Abstract
BackgroundThere 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. However, direct clinical evidence linking increased inspiratory effort to lung injury is scarce. 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. 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.ResultsSimulations 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. 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. Pleural pressure swing increased from 12.0 ± 0.3 cmH2O at baseline to 33.8 ± 0.4 cmH2O at VT/RR of 7 ml/kg/30 breaths/min and to 46.2 ± 0.5 cmH2O at 10 ml/kg/30 breaths/min. Transpulmonary pressure swing increased from 4.7 ± 0.1 cmH2O at baseline to 17.9 ± 0.3 cmH2O at VT/RR of 7 ml/kg/30 breaths/min and to 24.2 ± 0.3 cmH2O at 10 ml/kg/30 breaths/min. Total lung strain increased from 0.29 ± 0.006 at baseline to 0.65 ± 0.016 at 10 ml/kg/30 breaths/min. Mechanical power increased from 1.6 ± 0.1 J/min at baseline to 12.9 ± 0.2 J/min at VT/RR of 7 ml/kg/30 breaths/min, and to 24.9 ± 0.3 J/min at 10 ml/kg/30 breaths/min. Driving pressure increased from 7.7 ± 0.2 cmH2O at baseline to 19.6 ± 0.2 cmH2O at VT/RR of 7 ml/kg/30 breaths/min, and to 26.9 ± 0.3 cmH2O at 10 ml/kg/30 breaths/min.ConclusionsOur 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. Respiratory efforts in these patients should be carefully monitored and controlled to minimise the risk of lung injury.
Highlights
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 [1] and respiratory rates (RR) of 34 breaths/min [2] have been reported
The aim of the study was to quantify the levels of these indicators of lung injury that are generated in our model by breathing patterns that are frequently encountered in COVID-19 patients
The simulated patient population replicates levels of hypoxaemia that have frequently been reported in spontaneously breathing COVID-19 patients. SaO2, PaO2 and PaCO2 on 100% oxygen at baseline were 83.8 ± 5.1%, 52.6 ± 7.1 mmHg, and 51.8 ± 1.5 mmHg, respectively (Table 1)
Summary
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 [1] and respiratory rates (RR) of 34 breaths/min [2] have been reported. A number of studies have established the potential for injurious effects due to spontaneous breathing during mechanical ventilation in acute respiratory failure, see [15] and the review in [16]. In the context of COVID-19, a recent study [20], has asserted an association between increased respiratory effort and worsening of respiratory function during attempts to wean patients from mechanical ventilation, without definitively establishing a delineation between cause and effect [10, 11]. 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. 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
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