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

Abstract

Background 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. 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. Results 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. 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. Conclusions 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. Respiratory efforts in these patients should be carefully monitored and controlled to minimise the risk of lung injury.

Late Failure of High-Flow Nasal Cannula May Be Associated with High Mortality in COVID-19 Patients: A Multicenter Retrospective Study in the Republic of Korea

“…There is a concern regarding self-inflicted lung injury from the sustained high respiratory effort in spontaneously breathing patients [29]. A computational modeling study showed that the forces generated by increased inspiratory effort in acute hypoxic respiratory failure from COVID-19 are comparable to those involved in ventilator-induced lung injury [30]. Therefore, further prospective studies are needed to determine whether late failure causes diffuse alveolar damage.…”

Dynamic imaging for dynamic lung events

“…They found that elevated pixel values of DRRS were more frequent in COVID-19 patients as compared to healthy controls. As COVID-19 patients may be at increased risk for developing P-SILI [13], these data indicate that DRRS could prove to be a useful marker for early recognition of potentially injurious spontaneous efforts.…”

Pathophysiology of coronavirus-19 disease acute lung injury

“…A recently published study demonstrated that the median oesophageal pressure swing in non-COVID-19 patients with moderate or severe respiratory failure undergoing noninvasive ventilation trial was 34 cmH 2 O [ 72 ]. Although these phenomena have been identified in respiratory failure from any aetiology [ 74 , 75 ], including experimental lung oedema [ 76 ], modelling of data clearly shows that the forces generated by increased inspiratory effort are seen in COVID-19 are significant and compatible with the development of P-SILI [ 77 ]. Large inspiratory efforts – particularly when persisting despite noninvasive ventilation - are harbinger of physiological deterioration, failure of noninvasive support and need for invasive mechanical ventilation [ 72 ].…”