![]() ![]() ![]() As noted in, young, otherwise healthy adults can sustain tidal volumes of 20 ml/kg at a respiratory rate of 45 breaths/min almost indefinitely. On admission, some patients with COVID-19 acute hypoxaemic respiratory failure (AHRF) exhibit profound hypoxaemia, combined with relatively preserved lung compliance and lung gas volume on CT chest imaging, and substantial increases in respiratory effort-tidal volumes (VT) of 15–20 ml/kg and respiratory rates (RR) of 34 breaths/min have been reported. Respiratory efforts in these patients should be carefully monitored and controlled to minimise the risk of lung injury. Our results suggest that the forces generated by increased inspiratory effort commonly seen in COVID-19 acute hypoxaemic respiratory failure are comparable with those that have been associated with ventilator-induced lung injury during mechanical ventilation. Driving pressure increased from 7.7 ± 0.2 cmH 2O at baseline to 19.6 ± 0.2 cmH 2O at VT/RR of 7 ml/kg/30 breaths/min, and to 26.9 ± 0.3 cmH 2O at 10 ml/kg/30 breaths/min. Transpulmonary pressure swing increased from 4.7 ± 0.1 cmH 2O at baseline to 17.9 ± 0.3 cmH 2O at VT/RR of 7 ml/kg/30 breaths/min and to 24.2 ± 0.3 cmH 2O at 10 ml/kg/30 breaths/min. Pleural pressure swing increased from 12.0 ± 0.3 cmH 2O at baseline to 33.8 ± 0.4 cmH 2O at VT/RR of 7 ml/kg/30 breaths/min and to 46.2 ± 0.5 cmH 2O at 10 ml/kg/30 breaths/min. While oxygenation improved with higher respiratory efforts, significant increases in multiple indicators of the potential for lung injury were observed at all higher VT/RR combinations tested. 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 7/20, 7/30, 10/14, 10/20 and 10/30 ml/kg / breaths/min. In accordance with recent data, the simulator parameters were manually adjusted to generate a population of 10 patients that recapitulate clinical features exhibited by certain COVID-19 patients, i.e., severe hypoxaemia combined with relatively well-preserved lung mechanics, being treated with supplemental oxygen. We adapted a computational simulator of cardiopulmonary pathophysiology to quantify the mechanical forces that could lead to P-SILI at different levels of respiratory effort. However, direct clinical evidence linking increased inspiratory effort to lung injury is scarce. There is on-going 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 hypoxaemic respiratory failure.
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