Alveolar and Alveolar Duct Mechanics in the Acutely Injured Lung: Peeling Stress and Stress Multiplication

In Chap. 3 , we delved into the microanatomy of pulmonary parenchyma and explored the dynamic processes governing volume changes in alveoli and alveolar ducts. A pivotal aspect of comprehending the mechanisms behind alterations in lung volume is the intricate interconnection of alveoli, extending seamlessly from the alveolar walls to the pleural surface. This microarchitecture, coupled with a well-functioning surfactant system, ensures the even distribution of stress throughout the homogeneous lung tissue during tidal ventilation. This minimizes energy dissipation and prevents collapse during expiration, thereby maintaining a normal end-expiratory lung volume (EELV). Nevertheless, these micromechanics undergo profound alterations during acute lung injury (ALI). ALI induces a heterogeneous injury pattern, leading to areas of regional instability and collapse distributed across the lung. These initial lesions serve as focal points, facilitating the rapid propagation of ventilator-induced lung injury (VILI) throughout the pulmonary tissue. The fundamental stages in the pathogenesis of ALI include Endothelial Leakage → Surfactant Deactivation → Alveolar Edema → Repetitive Alveolar Collapse, and Re-expansion (RACE). Regional instability (RACE) and collapse, generating stress multipliers, constitute the mechanisms of VILI, giving rise to both atelectrauma and volutrauma within the microenvironment. This chapter will analyze how atelectrauma and volutrauma contribute to cellular damage and explore the interplay between the two. Additionally, the impact of regional alveolar instability and collapse on adjacent open alveoli will be assessed as an additional VILI mechanism. Finally, the progression of VILI over time will be examined.