The Acutely Injured Lung Becomes Time/Press Dependent

The pulmonary microstructure is stabilized by an architecture of interdependent, connected alveolar walls and parenchymal tethering and, when combined with a functioning surfactant system, results in a very stable homogeneous inflation pattern (Chap. 3 ). In the acutely injured lung, loss of these stabilizing factors renders the lung time- and pressure-dependent, meaning it will take more time for alveoli to open and less time for them to collapse at any given airway pressure. This can result in a heterogeneous inflation pattern with normal open alveoli, collapsed alveoli (atelectasis), and unstable alveoli scattered throughout the lung, all of which are known mechanisms of ventilator-induced lung injury (VILI) (Chap. 4). In addition, if the pulmonary parenchyma remains atelectatic for an extended period, it is associated with multiple lung pathologies (Chap. 2 , Problems caused by long-term atelectasis) and creates areas of stress multiplication that cause both atelectrauma and volutrauma. Unstable alveoli result in repetitive alveolar collapse and expansion (RACE), which is the mechanism of atelectrauma. If RACE is allowed to continue unchecked, the excessive shear or “peeling” stress in collapsed alveoli and small airways as they reopen would cause damage to the endothelial cells in apposition as they separate with each breath. The collapsed or edema-filled tissue also generates stress multipliers that will damage the normal surrounding tissue by both atelectrauma and volutrauma. Since alveolar and alveolar duct (acinar) opening and collapse are viscoelastic in nature and thus time-dependent, appropriate adjustment of ventilator inspiratory and expiratory time might be used to effectively stabilize and then reopen these pulmonary microstructures pulling them out of the VILI vortex. More importantly, the acutely injured lung becomes time- and pressure-dependent, suggesting longer inspiratory time to open collapsed tissue and less expiration to prevent re-collapse. Applying physiologic principles to understand the mechanics of dynamic acinar inflation and deflation and how these mechanics change in the acutely injured lung is critical to developing novel protective ventilation strategies.