Alveolar and Alveolar Duct (Acinar) Mechanics in the Normal Lung

Chapters 1 and 2 established the unifying hypothesis of ventilator-induced lung injury (VILI), emphasizing its predisposition by the pulmonary microenvironment’s pathophysiology in the context of acute respiratory distress syndrome (ARDS). The review extended to current mechanical ventilation strategies aimed at minimizing VILI. In Chap. 3 , we will backtrack and delve into the normal microanatomy of the pulmonary parenchyma. Our focus will be on comprehending the mechanisms governing the change in volume of alveoli and alveolar ducts during tidal ventilation. The significance lies in understanding the micromechanics of normal alveoli and alveolar ducts, specifically their alterations in size and shape during inflation and deflation. This comprehension is crucial because a homogeneous inflation pattern, characteristic of normal physiology, avoids energy dissipation and tissue injury. In contrast, the heterogeneous inflation patterns observed in acute lung injury, featuring regional alveolar instability and collapse, contribute to energy dissipation and tissue injury—known mechanisms of VILI. Armed with this knowledge, we can formulate logically derived, novel ventilator strategies designed to mitigate VILI by restoring normal alveolar mechanics (Bates and Smith, Ann Transl Med 6:378, 2018; Gattinoni et al., Intensive Care Med 42:1567–75, 2016). To address the consequences of altered alveolar mechanics-induced tissue injury, the applied physiology solution involves restoring normal alveolar mechanics through adjustments in mechanical ventilation. This approach is grounded in an understanding of dynamic alveolar inflation mechanisms. The impact of altered alveolar mechanics on tissue injury can be analyzed using engineering principles such as stress, strain, dissipated mechanical power, and energy (i.e., power or energy delivered to the lung that does not return during exhalation). This analysis is the basis for designing innovative protective ventilation strategies targeting the lung’s nano-, micro-, and macro-environmental levels). Altered alveolar mechanics in the acutely injured lung give rise to regional phenomena like repetitive alveolar collapse and expansion (RACE) and microatelectasis, generating stress multipliers. With each breath, these stress multipliers contribute to increased dissipated energy in the surrounding normal tissue. The viscoelastic nature of changes in alveolar and alveolar duct volume entails specific characteristics, including (i) a time lag when airway pressure is applied during tidal ventilation and lung volume increase begins, (ii) alveoli may continue to expand and recruit without an increase in airway pressure (referred to as creep), and (iii) there is a time lag when airway pressure is reduced during exhalation and lung volume begins to decrease. ARDS modifies viscoelastic alveolar mechanics, rendering the lung time- and pressure-dependent. This implies that alveoli take longer to recruit and less time to re-collapse at any given airway pressure (as discussed in Chap. 5 ). This understanding suggests that the Mechanical Breath Profile (MBP), encompassing all airway pressures, volumes, flows, rates, and the time they are applied during inspiration and expiration, can be leveraged to minimize VILI. Specifically, inspiratory and expiratory time components and pressure can be utilized to recruit alveoli and prevent re-collapse. Thus, time emerges as a crucial tool in normalizing alveolar micromechanics, a necessity for minimizing VILI.