Annual update in intensive care and emergency medicine 2022 / / edited by Jean-Louis Vincent

• Record Nr.: UNINA9910558490303321
• Pubbl/distr/stampa: Cham, Switzerland : , : Springer, , [2022]; ©2022
• ISBN: 9783030934330; 9783030934323
• Descrizione fisica: 1 online resource (398 pages)
• Collana: Annual Update in Intensive Care and Emergency Medicine
• Disciplina: 616.028
• Soggetti: Critical care medicine; Medicina intensiva; Medicina d'urgència; Llibres electrònics
• Lingua di pubblicazione: Inglese
• Formato: Materiale a stampa
• Livello bibliografico: Monografia
• Nota di bibliografia: Includes bibliographical references and index.
• Nota di contenuto: Intro -- Contents -- Abbreviations -- Part I: Sepsis and the Immune Response -- 1: The Role of Mitochondria in the Immune Response in Critical Illness -- 1.1 Introduction -- 1.2 Mitochondrial Machinery That Mediates and Regulates Immune Responses in Critical Illness -- 1.2.1 Metabolic Reprogramming -- 1.2.2 Mitochondrial ROS and mtDNA -- 1.2.3 Succinate and Itaconate -- 1.2.4 Mitochondrial Dynamics -- 1.3 Immunometabolism: The Perfect World Scenario vs. the Critical Illness Scenario -- 1.4 Potential of Mitochondria-Targeting Therapy in Critical Care -- 1.5 Challenges of Applying Mitochondria-Targeting Therapy in Critical Care -- 1.6 Conclusion -- References -- 2: Immunomodulation by Tetracyclines in the Critically Ill: An Emerging Treatment Option? -- 2.1 Introduction -- 2.2 Immunopathogenesis of Sepsis -- 2.3 Immunopathogenesis of ARDS -- 2.4 Mechanisms of Action of Tetracyclines in ARDS -- 2.4.1 In Vivo Models -- 2.4.1.1 Effects on Inflammatory Cytokines and NLRP3 Inflammasome Caspase-1 Signaling -- 2.4.1.2 Effects on MMPs -- 2.4.1.3 Effects on Neutrophil Transmigration -- 2.4.2 Human Data -- 2.5 Mechanisms of Action of Tetracyclines in Sepsis -- 2.5.1 In Vitro ; Models -- 2.5.1.1 Effects on Cytokine and Chemokine Production -- 2.5.1.2 Effects on Arachidonic Acid Metabolites and NO Production -- 2.5.2 In Vivo Models -- 2.5.2.1 Effects on MAPK Signaling Pathways and Inflammatory Mediators -- 2.5.2.2 Effects on Organ Dysfunction -- 2.5.3 Human Data -- 2.6 Future Research Perspectives -- 2.7 Conclusion -- References -- 3: Hit Early: Blocking Interleukin-1 in the Treatment of COVID-19 Pneumonia -- 3.1 Introduction -- 3.2 Cytokines and Disease Progression in COVID-19 -- 3.3 Contribution of Monocytes and Macrophages in Early Cytokine Response -- 3.4 How Can Early Activation of IL-1 Be Identified?.; 3.5 SAVE Strategy: Early Blockade of IL-1 Guided by Biomarkers -- 3.6 Conclusion -- References -- 4: Hemoadsorption Therapy During ECMO: Emerging Evidence -- 4.1 Introduction -- 4.2 Devices and Implementation -- 4.3 Hemoadsorption in Combination with ECMO -- 4.4 Hemoadsorption in Severe COVID-19 Supported with ECMO -- 4.5 Discussion and Outlook -- 4.6 Conclusion -- References -- Part II: Respiratory Issues -- 5: The Forgotten Circulation and Transpulmonary Pressure Gradients -- 5.1 Introduction -- 5.2 Pulmonary Vessel Anatomy -- 5.3 Pulmonary Vascular Dysfunction -- 5.4 Pulmonary Circulation and Its Components -- 5.4.1 The Transpulmonary Driving Pressure: A Small Gradient with Big Importance -- 5.4.2 Pulmonary Vascular Resistance and 'Closing Pressures' -- 5.5 Measuring the Transpulmonary Pressure Gradient -- 5.6 The Evolving Role of Pulmonary Arterial Compliance -- 5.7 Relevant Clinical Scenarios in Critical Illness -- 5.7.1 Pulmonary Hypertension -- 5.7.2 Right Ventricular Dysfunction -- 5.8 Can Right Ventricular-Pulmonary Arterial (RV-PA) Coupling Shed more Light on the RV-Pulmonary Circuit in Critical Illness? -- 5.9 Conclusion -- References -- 6: Oxygen: Origin, Physiology, Pathophysiology, and Use in the Critically Ill -- 6.1 Introduction -- 6.2 Origin of Oxygen in the Earth's Atmosphere -- 6.3 Measurements and Estimations of Oxygenation -- 6.4 Definition of Hypoxemia, Normoxemia, and Hyperoxemia -- 6.5 Physiology of Oxygen in Humans -- 6.6 Pathophysiology of Oxygen in Humans: Hypoxemia and Effects of Lack of O2 -- 6.7 Pathophysiology of Oxygen in Humans: Hyperoxia, Hyperoxemia, and O2 Toxicity -- 6.8 Effects of Normoxia, Hypoxia and Hyperoxia in Critically Ill Patients -- 6.9 Future Studies -- 6.10 Conclusion -- References -- 7: Nebulized Therapeutics for COVID-19 Pneumonia in Critical Care -- 7.1 Introduction.; 7.2 Nebulized Therapeutics for COVID-19 Pneumonia -- 7.3 Technical Aspects of Nebulized Drug Therapy -- 7.4 Current Clinical Trials on Nebulized COVID-19 Therapeutics in Critical Care -- 7.4.1 Antivirals -- 7.4.1.1 Chloroquine/Hydroxychloroquine -- 7.4.1.2 Remdesivir -- 7.4.1.3 Ivermectin -- 7.4.2 Immunomodulators -- 7.4.2.1 Granulocyte-Monocyte Colony-Stimulating Factor (GM-CSF) -- 7.4.3 Anticoagulants -- 7.4.3.1 Heparin -- 7.4.4 Fibrinolytics -- 7.4.4.1 Tissue Plasminogen Activator (t-PA) -- 7.4.5 Anti-Inflammatory Agents -- 7.4.5.1 Interferon -- 7.4.5.2 Steroids -- 7.4.5.3 Retinoic Acid -- 7.4.6 Mucokinetics/Mucolytics -- 7.4.6.1 Dornase Alfa -- 7.4.7 Pulmonary Vasodilators -- 7.4.7.1 Epoprostenol, Iloprost -- 7.4.8 Miscellaneous -- 7.4.8.1 Surfactant -- 7.5 Barriers to Safe and Effective Nebulized Therapy in COVID-19 Pneumonia in Critical Care -- 7.6 Conclusion -- References -- Part III: Mechanical Ventilation -- 8: Positive End-Expiratory Pressure in Invasive and Non-invasive Ventilation of COVID-19 Acute Respiratory Distress Syndrome -- 8.1 Introduction -- 8.2 Evidence for a Unique CARDS Pathophysiology -- 8.3 A Computational Simulator to Compare CARDS Versus ARDS Pathophysiology -- 8.4 Setting PEEP in Invasive ; Mechanical Ventilation of CARDS Patients -- 8.5 Setting PEEP in Non-invasive Pressure Support Ventilation of CARDS Patients -- 8.6 Conclusion -- References -- 9: Personalized Mechanical Ventilation Settings: Slower Is Better! -- 9.1 Introduction -- 9.2 Strain, Stress, and Strain Rate: Insights from Polymeric Material -- 9.3 Origins of the Mechanical Power Formula: The Components Must Respect Time -- 9.4 Slow the Changes in Tidal Volume during Mechanical Ventilation -- 9.5 Slow the Changes in Respiratory Rate during Mechanical Ventilation -- 9.5.1 Prolonged Versus Short Inspiratory Time?.; 9.5.2 High Versus Low Inspiratory Flow? -- 9.6 Stepwise Increase in Airway Pressure during Recruitment Maneuvers -- 9.7 Slow Decreases in PEEP Levels and Lung Damage -- 9.8 Smooth the Expiration Phase: Does It Matter? -- 9.9 Conclusion -- References -- 10: Spontaneous Breathing in Acute Respiratory Failure -- 10.1 Introduction -- 10.2 Acute Respiratory Distress Syndrome -- 10.3 Mechanical Ventilation and VILI -- 10.4 Stress, Strain, and Stress Raisers -- 10.5 P-SILI and Assisted Ventilation -- 10.6 Lung Mechanics and Pulmonary Heterogeneity -- 10.7 Conclusion -- References -- 11: Laryngeal Injury: Impact on Patients in the Acute and Chronic Phases -- 11.1 Introduction -- 11.2 Laryngeal Injury -- 11.2.1 Endotracheal Intubation -- 11.2.2 Identification and Management of Laryngeal Injury in the Acute Phase -- 11.3 Impact of Laryngeal Injury on the Patient in the Acute Phase -- 11.3.1 Swallowing and Return to Oral Intake -- 11.3.2 Communication in the ICU -- 11.4 Impact of Laryngeal Injury on the Patient in the Chronic Phase -- 11.5 Laryngeal Injury in the ICU and beyond -- 11.5.1 Clinical Assessment: Future Directions -- 11.5.2 Laryngeal Rehabilitation -- 11.5.3 Community Follow Up of Critical Illness Survivors -- 11.6 Conclusion -- References -- Part IV: Fluids and Electrolytes -- 12: Fluid Responsiveness as a Physiologic Endpoint to Improve Successful Weaning -- 12.1 Introduction -- 12.2 Weaning from Mechanical Ventilation -- 12.3 Weaning Failure -- 12.4 Weaning-Induced Pulmonary Edema -- 12.5 De-Resuscitation -- 12.6 Physiology-Based Fluid Depletion -- 12.7 Monitoring Fluid Responsiveness Prior to SBT -- 12.8 Conclusion -- References -- 13: Tidal Volume Challenge Test: Expanding Possibilities -- 13.1 Introduction -- 13.2 Rationale for Developing the Tidal Volume Challenge Test.; 13.3 Reliability of the Tidal Volume Challenge Test to Predict Fluid Responsiveness -- 13.4 How to Perform and Interpret the Tidal Volume Challenge Test -- 13.5 Applications of the Tidal Volume Challenge Test -- 13.5.1 In ICU Patients Mechanically Ventilated Using Low Tidal Volumes -- 13.5.2 In Mechanically Ventilated Patients with Spontaneous Breathing Activity -- 13.5.3 In Patients with Normal Lungs Ventilated Using Low Tidal Volumes in the Operating Room -- 13.5.3.1 In the Supine Position -- 13.5.3.2 In the Prone Position -- 13.5.4 During Laparoscopic Surgery Using Pneumoperitoneum in the Trendelenburg Position -- 13.6 Comparison of Tidal Volume Challenge with Other Tests Used to Predict Fluid Responsiveness -- 13.7 Advantages of the Tidal Volume Challenge -- 13.8 Limitations of the Tidal Volume Challenge -- 13.9 Future Directions -- 13.10 Conclusion -- References -- 14: Fluid Management in COVID-19 ICU Patients -- 14.1 Introduction -- 14.2 Why Patients with COVID-19 Can Develop Acute Circulatory Failure? -- 14.2.1 Hypovolemia -- 14.2.2 Vasoplegia -- 14.2.3 Impaired Left Heart Function -- 14.2.4 Right Ventricular (RV) Dysfunction or Failure -- 14.3 Consequences of Fluid Therapy in COVID-19 Patients with Shock -- 14.4 How to Assess the Benefits and the Risks of Fluid Administration in COVID-; 19 Patients with Shock? -- 14.5 Summary -- 14.6 Conclusion -- References -- 15: Electrolytes in the ICU -- 15.1 Introduction -- 15.2 Physiology and Pathophysiology -- 15.2.1 Sodium: Regulator of Osmolality -- 15.2.1.1 Physiology -- 15.2.1.2 Pathophysiology -- 15.2.2 Potassium: Determinant of Excitability -- 15.2.2.1 Physiology -- 15.2.2.2 Pathophysiology -- 15.2.3 Magnesium: Membrane Stabilizer -- 15.2.3.1 Physiology -- 15.2.3.2 Pathophysiology -- 15.2.4 Calcium: Conduction and Contraction -- 15.2.4.1 Physiology.; 15.2.4.2 Pathophysiology.