Airflow-Related Shear Stress: The Main Cause of VILI or not?

The physical basis of ventilator-induced lung injury has been explored extensively in the last decades. The three mechanisms named volutrauma (overdistension of alveoli), barotrauma (high airway pressure), and atelectrauma (cyclic opening and closing of alveoli) have been known as the main mechanisms of lung injury. Lowering tidal volume and applying positive end-expiratory pressure have been suggested to minimize these mechanisms. Besides, some researchers believe that elevated airflow-related shear stress on the epithelial cell layer could cause an inflammatory response.

In this study, a simplified 0-D model for air flow in human lungs has computed the airflow-related shear stress. The airway resistance, compliance, and inertance have been calculated using Womersley analysis and included in this model. Considering a constant flow, volume-controlled mechanical ventilation, the effect of ventilation parameters including tidal volume, respiratory rate, and inspiratory/expiratory ratio on the magnitude of shear stress has been investigated.

The results show that high tidal volume, high respiratory rate, and low inspiratory/expiratory ratio, increase the magnitude of wall shear stress but still in the safety range.

This result suggests that airflow-related shear stress is not the primary cause of mechanical damage. So far, it has been assumed that wall shear stress plays a critical role in ventilator-induced lung injury. This paper enhances our understanding of wall shear stress magnitude, indicating that the shear stress from airflow in mechanical ventilation is not high enough to inflict mechanical damage on pulmonary epithelial cells.