Role of Tissue Viscoelasticity in the Pathogenesis of Ventilator-induced Lung Injury

Abstract

Biomechanics is mechanics applied to biology. One of its goals is to quantify the effect of mechanical stimuli on living organs and tissues, based on the relationship between the microscopic structure and the macroscopic function of these biological systems [1]. Ventilator-induced lung injury (VILI) can be defined as damage to the lungs (the biological system) triggered by physical forces (the mechanical stimuli) generated by an external ventilator. Biomechanical concepts could then be used to understand and predict the harm of mechanical ventilation. Based on this rationale, we and other authors have started to refer to the amplitude of lung inflation as “volumetric strain”, the velocity of lung inflation as “strain rate”, the reactive pulmonary tissue tension as “stress” and lung inhomogeneities as “stress risers” [2–6]. Ventilator- induced air leaks, such as pneumothorax, pneumomediastinum, subcutaneous em- physema or gaseous embolism, could then be interpreted as the rupture of one lung region that has been stretched above its upper physiological limit, or “ultimate ten- sile stress” [7]. Other lung injuries induced by less extreme inflation, including pul- monary edema, apparently develop as cumulative damage or “fatigue”. They start from microscopic structural discontinuities, slowly propagate and then suddenly grow into macroscopic defects [7]. The probability of developing these other lung injuries increases with the number of cycles of deformation, that is with the respi- ratory rate and the overall duration of mechanical ventilation [8]. As a general rule, the larger the mechanical stimulus, the lower the number of cycles to failure [7].