechanically ventilated patients was considered routine care based on the study by Bendixen et al that showed improved oxygenation, less acidosis and atelectasis in anesthetized patients undergoing laparotomy ...

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