scholarly journals Imaging atelectrauma in Ventilator-Induced Lung Injury using 4D X-ray microscopy

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Luca Fardin ◽  
Ludovic Broche ◽  
Goran Lovric ◽  
Alberto Mittone ◽  
Olivier Stephanov ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Lung Parenchyma ◽  
Contrast Imaging ◽  
Barrier Dysfunction ◽  
Mechanically Ventilated ◽  
Ventilator Induced Lung Injury ◽  
Regional Lung ◽  
Ventilation Strategies ◽  
Protective Mechanical Ventilation

AbstractMechanical ventilation can damage the lungs, a condition called Ventilator-Induced Lung Injury (VILI). However, the mechanisms leading to VILI at the microscopic scale remain poorly understood. Here we investigated the within-tidal dynamics of cyclic recruitment/derecruitment (R/D) using synchrotron radiation phase-contrast imaging (PCI), and the relation between R/D and cell infiltration, in a model of Acute Respiratory Distress Syndrome in 6 anaesthetized and mechanically ventilated New-Zealand White rabbits. Dynamic PCI was performed at 22.6 µm voxel size, under protective mechanical ventilation [tidal volume: 6 ml/kg; positive end-expiratory pressure (PEEP): 5 cmH2O]. Videos and quantitative maps of within-tidal R/D showed that injury propagated outwards from non-aerated regions towards adjacent regions where cyclic R/D was present. R/D of peripheral airspaces was both pressure and time-dependent, occurring throughout the respiratory cycle with significant scatter of opening/closing pressures. There was a significant association between R/D and regional lung cellular infiltration (p = 0.04) suggesting that tidal R/D of the lung parenchyma may contribute to regional lung inflammation or capillary-alveolar barrier dysfunction and to the progression of lung injury. PEEP may not fully mitigate this phenomenon even at high levels. Ventilation strategies utilizing the time-dependence of R/D may be helpful in reducing R/D and associated injury.

scholarly journals Interaction between regional lung volumes and ventilator-induced lung injury in the normal and endotoxemic lung

2020 ◽  
Vol 318 (3) ◽  
pp. L494-L499 ◽  
Author(s):  
Seiha Yen ◽  
Melissa Preissner ◽  
Ellen Bennett ◽  
Stephen Dubsky ◽  
Richard Carnibella ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Tidal Volume ◽  
Lung Volumes ◽  
Mechanically Ventilated ◽  
Ventilator Induced Lung Injury ◽  
Computed Tomography Images ◽  
Gas Trapping ◽  
Regional Lung ◽  
The Relationship

Both overdistension and atelectasis contribute to lung injury and mortality during mechanical ventilation. It has been proposed that combinations of tidal volume and end-expiratory lung volume exist that minimize lung injury linked to mechanical ventilation. The aim of this study was to examine this at the regional level in the healthy and endotoxemic lung. Adult female BALB/c mice were injected intraperitoneally with 10 mg/kg lipopolysaccharide (LPS) in saline or with saline alone. Four hours later, mice were mechanically ventilated for 2 h. Regional specific end-expiratory volume (sEEV) and tidal volume (sVt) were measured at baseline and after 2 h of ventilation using dynamic high-resolution four-dimensional computed tomography images. The regional expression of inflammatory genes was quantified by quantitative PCR. There was a heterogenous response in regional sEEV whereby endotoxemia increased gas trapping at end-expiration in some lung regions. Within the healthy group, there was a relationship between sEEV, sVt, and the expression of Tnfa, where high Vt in combination with high EEV or very low EEV was associated with an increase in gene expression. In endotoxemia there was an association between low sEEV, particularly when this was combined with moderate sVt, and high expression of IL6. Our data suggest that preexisting systemic inflammation modifies the relationship between regional lung volumes and inflammation and that although optimum EEV-Vt combinations to minimize injury exist, further studies are required to identify the critical inflammatory mediators to assess and the effect of different injury types on the response.

scholarly journals Redox Balance and Cellular Inflammation in the Diaphragm, Limb Muscles, and Lungs of Mechanically Ventilated Rats

2010 ◽  
Vol 112 (2) ◽  
pp. 384-394 ◽  
Author(s):  
Judith Marín-Corral ◽  
Leticia Martínez-Caro ◽  
José A. Lorente ◽  
Marta de Paula ◽  
Lara Pijuan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mechanical Ventilation ◽  
Lung Injury ◽  
Protein Adducts ◽  
Organ Injury ◽  
Mechanically Ventilated ◽  
Ventilator Induced Lung Injury ◽  
Cellular Inflammation ◽  
Cell Counts ◽  
Limb Muscles

Background High tidal volume (VT) mechanical ventilation was shown to induce organ injury other than lung injury and systemic inflammation in animal models of ventilator-induced lung injury. The authors aimed to explore whether high VT mechanical ventilation per se induces early oxidative stress and inflammation in the diaphragm, limb muscles, and lungs of healthy rats exposed to ventilator-induced lung injury. Methods Protein carbonylation and nitration, antioxidants (immunoblotting), and inflammation (immunohistochemistry) were evaluated in the diaphragm, gastrocnemius, soleus, tibialis anterior, and lungs of mechanically ventilated healthy rats and in nonventilated control animals (n = 8/group) for 1 h, using two different strategies (moderate VT [VT = 9 ml/kg] and high VT [VT = 35 ml/kg]). Results The main findings are summarized as follows: compared with controls, (1) the diaphragms and gastrocnemius of high-VT rats exhibited a decrease in reactive carbonyls, (2) the soleus and tibialis of high- and moderate-VT rodents showed a reduction in reactive carbonyls and malondialdehyde-protein adducts, (3) the lungs of high-VT rats exhibited a significant rise in malondialdehyde-protein adducts, (4) the soleus and tibialis of both high- and moderate-VT rats showed a reduction in protein nitration, (5) the lungs of high- and moderate-VT rats showed a reduction in antioxidant enzyme levels, but not in the muscles, and (6) the diaphragms and gastrocnemius of all groups exhibited very low inflammatory cell counts, whereas the lungs of high-VT rats exhibited a significant increase in inflammatory infiltrates. Conclusions Although oxidative stress and inflammation increased in the lungs of rats exposed to high VT, the diaphragm and limb muscles exhibited a decline in oxidative stress markers and very low levels of cellular inflammation.

scholarly journals The Extent of Ventilator-Induced Lung Injury in Mice Partly Depends on Duration of Mechanical Ventilation

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Maria A. Hegeman ◽  
Sabrine N. T. Hemmes ◽  
Maria T. Kuipers ◽  
Lieuwe D. J. Bos ◽  
Geartsje Jongsma ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Capillary Permeability ◽  
Statistical Significance ◽  
Lung Compliance ◽  
Alveolar Cell ◽  
Mechanically Ventilated ◽  
Ventilator Induced Lung Injury ◽  
Cell Counts ◽  
Alveolar Capillary

Background. Mechanical ventilation (MV) has the potential to initiate ventilator-induced lung injury (VILI). The pathogenesis of VILI has been primarily studied in animal models using more or less injurious ventilator settings. However, we speculate that duration of MV also influences severity and character of VILI.Methods. Sixty-four healthy C57Bl/6 mice were mechanically ventilated for 5 or 12 hours, using lower tidal volumes with positive end-expiratory pressure (PEEP) or higher tidal volumes without PEEP. Fifteen nonventilated mice served as controls.Results. All animals remained hemodynamically stable and survived MV protocols. In both MV groups, PaO2to FiO2ratios were lower and alveolar cell counts were higher after 12 hours of MV compared to 5 hours. Alveolar-capillary permeability was increased after 12 hours compared to 5 hours, although differences did not reach statistical significance. Lung levels of inflammatory mediators did not further increase over time. Only in mice ventilated with increased strain, lung compliance declined and wet to dry ratio increased after 12 hours of MV compared to 5 hours.Conclusions. Deleterious effects of MV are partly dependent on its duration. Even lower tidal volumes with PEEP may initiate aspects of VILI after 12 hours of MV.

scholarly journals Current Applications for the Use of Extracorporeal Carbon Dioxide Removal in Critically Ill Patients

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Luigi Camporota ◽  
Nicholas Barrett
Keyword(s):  
Carbon Dioxide ◽  
Mechanical Ventilation ◽  
Respiratory Failure ◽  
Lung Injury ◽  
Carbon Dioxide Removal ◽  
Extracorporeal Carbon Dioxide Removal ◽  
Ventilator Induced Lung Injury ◽  
Patient Groups ◽  
Protective Mechanical Ventilation

Mechanical ventilation in patients with respiratory failure has been associated with secondary lung injury, termed ventilator-induced lung injury. Extracorporeal venovenous carbon dioxide removal (ECCO2R) appears to be a feasible means to facilitate more protective mechanical ventilation or potentially avoid mechanical ventilation in select patient groups. With this expanding role of ECCO2R, we aim to describe the technology and the main indications of ECCO2R.

scholarly journals The proteomic response is linked to regional lung volumes in ventilator-induced lung injury

2020 ◽  
Vol 129 (4) ◽  
pp. 837-845
Author(s):  
Seiha Yen ◽  
Yong Song ◽  
Melissa Preissner ◽  
Ellen Bennett ◽  
Richard Wilson ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Complex Interaction ◽  
Lung Volumes ◽  
Ventilator Induced Lung Injury ◽  
Regional Lung ◽  
Altered Regulation ◽  
Proteomic Response

This study provides novel insights into the regional response to mechanical ventilation in the setting of acid-induced lung injury and highlights the complex interaction between tidal stretch and low end-expiratory lung volumes; both of which caused altered regulation of different injury pathways.

Intraoperative Protective Mechanical Ventilation for Prevention of Postoperative Pulmonary Complications

2015 ◽  
Vol 123 (3) ◽  
pp. 692-713 ◽  
Author(s):  
Andreas Güldner ◽  
Thomas Kiss ◽  
Ary Serpa Neto ◽  
Sabrine N. T. Hemmes ◽  
Jaume Canet ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Relevant Literature ◽  
Length Of Hospital Stay ◽  
Pulmonary Complications ◽  
Major Surgery ◽  
Postoperative Pulmonary Complication ◽  
Postoperative Pulmonary Complications ◽  
Ventilator Induced Lung Injury ◽  
Ventilation Strategies ◽  
Protective Mechanical Ventilation

Abstract Postoperative pulmonary complications are associated with increased morbidity, length of hospital stay, and mortality after major surgery. Intraoperative lung-protective mechanical ventilation has the potential to reduce the incidence of postoperative pulmonary complications. This review discusses the relevant literature on definition and methods to predict the occurrence of postoperative pulmonary complication, the pathophysiology of ventilator-induced lung injury with emphasis on the noninjured lung, and protective ventilation strategies, including the respective roles of tidal volumes, positive end-expiratory pressure, and recruitment maneuvers. The authors propose an algorithm for protective intraoperative mechanical ventilation based on evidence from recent randomized controlled trials.

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 Simultaneous Pretreatment of Aspirin and Omega-3 Fatty Acid Attenuates Nuclear Factor-κB Activation in a Murine Model with Ventilator-Induced Lung Injury

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2258
Author(s):  
Won-Gun Kwack ◽  
Yoon-Je Lee ◽  
Eun-Young Eo ◽  
Jin-Haeng Chung ◽  
Jae-Ho Lee ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Fatty Acid ◽  
Lung Injury ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Omega 3 ◽  
Omega 3 Fatty Acid ◽  
Ventilator Induced Lung Injury ◽  
Sequential Administration ◽  
Pretreated Group

Ventilator-induced lung injury (VILI) is an important critical care complication. Nuclear factor-κB (NF-κB) activation, a critical signaling event in the inflammatory response, has been implicated in the tracking of the lung injury. The present study aimed to determine the effect of simultaneous pretreatment with enteral aspirin and omega-3 fatty acid on lung injury in a murine VILI model. We compared the lung inflammation after the sequential administration of lipopolysaccharides and mechanical ventilation between the pretreated simultaneous enteral aspirin and omega-3 fatty acid group and the non-pretreatment group, by quantifying NF-κB activation using an in vivo imaging system to detect bioluminescence signals. The pretreated group with enteral aspirin and omega-3 fatty acid exhibited a smaller elevation of bioluminescence signals than the non-pretreated group (p = 0.039). Compared to the non-pretreated group, the pretreatment group with simultaneous enteral aspirin and omega-3 fatty acid showed reduced expression of the pro-inflammatory cytokine, tumor necrosis factor-α, in bronchoalveolar lavage fluid (p = 0.038). Histopathological lung injury scores were also lower in the pretreatment groups compared to the only injury group. Simultaneous pretreatment with enteral administration of aspirin and omega-3 fatty acid could be a prevention method for VILI in patients with impending mechanical ventilation therapy.

scholarly journals Brain injury after 50 h of lung-protective mechanical ventilation in a preclinical model

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Thiago G. Bassi ◽  
Elizabeth C. Rohrs ◽  
Karl C. Fernandez ◽  
Marlena Ornowska ◽  
Michelle Nicholas ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Brain Injury ◽  
Neuronal Damage ◽  
Normal Lung ◽  
Preclinical Model ◽  
Negative Consequences ◽  
Mechanically Ventilated ◽  
Protective Mechanical Ventilation ◽  
Hippocampal Apoptosis ◽  
Lung Protective Mechanical Ventilation

AbstractMechanical ventilation is the cornerstone of the Intensive Care Unit. However, it has been associated with many negative consequences. Recently, ventilator-induced brain injury has been reported in rodents under injurious ventilation settings. Our group wanted to explore the extent of brain injury after 50 h of mechanical ventilation, sedation and physical immobility, quantifying hippocampal apoptosis and inflammation, in a normal-lung porcine study. After 50 h of lung-protective mechanical ventilation, sedation and immobility, greater levels of hippocampal apoptosis and neuroinflammation were clearly observed in the mechanically ventilated group, in comparison to a never-ventilated group. Markers in the serum for astrocyte damage and neuronal damage were also higher in the mechanically ventilated group. Therefore, our study demonstrated that considerable hippocampal insult can be observed after 50 h of lung-protective mechanical ventilation, sedation and physical immobility.

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