Fifty Years of Research in ARDS. Vt Selection in Acute Respiratory Distress Syndrome

Abstract

Mechanical ventilation (MV) is critical in the management of many patients with acute respiratory distress syndrome (ARDS). However, MV can also cause ventilator-induced lung injury (VILI). The selection of an appropriate Vt is an essential part of a lung-protective MV strategy. Since the publication of a large randomized clinical trial demonstrating the benefit of lower Vts, the use of Vts of 6 ml/kg predicted body weight (based on sex and height) has been recommended in clinical practice guidelines. However, the predicted body weight approach is imperfect in patients with ARDS because the amount of aerated lung varies considerably due to differences in inflammation, consolidation, flooding, and atelectasis. Better approaches to setting Vt may include limits on end-inspiratory transpulmonary pressure, lung strain, and driving pressure. The limits of lowering Vt have not yet been established, and some patients may benefit from Vts that are lower than those in current use. However, lowering Vts may result in respiratory acidosis. Tactics to reduce respiratory acidosis include reductions in ventilation circuit dead space, increases in respiratory rate, higher positive end-expiratory pressures in patients who recruit lung in response to positive end-expiratory pressure, recruitment maneuvers, and prone positioning. Mechanical adjuncts such as extracorporeal carbon dioxide removal may be useful to normalize pH and carbon dioxide levels, but further studies will be necessary to demonstrate benefit with this technology.

Keywords: acute respiratory distress syndrome; mechanical ventilation; tidal volume.

Figure 1.

Patient–ventilator dyssynchrony with triggering of double breaths from the ventilator in volume-assist control mode. The first channel demonstrates airway pressure with a normal breath followed by a double breath triggered by the patient. The second channel shows flow during a normal breath followed by a double breath. Patient inspiratory effort continues beyond the set ventilator inspiratory time, resulting in airway pressure decreasing below the positive end-expiratory pressure and triggering a second breath during the same patient effort. This may result in high lung pressures (during the double breath: top panel) and high volumes. The third channel demonstrates increased volumes during double-triggered breaths. If patients consistently trigger double breaths, they will not be receiving low Vts for lung protection during the double breaths and are at increased risk for overdistention.

Figure 2.

Relative risk of death in the hospital versus driving pressure in the combined cohort after multivariate adjustment. Even below the median driving pressure of 14 cm H₂O, there is still a significant risk of death in the hospital. Reprinted by permission from Reference .