Liam Weaver1, Anup Das1, Sina Saffaran2, Nadir Yehya3, Timothy E Scott4, Marc Chikhani5, John G Laffey6, Jonathan G Hardman7,5, Luigi Camporota8, Declan G Bates9. 1. School of Engineering, University of Warwick, Coventry, CV4 7AL, UK. 2. Faculty of Engineering Science, University College London, London, WC1E 6BT, UK. 3. Department of Anaesthesiology and Critical Care Medicine, Children's Hospital of Philadelphia, University of Pennsylvania, Philadelphia, PA, USA. 4. Academic Department of Military Anaesthesia and Critical Care, Royal Centre for Defence Medicine, ICT Centre, Birmingham, B15 2SQ, UK. 5. Nottingham University Hospitals NHS Trust, Nottingham, NG7 2UH, UK. 6. Anaesthesia and Intensive Care Medicine, School of Medicine, NUI Galway, Galway, Ireland. 7. Anaesthesia & Critical Care, Division of Clinical Neuroscience, School of Medicine, University of Nottingham, Nottingham, NG7 2UH, UK. 8. Department of Critical Care, Guy's and St Thomas' NHS Foundation Trust, London, UK. luigi.camporota@gstt.nhs.uk. 9. School of Engineering, University of Warwick, Coventry, CV4 7AL, UK. d.bates@warwick.ac.uk.
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.
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-19acute 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-19patients, 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-19acute 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.
Authors: Pablo Cruces; Jaime Retamal; Daniel E Hurtado; Benjamín Erranz; Pablo Iturrieta; Carlos González; Franco Díaz Journal: Crit Care Date: 2020-08-10 Impact factor: 9.097
Authors: Abdul Rahman Al Armashi; Francisco J Somoza-Cano; Kanchi Patell; Mohamed Homeida; Omkar Desai; Anas Al Zubaidi; Basel Altaqi; Keyvan Ravakhah Journal: Radiol Case Rep Date: 2021-10-04
Authors: Liam Weaver; Anup Das; Sina Saffaran; Nadir Yehya; Marc Chikhani; Timothy E Scott; John G Laffey; Jonathan G Hardman; Luigi Camporota; Declan G Bates Journal: Br J Anaesth Date: 2022-03-18 Impact factor: 11.719
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