High risk of patient self-inflicted lung injury in COVID-19 with frequently encountered spontaneous breathing patterns: a computational modelling study

Das, A.; Weaver, L.; Saffaran, S.; Yehya, N.; Scott, T. E.; Chikhani, M.; Laffey, J. G.; Hardman, J. G.; Camporota, L.; Bates, D.

There is ongoing controversy regarding the potential for increased respiratory effort to generate patient self-inflicted lung injury (P-SILI) in spontaneously breathing patients with COVID-19 acute respiratory failure. However, direct clinical evidence linking increased inspiratory effort to lung injury is scarce. We adapted a recently developed computational simulator that replicates distinctive features of COVID-19 pathophysiology to quantify the mechanical forces that could lead to P-SILI at different levels of respiratory effort. In accordance with recent data, the simulator was calibrated to represent a spontaneously breathing COVID-19 patient with severe hypoxaemia (SaO2 80.6%) and relatively well-preserved lung mechanics (lung compliance of 47.5 ml/cmH2O), being treated with supplemental oxygen (FiO2 = 100%). Simulations were conducted at tidal volumes (VT) and respiratory rates (RR) of 7 ml/kg and 14 breaths/min (representing normal respiratory effort) and at VT/RR of 15/14, 7/20, 15/20, 10/30, 12/30, 10/35, 12/35, 10/40, 12/40 ml/kg / breaths/min. Lung compliance was unaffected by increased VT but decreased significantly at higher RR. While oxygenation improved, significant increases in multiple indicators of the potential for lung injury were observed at all higher VT/RR combinations tested. Pleural pressure swing increased from 10.1 cmH2O at baseline to 30 cmH2O at VT/RR of 15 ml/kg / 20 breaths/min and to 54.6 cmH2O at 12 ml/kg / 40 breaths/min. Dynamic strain increased from 0.3 to 0.49 at VT/RR of 12 ml/kg / 30 breaths/min, and to 0.6 at 15 ml/kg / 20 breaths/min. Mechanical power increased from 7.83 J/min to 17.7 J/min at VT/RR of 7 ml/kg / 20 breaths/min, and to 240.5 7 J/min at 12 ml/kg / 40 breaths/min. Our results suggest that the forces generated during increased inspiratory effort in severe COVID-19 are compatible with the development of P-SILI. If conventional oxygen therapy or non-invasive ventilation is ineffective in reducing respiratory effort, control of driving and transpulmonary pressures with invasive ventilation may reduce the risk of P-SILI and allow time for the resolution of the underlying condition.