Ventilator-induced lung injury /

Ventilator-induced lung injury /

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Bibliographic Details
Imprint:New York : Taylor & Francis, 2006.
Description:xxiii, 738 p. : ill. ; 24 cm.
Language:English
Series:Lung biology in health and disease ; v. 215
Subject:
Lungs -- Wounds and injuries.
Respiratory distress syndrome, Adult.
Artificial respiration.
Respirators (Medical equipment)
Lung -- injuries.
Respiratory Distress Syndrome, Adult -- etiology.
Respiratory Distress Syndrome, Adult -- prevention & control.
Ventilators, Mechanical -- adverse effects.
Artificial respiration.
Lungs -- Wounds and injuries.
Respirators (Medical equipment)
Respiratory distress syndrome, Adult.
Format: Print Book
URL for this record:http://pi.lib.uchicago.edu/1001/cat/bib/5899465
Hidden Bibliographic Details
Other authors / contributors:Dreyfuss, Didier.
Saumon, Georges.
Hubmayr, Rolf.
ISBN:9780849337161 (alk. paper)
084933716X (alk. paper)
Notes:Includes bibliographical references and index.
Table of Contents:
  • Introduction
  • Preface
  • Contributors
  • Part I. Acute Manifestations of VILI
  • 1. Shear and Pressure-Induced Mechanotransduction
  • I. Introduction
  • II. Mechanical Forces
  • III. Membrane Signal Transduction
  • IV. Intracellular Signal Transduction
  • V. Conclusion
  • References
  • 2. Pulmonary Micromechanics of Injured Lungs
  • I. Introduction
  • II. Determinants of Regional Pressure and Volume in Health and Disease
  • III. Micromechanics of the Normal Lung
  • IV. Alveolar Micromechanics in Injury States
  • V. Mechanisms by Which Ventilators Injure Lungs
  • VI. Concluding Remarks
  • References
  • 3. Response of Cellular Plasma Membrane to Mechanical Stress
  • I. Introduction
  • II. The Histology of VILI
  • III. Cellular Stress Failure in Ventilator-Injured Lungs
  • IV. Determinants of PM Tension
  • V. Cell Deformation-Associated PM Remodeling
  • VI. PM Repair
  • VII. Effects of PM Wounding on Gene Expression and Cell Survival
  • VIII. Conclusion
  • References
  • 4. Acute Passive and Active Changes in Microvascular Permeability During Lung Distention
  • I. Introduction
  • II. Passive Effects of Lung Distention
  • III. Active Endothelial Control of Vascular Permeability
  • IV. Conclusion
  • References
  • 5. Hemodynamic Interactions During Ventilator-Induced Lung Injury
  • I. Introduction
  • II. Effect of Pulmonary Expansion on the Pulmonary Vascular Tree
  • III. Response of the Endothelial Cell to Shear Forces
  • IV. Interactions Between Airway and Pulmonary Vascular Pressures
  • V. Mechanisms Disrupting the Blood-Gas Barrier
  • VI. Behavior of Airway and Vascular Pressures in Heterogeneous Areas
  • VII. Role of Vascular Pressure and Flow on Genesis of VILI
  • VIII. Effect of Respiratory Rate and Flow on Expression of VILI 107 IX Cyclic Effect on the Microvascular Environment Induced by Mechanical Ventilation
  • X. Effect of Postalveolar Vascular Pressure on the Development of VILI
  • XI. Potential Clinical Implications
  • XII. Conclusions
  • References
  • 6. Lung Mechanics and Pathological Features During Ventilation-Induced Lung Injury
  • I. Introduction
  • II. Acute Pulmonary Edema Consecutive to High-Lung-Volume Ventilation
  • III. Respiratory Mechanics and Severity of VILI
  • IV. Respiratory System PV Curve Changes During Lung Injury
  • V. Improvement of Lung Mechanical Properties and Protection from VILI
  • VI. Clinical Considerations
  • References
  • 7. The Significance of Air-Liquid Interfacial Stresses on Low-Volume Ventilator-Induced Lung Injury
  • I. Introduction
  • II. Background
  • III. Introduction to Pulmonary Fluid-Structure Interactions
  • IV. Microscale Fluid-Structure Interactions Leading to VILI
  • V. The Protective Effect of Pulmonary Surfactant
  • VI. Future Directions
  • References
  • 8. Cellular and Molecular Basis for Ventilator-Induced Lung Injury
  • I. Introduction
  • II. Ventilator-Induced Lung Inflammation
  • III. Cells Submitted to Mechanical Stress
  • IV. What Happens to Cells When They Are Submitted to Cyclic Stretch?
  • V. Mechanosensing
  • VI. Cyclic Stretch of Lung Epithelial Cells
  • VII. Cyclic Stretch-Induced Cell Activation
  • VIII. Synergy Between Cyclic Stretch and Inflammatory Stimuli
  • IX. Genes Activated by Cyclic Stretch
  • X. Conclusions and Perspectives
  • References
  • Part II. Subacute VILI
  • 9. The Role of Cytokines During the Pathogenesis of Ventilator-Associated and Ventilator-Induced Lung Injury
  • I. Introduction
  • II. Mechanical Ventilation of the ALI/ARDS Lung
  • III. Mechanotransduction Leads to Lung Injury
  • IV. Cytokines and the Pathogenesis of VALI/VILI
  • V. The Role of TNF-[alpha] During the Pathogenesis of VALI/VILI
  • VI. The Role of IL-1[beta] During the Pathogenesis of VALI/VILI
  • VII. The Role of IL-6 During the Pathogenesis of VALI/VILI
  • VIII. The Role of IFN-[gamma] During the Pathogenesis of VALI/VILI
  • IX. The Role of IL-10 During the Pathogenesis of VALI/VILI
  • X. The Role of TGF-[beta] During the Pathogenesis of VALI/VILI
  • XI. The Role of Chemokines and Chemokine Receptors During the Pathogenesis of VALI/VILI
  • XII. The Role of CC Chemokines During the Pathogenesis of VALI/VILI
  • XIII. Conclusion
  • References
  • 10. Systemic Effects of Mechanical Ventilation
  • I. Introduction
  • II. Physiological Effects of MV
  • III. Mechanical Strain-Induced Release of Inflammatory Mediators In Vitro
  • IV. Pulmonary and Systemic Release of Inflammatory Mediators in Ex Vivo and In Vivo Models of VILI
  • V. Passage of Mediators from Lung to Bloodstream
  • VI. Injurious Ventilatory Strategies Can Enhance End-Organ Dysfunction, Apoptosis, and Inflammation
  • VII. Bacterial Translocation in MV
  • VIII. Does the Release of Mediators by VILI Have Any Pathophysiologic Relevance?
  • IX. Pulmonary and Systemic Inflammatory Mediators in VILI in Clinical Studies
  • X. Multiple Organ Dysfunction and VILI in Clinical Studies
  • XI. Conclusions
  • References
  • 11. Alveolar Fluid Reabsorption During VILI
  • I. Introduction
  • II. Alveolar Epithelial Sodium Transport
  • III. Alveolar Fluid Reabsorption During VILI
  • IV. Summary
  • References
  • 12. Interaction of VILI with Previous Lung Alterations
  • I. Introduction
  • II. Surfactant Depletion and Deactivation
  • III. Toxic Lung Injuries
  • IV. Inflammation and Infection: The Importance of Lung Priming and the Two-Hit Theory
  • V. Consequences of Previous Lung Injury on Lung Mechanics
  • VI. Counteracting Previous Lung Injury
  • VII. Clinical Considerations
  • References
  • 13. Biological Markers of Ventilator-Induced Lung Injury
  • I. Introduction
  • II. Rationale for Biological Markers of VILI
  • III. Recent Progress in Identifying Biological Markers of VILI
  • IV. Future Approaches to Identifying Markers of VILI
  • V. Summary and Conclusions
  • References
  • 14. Modulation of Lung Injury by Hypercapnia
  • I. Introduction-Historical Context
  • II. Hypercapnia-Definitions and Terminology
  • III. Hypercapnia-Physiologic Effects
  • IV. Acute Organ Injury: Evidence That CO[subscript 2] Is Protective
  • V. Mechanisms of CO[subscript 2]-Induced Protection
  • VI. Molecular Mechanisms of Hypercapnia-Induced Tissue Injury
  • VII. Administration and Dose Response
  • VIII. Role of Buffering
  • IX. Hypercapnia-Clinical Studies
  • X. Future Directions
  • XI. Summary
  • References
  • 15. Alveolar Epithelial Function in Ventilator-Injured Lungs
  • I. Introduction
  • II. Effects of Mechanical Ventilation on Alveolar Epithelial Barrier Function
  • III. Alveolar Epithelial Ion and Fluid Transport
  • IV. Effects of Mechanical Strain on Epithelial Inflammatory Mediators
  • V. Consequences of the Loss of Epithelial Barrier Function
  • VI. Effects of VILI on Surfactants
  • VII. Summary
  • References
  • 16. Genomic Insights into Ventilator-Induced Lung Injury
  • I. Introduction-VALI and Genome Medicine
  • II. Challenges to Unraveling the Genetics of VALI
  • III. Current Status of VALI/VILI Genetics and the Candidate Gene Approach
  • IV. Gene Expression in Animal Models of VILI
  • V. Ortholog Gene Database in VALI and Mechanical Stress
  • VI. Regional Heterogeneity in Ventilator-Associated Mechanical Stress
  • VII. Pre-B-Cell Colony-Enhancing Factor as an ALI Candidate Gene
  • VIII. Preliminary PBEF Genotyping in ALI Patients
  • IX. Preliminary IL-6 Genotyping in VALI
  • X. Summary
  • References
  • Part III. Clinical Implications and Treatment of VILI
  • 17. Lung Imaging of Ventilator-Associated Injury
  • I. Introduction
  • II. Histological Evidence of Mechanical Ventilation-Induced Lung Distortion/Overinflation
  • III. CT Evidence of Mechanical Ventilation-Induced Lung Distortion/Overinflation
  • References
  • 18. Imaging Ventilator-Induced Lung Injury: Present and Future Possibilities
  • I. Introduction
  • II. Anatomic Imaging of VILI: Quantifying Edema Accumulation
  • III. Functional Imaging of VILI
  • IV. Molecular Imaging of VILI
  • V. Summary
  • References
  • 19. Modulation of the Cytokine Network by Lung-Protective Mechanical Ventilation Strategies
  • I. Introduction
  • II. MV and the Cytokine Network
  • III. Modulation of the Cytokine Network in ALI: Evidence from Studies
  • IV. Impact of MV on the Cytokine Network in Healthy Lungs
  • V. Conclusion
  • References
  • 20. Role of Tidal Volume and PEEP in the Reduction of VILI
  • I. Introduction
  • II. Traditional Approach to MV in ALI/ARDS
  • III. Mechanisms of VILI
  • IV. Lung-Protective Ventilation
  • V. Clinical Trials of Lung-Protective MV Strategies
  • VI. Controversies
  • VII. Summary
  • References
  • 21. A Critical Review of RCTs of Tidal Volume Reduction in Patients with ARDS and Their Impact on Practice
  • I. Introduction
  • II. Randomized, Controlled Trials of Tidal Volume Reduction in ARDS
  • III. Meta-Analyses of the RCTs of Tidal Volume Reduction During ARDS
  • IV. Impact of the Low Tidal Volume Trials on Practice Patterns
  • V. Conclusions
  • References
  • 22. The Importance of Protocol-Directed Patient Management for Research on Lung-Protective Ventilation
  • I. Introduction
  • II. Experimental Scientific Principles
  • III. Computerized Protocol Experience
  • IV. Summary
  • References
  • 23. Crossing the Quality Chasm in Critical Care: Changing Ventilator Management in Patients with ALI
  • I. Introduction
  • II. Understanding Current Practice
  • III. Do We Know Why Clinicians Do Not Follow Practice Guidelines?
  • IV. Barriers to Changing Practice in the ICU
  • V. Models of Changing Clinical Practice
  • VI. Effective Strategies to Change Practice in the ICU
  • VII. Conclusions
  • References
  • 24. How to Design Clinical Studies for Preventing Ventilator-Induced Lung Injury
  • I. Introduction-Questions to Be Addressed
  • II. Inclusion and Exclusion Criteria
  • III. Outcomes
  • IV. Study Designs
  • V. The RCT
  • VI. Ethical Issues in a Clinical Trial
  • VII. Understanding the Results of a Clinical Trial
  • VIII. Nonrandomized Cohort Studies
  • IX. Evidence-Based Medicine and Hierarchy of Study Designs
  • References
  • 25. Perfluorocarbons and Acute Lung Injury
  • I. Introduction
  • II. Perfluorocarbon Liquids as Media for Breathing
  • III. Effects of Perfluorocarbons on Inflammation and Oxidative Injury
  • IV. In Vitro Effects of Neat Perfluorocarbon Liquids Involving Surface Tension
  • V. Effects of Ventilation with Perfluorocarbons on Lung Injury
  • VI. Mechanical Protection from Lung Injury by Perfluorocarbon Ventilation
  • VII. Conclusions
  • References
  • 26. Prospects for Reduction of Ventilator-Induced Lung Injury with Surfactant
  • I. Introduction-The Pulmonary Surfactant System
  • II. Surfactant Alterations and Replacement Treatment in ALI/ARDS
  • III. Role of the Pulmonary Surfactant System in VILI
  • IV. Conclusions
  • References
  • 27. Rationale for High-Frequency Oscillatory Ventilation in Acute Lung Injury
  • I. Introduction
  • II. Background
  • III. Rationale for HFOV
  • IV. Clinical Experience with HFOV
  • V. Future Directions in the Application of HFOV
  • VI. Conclusion
  • References
  • 28. Gene Therapy for Ventilator-Induced Lung Injury
  • I. Introduction
  • II. Gene Therapy for ALI
  • III. Gene Therapy for VILI
  • IV. Conclusions
  • References
  • Index
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