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Ventilator-induced Lung Injury (ventilator-induced + lung_injury)
Selected AbstractsEffects of surfactant replacement on alveolar overdistension and plasma cytokines in ventilator-induced lung injuryACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 3 2010H. WU Background: Overdistension of the lung causes ventilator-induced lung injury (VILI) accompanied by surfactant abnormalities and inflammatory changes. We investigated the effects of surfactant replacement on overdistension of the terminal airspaces and plasma cytokine levels in VILI. Methods: VILI was induced by high-pressure ventilation (HPV) in rats anesthetized with pentobarbital, followed by ventilation for 2 h in the maintenance mode (tidal volume=10 ml/kg, positive end-expiratory pressure=7.5 cmH2O) with or without surfactant replacement. The sizes of the terminal airspaces were determined after fixing the lungs at an airway pressure of 10 cmH2O on deflation. Cytokine levels were assessed by enzyme-linked immunosorbent assay. Results: The mean ratio of the largest terminal airspace size class (,64,000 ,m2) was increased from 13.4% to 32.0% by HPV (P<0.05). After maintenance-mode ventilation, the ratio decreased to 16.1% with surfactant replacement (P<0.05), but increased to 44.6% without surfactant replacement (P<0.05). Mean macrophage inflammatory protein-2 (MIP-2) levels in the plasma increased from <0.02 to 6.9 ng/ml with HPV (P<0.05), and further increased to ,11.8 ng/ml, regardless of surfactant replacement after maintenance-mode ventilation. Similar tendencies were observed in the interleukin (IL)-6 and IL-10 levels. Tumor necrosis factor-, levels were almost negligible during the experiment. Conclusion: In rats with VILI, surfactant replacement reversed overdistension of the terminal airspaces that may induce barotrauma, but not upregulation of MIP-2, IL-6, and IL-10 within 2 h. [source] Isoflurane attenuates pulmonary interleukin-1, and systemic tumor necrosis factor-, following mechanical ventilation in healthy miceACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 6 2009M. VANEKER Background: Mechanical ventilation (MV) induces an inflammatory response in healthy lungs. The resulting pro-inflammatory state is a risk factor for ventilator-induced lung injury and peripheral organ dysfunction. Isoflurane is known to have protective immunological effects on different organ systems. We tested the hypothesis that the MV-induced inflammatory response in healthy lungs is reduced by isoflurane. Methods: Healthy C57BL6 mice (n=34) were mechanically ventilated (tidal volume, 8 ml/kg; positive end-expiratory pressure, 4 cmH2O; and fraction of inspired oxygen, 0.4) for 4 h under general anesthesia using a mix of ketamine, medetomidine and atropine (KMA). Animals were divided into four groups: (1) Unventilated control group; (2) MV group using KMA anesthesia; (3) MV group using KMA with 0.25 MAC isoflurane; (4) MV group using KMA with 0.75 MAC isoflurane. Cytokine levels were measured in lung homogenate and plasma. Leukocytes were counted in lung tissue. Results: Lung homogenates: MV increased pro-inflammatory cytokines. In mice receiving KMA+ isoflurane 0.75 MAC, no significant increase in interleukin (IL)-1, was found compared with non-ventilated control mice. Plasma: MV induced a systemic pro-inflammatory response. In mice anesthetized with KMA+ isoflurane (both 0.25 and 0.75 MAC), no significant increase in tumor necrosis factor (TNF)-, was found compared with non-ventilated control mice. Conclusions: The present study is the first to show that isoflurane attenuates the pulmonary IL-1, and systemic TNF-, response following MV in healthy mice. [source] Effects of PEEP levels following repeated recruitment maneuvers on ventilator-induced lung injuryACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 4 2008S.-C. KO Background: Different levels of positive end-expiratory pressure (PEEP) with and without a recruitment maneuver (RM) may have a significant impact on ventilator-induced lung injury but this issue has not been well addressed. Methods: Anesthetized rats received hydrochloric acid (HCl, pH 1.5) aspiration, followed by mechanical ventilation with a tidal volume of 6 ml/kg. The animals were randomized into four groups of 10 each: (1) high PEEP at 6 cm H2O with an RM by applying peak airway pressure at 30 cm H2O for 10 s every 15 min; (2) low PEEP at 2 cm H2O with RM; (3) high PEEP alone; and (4) low PEEP alone. Results: The mean arterial pressure and the amounts of fluid infused were similar in the four groups. Application of the higher PEEP improved oxygenation compared with the lower PEEP groups (P<0.05). The lung compliance was better reserved, and the systemic cytokine responses and lung wet to dry ratio were lower in the high PEEP than in the low PEEP group for a given RM (P<0.05). Conclusions: The use of a combination of periodic RM and the higher PEEP had an additive effect in improving oxygenation and pulmonary mechanics and attenuation of inflammation. [source] Mechanical Ventilation Exacerbates Alveolar Macrophage Dysfunction in the Lungs of Ethanol-Fed RatsALCOHOLISM, Issue 8 2005Pradip P. Kamat Background: Patients with alcohol abuse have a two- to three-fold increased risk of acute lung injury and respiratory failure after sepsis or trauma but are also at increased risk of nosocomial pneumonia. Mechanical ventilation exacerbates lung injury during critical illnesses. In this study we tested whether mechanical ventilation of the alcoholic lung promotes on balance a proinflammatory phenotype favoring ventilator-induced lung injury or an immunosuppressive phenotype favoring ventilator-associated pneumonia. Methods: Lungs from rats fed an isocaloric diet with or without ethanol (six weeks) were isolated and ventilated ex vivo with a low-volume (protective) or high-volume (injurious) strategy for two hours with or without prior endotoxemia (two hours). In other experiments, rats were subjected to high-volume ventilation in vivo. Airway levels of the proinflammatory cytokines tumor necrosis factor-,, macrophage inflammatory protein-2, and interleukin-1, were determined after mechanical ventilation ex vivo and compared with edematous lung injury after high-volume ventilation in vivo. In parallel, alveolar macrophage phagocytosis of bacteria and secretion of interleukin-12 during ventilation ex vivo and endotoxin-stimulated alveolar macrophage phagocytosis and tumor necrosis factor-, secretion in vitro were determined. Results: Ethanol ingestion suppressed the proinflammatory response to injurious mechanical ventilation and did not increase experimental ventilator-induced lung injury. In parallel, ethanol ingestion blunted the innate immune response of alveolar macrophages during injurious ventilation ex vivo and after endotoxin stimulation in vitro. Conclusions: Ethanol ingestion dampens ventilator-induced inflammation but exacerbates macrophage immune dysfunction. These findings could explain at least in part why alcoholic patients are at increased risk of ventilator-associated pneumonia. [source] From ventilator-induced lung injury to physician-induced lung injury: Why the reluctance to use small tidal volumes?ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 3 2004J. Villar First page of article [source] Relationship between endotracheal tube leakage and under-reading of tidal volume in neonatal ventilatorsACTA PAEDIATRICA, Issue 7 2009RA Mahmoud Abstract Aim:, Protective ventilation in neonates requires careful volume monitoring to prevent ventilator-induced lung injury caused by baro/volutrauma and hence chronic lung disease. This study investigated the effect of endotracheal tube (ET) leakage on the displayed tidal volume using an in vitro model. Methods:, A neonatal lung model was ventilated via a 3 mm ET using three ventilators [Babylog 8000 (BL), Leoni (LE) and Stephanie (ST)]. Tidal volume was measured by each ventilator at the Y-piece and by a pneumotach (CO2SMO+) in the model. ET leaks were simulated by open tubes of different lengths. PIP (20 cmH2O) and PEEP (5 cmH2O) were kept constant, and the respiratory rate (RR) was varied between 20/min and 70/min (Ti:Te = 1:1). Results:, Tidal volume displayed by a ventilator decreased independently of RR with increasing leakage up to 21% (BL), 30% (LE) and 33% (ST). However, the volume delivered to the lung was nearly constant. The displayed leakage varied between 0 and 78% and was dependent on RR and leakage resistance. There were distinct differences between the three ventilators in the relationship between displayed leakage and volume error. Accepting a volume error <10% for RR between 20 and 70/min, ET leakage of up to 20% for BL, 12% for LE, but only <5% for ST, was acceptable. Conclusion:, Tidal volume underestimation arising from ET leakage depends on ventilator pressures, timing parameters and ventilator-specific algorithms for signal processing. Therefore, neonatologists should be aware of these issues to prevent lung over-inflation when adjusting target volume in the presence of ET leakage. [source] | ||||||||||