Abstract
The pathophysiology of acute respiratory distress syndrome (ARDS) results in heterogeneous lung collapse, edema-flooded airways and unstable alveoli. These pathologic alterations in alveolar mechanics (i.e. dynamic change in alveolar size and shape with each breath) predispose the lung to secondary ventilator-induced lung injury (VILI). It is our viewpoint that the acutely injured lung can be recruited and stabilized with a mechanical breath until it heals, much like casting a broken bone until it mends. If the lung can be “casted” with a mechanical breath, VILI could be prevented and ARDS incidence significantly reduced.
Highlights
The pathophysiology of acute respiratory distress syndrome (ARDS) results in heterogeneous lung collapse, edema-flooded airways and unstable alveoli
After the healing takes place will the cast be removed; otherwise the bone will re-fracture, exacerbating the original injury and causing further tissue injury. This analogy illustrates the possibility that acute respiratory distress syndrome (ARDS), resulting in repetitive alveolar collapse and expansion (RACE) [1], would result in progressive tissue damage known as ventilator-induced lung injury (VILI), unless a mechanical ventilation “cast”
This is exemplified in clinical trials testing the efficacy of open-lung ventilation strategies where normalized oxygenation is equated with alveolar stability, triggering a reduction in airway pressure or ventilation mode change, which occurred in the high frequency oscillatory ventilation (HFOV) trials or when using the positive end-expiratry pressure (PEEP)/fraction of inspired oxygen (FiO2) scale of low tidal volume (Vt) strategy [6, 7]
Summary
The pathophysiology of acute respiratory distress syndrome (ARDS) results in heterogeneous lung collapse, edema-flooded airways and unstable alveoli. During ARDS, the lung is pressure dependent (i.e. will collapse at atmospheric pressure) and both time to recover and an environment conducive to regaining inherit lung stability are required before the pressure stabilizing (casting) the lung can be withdrawn This is exemplified in clinical trials testing the efficacy of open-lung ventilation strategies where normalized oxygenation is equated with alveolar stability, triggering a reduction in airway pressure or ventilation mode change, which occurred in the high frequency oscillatory ventilation (HFOV) trials or when using the positive end-expiratry pressure (PEEP)/fraction of inspired oxygen (FiO2) scale of low tidal volume (Vt) strategy [6, 7]. All too often following recruitment of the acutely injured lung there is a compulsion to reduce airway pressure as soon as oxygenation increases and the “casted” lung becomes “unstable” again with VILI-induced tissue damage recurring
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