IntroductionBased on the hypothesis that failure of weaning from mechanical ventilation is caused by respiratory demand exceeding the capacity of the respiratory muscles, we evaluated whether extubation failure could be characterized by increased respiratory drive and impaired efficiency to generate inspiratory pressure and ventilation.MethodsAirway pressure, flow, volume, breathing frequency, and diaphragm electrical activity were measured in a heterogeneous group of patients deemed ready for a spontaneous breathing trial. Efficiency to convert neuromuscular activity into inspiratory pressure was calculated as the ratio of negative airway pressure and diaphragm electrical activity during an inspiratory occlusion. Efficiency to convert neuromuscular activity into volume was calculated as the ratio of the tidal volume to diaphragm electrical activity. All variables were obtained during a 30-minute spontaneous breathing trial on continuous positive airway pressure (CPAP) of 5 cm H2O and compared between patients for whom extubation succeeded with those for whom either the spontaneous breathing trial failed or for those who passed, but then the extubation failed.ResultsOf 52 patients enrolled in the study, 35 (67.3%) were successfully extubated, and 17 (32.7%) were not. Patients for whom it failed had higher diaphragm electrical activity (48%; P < 0.001) and a lower efficiency to convert neuromuscular activity into inspiratory pressure and tidal volume (40% (P < 0.001) and 53% (P < 0.001)), respectively. Neuroventilatory efficiency demonstrated the greatest predictability for weaning success.ConclusionsThis study shows that a mixed group of critically ill patients for whom weaning fails have increased neural respiratory drive and impaired ability to convert neuromuscular activity into tidal ventilation, in part because of diaphragm weakness.Trial RegistrationClinicaltrials.gov identifier NCT01065428. ©2012 Liu et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

IntroductionThe aim of this study was to validate an automated, objective and standardized algorithm for quantifying and displaying patient-ventilator interaction.MethodsUsing a new method to detect patient-ventilator synchrony, the present study re-analyzed previously acquired and published data from 24 mechanically ventilated adult patients (Colombo et al., Crit Care Med. 2011 Nov;39(11):2452–7). Patient-ventilator interactions were evaluated by comparing ventilator pressure and diaphragm electrical activity (EAdi) waveforms, recorded during pressure support ventilation. The EAdi and ventilator pressure waveforms were analyzed for their timings (manually and automatically determined), and the error between the two waveforms was quantified. A new index of patient-ventilator interaction (NeuroSync index), which is standardized and automated, was validated and compared to manual analysis and previously published indices of asynchrony.ResultsThe comparison of manual and automated detection methods produced high test-retest and inter-rater reliability (Intraclass correlation coefficient = 0.95). The NeuroSync index increased the sensitivity of detecting dyssynchronies, compared to previously published indices, which were found to only detect asynchronies.ConclusionThe present study introduces an automated method and the NeuroSync index to determine patient-ventilator interaction with a more sensitive analysis method than those previously described. A dashboard-style of graphical display allows a rapid overview of patient-ventilator interaction and breathing pattern at the bedside.

Rationale: Chest computed tomography (CT) has been used for the coronavirus disease 2019 (COVID-19) monitoring. However, the imaging risk factors for poor clinical outcomes remain unclear. In this study, we aimed to assess the imaging characteristics and risk factors associated with adverse composite endpoints in patients with COVID-19 pneumonia. Methods: This retrospective cohort study enrolled patients with laboratory-confirmed COVID-19 from 24 designated hospitals in Jiangsu province, China, between 10 January and 18 February 2020. Clinical and initial CT findings at admission were extracted from medical records. Patients aged < 18 years or without available clinical or CT records were excluded. The composite endpoints were admission to ICU, acute respiratory failure occurrence, or shock during hospitalization. The volume, density, and location of lesions, including ground-glass opacity (GGO) and consolidation, were quantitatively analyzed in each patient. Multivariable logistic regression models were used to identify the risk factors among age and CT parameters associated with the composite endpoints. Results: In this study, 625 laboratory-confirmed COVID-19 patients were enrolled; among them, 179 patients without an initial CT at admission and 25 patients aged < 18 years old were excluded and 421 patients were included in analysis. The median age was 48.0 years and the male proportion was 53% (224/421). During the follow-up period, 64 (15%) patients had a composite endpoint. There was an association of older age (odds ratio [OR], 1.04; 95% confidence interval [CI]: 1.01-1.06; P = 0.003), larger consolidation lesions in the upper lung (Right: OR, 1.13; 95%CI: 1.03-1.25, P =0.01; Left: OR,1.15; 95%CI: 1.01-1.32; P = 0.04) with increased odds of adverse endpoints. Conclusion:There was an association of older age and larger consolidation in upper lungs on admission with higher odds of poor outcomes in patients with COVID-19.

BackgroundAcute respiratory distress syndrome (ARDS) is a life-threatening condition in critically ill patients. Recently, we have found that mesenchymal stem cells (MSC) improved the permeability of human lung microvascular endothelial cells by secreting hepatocyte growth factor (HGF) in vitro. However, the properties and functions of MSC may change under complex circumstances in vivo. Here, we sought to determine the role of the HGF-expressing character of MSC in the therapeutic effects of MSC on ARDS in vivo.MethodsMSC with HGF gene knockdown (MSC-ShHGF) were constructed using lentiviral transduction. The HGF mRNA and protein levels in MSC-ShHGF were detected using quantitative real-time polymerase chain reaction and Western blotting analysis, respectively. HGF levels in the MSC culture medium were measured by enzyme-linked immunosorbent assay (ELISA). Rats with ARDS induced by lipopolysaccharide received MSC infusion via the tail vein. After 1, 6, and 24 h, rats were sacrificed. MSC retention in the lung was assessed by immunohistochemical assay. The lung wet weight to body weight ratio (LWW/BW) and Evans blue dye extravasation were obtained to reflect lung permeability. The VE-cadherin was detected with inmmunofluorescence, and the lung endothelial cell apoptosis was assessed by TUNEL assay. The severity of lung injury was evaluated using histopathology. The cytokines and HGF levels in the lung were measured by ELISA.ResultsMSC-ShHGF with markedly lower HGF expression were successfully constructed. Treatment with MSC or MSC carrying green fluorescent protein (MSC-GFP) maintained HGF expression at relatively high levels in the lung at 24 h. MSC or MSC-GFP decreased the LWW/BW and the Evans Blue Dye extravasation, protected adherens junction VE-cadherin, and reduced the lung endothelial cell apoptosis. Furthermore, MSC or MSC-GFP reduced the inflammation and alleviated lung injury based on histopathology. However, HGF gene knockdown significantly decreased the HGF levels without any changes in the MSC retention in the lung, and diminished the protective effects of MSC on the injured lung, indicating the therapeutic effects of MSC on ARDS were partly associated with the HGF-expressing character of MSC.ConclusionsMSC restores lung permeability and lung injury in part by maintaining HGF levels in the lung and the HGF-expressing character is required for MSC to protect the injured lung.Electronic supplementary materialThe online version of this article (doi:10.1186/s13287-016-0320-5) contains supplementary material, which is available to authorized users.

Purpose: Noninvasive ventilation (NIV) may facilitate withdrawal of invasive mechanical ventilation (i-MV) and shorten intensive care unit (ICU) length of stay (LOS) in hypercapnic patients, while data are lacking on hypoxemic patients. We aim to determine whether NIV after early extubation reduces the duration of i-MV and ICU LOS in patients recovering from hypoxemic acute respiratory failure. Methods: Highly selected non-hypercapnic hypoxemic patients were randomly assigned to receive NIV after early or standard extubation. Co-primary end points were duration of i-MV and ICU LOS. Secondary end points were treatment failure, severe events (hemorrhagic, septic, cardiac, renal or neurologic episodes, pneumothorax or pulmonary embolism), ventilator-associated pneumonia (VAP) or tracheobronchitis (VAT), tracheotomy, percent of patients receiving sedation after study enrollment, hospital LOS, and ICU and hospital mortality. Results: We enrolled 130 consecutive patients, 65 treatments and 65 controls. Duration of i-MV was shorter in the treatment group than for controls [4.0 (3.0-7.0) vs. 5.5 (4.0-9.0) days, respectively, p = 0.004], while ICU LOS was not significantly different [8.0 (6.0-12.0) vs. 9.0 (6.5-12.5) days, respectively (p = 0.259)]. Incidence of VAT or VAP (9% vs. 25%, p = 0.019), rate of patients requiring infusion of sedatives after enrollment (57% vs. 85%, p = 0.001), and hospital LOS, 20 (13-32) vs. 27(18-39) days (p = 0.043) were all significantly reduced in the treatment group compared with controls. There were no significant differences in ICU and hospital mortality or in the number of treatment failures, severe events, and tracheostomies. Conclusions: In highly selected hypoxemic patients, early extubation followed by immediate NIV application reduced the days spent on invasive ventilation without affecting ICU LOS.