Expiratory flow-limitation in mechanically ventilated patients: A risk for ventilator-induced lung injury?

Abstract

Expiratory flow limitation (EFL), that is the inability of expiratory flow to increase in spite of an increase of the driving pressure, is a common and unrecognized occurrence during mechanical ventilation in a variety of intensive care unit conditions. Recent evidence suggests that the presence of EFL is associated with an increase in mortality, at least in acute respiratory distress syndrome (ARDS) patients, and in pulmonary complications in patients undergoing surgery. EFL is a major cause of intrinsic positive end-expiratory pressure (PEEPi), which in ARDS patients is heterogeneously distributed, with a consequent increase of ventilation/perfusion mismatch and reduction of arterial oxygenation. Airway collapse is frequently concomitant to the presence of EFL. When airways close and reopen during tidal ventilation, abnormally high stresses are generated that can damage the bronchiolar epithelium and uncouple small airways from the alveolar septa, possibly generating the small airways abnormalities detected at autopsy in ARDS. Finally, the high stresses and airway distortion generated downstream the choke points may contribute to parenchymal injury, but this possibility is still unproven. PEEP application can abolish EFL, decrease PEEPi heterogeneity, and limit recruitment/derecruitment. Whether increasing PEEP up to EFL disappearance is a useful criterion for PEEP titration can only be determined by future studies.

Keywords: Expiratory flow-limitation; Mechanical ventilation; Ventilator-induced lung injury; Acute respiratory distress syndrome; Positive end-expiratory pressure; Intrinsic positive end-expiratory pressure

Core tip: Expiratory flow limitation (EFL), the inability of expiratory flow to increase despite increasing driving pressure, is a common unrecognized occurrence during mechanical ventilation in a variety of intensive care unit conditions. It implies cyclic compression/decompression of the airways, is associated with intrinsic positive end-expiratory pressure (PEEPi) and inhomogeneous filling, and is often concomitant with cyclic recruitment/derecruitment. In acute respiratory distress syndrome, the development of abnormally high stresses is potentially injurious for the lung. External PEEP abolishes EFL and decreases ventilation and intrinsic PEEP heterogeneity, improving gas exchange. Moreover, external PEEP prevents cyclic airway collapse/reopening, possibly protecting the parenchyma from low lung volume ventilator-induced lung injury.