Ventilator-induced Lung Injury Research Articles

Pressure- and time-dependent alveolar recruitment/derecruitment in a spatially resolved patient-specific computational model for injured human lungs.

We present a novel computational model for the dynamics of alveolar recruitment/derecruitment (RD), which reproduces the underlying characteristics typically observed in injured lungs. The basic idea is a pressure- and time-dependent variation of the stress-free reference volume in reduced dimensional viscoelastic elements representing the acinar tissue. We choose a variable reference volume triggered by critical opening and closing pressures in a time-dependent manner from a straightforward mechanical point of view. In the case of (partially and progressively) collapsing alveolar structures, the volume available for expansion during breathing reduces and vice versa, eventually enabling consideration of alveolar collapse and reopening in our model. We further introduce a method for patient-specific determination of the underlying critical parameters of the new alveolar RD dynamics when integrated into the tissue elements, referred to as terminal units, of a spatially resolved physics-based lung model that simulates the human respiratory system in an anatomically correct manner. Relevant patient-specific parameters of the terminal units are herein determined based on medical image data and the macromechanical behavior of the lung during artificial ventilation. We test the whole modeling approach for a real-life scenario by applying it to the clinical data of a mechanically ventilated patient. The generated lung model is capable of reproducing clinical measurements such as tidal volume and pleural pressure during various ventilation maneuvers. We conclude that this new model is an important step toward personalized treatment of ARDS patients by considering potentially harmful mechanisms-such as cyclic RD and overdistension-and might help in the development of relevant protective ventilation strategies to reduce ventilator-induced lung injury (VILI).

A 16-year-old man with leptospirosis and atypical disseminated intravascular coagulation: a case report

BackgroundLeptospirosis is known for its pulmonary form characterized by intra-alveolar hemorrhage, exhibiting a high mortality rate. Management by venous–venous extracorporeal membrane oxygenation has been reported in a small number of cases.Case presentationWe report herein the case of a 16-year-old Caucasian male who was admitted with rapidly deteriorating respiratory and digestive complaints. He developed severe acute respiratory distress syndrome secondary to disseminated intravascular coagulation and intra-alveolar hemorrhage, requiring initiation of venous–venous extracorporeal membrane oxygenation. Initial infectious and immunological assessments were inconclusive, but repeat serology on the tenth day of admission confirmed a diagnosis of leptospirosis. The patient received multiple transfusions, and upon favorable response to treatment with corticosteroids and antibiotics, he was successfully weaned off venous–venous extracorporeal membrane oxygenation, which was discontinued after 12 days.ConclusionLeptospirosis is a rare cause of severe acute respiratory failure following pulmonary hemorrhage. It is typically diagnosed by serology, with detectable IgM antibodies 5–7 days after the onset of symptoms. We report that early support with respiratory extracorporeal membrane oxygenation favors timely clearance of endobronchial clotting, parenchymal recovery, and prevention of ventilator-induced lung injury. Major hypofibrinogenemia, which did not seem to worsen during extracorporeal membrane oxygenation application, was managed by repeated transfusions. Further studies investigating the pathogenesis of this coagulopathy are required to further optimize the management of this rare and severe complication.

Sphingosine-1-Phosphate Receptor 3 Induces Endothelial Barrier Loss via ADAM10-Mediated Vascular Endothelial-Cadherin Cleavage.

Mechanical ventilation (MV) is a life-supporting strategy employed in the Intensive Care Unit (ICU). However, MV-associated mechanical stress exacerbates existing lung inflammation in ICU patients, resulting in limited improvement in mortality and a condition known as Ventilator-Induced Lung Injury (VILI). Sphingosine-1-phosphate (S1P) is a circulating bioactive lipid that maintains endothelial integrity primarily through S1P receptor 1 (S1PR1). During VILI, mechanical stress upregulates endothelial S1PR3 levels. Unlike S1PR1, S1PR3 mediates endothelial barrier disruption through Rho-dependent pathways. However, the specific impact of elevated S1PR3 on lung endothelial function, apart from Rho activation, remains poorly understood. In this study, we investigated the effects of S1PR3 in endothelial pathobiology during VILI using an S1PR3 overexpression adenovirus. S1PR3 overexpression caused cytoskeleton rearrangement, formation of paracellular gaps, and a modified endothelial response towards S1P. It resulted in a shift from S1PR1-dependent barrier enhancement to S1PR3-dependent barrier disruption. Moreover, S1PR3 overexpression induced an ADAM10-dependent cleavage of Vascular Endothelial (VE)-cadherin, which hindered endothelial barrier recovery. S1PR3-induced cleavage of VE-cadherin was at least partially regulated by S1PR3-mediated NFκB activation. Additionally, we employed an S1PR3 inhibitor TY-52156 in a murine model of VILI. TY-52156 effectively attenuated VILI-induced increases in bronchoalveolar lavage cell counts and protein concentration, suppressed the release of pro-inflammatory cytokines, and inhibited lung inflammation as assessed via a histological evaluation. These findings confirm that mechanical stress associated with VILI increases S1PR3 levels, thereby altering the pulmonary endothelial response towards S1P and impairing barrier recovery. Inhibiting S1PR3 is validated as an effective therapeutic strategy for VILI.

The Impact of Tracheal Stenosis on Distal Airway Pressure with Jet Ventilation.

This study investigates the effects of tracheal stenosis on distal airway pressure during low-frequency jet ventilation (LFJV) in tracheal stenosis resection procedures, focusing on variables like stenosis size, depth, scope type, and inlet pressure. A 3D-printed human airway model was employed, featuring inserted tracheal stenoses of varied sizes and depths. Distal airway pressure was measured with 16 pressure transducers, and data were processed via MATLAB. The study varied stenosis size, depth, scope type, and inlet pressure during five sequential jet bursts under LFJV. Using a subglottiscope resulted in significantly reduced distal airway pressure compared to a laryngoscope. Interestingly, neither stenosis size nor depth significantly influenced distal airway pressure. However, increased distance between the scope and stenosis raised normalized pressure. A linear rise in normalized distal airway pressure was noted with increased inlet pressure, regardless of stenosis dimensions. In this model, scope type and inlet pressure were noted to be significant determinants of distal airway pressure, while stenosis size and depth were not. The distance between the scope and the stenosis did influence distal pressures. These findings may have clinical implications for managing airway pressures in patients undergoing LFJV, potentially reducing the risk of ventilator-induced lung injury. NA (Basic Research) Laryngoscope, 134:2300-2305, 2024.

Effect and mechanical mechanism of spontaneous breathing on oxygenation and lung injury in mild or moderate animal ARDS

ObjectiveThe present study aimed to determine the effect and mechanical mechanism of spontaneous breathing during mechanical ventilation on oxygenation and lung injury using Beagles dogs mild or moderate acute respiratory distress syndrome (ARDS) model.MethodsAfter inducing mild or moderate ARDS by infusion of oleic acid, Eighteen Beagles dogs were randomly split into Spontaneous breathing group (BIPAPSB, n = 6), and Complete muscle paralysis group (BIPAPPC, n = 6),Six Beagles without ventilator support comprised the control group. Both groups were ventilated for 8 h under BIPAP mode. High-pressure was titrated TV to 6 ml/kg. A multi-pair esophageal balloon electrode catheter was used to measure respiratory mechanics and electromyogram. End-expiratory lung volume (EELV), gas exchange and respiratory variables were recorded in the process of mechanical ventilation. The contents of Interleukin (IL)-6 and IL-8 in lung tissue were measure using qRT-PCR. Besides, lung injury score was calculated in the end of mechanical ventilation.ResultsBased on the comparable setting of ventilator, BIPAPSB group exhibited higher safety peak transpulmonary pressure, abdominal pressure, EELV and P/F(PaO2/FiO2) than BIPAPPC group, whereas mean transpulmonary pressure, the mRNA levels of the IL-6 and IL-8 in the lung tissues and lung injury score in BIPAPSB group were lower than those in BIPAPPC group.ConclusionIn mild to moderate ARDS animal models, during mechanical ventilation, SB may improve respiratory function and reduce ventilator-induced lung injury. The mechanism may be that spontaneous inspiration up-regulates peak transpulmonary pressure and EELV; Spontaneous expiration decreases mean transpulmonary pressure by up-regulating intra-abdominal pressure, thereby reducing stress and strain.

Ratchet recruitment in the acute respiratory distress syndrome: lessons from the newborn cry.

Patients with acute respiratory distress syndrome (ARDS) have few treatment options other than supportive mechanical ventilation. The mortality associated with ARDS remains unacceptably high, and mechanical ventilation itself has the potential to increase mortality further by unintended ventilator-induced lung injury (VILI). Thus, there is motivation to improve management of ventilation in patients with ARDS. The immediate goal of mechanical ventilation in ARDS should be to prevent atelectrauma resulting from repetitive alveolar collapse and reopening. However, a long-term goal should be to re-open collapsed and edematous regions of the lung and reduce regions of high mechanical stress that lead to regional volutrauma. In this paper, we consider the proposed strategy used by the full-term newborn to open the fluid-filled lung during the initial breaths of life, by ratcheting tissues opened over a series of initial breaths with brief expirations. The newborn's cry after birth shares key similarities with the Airway Pressure Release Ventilation (APRV) modality, in which the expiratory duration is sufficiently short to minimize end-expiratory derecruitment. Using a simple computational model of the injured lung, we demonstrate that APRV can slowly open even the most recalcitrant alveoli with extended periods of high inspiratory pressure, while reducing alveolar re-collapse with brief expirations. These processes together comprise a ratchet mechanism by which the lung is progressively recruited, similar to the manner in which the newborn lung is aerated during a series of cries, albeit over longer time scales.

Research advances on neurally adjusted ventilatory assist

Mechanical ventilation has, since its introduction into clinical practice, undergone a major evolution from controlled ventilation to diverse modes of assisted ventilation. Conventional mechanical ventilators depend on flow sensors and pneumatic pressure and controllers to complete the respiratory cycle. Neurally adjusted ventilatory assist (NAVA) is a new form of assisted ventilation in recent years, which monitors the electrical activity of the diaphragm (EAdi) to provide an appropriately level of pressure support. And EAdi is the best available signal to sense central respiratory drive and trigger ventilatory assist. Unlike other ventilation modes, NAVA breathing instructions come from the center. Therefore, NAVA have the synchronous nature of the breaths and the patient-adjusted nature of the support. Compared with traditional ventilation mode, NAVA can efficiently unload respiratory muscles, relieve the risk of ventilator-induced lung injury (VILI), improve patient-ventilator coordination, enhance gas exchange, increase the success rate of weaning, etc. This article reviews the research progress of NAVA in order to provide theoretical guidance for clinical applications.

Targeting the mitochondrial fission-mediator Drp1 is a potential therapeutic strategy for ventilator induced lung injury

Targeting the mitochondrial fission-mediator Drp1 is a potential therapeutic strategy for ventilator induced lung injury

Pulmonary MicroRNA Profiling in a Rat Model of Ventilator-Induced Lung Injury

Pulmonary MicroRNA Profiling in a Rat Model of Ventilator-Induced Lung Injury

Sigh Ventilation in Patients With Trauma

Among patients receiving mechanical ventilation, tidal volumes with each breath are often constant or similar. This may lead to ventilator-induced lung injury by altering or depleting surfactant. The role of sigh breaths in reducing ventilator-induced lung injury among trauma patients at risk of poor outcomes is unknown. To determine whether adding sigh breaths improves clinical outcomes. A pragmatic, randomized trial of sigh breaths plus usual care conducted from 2016 to 2022 with 28-day follow-up in 15 academic trauma centers in the US. Inclusion criteria were age older than 18 years, mechanical ventilation because of trauma for less than 24 hours, 1 or more of 5 risk factors for developing acute respiratory distress syndrome, expected duration of ventilation longer than 24 hours, and predicted survival longer than 48 hours. Sigh volumes producing plateau pressures of 35 cm H2O (or 40 cm H2O for inpatients with body mass indexes >35) delivered once every 6 minutes. Usual care was defined as the patient's physician(s) treating the patient as they wished. The primary outcome was ventilator-free days. Prespecified secondary outcomes included all-cause 28-day mortality. Of 5753 patients screened, 524 were enrolled (mean [SD] age, 43.9 [19.2] years; 394 [75.2%] were male). The median ventilator-free days was 18.4 (IQR, 7.0-25.2) in patients randomized to sighs and 16.1 (IQR, 1.1-24.4) in those receiving usual care alone (P = .08). The unadjusted mean difference in ventilator-free days between groups was 1.9 days (95% CI, 0.1 to 3.6) and the prespecified adjusted mean difference was 1.4 days (95% CI, -0.2 to 3.0). For the prespecified secondary outcome, patients randomized to sighs had 28-day mortality of 11.6% (30/259) vs 17.6% (46/261) in those receiving usual care (P = .05). No differences were observed in nonfatal adverse events comparing patients with sighs (80/259 [30.9%]) vs those without (80/261 [30.7%]). In a pragmatic, randomized trial among trauma patients receiving mechanical ventilation with risk factors for developing acute respiratory distress syndrome, the addition of sigh breaths did not significantly increase ventilator-free days. Prespecified secondary outcome data suggest that sighs are well-tolerated and may improve clinical outcomes. ClinicalTrials.gov Identifier: NCT02582957.

CircUBR1 knockdown relieves ventilator-induced lung injury through regulating miR-20a-5p/GGPPS1 pathway

ObjectiveTo assess the influences and underlying mechanism of circular RNA UBR1 (circUBR1) in ventilator-induced lung injury (VILI). MethodsIn mice and mouse alveolar epithelial cells, VILI model was established. CircUBR1 and miR-20a-5p expression was assessed via quantitative real time polymerase chain reaction. Western blot and immunohistochemistry were applied to assess geranylgeranyl diphosphate synthase 1 (GGPPS1) protein expression. In lung tissues, the histopathological changes were utilized using hematoxylin and eosin staining. Cell counting kit-8 assay and flow cytometer were applied to detect cell proliferation and apoptosis. The levels of inflammatory cytokines [interleukin (IL)-1β, IL-18, IL-6, and tumor necrosis factor (TNF)-α] were measured by western blot and enzyme-linked immunosorbent assay. ResultsIn lung tissues of VILI mice, circUBR1 and GGPPS1 expression were upregulated, while miR-20a-5p expression was downregulated. In vivo, circUBR1 knockdown alleviated lung injury, inhibited cell apoptosis, and decreased the levels of inflammatory cytokines. In cells treated with cyclic stretch (CS), circUBR1 knockdown promoted cell viability, inhibited cell apoptosis, and reduced inflammatory cytokines. CircUBR1 could sponge miR-20a-5p, and GGPPS1 was the target gene of miR-20a-5p. In addition, in cells treated with CS, downregulation of miR-20a-5p or the overexpression of GGPPS1 reversed the promotive effect of circUBR1 knockdown on cell viability and the inhibitive effect of circUBR1 knockdown on cell apoptosis and inflammation production. ConclusionsIn VILI, knockdown of circUBR1 attenuated lung injury and inflammation via regulating the miR-20a-5p/GGPPS1 pathway. Our study may provide a potential therapeutic target for treatment of VILI.

Modulation of the hippo-YAP pathway by cyclic stretch in rat type 2 alveolar epithelial cells-a proof-of-concept study.

Background: Mechanical ventilation (MV) is a life supporting therapy but may also cause lung damage. This phenomenon is known as ventilator-induced lung injury (VILI). A potential pathomechanisms of ventilator-induced lung injury may be the stretch-induced production and release of cytokines and pro-inflammatory molecules from the alveolar epithelium. Yes-associated protein (YAP) might be regulated by mechanical forces and involved in the inflammation cascade. However, its role in stretch-induced damage of alveolar cells remains poorly understood. In this study, we explored the role of YAP in the response of alveolar epithelial type II cells (AEC II) to elevated cyclic stretch in vitro. We hypothesize that Yes-associated protein activates its downstream targets and regulates the interleukin-6 (IL-6) expression in response to 30% cyclic stretch in AEC II. Methods: The rat lung L2 cell line was exposed to 30% cyclic equibiaxial stretch for 1 or 4h. Non-stretched conditions served as controls. The cytoskeleton remodeling and cell junction integrity were evaluated by F-actin and Pan-cadherin immunofluorescence, respectively. The gene expression and protein levels of IL-6, Yes-associated protein, Cysteine-rich angiogenic inducer 61 (Cyr61/CCN1), and connective tissue growth factor (CTGF/CCN2) were studied by real-time polymerase chain reaction (RT-qPCR) and Western blot, respectively. Verteporfin (VP) was used to inhibit Yes-associated protein activation. The effects of 30% cyclic stretch were assessed by two-way ANOVA. Statistical significance as accepted at p < 0.05. Results: Cyclic stretch of 30% induced YAP nuclear accumulation, activated the transcription of Yes-associated protein downstream targets Cyr61/CCN1 and CTGF/CCN2 and elevated IL-6 expression in AEC II after 1hour, compared to static control. VP (2µM) inhibited Yes-associated protein activation in response to 30% cyclic stretch and reduced IL-6 protein levels. Conclusion: In rat lung L2 AEC II, 30% cyclic stretch activated YAP, and its downstream targets Cyr61/CCN1 and CTGF/CCN2 and proinflammatory IL-6 expression. Target activation was blocked by a Yes-associated protein inhibitor. This novel YAP-dependent pathway could be involved in stretch-induced damage of alveolar cells.

Regulation of cell proliferation and transdifferentiation compensates for ventilator-induced lung injury mediated by NLRP3 inflammasome activation.

Mechanical ventilation is an important means of respiratory support and treatment for various diseases. However, its use can lead to serious complications, especially ventilator-induced lung injury (VILI). The mechanisms underlying this disease are complex, but activation of inflammatory signalling pathways results in activation of cytokines and inflammatory mediators, which play key roles in VILI. Recent studies have demonstrated that nod-like receptor protein 3 (NLRP3) inflammasome activation mediates VILI and also accompanied by cell proliferation and transdifferentiation to compensate for alveolar membrane damage. Type I alveolar epithelial cells (AECs I), which are involved in the formation of the blood-air barrier, are vulnerable to damage but cannot proliferate by themselves; thus, replacing AECs I relies on type II alveolar epithelial cells (AECs II). The review aims to introduce the mechanisms of NLRP3 inflammasome activation and its inhibitors, as well as the mechanisms that regulate cell proliferation and transdifferentiation. A large number of relevant literature was searched, then the key content was summarized and figures were also made. The mechanism of NLRP3 inflammasome activation has been further explored, including but not limited to pathogenic and aseptic inflammatory signals, such as, pathogenic molecular patterns and host-derived danger-associated molecular patterns activate toll-like receptor 4/nuclear factor-kappaB pathway or reactive oxygen species, cyclic stretch, adenosine triphosphate induce K+ efflux through P2X7, Ca2+ inflow, mitochondrial damage, etc, eventually induce NIMA-related kinase 7/NLRP3 binding and NLRP3 inflammasome activation. Not only that, the review also described in detail the inhibitors of NLRP3 inflammasome. And the mechanisms regulating cell proliferation and transdifferentiation are complex and unclear, including the Wnt/β-catenin, Yap/Taz, BMP/Smad and Notch signalling pathways. NLRP3 inflammasome activation mediated VILI, and VILI is alleviated after interfering with its activation, and inflammation and repair exist simultaneously in VILI. Clarifying these mechanisms is expected to provide theoretical guidance for alleviating VILI by inhibiting the inflammatory response and accelerating alveolar epithelial cell regeneration in the early stage.

Updated Guidelines for Acute Respiratory Distress Syndrome

Acute respiratory distress syndrome (ARDS) accounts for 10% of patients admitted to the intensive care unit and 23% of patients using mechanical ventilation, with a mortality rate of 45% in severe cases. The perception that patients with ARDS are vulnerable to ventilator-induced lung injury has led to lung-protective ventilation strategies. Accordingly, the American Thoracic Society, the European Society of Intensive Care Medicine (ESICM), and the Society of Critical Care Medicine announced ARDS mechanical ventilation guidelines in 2017. Since then, based on the results of newly reported research and data accumulated throughout the coronavirus disease 2019 pandemic, the ESICM announced an amendment to the previous guidelines in 2023. The revised ARDS guidelines discuss extending the ARDS definition and its phenotypes that were not mentioned in the previous guidelines. The new guidelines encompass ventilation strategies, including positive end-expiratory pressure and recruitment maneuvers in patients receiving mechanical ventilation. In addition, various oxygenation devices, such as high-flow nasal cannulated oxygen and continuous positive airway pressure in nonmechanically ventilated patients, are introduced. This review discusses new changes in the diagnosis and treatment of ARDS based on the new ESICM guidelines, providing a supportive background and rationale.

Mechanical Power Correlates With Stress, Strain, and Atelectrauma Only When Normalized to Aerated Lung Size in Patients With Acute Respiratory Distress Syndrome.

First, to investigate whether the severity of acute respiratory distress syndrome (ARDS) influences ventilator-induced lung injury (VILI) risk in ventilated patients with similar mechanical power of respiratory system (MPRS). Second, to determine whether, under these circumstances, there is a relationship between transpulmonary mechanical power (MPTp) normalized to the aerated lung (specific lung mechanical power or SLMP) and VILI risk, and third, to determine whether normalizing MPRS to compliance of respiratory system (CRS) can replace SLMP to bedside. Prospective cohort study. The study was conducted in a tertiary academic ICU. The study included 18 patients with ARDS. Ventilatory settings were adjusted to achieve a similar MPRS. Mechanical power was normalized to CRS (specific mechanical power or SMP = MPRS/CRS), and SLMP was calculated as the ratio between MPTp and end-expiratory lung volume (SLMP = MPTp/EELV). The strain was defined as the ratio between tidal volume and EELV (strain = Vt/EELV), stress as transpulmonary pressure at the end of inspiration, and atelectrauma as the difference between expiration and inspiration in the nonaerated lung. Although patients had been ventilated with similar MPRS = 23.75 (23-24) J/min and MPTp = 11.6 (10.8-12.8) J/min, SLMP increased linearly with the fall in Pao2/Fio2 (R = -0.83, p = 0.0001). MPRS only correlated positively with VILI-associated mechanisms when normalized to aerated lung size: correlations between SLMP and stress (R = 0.9, R2 = 0.84, p = 0.00004), strain (R = 0.97, R2 = 0.94, p < 0.00001) and atelectrauma (R = 0.82, R2 = 0.70, p = 0.00002), and correlations between SMP and stress (R = 0.86, R2 = 0.75, p = 0.00001), strain (R = 0.68, R2 = 0.47, p = 0.001) and atelectrauma (R = 0.67, R2 = 0.46, p = 0.002). The results suggest that normalizing mechanical power to lung-aerated size or CRS may correlate positively with stress, strain, and atelectrauma.

Hyperoxia but not high tidal volume contributes to ventilator-induced lung injury in healthy mice

BackgroundMechanical ventilation is a supportive therapy used to maintain respiratory function in several clinical and surgical cases but is always accompanied by lung injury risk due to improper treatment. We investigated how tidal volume and oxygen delivery would contribute independently or synergistically to ventilator-induced lung injury (VILI).MethodsUnder general anesthesia and tracheal intubation, healthy female C57BL/6 N mice (9 weeks old) were randomly ventilated for 2 h by standard (7 ml/kg) or high (14 ml/kg) tidal volume at positive end-expiratory pressure (PEEP) of 2 cmH2O, with room air, 50% O2 (moderate hyperoxia), or 100% O2 (severe hyperoxia); respectively. Mice were sacrificed 4 h after mechanical ventilation, and lung tissues were collected for experimental assessments on lung injury.ResultsCompared with the healthy control, severe hyperoxia ventilation by either standard or high tidal volume resulted in significantly higher wet-to-dry lung weight ratio and higher levels of IL-1β and 8-OHdG in the lungs. However, moderate hyperoxia ventilation, even by high tidal volume did not significantly increase the levels of IL-1β and 8-OHdG in the lungs. Western blot analysis showed that the expression of RhoA, ROCK1, MLC2, and p-MLC2 was not significantly induced in the ventilated lungs, even by high tidal volume at 2 cmH2O PEEP.ConclusionSevere hyperoxia ventilation causes inflammatory response and oxidative damage in mechanically ventilated lungs, while high tidal volume ventilation at a reasonable PEEP possibly does not cause VILI.

Mechanical Power and Ventilator-induced Lung Injury: What Does Physics Have to Say?

Mechanical Power and Ventilator-induced Lung Injury: What Does Physics Have to Say?

The forgotten tale of spontaneous plateau pressure

This article highlights the significance of measuring plateau pressure in spontaneously breathing patients as it provides valuable information about PMI (Pmusc Index), which serves as a surrogate for the patient's efforts during mechanical ventilation. The PMI value obtained from the difference between the end-inspiratory occlusion plateau pressure and the airway pressure before the occlusion (PEEP + PS) enables clinicians to estimate the patient's inspiratory effort accurately. The accurate measurement of patient efforts is crucial in optimizing pressure support during lung protective weaning strategies. By titrating pressure support based on PMI values, clinicians can provide personalized care to patients, reducing the risk of ventilator-induced lung injury and enhancing the likelihood of successful weaning. Keywords: PMI, Pmus, Plateau pressure

Machine learning prediction of the total duration of invasive and non-invasive ventilation During ICU Stay.

Predicting the duration of ventilation in the ICU helps in assessing the risk of ventilator-induced lung injury, ensuring sufficient oxygenation, and optimizing resource allocation. Prior models provided a prediction of total duration without distinguishing between invasive and non-invasive ventilation. This work proposes two independent gradient boosting regression models for predicting the duration of invasive and non-invasive ventilation based on commonly available ICU features. These models are trained on 2.6 million patient stays across 350 US hospitals between 2010 to 2019. The mean absolute error (MAE) for the prediction of duration was 2.08 days for invasive ventilation and 0.36 days for non-invasive ventilation. The total ventilation duration predicted by our model had MAE of 2.38 days, which outperformed the gold standard (APACHE) with MAE of 3.02 days. The feature importance analysis of the trained models showed that, for invasive ventilation, high average heart rate, diagnosis of respiratory infection and admissions from locations other than the operating room were associated with longer ventilation durations. For non-invasive ventilation, higher respiratory rates and having any GCS measurement were associated with longer durations.

Ventilator-induced lung injury in ARDS

Acute respiratory distress syndrome (ARDS) develops in nearly 2 to 19 patients in every 100 critically ill patients, and the incidence of ARDS demands the implementation of mechanical ventilation to support the respiratory distress in the patients. However, mechanical ventilation is the primary cause that leads to ventilator- induced lung injury. A sequence of pathophysiological mechanisms involving volutrauma/barotrauma results in ventilator-induced injury in the later stages. In other words, ventilator-induced lung injury is an outcome experienced as a result of physiological and morphological alterations of the lungs due to mechanical ventilation. Among all factors, VILI primarily occurs as a result of improper ventilation, and further continuation of improper ventilation can even result in a secondary ventilator-induced lung injury. Furthermore, ventilator-induced lung injury can result in hypoxia, pulmonary edema, and multi-organ dysfunction and can even risk the life of the patient. This makes it essential to identify some effective strategies that can act as a measure to support protective ventilation to prevent ventilation-induced lung injuries. This review explores the clinical aspects of barotrauma to gather proper information about the aspects that contribute to ventilator- induced lung injury so that the recommendations can be suggested to prevent the increasing incidences of these injuries during ventilation. To conduct this review, an extensive search of multiple databases, including PubMed, ScienceDirect, Medline, etc., was conducted with the mentioned keywords, and 15 articles were shortlisted to be reviewed within this article. The findings of this review have indicated that protective ventilation is the most effective strategy that can support the survival of patients suffering from ventilator- induced lung injury. Protective ventilation not only helps in saving lives, but was also found to be a useful measure in preventing lung injuries experienced by the patients due to mismatch between actual and required optimum ventilator settings for the patient. Further findings of the review also indicate that ventilator-induced lung injuries could be prevented by ensuring the transpulmonary pressure is within the physiological range and the position of the patient is maintained supine for the majority of the time to support homogeneity in the distribution of the transpulmonary pressure.