Personalized mechanical ventilation strategy minimizes ventilator-induced lung injury in experimental acute respiratory distress syndrome

2017 ◽  
Vol 42 ◽  
pp. 389
Author(s):  
Raquel Ferreira de Magalhães ◽  
Pedro Leme Silva ◽  
Fernanda Ferreira Cruz ◽  
Cynthia dos Santos Samary ◽  
Lilian Moraes ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Acute Respiratory Distress Syndrome ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Ventilation Strategy ◽  
Ventilator Induced Lung Injury

scholarly journals Mechanosensitive activation of mTORC1 mediates ventilator induced lung injury during the acute respiratory distress syndrome

2020 ◽  
Author(s):  
Hyunwook Lee ◽  
Qinqin Fei ◽  
Adam Streicher ◽  
Wenjuan Zhang ◽  
Colleen Isabelle ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Acute Respiratory Distress Syndrome ◽  
Epithelial Cells ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Lung Epithelial Cells ◽  
Ventilator Induced Lung Injury ◽  
Lung Epithelial

AbstractAcute respiratory distress syndrome (ARDS) is a highly lethal condition that impairs lung function and causes respiratory failure. Mechanical ventilation maintains gas exchange in patients with ARDS, but exposes lung cells to physical forces that exacerbate lung injury. Our data demonstrate that mTOR complex 1 (mTORC1) is a mechanosensor in lung epithelial cells and that activation of this pathway during mechanical ventilation exacerbates lung injury. We found that mTORC1 is activated in lung epithelial cells following volutrauma and atelectrauma in mice and humanized in vitro models of the lung microenvironment. mTORC1 is also activated in lung tissue of mechanically ventilated patients with ARDS. Deletion of Tsc2, a negative regulator of mTORC1, in epithelial cells exacerbates physiologic lung dysfunction during mechanical ventilation. Conversely, treatment with rapamycin at the time mechanical ventilation is initiated prevents physiologic lung injury (i.e. decreased compliance) without altering lung inflammation or barrier permeability. mTORC1 inhibition mitigates physiologic lung injury by preventing surfactant dysfunction during mechanical ventilation. Our data demonstrate that in contrast to canonical mTORC1 activation under favorable growth conditions, activation of mTORC1 during mechanical ventilation exacerbates lung injury and inhibition of this pathway may be a novel therapeutic target to mitigate ventilator induced lung injury during ARDS.

scholarly journals Acute Respiratory Distress Syndrome: Insights Gained from Clinical and Translational Research

2009 ◽  
Vol 9 (1) ◽  
pp. S59-S68 ◽  
Author(s):  
Marija Kojicic ◽  
Emir Festic ◽  
Ognjen Gajic
Keyword(s):  
Mechanical Ventilation ◽  
Acute Respiratory Distress Syndrome ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Severe Form ◽  
Ventilator Induced Lung Injury ◽  
Protective Mechanical Ventilation ◽  
Lung Protective Mechanical Ventilation

Acute lung injury and its more severe form acute respiratory distress syndrome (ARDS) are characterized by diffuse impairment of alveolocapillary membrane in the settings of different predisposing conditions such as sepsis, trauma and shock. Many intrahospital exposures, including aspiration, delayed resuscitation, high tidal volume mechanical ventilation and non critical use of transfusions may contribute or worsen ARDS. Therapy is targeted to treatment of predisposing condition, life supportive measures and prevention of nosocomial complications. Rigorous adherence to lung-protective mechanical ventilation is critical to prevent ventilator induced lung injury and decrease mortality. Although survival of ARDS patients has improved in the last decades ARDS mortality rates are still high and survivors encounter significant physical and psychological impairments

scholarly journals Desflurane Attenuates Ventilator-Induced Lung Injury in Rats with Acute Respiratory Distress Syndrome

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Xue Lin ◽  
Ying-nan Ju ◽  
Wei Gao ◽  
Dong-mei Li ◽  
Chang-chun Guo
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Tidal Volume ◽  
Lung Tissue ◽  
Rat Model ◽  
Distress Syndrome ◽  
Inflammatory Factors ◽  
Ventilator Induced Lung Injury

Ventilator-induced lung injury aggravates the existing lung injury. This study investigated the effect of desflurane on VILI in a rat model of acute respiratory distress syndrome. Forty-eight rats were randomized into a sham (S) group, control (C) group, lipopolysaccharide/ventilation (LV) group, lipopolysaccharide/ventilation/desflurane (LVD) group, or lipopolysaccharide/low ventilation with and without desflurane (LLV and LLVD) groups. Rats in the S group received anesthesia only. Rats in the LV and LVD groups received lipopolysaccharide and were ventilated with a high tidal volume. Rats in LLV and LLVD groups were treated as the LV and LVD groups and ventilated with a low tidal volume. PaO2/FiO2, lung wet-to-dry weight ratios, concentrations of inflammatory factors in serum and BALF, histopathologic analysis of lung tissue, and levels of nuclear factor- (NF-) κB protein in lung tissue were investigated. PaO2/FiO2 was significantly increased by desflurane. Total cell count, macrophages, and neutrophils in BALF and proinflammatory factors in BALF and serum were significantly decreased by desflurane, while IL-10 was increased. The histopathological changes and levels of NF-κB protein in lung tissue were decreased by desflurane. The results indicated that desflurane ameliorated VILI in a rat model of acute respiratory distress syndrome.

Does Earlier Cannulation With Veno-Venous Extracorporeal Membrane Oxygenation in Adult Patients With Acute Respiratory Distress Syndrome Decrease Duration of Artificial Mechanical Ventilation?

2020 ◽  
Vol 13 (2) ◽  
pp. 148-155
Author(s):  
Christine Hartner ◽  
Jacqueline Ochsenreither ◽  
Kenneth Miller ◽  
Michael Weiss
Keyword(s):  
Mechanical Ventilation ◽  
Acute Respiratory Distress Syndrome ◽  
Lung Injury ◽  
Extracorporeal Membrane Oxygenation ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Adult Patients ◽  
Membrane Oxygenation ◽  
Vv Ecmo

BackgroundAcute respiratory distress syndrome (ARDS) is characterized by an acute, diffuse, inflammatory lung injury, leading to increased alveolar capillary permeability, increased lung weight, and loss of aerated lung tissue (Fan, Brodie, & Slutsky, 2018). Primary treatment for ARDS is artificial mechanical ventilation (AMV) (Wu, Huang, Wu, Wang, & Lin, 2016). Given recent advances in technology, the use of veno-venous extracorporeal membrane oxygenation (VV-ECMO) to treat severe ARDS is growing rapidly (Combes et al., 2014).ObjectiveThis 49-month quantitative, retrospective inpatient EMR chart review compared if cannulation with VV-ECMO up to and including 48 hours of admission and diagnosis in adult patients 30 to 65 years of age diagnosed with ARDS, decreased duration on AMV, as compared to participants who were cannulated after 48 hours of admission and diagnosis with ARDS.MethodsA total of 110 participants were identified as receiving VV-ECMO during the study timeframe. Of the 58 participants who met all inclusion criteria, 39 participants were cannulated for VV-ECMO within 48 hours of admission and diagnosis with ARDS, and 19 participants were cannulated with VV-ECMO after 48 hours of admission and diagnosis with ARDS.ResultsData collected identified no statistically significant (p < 0.579) difference in length of days on AMV between participant groups.ConclusionsFurther studies are needed to determine if earlier initiation of VV-ECMO in adult patients with ARDS decrease time on AMV.Implications for NursingAlthough the results related to length of time on AMV did not produce statistical significance, the decreased duration of AMV in the participants who were cannulated within 48 hours (21 days vs. 27 days) may support several benefits associated with this participant population including increased knowledge of healthcare providers, decreased lung injury, earlier discharge which decreases hospital and patient cost, ability for patients to communicate sooner, decreased risk of pulmonary infection, decreased length of stay, decreased cost, and improved patient and family satisfaction.

Biological Impact of Transpulmonary Driving Pressure in Experimental Acute Respiratory Distress Syndrome

2015 ◽  
Vol 123 (2) ◽  
pp. 423-433 ◽  
Author(s):  
Cynthia S. Samary ◽  
Raquel S. Santos ◽  
Cíntia L. Santos ◽  
Nathane S. Felix ◽  
Maira Bentes ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Peep Level ◽  
Transpulmonary Pressure ◽  
Plateau Pressure ◽  
Driving Pressure ◽  
Ventilator Induced Lung Injury

Abstract Background: Ventilator-induced lung injury has been attributed to the interaction of several factors: tidal volume (VT), positive end-expiratory pressure (PEEP), transpulmonary driving pressure (difference between transpulmonary pressure at end-inspiration and end-expiration, ΔP,L), and respiratory system plateau pressure (Pplat,rs). Methods: Forty-eight Wistar rats received Escherichia coli lipopolysaccharide intratracheally. After 24 h, animals were randomized into combinations of VT and PEEP, yielding three different ΔP,L levels: ΔP,LLOW (VT = 6 ml/kg, PEEP = 3 cm H2O); ΔP,LMEAN (VT = 13 ml/kg, PEEP = 3 cm H2O or VT = 6 ml/kg, PEEP = 9.5 cm H2O); and ΔP,LHIGH (VT = 22 ml/kg, PEEP = 3 cm H2O or VT = 6 ml/kg, PEEP = 11 cm H2O). In other groups, at low VT, PEEP was adjusted to obtain a Pplat,rs similar to that achieved with ΔP,LMEAN and ΔP,LHIGH at high VT. Results: At ΔP,LLOW, expressions of interleukin (IL)-6, receptor for advanced glycation end products (RAGE), and amphiregulin were reduced, despite morphometric evidence of alveolar collapse. At ΔP,LHIGH (VT = 6 ml/kg and PEEP = 11 cm H2O), lungs were fully open and IL-6 and RAGE were reduced compared with ΔP,LMEAN (27.4 ± 12.9 vs. 41.6 ± 14.1 and 0.6 ± 0.2 vs. 1.4 ± 0.3, respectively), despite increased hyperinflation and amphiregulin expression. At ΔP,LMEAN (VT = 6 ml/kg and PEEP = 9.5 cm H2O), when PEEP was not high enough to keep lungs open, IL-6, RAGE, and amphiregulin expression increased compared with ΔP,LLOW (41.6 ± 14.1 vs. 9.0 ± 9.8, 1.4 ± 0.3 vs. 0.6 ± 0.2, and 6.7 ± 0.8 vs. 2.2 ± 1.0, respectively). At Pplat,rs similar to that achieved with ΔP,LMEAN and ΔP,LHIGH, higher VT and lower PEEP reduced IL-6 and RAGE expression. Conclusion: In the acute respiratory distress syndrome model used in this experiment, two strategies minimized ventilator-induced lung injury: (1) low VT and PEEP, yielding low ΔP,L and Pplat,rs; and (2) low VT associated with a PEEP level sufficient to keep the lungs open.

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