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Objectives: Lung ultrasound is commonly used to evaluate lung morphology in patients with acute respiratory distress syndrome. Aim of this study was to determine lung ultrasound reliability in assessing lung aeration and positive end-expiratory pressure-induced recruitment compared with CT., Design: Randomized crossover study., Setting: University hospital ICU., Patients: Twenty sedated paralyzed acute respiratory distress syndrome patients: age 56 years (43-72 yr), body mass index 25 kg/m (22-27 kg/m), and PaO2/FIO2 160 (113-218)., Interventions: Lung CT and lung ultrasound examination were performed at positive end-expiratory pressure 5 and 15 cm H2O., Measurements and Main Results: Global and regional Lung Ultrasound scores were compared with CT quantitative analysis. Lung recruitment (i.e., decrease in not aerated tissue as assessed with CT) was compared with global Lung Ultrasound score variations. Global Lung Ultrasound score was strongly associated with average lung tissue density at positive end-expiratory pressure 5 (R = 0.78; p < 0.0001) and positive end-expiratory pressure 15 (R = 0.62; p < 0.0001). Regional Lung Ultrasound score strongly correlated with tissue density at positive end-expiratory pressure 5 (rs = 0.79; p < 0.0001) and positive end-expiratory pressure 15 (rs = 0.79; p < 0.0001). Each step increase of regional Lung Ultrasound score was associated with significant increase of tissue density (p < 0.005). A substantial agreement was found between regional Lung Ultrasound score and CT classification at positive end-expiratory pressure 5 (k = 0.69 [0.63-0.75]) and at positive end-expiratory pressure 15 (k = 0.70 [0.64-0.75]). At positive end-expiratory pressure 15, both global Lung Ultrasound score (22 [16-27] vs 26 [21-29]; p < 0.0001) and not aerated tissue (42% [25-57%] vs 52% [39-67%]; p < 0.0001) decreased. However, Lung Ultrasound score variations were not associated with lung recruitment (R = 0.01; p = 0.67)., Conclusions: Lung Ultrasound score is a valid tool to assess regional and global lung aeration. Global Lung Ultrasound score variations should not be used for bedside assessment of positive end-expiratory pressure-induced recruitment.

Background: The leading cause of early mortality after lung transplantation is Primary graft dysfunction (PGD). We assessed the lung inflammation, inflation status and inhomogeneities after lung transplantation. Our purpose was to investigate the possible differences between patients who did or did not develop PGD., Methods: We designed a prospective observational study enrolling patients who underwent a CT-PET study within 1 week after lung transplantation. Twenty-four patients (10 after double- and 14 after single-lung) were enrolled. Respiratory and hemodynamic data were collected before, during and after lung transplantation. Each patient underwent computed tomography-positron emission tomography (CT-PET) scan early after surgery. Broncho-alveolar lavage (BAL) fluid collection was performed to analyze inflammatory mediators., Results: The grafts showed a [18F]fluoro-2-deoxy-D-glucose ([18F]FDG) uptake rate of 26[18-33]*10-4 mLblood/mLtissue/min (reference values 11[7-15]*10-4). Three double- and six single-lung recipients developed PGD. The grafts of patients who developed PGD had similar [18F]FDG uptake than grafts of patients who did not (28[18-26]*10-4 versus 26[22-31]*10-4, P=0.79). Not-inflated tissue fraction was significantly higher (28[20-38]% versus 14[7-21]%, P=0.01) while well-inflated fraction was significantly lower (29[25-41]% versus 53[39-65]%, P<0.01). Inhomogeneity extent was higher in patients who developed PGD (23[18-26]% versus 14[10-20]%, P=0.01)The lung weight was 650[591-820]g versus 597[480-650]g (P=0.09)). BAL fluid analysis for inflammatory mediators did not detect a difference between the study groups., Conclusions: Compared to healthy lungs, all the grafts showed increased [18F]FDG uptake rate, but there were no differences between patients who developed PGD and patients who did not. Of note, the PGD patients showed a worse inflation status of lungs and a higher inhomogeneity extent.

Purpose: Open lung strategy during ARDS aims to decrease the ventilator-induced lung injury by minimizing the atelectrauma and stress/strain maldistribution. We aim to assess how much of the lung is opened and kept open within the limits of mechanical ventilation considered safe (i.e., plateau pressure 30 cmH 2 O, PEEP 15 cmH 2 O)., Methods: Prospective study from two university hospitals. Thirty-three ARDS patients (5 mild, 10 moderate, 9 severe without extracorporeal support, ECMO, and 9 severe with it) underwent two low-dose end-expiratory CT scans at PEEP 5 and 15 cmH 2 O and four end-inspiratory CT scans (from 19 to 40 cmH 2 O). Recruitment was defined as the fraction of lung tissue which regained inflation. The atelectrauma was estimated as the difference between the intratidal tissue collapse at 5 and 15 cmH 2 O PEEP. Lung ventilation inhomogeneities were estimated as the ratio of inflation between neighboring lung units., Results: The lung tissue which is opened between 30 and 45 cmH 2 O (i.e., always closed at plateau 30 cmH 2 O) was 10 ± 29, 54 ± 86, 162 ± 92, and 185 ± 134 g in mild, moderate, and severe ARDS without and with ECMO, respectively (p < 0.05 mild versus severe without or with ECMO). The intratidal collapses were similar at PEEP 5 and 15 cmH 2 O (63 ± 26 vs 39 ± 32 g in mild ARDS, p = 0.23; 92 ± 53 vs 78 ± 142 g in moderate ARDS, p = 0.76; 110 ± 91 vs 89 ± 93, p = 0.57 in severe ARDS without ECMO; 135 ± 100 vs 104 ± 80, p = 0.32 in severe ARDS with ECMO). Increasing the applied airway pressure up to 45 cmH 2 O decreased the lung inhomogeneity slightly (but significantly) in mild and moderate ARDS, but not in severe ARDS., Conclusions: Data show that the prerequisites of the open lung strategy are not satisfied using PEEP up to 15 cmH 2 O and plateau pressure up to 30 cmH 2 O. For an effective open lung strategy, higher pressures are required. Therefore, risks of atelectrauma must be weighted versus risks of volutrauma., Trial Registration: Clinicaltrials.gov identifier: NCT01670747 ( www.clinicaltrials.gov ).

Rationale: The assessment of lung recruitability in patients with acute respiratory distress syndrome (ARDS) may be important for planning recruitment maneuvers and setting positive end-expiratory pressure (PEEP)., Objectives: To determine whether lung recruitment measured by respiratory mechanics is comparable with lung recruitment measured by computed tomography (CT)., Methods: In 22 patients with ARDS, lung recruitment was assessed at 5 and 15 cm H2O PEEP by using respiratory mechanics-based methods: (1) increase in gas volume between two pressure-volume curves (P-Vrs curve); (2) increase in gas volume measured and predicted on the basis of expected end-expiratory lung volume and static compliance of the respiratory system (EELV-Cst,rs); as well as by CT scan: (3) decrease in noninflated lung tissue (CT [not inflated]); and (4) decrease in noninflated and poorly inflated tissue (CT [not + poorly inflated])., Measurements and Main Results: The P-Vrs curve recruitment was significantly higher than EELV-Cst,rs recruitment (423 ± 223 ml vs. 315 ± 201 ml; P < 0.001), but these measures were significantly related to each other (R(2) = 0.93; P < 0.001). CT (not inflated) recruitment was 77 ± 86 g and CT (not + poorly inflated) was 80 ± 67 g (P = 0.856), and these measures were also significantly related to each other (R(2) = 0.20; P = 0.04). Recruitment measured by respiratory mechanics was 54 ± 28% (P-Vrs curve) and 39 ± 25% (EELV-Cst,rs) of the gas volume at 5 cm H2O PEEP. Recruitment measured by CT scan was 5 ± 5% (CT [not inflated]) and 6 ± 6% (CT [not + poorly inflated]) of lung tissue., Conclusions: Respiratory mechanics and CT measure-under the same term, "recruitment"-two different entities. The respiratory mechanics-based methods include gas entering in already open pulmonary units that improve their mechanical properties at higher PEEP. Consequently, they can be used to assess the overall improvement of inflation. The CT scan measures the amount of collapsed tissue that regains inflation. Clinical trial registered with www.clinicaltrials.gov (NCT00759590).

Background: The ventilator works mechanically on the lung parenchyma. The authors set out to obtain the proof of concept that ventilator-induced lung injury (VILI) depends on the mechanical power applied to the lung., Methods: Mechanical power was defined as the function of transpulmonary pressure, tidal volume (TV), and respiratory rate. Three piglets were ventilated with a mechanical power known to be lethal (TV, 38 ml/kg; plateau pressure, 27 cm H2O; and respiratory rate, 15 breaths/min). Other groups (three piglets each) were ventilated with the same TV per kilogram and transpulmonary pressure but at the respiratory rates of 12, 9, 6, and 3 breaths/min. The authors identified a mechanical power threshold for VILI and did nine additional experiments at the respiratory rate of 35 breaths/min and mechanical power below (TV 11 ml/kg) and above (TV 22 ml/kg) the threshold., Results: In the 15 experiments to detect the threshold for VILI, up to a mechanical power of approximately 12 J/min (respiratory rate, 9 breaths/min), the computed tomography scans showed mostly isolated densities, whereas at the mechanical power above approximately 12 J/min, all piglets developed whole-lung edema. In the nine confirmatory experiments, the five piglets ventilated above the power threshold developed VILI, but the four piglets ventilated below did not. By grouping all 24 piglets, the authors found a significant relationship between the mechanical power applied to the lung and the increase in lung weight (r = 0.41, P = 0.001) and lung elastance (r = 0.33, P < 0.01) and decrease in PaO2/FIO2 (r = 0.40, P < 0.001) at the end of the study., Conclusion: In piglets, VILI develops if a mechanical power threshold is exceeded.

The use of low tidal volume ventilation and low to moderate positive end-expiratory pressure (PEEP) levels is a widespread strategy to ventilate patients with non-injured lungs during general anesthesia and in intensive care as well with mild to moderate acute respiratory distress syndrome (ARDS). Higher PEEP levels have been recommended in severe ARDS. Due to the presence of alveolar collapse, recruitment maneuvers (RMs) by causing a transient elevation in airway pressure (i.e. transpulmonary pressure) have been suggested to improve lung inflation in non-inflated and poorly-inflated lung regions. Various types of RMs such as sustained inflation at high pressure, intermittent sighs and stepwise increases of PEEP and/or airway plateau inspiratory pressure have been proposed. The use of RMs has been associated with mixed results in terms of physiological and clinical outcomes. The optimal method for RMs has not yet been identified. The use of RMs is not standardized and left to the individual physician based on his/her experience. Based on the same grounds, RMs have been proposed to improve lung aeration during general anesthesia. The aim of this review was to present the clinical evidence supporting the use of RMs in patients with ARDS and during general anesthesia and as well their potential biological effects in experimental models of acute lung injury.

Background: Obesity is associated in healthy subjects with a great reduction in functional residual capacity and with a stiffening of lung and chest wall elastance, which promote alveolar collapse and hypoxaemia. Likewise, obese patients with acute respiratory distress syndrome (ARDS) could present greater derangements of respiratory mechanics than patients of normal weight., Methods: One hundred and one ARDS patients were enrolled. Partitioned respiratory mechanics and gas exchange were measured at 5 and 15 cm H2O of PEEP with a tidal volume of 6-8 ml kg(-1) of predicted body weight. At 5 and 45 cm H2O of PEEP, two lung computed tomography scans were performed., Results: Patients were divided as follows according to BMI: normal weight (BMI≤25 kg m(-2)), overweight (BMI between 25 and 30 kg m(-2)), and obese (BMI>30 kg m(-2)). Obese, overweight, and normal-weight groups presented a similar lung elastance (median [interquartile range], respectively: 17.7 [14.2-24.8], 20.9 [16.1-30.2], and 20.5 [15.2-23.6] cm H2O litre(-1) at 5 cm H2O of PEEP and 19.3 [15.5-26.3], 21.1 [17.4-29.2], and 17.1 [13.4-20.4] cm H2O litre(-1) at 15 cm H2O of PEEP) and chest elastance (respectively: 4.9 [3.1-8.8], 5.9 [3.8-8.7], and 7.8 [3.9-9.8] cm H2O litre(-1) at 5 cm H2O of PEEP and 6.5 [4.5-9.6], 6.6 [4.2-9.2], and 4.9 [2.4-7.6] cm H2O litre(-1) at 15 cm H2O of PEEP). Lung recruitability was not affected by the body weight (15.6 [6.3-23.4], 15.7 [9.8-22.2], and 11.3 [6.2-15.6]% for normal-weight, overweight, and obese groups, respectively). Lung gas volume was significantly lower whereas total superimposed pressure was significantly higher in the obese compared with the normal-weight group (1148 [680-1815] vs 827 [686-1213] ml and 17.4 [15.8-19.3] vs 19.3 [18.6-21.7] cm H2O, respectively)., Conclusions: Obese ARDS patients do not present higher chest wall elastance and lung recruitability., (© The Author 2015. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

The aim of the study was to determine the size and location of homogeneous inflamed/noninflamed and inhomogeneous inflamed/noninflamed lung compartments and their association with acute respiratory distress syndrome (ARDS) severity.In total, 20 ARDS patients underwent 5 and 45 cmH2O computed tomography (CT) scans to measure lung recruitability. [(18)F]2-fluoro-2-deoxy-d-glucose ([(18)F]FDG) uptake and lung inhomogeneities were quantified with a positron emission tomography-CT scan at 10 cmH2O. We defined four compartments with normal/abnormal [(18)F]FDG uptake and lung homogeneity.The homogeneous compartment with normal [(18)F]FDG uptake was primarily composed of well-inflated tissue (80±16%), double-sized in nondependent lung (32±27% versus 16±17%, p<0.0001) and decreased in size from mild, moderate to severe ARDS (33±14%, 26±20% and 5±9% of the total lung volume, respectively, p=0.05). The homogeneous compartment with high [(18)F]FDG uptake was similarly distributed between the dependent and nondependent lung. The inhomogeneous compartment with normal [(18)F]FDG uptake represented 4% of the lung volume. The inhomogeneous compartment with high [(18)F]FDG uptake was preferentially located in the dependent lung (21±10% versus 12±10%, p<0.0001), mostly at the open/closed interfaces and related to recruitability (r(2)=0.53, p<0.001).The homogeneous lung compartment with normal inflation and [(18)F]FDG uptake decreases with ARDS severity, while the inhomogeneous poorly/not inflated compartment increases. Most of the lung inhomogeneities are inflamed. A minor fraction of healthy tissue remains in severe ARDS., (Copyright ©ERS 2016.)

Background: During mechanical ventilation, stress and strain may be locally multiplied in an inhomogeneous lung. The authors investigated whether, in healthy lungs, during high pressure/volume ventilation, injury begins at the interface of naturally inhomogeneous structures as visceral pleura, bronchi, vessels, and alveoli. The authors wished also to characterize the nature of the lesions (collapse vs. consolidation)., Methods: Twelve piglets were ventilated with strain greater than 2.5 (tidal volume/end-expiratory lung volume) until whole lung edema developed. At least every 3 h, the authors acquired end-expiratory/end-inspiratory computed tomography scans to identify the site and the number of new lesions. Lung inhomogeneities and recruitability were quantified., Results: The first new densities developed after 8.4 ± 6.3 h (mean ± SD), and their number increased exponentially up to 15 ± 12 h. Afterward, they merged into full lung edema. A median of 61% (interquartile range, 57 to 76) of the lesions appeared in subpleural regions, 19% (interquartile range, 11 to 23) were peribronchial, and 19% (interquartile range, 6 to 25) were parenchymal (P < 0.0001). All the new densities were fully recruitable. Lung elastance and gas exchange deteriorated significantly after 18 ± 11 h, whereas lung edema developed after 20 ± 11 h., Conclusions: Most of the computed tomography scan new densities developed in nonhomogeneous lung regions. The damage in this model was primarily located in the interstitial space, causing alveolar collapse and consequent high recruitability.

Background: The aim of this study was to evaluate in vitro the accuracy of second generation esophageal catheters at different surrounding pressures and filling volumes and to suggest appropriate catheter management in clinical practice., Methods: Six different esophageal catheters were placed in an experimental chamber at four chamber pressures (0, 10, 20 and 30 cmH2O) and at filling volumes ranging from 0 to 10 mL. The working volume was defined as the volume range between the maximum (Vmax) and minimum (Vmin) volumes achieving acceptable accuracy (defined by a balloon transmural pressure ± 1 cmH2O). Accuracy was evaluated for a standard volume of 0.5 mL and for volumes recommended by manufacturers. Data are shown as median and interquartile range., Results: In the four conditions of chamber pressure Vmin, Vmax and working volume were 1.0 (0.5, 1.5), 5.3 (3.8, 7.1), and 3.5 (2.9, 6.1) mL. Increasing chamber pressure increased Vmin (rho=0.9; P<0.0001), that reached 2.0 mL (1.6-2.0) at 30 cmH2O. Vmax and working volumes differed among catheters, whereas Vmin did not. By injecting 0.5 mL and the minimum recommended volume by manufacturer, balloon transmural pressure was <-1 cmH2O in 71% and 53% of cases, it was negatively related to chamber pressure (rho=-0.97 and -0.71; P<0.0001) and reached values of -10.4 (-12.4, -9.7) and -9.8 (-10.6, -3.4) at 30 cmH2O., Conclusion: Measuring positive esophageal pressures needs higher injected volumes than usually recommended. The range of appropriate filling volumes is catheter-specific. Both absolute values and respiratory changes of esophageal pressure can be underestimated by an underfilled balloon.