How ARDS should be treated

Gattinoni, Luciano; Quintel, Michael

doi:10.1186/s13054-016-1268-7

Cited by 34 publications

(22 citation statements)

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“…Management of patients with ARDS is an ongoing process that combines physiologic [14] and pragmatic information [17]. The use of ΔPrs to manage patients as a therapeutic target should be part of the research agenda in ARDS [18].…”

Section: Discussionmentioning

confidence: 99%

Effect of driving pressure on mortality in ARDS patients during lung protective mechanical ventilation in two randomized controlled trials

Guérin¹,

Papazian²,

Reignier³

et al. 2016

Crit Care

184

134

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BackgroundDriving pressure (ΔPrs) across the respiratory system is suggested as the strongest predictor of hospital mortality in patients with acute respiratory distress syndrome (ARDS). We wonder whether this result is related to the range of tidal volume (VT). Therefore, we investigated ΔPrs in two trials in which strict lung-protective mechanical ventilation was applied in ARDS. Our working hypothesis was that ΔPrs is a risk factor for mortality just like compliance (Crs) or plateau pressure (Pplat,rs) of the respiratory system.MethodsWe performed secondary analysis of data from 787 ARDS patients enrolled in two independent randomized controlled trials evaluating distinct adjunctive techniques while they were ventilated as in the low VT arm of the ARDSnet trial. For this study, we used VT, positive end-expiratory pressure (PEEP), Pplat,rs, Crs, ΔPrs, and respiratory rate recorded 24 hours after randomization, and compared them between survivors and nonsurvivors at day 90. Patients were followed for 90 days after inclusion. Cox proportional hazard modeling was used for mortality at day 90. If colinearity between ΔPrs, Crs, and Pplat,rs was verified, specific Cox models were used for each of them.ResultsBoth trials enrolled 805 patients of whom 787 had day-1 data available, and 533 of these survived. In the univariate analysis, ΔPrs averaged 13.7 ± 3.7 and 12.8 ± 3.7 cmH2O (P = 0.002) in nonsurvivors and survivors, respectively. Colinearity between ΔPrs, Crs and Pplat,rs, which was expected as these variables are mathematically coupled, was statistically significant. Hazard ratios from the Cox models for day-90 mortality were 1.05 (1.02–1.08) (P = 0.005), 1.05 (1.01–1.08) (P = 0.008) and 0.985 (0.972–0.985) (P = 0.029) for ΔPrs, Pplat,rs and Crs, respectively. PEEP and VT were not associated with death in any model.ConclusionsWhen ventilating patients with low VT, ΔPrs is a risk factor for death in ARDS patients, as is Pplat,rs or Crs. As our data originated from trials from which most ARDS patients were excluded due to strict inclusion and exclusion criteria, these findings must be validated in independent observational studies in patients ventilated with a lung protective strategy.Trial registrationClinicaltrials.gov NCT00299650. Registered 6 March 2006 for the Acurasys trial.Clinicaltrials.gov NCT00527813. Registered 10 September 2007 for the Proseva trial.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-016-1556-2) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Effect of driving pressure on mortality in ARDS patients during lung protective mechanical ventilation in two randomized controlled trials

Guérin¹,

Papazian²,

Reignier³

et al. 2016

Crit Care

184

134

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“…However, it is still unclear which is the optimal PEEP that has to be used to avoid overdistension of the alveoli and de-recruitment, and to minimize VILI [30,31].…”

Section: Rationale Strategy For Lung Protective Ventilationmentioning

confidence: 99%

Synergistic Effect of Hyperoxia and Biotrauma On Ventilator-Induced Lung Injury

Shosholcheva

Јankulovski

Карталов

et al. 2017

Prilozi

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Patients undergoing mechanical ventilation in intensive care units (ICUs) may develop ventilator-induced lung injury (VILI). Beside the high tidal volume (Vt) and plateau pressure (Pplat), hyperoxia is supposed to precipitate lung injury. Oxygen toxicity is presumed to occur at levels of fraction of inspired oxygen (FiO 2 ) exceeding 0.40. The exposure time to hyperoxia is certainly very important and patients who spend extended time on mechanical ventilation (MV) are probably more exposed to severe hyperoxic acute lung injury (HALI). Together, hyperoxia and biotrauma (release of cytokines) have a synergistic effect and can induce VILI. In the clinical practice, the reduction of FiO 2 to safe levels through the appropriate use of the positive end expiratory pressure (PEEP) and the alignment of mean airway pressure is an appropriate goal. The strategy for lung protective ventilation must include setting up FiO 2 to a safe level that is accomplished by using PaO 2 /FiO 2 ratio with a lower limit of FiO 2 to achieve acceptable levels of PaO 2 , which will be safe for the patient without local (lungs) or systemic inflammatory response. The protocol from the ARDS-net study is used for ventilator setup and adjustment. Cytokines (IL-1, IL-6, TNFα and MIP-2) that are involved in the inflammatory response are determined in order to help the therapeutic approach in counteracting HALI. Computed tomography findings reflect the pathological phases of the diffuse alveolar damage. At least preferably the lowest level of FiO 2 should be used in order to provide full lung protection against the damage induced by MV.

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“…From the physiopathological point of view, when applying positive pressure in a patient with heterogeneous alteration of the pulmonary parenchyma, the recruitment of previously collapsed areas is favored, with the disadvantage that there is overdistension of the alveolar units that have a conserved compliance or "normal" [4]. The pronation of the patients would allow adapting the V / Q ratio within the lung, since it produces a better distribution of oxygenated air during ventilation, which results in an overall improvement of oxygenation.…”

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confidence: 99%