Parameter updating of a patient-specific lung mechanics model for optimising mechanical ventilation

2020 ◽  
Vol 60 ◽  
pp. 102003
Author(s):  
Qianhui Sun ◽  
Cong Zhou ◽  
J. Geoffrey Chase
Keyword(s):  
Mechanical Ventilation ◽  
Lung Mechanics ◽  
Patient Specific ◽  
Mechanics Model

scholarly journals Inflammatory cellular response to mechanical ventilation in elastase-induced experimental emphysema: role of pre-existing alveolar macrophages infiltration

2017 ◽  
Author(s):  
Anahita Rouze ◽  
Guillaume Voiriot ◽  
Elise Guivarch ◽  
Françoise Roux ◽  
Jeanne Tran Van Nhieu ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Alveolar Macrophages ◽  
Pulmonary Emphysema ◽  
Lung Inflammation ◽  
Cellular Response ◽  
Invasive Mechanical Ventilation ◽  
Inflammatory Cells ◽  
Chord Length ◽  
Lung Mechanics ◽  
Chronic Obstructive

ABSTRACTBackgroundAn excessive pulmonary inflammatory response could explain the poor prognosis of chronic obstructive pulmonary disease (COPD) patients submitted to invasive mechanical ventilation. The aim of this study was to evaluate the response to normal tidal volume (Vt) mechanical ventilation in a murine model of pulmonary emphysema, which represents the alveolar component of COPD. In this model, two time points associated with different levels of lung inflammation but similar lung destruction, were analyzed.MethodsC57BL/6 mice received a tracheal instillation of 5 IU of porcine pancreatic elastase (Elastase mice) or the same volume of saline (Saline mice). Fourteen (D14) and 21 (D21) days after instillation, mice were anesthetized, intubated, and either mechanically ventilated (MV) with a normal Vt (8 mL/kg) or maintained on spontaneous ventilation (SV) during two hours. We analyzed respiratory mechanics, emphysema degree (mean chord length by lung histological analysis), and lung inflammation (bronchoalveolar lavage (BAL) cellularity, proportion and activation of total lung inflammatory cells by flow cytometry).ResultsAs compared with Saline mice, Elastase mice showed a similarly increased mean chord length and pulmonary compliance at D14 and D21, while BAL cellularity was comparable between groups. Lung mechanics was similarly altered during mechanical ventilation in Elastase and Saline mice. Activated alveolar macrophages CD11bmid were present in lung parenchyma in both Elastase SV mice and Elastase MV mice at D14 but were absent at D21 and in Saline mice, indicating an inflammatory state with elastase at D14 only. At D14, Elastase MV mice showed a significant increase in percentage of neutrophils concomitant with a decrease in percentage of alveolar macrophages in total lung, as compared with Elastase SV mice. Furthermore, alveolar macrophages of Elastase MV mice at D14 overexpressed Gr1, and monocytes showed a trend to overexpression of CD62L, compared with Elastase SV mice.ConclusionsIn an elastase-induced model of pulmonary emphysema, normal Vt mechanical ventilation produced an increase in the proportion of pulmonary neutrophils, and an activation of alveolar macrophages and pulmonary monocytes. This response was observed only when the emphysema model showed an underlying inflammation (D14), reflected by the presence of activated alveolar macrophages CD11bmid.

Case studies in terminal weaning from mechanical ventilation

1993 ◽  
Vol 2 (5) ◽  
pp. 354-358 ◽  
Author(s):  
ML Campbell
Keyword(s):  
Mechanical Ventilation ◽  
Supportive Care ◽  
Case Studies ◽  
Significant Others ◽  
Care Team ◽  
Patient Specific ◽  
Healthcare Team ◽  
Weaning From Mechanical Ventilation ◽  
Terminal Weaning

Terminal weaning, withdrawal of mechanical ventilation when the patient is not expected to survive the process, must not be burdensome to the patient or significant others. The healthcare team must individualize the weaning process, considering the physiologic comfort of the patient and the psychoemotional comfort of both the patient and family. The following case studies illustrate variations in a method for terminal weaning that are patient-specific and are based on the experience of a supportive care team.

scholarly journals 2045 The role of TGFβ in driving early cystic fibrosis lung disease

2018 ◽  
Vol 2 (S1) ◽  
pp. 33-33
Author(s):  
Elizabeth L. Kramer ◽  
William Hardie ◽  
Kristin Hudock ◽  
Cynthia Davidson ◽  
Alicia Ostmann ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Bronchoalveolar Lavage ◽  
Lung Disease ◽  
Bronchoalveolar Lavage Fluid ◽  
Transforming Growth Factor ◽  
Genetic Modifier ◽  
Lavage Fluid ◽  
Lung Mechanics ◽  
Patient Specific

OBJECTIVES/SPECIFIC AIMS: Transforming growth factor-beta (TGFβ) is a genetic modifier of cystic fibrosis (CF) lung disease. TGFβ’s pulmonary levels in young CF patients and its mechanism of action in CF are unknown. We examined TGFβ levels in children with CF and investigated responses of human airway epithelial cells (AECs) and mice to TGFβ. METHODS/STUDY POPULATION: TGFβ levels in bronchoalveolar lavage fluid from CF patients (n=15) and non-CF control patients (n=21)<6 years old were determined by ELISA. CF mice and non-CF mice were intratracheally treated with an adenoviral TGFβ1 vector or PBS; lungs were collected for analysis at day 7. Human CF and non-CF AECs were treated with TGFβ or PBS for 24 hours then collected for analysis. RESULTS/ANTICIPATED RESULTS: Young CF patients had higher bronchoalveolar lavage fluid TGFβ than non-CF controls (p=0.03). Mouse lungs exposed to TGFβ demonstrated inflammation, goblet cell hyperplasia, and decreased CFTR expression. CF mice had greater TGFβ-induced lung mechanics abnormalities than controls; both CF human AECs and CF mice showed higher TGFβ induced MAPK and PI3K signaling compared with controls. DISCUSSION/SIGNIFICANCE OF IMPACT: For the first time, we show increased TGFβ levels very early in CF. TGFβ drives CF lung abnormalities in mouse and human models; CF models are more sensitive to TGFβ’s effects. Understanding the role of TGFβ in promoting CF lung disease is critical to developing patient specific treatments.

scholarly journals Effects of Various Modes of Mechanical Ventilation in Normal Rats

2014 ◽  
Vol 120 (4) ◽  
pp. 943-950 ◽  
Author(s):  
Matteo Pecchiari ◽  
Ario Monaco ◽  
Antonia Koutsoukou ◽  
Patrizia Della Valle ◽  
Guendalina Gentile ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Negative Pressure ◽  
Positive Pressure Ventilation ◽  
Lung Mechanics ◽  
Whole Body ◽  
Positive Pressure ◽  
Negative Pressure Ventilation ◽  
Cytokine Levels

Abstract Background: Recent studies in healthy mice and rats have reported that positive pressure ventilation delivered with physiological tidal volumes at normal end-expiratory volume worsens lung mechanics and induces cytokine release, thus suggesting that detrimental effects are due to positive pressure ventilation per se. The aim of this study in healthy animals is to assess whether these adverse outcomes depend on the mode of mechanical ventilation. Methods: Rats were subjected to 4 h of spontaneous, positive pressure, and whole-body or thorax-only negative pressure ventilation (N = 8 per group). In all instances the ventilatory pattern was that of spontaneous breathing. Lung mechanics, cytokines concentration in serum and broncho–alveolar lavage fluid, lung wet-to-dry ratio, and histology were assessed. Values from eight animals euthanized shortly after anesthesia served as control. Results: No evidence of mechanical ventilation–dependent lung injury was found in terms of lung mechanics, histology, or wet-to-dry ratio. Relative to control, cytokine levels and recruitment of polymorphonuclear leucocytes increased slightly, and to the same extent with spontaneous, positive pressure, and whole-body negative pressure ventilation. Thorax-only negative pressure ventilation caused marked chest and lung distortion, reversible increase of lung elastance, and higher polymorphonuclear leucocyte count and cytokine levels. Conclusion: Both positive and negative pressure ventilation performed with tidal volumes and timing of spontaneous, quiet breathing neither elicit an inflammatory response nor cause morpho-functional alterations in normal animals, thus supporting the notion of the presence of a critical volume threshold above which acute lung injury ensues. Distortion of lung parenchyma can induce an inflammatory response, even in the absence of volotrauma.

Managing Patient-Specific Mechanical Ventilation: Clinical Utilisation of Respiratory Elastance (CURE) – Model and Software Development

2014 ◽  
Vol 47 (3) ◽  
pp. 3875-3880 ◽  
Author(s):  
Daniel P. Redmond ◽  
Shaun M. Davidson ◽  
Hamish A. Laing ◽  
Richard H. White ◽  
Faizi Radzi ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Software Development ◽  
Patient Specific ◽  
Cure Model ◽  
Clinical Utilisation

Ventilator-Induced Airway Injury: A Critical Consideration During Mechanical Ventilation of the Infant

2006 ◽  
Vol 25 (3) ◽  
pp. 159-166 ◽  
Author(s):  
Jay Greenspan ◽  
Thomas Shaffer
Keyword(s):  
Health Care ◽  
Mechanical Ventilation ◽  
Respiratory Failure ◽  
Gas Exchange ◽  
Developmental Changes ◽  
Lung Mechanics ◽  
Optimal Outcomes ◽  
Airway Injury ◽  
Chronic Course ◽  
Critical Consideration

The clinical management of respiratory failure in the newborn often focuses on lung parenchymal stiffness due to immaturity, surfactant deficiency, infiltrates, and other causes. However, health care personnel should also consider the airway, which plays an important role in gas exchange and lung mechanics. The airway can be easily injured, and an injured airway can significantly alter both the acute and chronic course of lung disease in infants. Further, there are developmental changes that affect the susceptibility of the neonatal airway to injury. Recognizing and preventing causes of airway injury can help to ensure optimal outcomes for the critically ill neonate.

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