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Purpose While our understanding of the pathogenesis and management of acute respiratory distress syndrome (ARDS) has improved over the past decade, estimates of its incidence have been controversial. The goal of this study was to examine ARDS incidence and outcome under current lung protective ventilatory support practices before and after the diagnosis of ARDS. Methods This was a 1-year prospective, multicenter, observational study in 13 geographical areas of Spain (serving a population of 3.55 million at least 18 years of age) between November 2008 and October 2009. Subjects comprised all consecutive patients meeting American-European Consensus Criteria for ARDS. Data on ventilatory management, gas exchange, hemodynamics, and organ dysfunction were collected. Results A total of 255 mechanically ventilated patients fulfilled the ARDS definition, representing an incidence of 7.2/100,000 population/year. Pneumonia and sepsis were the most common causes of ARDS. At the time of meeting ARDS criteria, mean PaO 2 /FiO 2 was 114 ± 40 mmHg, mean tidal volume was 7.2 ± 1.1 ml/kg predicted body weight, mean plateau pressure was 26 ± 5 cmH 2 O, and mean positive end-expiratory pressure (PEEP) was 9.3 ± 2.4 cmH 2 O. Overall ARDS intensive care unit (ICU) and hospital mortality was 42.7% (95%CI 37.7–47.8) and 47.8% (95%CI 42.8–53.0), respectively. Conclusions This is the first study to prospectively estimate the ARDS incidence during the routine application of lung protective ventilation. Our findings support previous estimates in Europe and are an order of magnitude lower than those reported in the USA and Australia. Despite use of lung protective ventilation, overall ICU and hospital mortality of ARDS patients is still higher than 40%.

Purpose The PaO 2 /FiO 2 is an integral part of the assessment of patients with acute respiratory distress syndrome (ARDS). The American-European Consensus Conference definition does not mandate any standardization procedure. We hypothesized that the use of PaO 2 /FiO 2 calculated under a standard ventilatory setting within 24 h of ARDS diagnosis allows a more clinically relevant ARDS classification. Methods We studied 452 ARDS patients enrolled prospectively in two independent, multicenter cohorts treated with protective mechanical ventilation. At the time of ARDS diagnosis, patients had a PaO 2 /FiO 2  ≤ 200. In the derivation cohort ( n  = 170), we measured PaO 2 /FiO 2 with two levels of positive end-expiratory pressure (PEEP) (≥5 and ≥10 cmH 2 O) and two levels of FiO 2 (≥0.5 and 1.0) at ARDS onset and 24 h later. Dependent upon PaO 2 response, patients were reclassified into three groups: mild (PaO 2 /FiO 2  > 200), moderate (PaO 2 /FiO 2 101–200), and severe (PaO 2 /FiO 2  ≤ 100) ARDS. The primary outcome measure was ICU mortality. The standard ventilatory setting that reached the highest significance difference in mortality among these categories was tested in a separate cohort ( n  = 282). Results The only standard ventilatory setting that identified the three PaO 2 /FiO 2 risk categories in the derivation cohort was PEEP ≥ 10 cmH 2 O and FiO 2  ≥ 0.5 at 24 h after ARDS onset ( p  = 0.0001). Using this ventilatory setting, patients in the validation cohort were reclassified as having mild ARDS ( n  = 47, mortality 17 %), moderate ARDS ( n  = 149, mortality 40.9 %), and severe ARDS ( n  = 86, mortality 58.1 %) ( p  = 0.00001). Conclusions Our method for assessing PaO 2 /FiO 2 greatly improved risk stratification of ARDS and could be used for enrolling appropriate ARDS patients into therapeutic clinical trials.

Background Limited data exist regarding ventilation in patients with class III obesity [body mass index (BMI) > 40 kg/m 2 ] and acute respiratory distress syndrome (ARDS). The aim of the present study was to determine whether an individualized titration of mechanical ventilation according to cardiopulmonary physiology reduces the mortality in patients with class III obesity and ARDS. Methods In this retrospective study, we enrolled adults admitted to the ICU from 2012 to 2017 who had class III obesity and ARDS and received mechanical ventilation for > 48 h. Enrolled patients were divided in two cohorts: one cohort (2012–2014) had ventilator settings determined by the ARDSnet table for lower positive end-expiratory pressure/higher inspiratory fraction of oxygen ( standard protocol-based cohort ); the other cohort (2015–2017) had ventilator settings determined by an individualized protocol established by a lung rescue team ( lung rescue team cohort ). The lung rescue team used lung recruitment maneuvers, esophageal manometry, and hemodynamic monitoring. Results The standard protocol-based cohort included 70 patients (BMI = 49 ± 9 kg/m 2 ), and the lung rescue team cohort included 50 patients (BMI = 54 ± 13 kg/m 2 ). Patients in the standard protocol-based cohort compared to lung rescue team cohort had almost double the risk of dying at 28 days [31% versus 16%, P  = 0.012; hazard ratio (HR) 0.32; 95% confidence interval (CI95%) 0.13–0.78] and 3 months (41% versus 22%, P  = 0.006; HR 0.35; CI95% 0.16–0.74), and this effect persisted at 6 months and 1 year (incidence of death unchanged 41% versus 22%, P  = 0.006; HR 0.35; CI95% 0.16–0.74). Conclusion Individualized titration of mechanical ventilation by a lung rescue team was associated with decreased mortality compared to use of an ARDSnet table.

Plan Nacional de R+D+I [PI09/91074, PI13/02204, PI16/01606]; ISCIII-Subdireccion General de Evaluacion y el Fondo Europeo de Desarrollo Regional (FEDER); Fundacio Parc Tauli, Plan Avanza [TSI-020302-2008-38]; AEI/FEDER UE [RTC-2017-6193-1]

To investigate if respiratory mechanics and other baseline characteristics are predictors of patient-ventilator asynchrony and to evaluate the relationship between asynchrony during assisted ventilation and clinical outcomes. We performed a prospective cohort study in patients under mechanical ventilation (MV). Baseline measurements included severity of illness and respiratory mechanics. The primary outcome was the Asynchrony Index (AI), defined as the number of asynchronous events divided by the number of ventilator cycles and wasted efforts. We recorded ventilator waveforms throughout the entire period of MV. We analyzed 11,881 h of MV from 103 subjects. Median AI during the entire period of MV was 5.1% (IQR:2.6–8.7). Intrinsic PEEP was associated with AI (OR:1.72, 95%CI:1.1–2.68), but static compliance and airway resistance were not. Simplified Acute Physiology Score 3 (OR:1.03, 95%CI:1–1.06) was also associated with AI. Median AI was higher during assisted (5.4%, IQR:2.9–9.1) than controlled (2%, IQR:0.6–4.9) ventilation, and 22% of subjects had high incidence of asynchrony (AI≥10%). Subjects with AI≥10% had more extubation failure (33%) than patients with AI<10% (6%), p = .01. Predictors of high incidence of asynchrony were severity of illness and intrinsic PEEP. High incidence of asynchrony was associated with extubation failure, but not mortality. Trial registration: ClinicalTrials.gov, NCT02687802 •Intrinsic PEEP at intubation was a predictor of high incidence of asynchrony (AI≥10%), but static compliance and airway resistance were not•Severity of illness was also associated with high incidence of asynchrony•Double triggering was the most frequent type of asynchrony in subjects under controlled ventilation.•During assisted ventilation, ineffective efforts were more common.•AI≥10% during assisted ventilation was associated with extubation failure, but not with mortality

Purpose To determine if neurally adjusted ventilatory assist (NAVA) improves asynchrony, ventilatory drive, breath-to-breath variability and COMFORT score when compared to pressure support (PS). Methods This is a non-randomized short-term cross-over trial in which 12 pediatric patients with asynchrony (auto-triggering, double triggering or non-triggered breaths) were enrolled. Four sequential 10-min periods of data were recorded after 20 min of ventilatory stabilization (wash-out) at each of the following settings: baseline PS with the ventilator settings determined by the attending physician (1-PS b ); PS after optimization (2-PS opt ); NAVA level set so that maximum inspiratory pressure ( P max ) equaled P max in PS (3-NAVA); same settings as in 2-PS opt (4-PS opt ). Results The median asynchrony index was significantly lower during NAVA (2.0 %) than during 2-PS opt (8.5 %, p  = 0.017) and 4-PS opt (7.5 %, p  = 0.008). In NAVA mode, the NAVA trigger accounted on average for 66 % of triggered breaths. The median trigger delay with respect to neural inspiratory time was significantly lower during NAVA (8.6 %) than during 2-PS opt (25.2 %, p  = 0.003) and 4-PS opt (28.2 %, p  = 0.0005). The median electrical activity of the diaphragm (EAdi) change during trigger delay normalized to maximum inspiratory EAdi difference was significantly lower during NAVA (5.3 %) than during 2-PS opt (21.7 %, p  = 0.0005) and 4-PS opt (24.6 %, p  = 0.001). The coefficient of variation of tidal volume was significantly higher during NAVA (44.2 %) than during 2-PS opt (19.8 %, p  = 0.0002) and 4-PS opt (23.0 %, p  = 0.0005). The median COMFORT score during NAVA (15.0) was lower than that during 2-PS opt (18.0, p  = 0.0125) and 4-PS opt (17.5, p  = 0.039). No significant changes for any variable were observed between 1-PS b and 2-PS opt . Conclusions Neurally adjusted ventilatory assist as compared to optimized PS results in improved synchrony, reduced ventilatory drive, increased breath-to-breath mechanical variability and improved patient comfort.

The patient was successfully extubated to 16 cm H2O continuous positive airway pressure, discharged from the ICU, and eventually discharged from the hospital without the need for reintubation. The elevated pleural pressure in these patients works as a mechanical load, reducing lung volumes and causing airway closure, increased airway resistance, and development of atelectasis, especially within dependent lung regions. Liberation from mechanical ventilation in critically ill adults: an official American College of Chest Physicians/American Thoracic Society Clinical Practice Guideline: inspiratory pressure augmentation during spontaneous breathing trials, protocols minimizing sedation, and noninvasive ventilation immediately after extubation.

ARDS: Acute respiratory distress syndrome LUNG-SAFE: Large Observational Study to Understand the Global Impact of Severe Acute Respiratory Failure

The hypothesis that lung collapse is detrimental during the acute respiratory distress syndrome is still debatable. One of the difficulties is the lack of an efficient maneuver to minimize it. To test if a bedside recruitment strategy, capable of reversing hypoxemia and collapse in > 95% of lung units, is clinically applicable in early acute respiratory distress syndrome. Prospective assessment of a stepwise maximum-recruitment strategy using multislice computed tomography and continuous blood-gas hemodynamic monitoring. Twenty-six patients received sequential increments in inspiratory airway pressures, in 5 cm H(2)O steps, until the detection of Pa(O(2)) + Pa(CO(2)) >or= 400 mm Hg. Whenever this primary target was not met, despite inspiratory pressures reaching 60 cm H(2)O, the maneuver was considered incomplete. If there was hemodynamic deterioration or barotrauma, the maneuver was to be interrupted. Late assessment of recruitment efficacy was performed by computed tomography (9 patients) or by online continuous monitoring in the intensive care unit (15 patients) up to 6 h. It was possible to open the lung and to keep the lung open in the majority (24/26) of patients, at the expense of transient hemodynamic effects and hypercapnia but without major clinical consequences. No barotrauma directly associated with the maneuver was detected. There was a strong and inverse relationship between arterial oxygenation and percentage of collapsed lung mass (R = - 0.91; p < 0.0001). It is often possible to reverse hypoxemia and fully recruit the lung in early acute respiratory distress syndrome. Due to transient side effects, the required maneuver still awaits further evaluation before routine clinical application.

Mechanical ventilation (MV) with high tidal volumes (V(T)) can cause or aggravate lung damage, so-called ventilator induced lung injury (VILI). The relationship between specific mechanical events in the lung and the cellular responses that result in VILI remains incomplete. Since activation of Wnt/β-catenin signaling has been suggested to be central to mechanisms of lung healing and fibrosis, we hypothesized that the Wnt/β-catenin signaling plays a role during VILI. Prospective, randomized, controlled animal study using adult, healthy, male Sprague-Dawley rats. Animals (n = 6/group) were randomized to spontaneous breathing or two strategies of MV for 4 hours: low tidal volume (V(T)) (6 mL/kg) or high V(T) (20 mL/kg). Histological evaluation of lung tissue, measurements of WNT5A, total β-catenin, non-phospho (Ser33/37/Thr41) β-catenin, matrix metalloproteinase-7 (MMP-7), cyclin D1, vascular endothelial growth factor (VEGF), and axis inhibition protein 2 (AXIN2) protein levels by Western blot, and WNT5A, non-phospho (Ser33/37/Thr41) β-catenin, MMP-7, and AXIN2 immunohistochemical localization in the lungs were analyzed. High-V(T) MV caused lung inflammation and perivascular edema with cellular infiltrates and collagen deposition. Protein levels of WNT5A, non-phospho (Ser33/37/Thr41) β-catenin, MMP-7, cyclin D1, VEGF, and AXIN2 in the lungs were increased in all ventilated animals although high-V(T) MV was associated with significantly higher levels of WNT5A, non-phospho (Ser33/37/Thr41) β-catenin, MMP-7, cyclin D1, VEGF, and AXIN2 levels. Our findings demonstrate that the Wnt/β-catenin signaling pathway is modulated very early by MV in lungs without preexistent lung disease, suggesting that activation of this pathway could play an important role in both VILI and lung repair. Modulation of this pathway might represent a therapeutic option for prevention and/or management of VILI.