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

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...

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Veröffentlicht in:Canadian Journal of Respiratory Therapy 2023-01, Vol.59, p.103-110
Hauptverfasser: Rohrs, Elizabeth C, Bassi, Thiago G, Nicholas, Michelle, Wittmann, Jessica, Ornowska, Marlena, Fernandez, Karl C, Gani, Matt, Reynolds, Steven C
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container_title Canadian Journal of Respiratory Therapy
container_volume 59
creator Rohrs, Elizabeth C
Bassi, Thiago G
Nicholas, Michelle
Wittmann, Jessica
Ornowska, Marlena
Fernandez, Karl C
Gani, Matt
Reynolds, Steven C
description 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. 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 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. End-expiratory lung-volume loss was greater in the 50-Hour MV group (P
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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. 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 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. End-expiratory lung-volume loss was greater in the 50-Hour MV group (P&lt;0.05). Plateau pressure, driving pressure and lung injury score were higher in the LI MV group, (P&lt;0.05). 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subjects acute lung injury
Lung cancer
Lung diseases
mechanical ventilation
Risk factors
Ventilation
ventilator-induced lung injury
Ventilators
title Risk factors for ventilator-induced-lung injury develop three to five times faster after a single episode of lung injury
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