Determinants and Prevention of Ventilator-Induced Lung Injury

Vasques, Francesco; Duscio, Eleonora; Cipulli, Francesco; Romitti, Federica; Quintel, Michael; Gattinoni, Luciano

doi:10.1016/j.ccc.2018.03.004

Cited by 35 publications

(26 citation statements)

References 31 publications

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“…[38][39][40] High F IO 2 contributes to ventilator-induced lung injury through the production of reactive oxygen species and atelectrauma. 4,5 The association between ventilator F IO 2 and mortality observed in our study may be due to the direct toxic effects of F IO 2 . However, there are potential confounders that could drive this association, such as severity of disease or inadequacy of ECMO support.…”

Section: Discussionmentioning

confidence: 59%

“…When initiated, venovenous extracorporeal membrane oxygenation (VV-ECMO) relieves the lungs from their usual functions of oxygenation and ventilation, allowing for a reduction of high ventilator settings, which are associated with ventilator-induced lung injury. 4,5 Mechanical ventilation strategies in adult and neonatal subjects with acute respiratory failure have been studied. [6][7][8][9][10][11][12][13][14] Conversely, there has been little study of mechanical ventilation in children on ECMO support for respiratory failure, and there are no evidence-based or expert consensus guidelines.…”

Section: Introductionmentioning

confidence: 99%

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Mechanical Ventilation in Children on Venovenous ECMO

et al. 2020

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BACKGROUND: Venovenous extracorporeal membrane oxygenation (VV-ECMO) is used when mechanical ventilation can no longer support oxygenation or ventilation, or if the risk of ventilator-induced lung injury is considered excessive. The optimum mechanical ventilation strategy once on ECMO is unknown. We sought to describe the practice of mechanical ventilation in children on VV-ECMO and to determine whether mechanical ventilation practices are associated with clinical outcomes. METHODS: We conducted a multicenter retrospective cohort study in 10 pediatric academic centers in the United States. Children age 14 d through 18 y on VV-ECMO from 2011 to 2016 were included. Exclusion criteria were preexisting chronic respiratory failure, primary diagnosis of asthma, cyanotic heart disease, or ECMO as a bridge to lung transplant. RESULTS: Conventional mechanical ventilation was used in about 75% of children on VV-ECMO; the remaining subjects were managed with a variety of approaches. With the exception of PEEP, there was large variation in ventilator settings. Ventilator mode and pressure settings were not associated with survival. Mean ventilator F IO 2 on days 1-3 was higher in nonsurvivors than in survivors (0.5 vs 0.4, P 5 .009). In univariate analysis, other risk factors for mortality were female gender, higher Pediatric Risk Estimate Score for Children Using Extracorporeal Respiratory Support (Ped-RESCUERS), diagnosis of cancer or stem cell transplant, and number of days intubated prior to initiation of ECMO (all P < .05). In multivariate analysis, ventilator F IO 2 was significantly associated with mortality (odds ratio 1.38 for each 0.1 increase in F IO 2 , 95% CI 1.09-1.75). Mortality was higher in subjects on high ventilator F IO 2 (6 0.5) compared to low ventilator F IO 2 (> 0.5) (46% vs 22%, P 5 .001). CONCLUSIONS: Ventilator mode and some settings vary in practice. The only ventilator setting associated with mortality was F IO 2 , even after adjustment for disease severity. Ventilator F IO 2 is a modifiable setting that may contribute to mortality in children on VV-ECMO.

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Section: Discussionmentioning

confidence: 59%

Section: Introductionmentioning

confidence: 99%

Mechanical Ventilation in Children on Venovenous ECMO

et al. 2020

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“…An era of research into how mechanical ventilation could injure the lungs of ARDS patients de novo culminated in the NHLBI ARDS Network ARMA trial that made low tidal volume ventilation the cornerstone strategy of provision of this therapy worldwide 30 . Clinically, VILI has two major manifestations, volutrauma and atelectrauma, both intricately linked to lung stress and strain 29 , 31 . Lung stress refers to transpulmonary pressure (alveolar pressure – pleural pressure), and strain refers to the change in lung volume indexed to functional residual capacity of the ARDS lung at zero PEEP.…”

Section: Therapymentioning

confidence: 99%

“…Lung stress refers to transpulmonary pressure (alveolar pressure – pleural pressure), and strain refers to the change in lung volume indexed to functional residual capacity of the ARDS lung at zero PEEP. Thus, lung stress is nothing but the specific lung elastance multiplied by lung strain 29 , 31 . Volutrauma therefore refers to excessive generalized stress/strain on the lung 29 , 31 .…”

Section: Therapymentioning

confidence: 99%

“…Thus, lung stress is nothing but the specific lung elastance multiplied by lung strain 29 , 31 . Volutrauma therefore refers to excessive generalized stress/strain on the lung 29 , 31 . Sophisticated CT scan studies and elegant physiological investigations have shown that lung injury in ARDS is heterogeneous, with injured or atelectatic areas adjacent to relatively normal aerated areas 32 .…”

Section: Therapymentioning

confidence: 99%

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Recent advances in understanding and treating acute respiratory distress syndrome

Nanchal

Truwit

2018

F1000Res

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Acute respiratory distress syndrome (ARDS) is a clinically and biologically heterogeneous disorder associated with many disease processes that injure the lung, culminating in increased non-hydrostatic extravascular lung water, reduced compliance, and severe hypoxemia. Despite enhanced understanding of molecular mechanisms, advances in ventilatory strategies, and general care of the critically ill patient, mortality remains unacceptably high. The Berlin definition of ARDS has now replaced the American-European Consensus Conference definition. The recently concluded Large Observational Study to Understand the Global Impact of Severe Acute Respiratory Failure (LUNG-SAFE) provided worldwide epidemiological data of ARDS including prevalence, geographic variability, mortality, and patterns of mechanical ventilation use. Failure of clinical therapeutic trials prompted the investigation and subsequent discovery of two distinct phenotypes of ARDS (hyper-inflammatory and hypo-inflammatory) that have different biomarker profiles and clinical courses and respond differently to the random application of positive end expiratory pressure (PEEP) and fluid management strategies. Low tidal volume ventilation remains the predominant mainstay of the ventilatory strategy in ARDS. High-frequency oscillatory ventilation, application of recruitment maneuvers, higher PEEP, extracorporeal membrane oxygenation, and alternate modes of mechanical ventilation have failed to show benefit. Similarly, most pharmacological therapies including keratinocyte growth factor, beta-2 agonists, and aspirin did not improve outcomes. Prone positioning and early neuromuscular blockade have demonstrated mortality benefit, and clinical guidelines now recommend their use. Current ongoing trials include the use of mesenchymal stem cells, vitamin C, re-evaluation of neuromuscular blockade, and extracorporeal carbon dioxide removal. In this article, we describe advances in the diagnosis, epidemiology, and treatment of ARDS over the past decade.

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The Elusive Search for “Best PEEP” and Whether Esophageal Pressure Monitoring Helps

Cavalcanti¹,

Amato

Neto

2019

JAMA

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Acute respiratory distress syndrome (ARDS) was described more than 50 years ago. 1 In that first description, Ashbaugh et al 1 framed ARDS as an acute lung injury that arises from several underlying causes, such as severe trauma or pneumonia, and can lead to catastrophic hypoxemia and death. The authors considered several potential therapies that might modulate the underlying disease process, but concluded the only demonstrably useful intervention was optimal titration of positive end-expiratory pressure (PEEP). They acknowledged, however, that PEEP worked principally by improving oxygenation as a temporizing measure while waiting for the underlying cause of ARDS to resolve. ARDS rarely occurs in isolation, and the precipitating causes often contribute not only to respiratory failure, but also to multisystem organ failure. Thus, with advances in mechanical ventilation, such as better use of PEEP, refractory hypoxemia is now rarely the cause of death for patients with ARDS. 2 In recent decades, however, it has become increasingly apparent that lifesaving mechanical ventilation is, paradoxically, injurious in its own right, causing ventilator-induced lung injury (VILI). VILI is caused by pressure-and volumemediated trauma to the airways and alveoli from ventilatorgenerated breaths, inducing a systemic inflammatory response that in turn contributes to multiple organ failure and death. 3 The recognition of the potentially harmful effects of mechanical ventilation has shifted the goal of optimal PEEP away from just improving oxygenation toward preventing VILI. 4 "Optimizing" PEEP is not easy. PEEP splints the lung open at the end of expiration. It can therefore minimize atelectrauma by decreasing cyclic opening and closing of lung units, but can also lead to overdistention. 3 The effect of PEEP on driving pressure, an important determinant of VILI, therefore depends on the balance of its effects on recruitment of nonaerated areas vs overdistention of normally aerated ones. 5 In addition, higher PEEP can impede venous return, compromising right ventricular function and central hemodynamics. In other words, some level of PEEP is needed to maintain oxygenation and to avoid VILI, but how much? And which is the best method to find it? Several randomized trials have compared higher vs lower levels of PEEP in patients with ARDS. [6][7][8][9] Individual trials did not show a beneficial effect of higher levels of PEEP on mortality, although an individual patient data meta-analysis suggested higher PEEP reduced mortality in patients with ARDS

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Determinants and Prevention of Ventilator-Induced Lung Injury

Cited by 35 publications

References 31 publications

Mechanical Ventilation in Children on Venovenous ECMO

Mechanical Ventilation in Children on Venovenous ECMO

Recent advances in understanding and treating acute respiratory distress syndrome

The Elusive Search for “Best PEEP” and Whether Esophageal Pressure Monitoring Helps

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