Risk factors for ventilator-induced-lung injury develop three to five times faster after a single episode of lung injury.

Autor: Rohrs EC; Advancing Innovation in Medicine Institute, New Westminster, BC, Canada.; Fraser Health Authority, Royal Columbian Hospital, New Westminster, BC, Canada.; Simon Fraser University, Burnaby, BC, Canada., Bassi TG; Simon Fraser University, Burnaby, BC, Canada.; Lungpacer Medical USA Inc., Exton, PA, USA., Nicholas M; Fraser Health Authority, Royal Columbian Hospital, New Westminster, BC, Canada.; Simon Fraser University, Burnaby, BC, Canada., Wittmann J; Fraser Health Authority, Royal Columbian Hospital, New Westminster, BC, Canada., Ornowska M; Simon Fraser University, Burnaby, BC, Canada., Fernandez KC; Fraser Health Authority, Royal Columbian Hospital, New Westminster, BC, Canada.; Simon Fraser University, Burnaby, BC, Canada., Gani M; Lungpacer Medical USA Inc., Exton, PA, USA., Reynolds SC; Advancing Innovation in Medicine Institute, New Westminster, BC, Canada.; Fraser Health Authority, Royal Columbian Hospital, New Westminster, BC, Canada.; Simon Fraser University, Burnaby, BC, Canada.
Jazyk: angličtina
Zdroj: Canadian journal of respiratory therapy : CJRT = Revue canadienne de la therapie respiratoire : RCTR [Can J Respir Ther] 2023 Apr 11; Vol. 59, pp. 103-110. Date of Electronic Publication: 2023 Apr 11 (Print Publication: 2023).
DOI: 10.29390/cjrt-2022-075
Abstrakt: Introduction: Mechanical ventilator breaths provided to deeply sedated patients have an abnormal volume distribution, encouraging alveolar collapse in dependent regions and promoting alveolar overdistention in non-dependent regions. Collapse and overdistention both start with the first breath and worsen over time, driving ventilator-induced lung injury (VILI). This is exacerbated when the lung is already injured or has increased heterogeneity. Our study investigated the impact of a single episode of lung injury on lung mechanics and the risk factors for ventilator-induced injury, compared with non-injured lungs.
Methods: Two groups of pigs were sedated and ventilated using lung-protective volume-controlled mode at 8 mL/kg, positive end-expiratory pressure (PEEP) 5 cmH 2 O, with respiratory rate and FiO2 set to maintain normal blood gas values. Animals in one group were ventilated for 50 h (50-Hour MV group, n=10). Animals in the second group had lung injury induced using oleic acid and were ventilated for 12 h post-injury (LI MV group, n=6). Both groups were compared with a never-ventilated control group (NV, n=6). Lung mechanics and injury were measured using electrical impedance tomography, esophageal pressure monitoring and tissue histology.
Results: End-expiratory lung-volume loss was greater in the 50-Hour MV group (P<0.05). Plateau pressure, driving pressure and lung injury score were higher in the LI MV group, (P<0.05).
Conclusion: Risk factors for VILI developed three- to five-times faster in the group with injured lungs, demonstrating that a single lung-injury episode substantially increased the risk of VILI, compared with normal lungs, despite using a lung-protective mechanical ventilation protocol.
Competing Interests: MG and TGB are employees of Lungpacer Medical Inc. SCR is a shareholder and has interest in patents with Lungpacer Medical Inc. All other authors have received consulting fees from Lungpacer Medical Inc. Elizabeth Rohrs is Editor-in-Chief of the CJRT, but was blinded to the decision-making process.
Databáze: MEDLINE
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