Mechanical ventilation

Engineering

Ventilation (architecture)

Anesthesiology

Oxygenation

Cardiology

Heart rate

Anesthesia

Environmental health

Mechanical engineering

Lung volumes

Respiratory rate

Blood pressure

Population

Internal medicine

Respiratory system

Medicine

Respiratory physiology

Lung

Transpulmonary pressure

Annals of Intensive Care

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 cmH 2 O at baseline to 33.8 ± 0.4 cmH 2 O at VT/RR of 7 ml/kg/30 breaths/min and to 46.2 ± 0.5 cmH 2 O at 10 ml/kg/30 breaths/min. Transpulmonary pressure swing increased from 4.7 ± 0.1 cmH 2 O at baseline to 17.9 ± 0.3 cmH 2 O at VT/RR of 7 ml/kg/30 breaths/min and to 24.2 ± 0.3 cmH 2 O 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 cmH 2 O at baseline to 19.6 ± 0.2 cmH 2 O at VT/RR of 7 ml/kg/30 breaths/min, and to 26.9 ± 0.3 cmH 2 O 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.

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