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Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
Ards atef
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Ards atef

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  • 1. ARDSAtef Kamel
  • 2. Outline Define ARDS and describe the pathological process Know causes of ARDS, and differential diagnosis Understand specific challenges in mechanical ventilation of patients with ARDS Understand treatment strategies and evidence behind
  • 3. ARDSSevere lung injury characterized by non- cardiogenic pulmonary edema, decreased lung compliance, refractory hypoxemiaDefinition  Acute onset (<2 weeks)  Bilateral infiltrates on chest x ray  PCWP ≤18mmHg  Acute lung injury if PaO2/FiO2 ≤300  ARDS if PaO2/FiO2 ≤200
  • 4. Most common causes ARDSPneumonia (34%)Sepsis (27%)Aspiration (15%)Trauma (11%)  Pulmonary contusion  Multiple fractures
  • 5. Causes cont.
  • 6. Risk factors for ARDS Preexisting lung disease Chronic alcohol use Low serum pH Sepsis 40% of patients with sepsis develop ARDS
  • 7. Differential diagnosisPulmonary edema from left heart failureDiffuse alveolar hemorrhageLupus pneumonitisDrug-induced pulmonary edema and pneumonitisAcute major pulmonary embolusSarcoidosisInterstitial pulmonary fibrosis
  • 8. Excluding other diagnoses Echo Central venous catheter Bronchoscopy with bronchoalveolar lavage (to evaluate for hemorrhage, etc) Chest CT
  • 9. Pathogenesis
  • 10. Pathophysiology Diffuse alveolar damage Lung capillary damage Inflammation/pulm edema Resulting severe hypoxemia and decreased lung compliance
  • 11. Phases of ARDS Acute - exudative, inflammatory (0 - 3 days) Subacute - proliferative (4 - 10 days) Chronic - fibrosing alveolitis ( > 10 days)
  • 12. Phases of ARDS
  • 13. Exudative phase (Acute Phase) Alveolar-capillary barrier is formed by microvascular endothelium and alveolar epithelium Under normal conditions epithelial barrier is much less permeable than endothelium Epithelium is made up of type I and II cells Type I cells are injured easily and Type II cells are more resistant
  • 14. Exudative PhaseIn ALI/ARDS – damage to either one occurs resulting in increased permeability of the barrierinflux of protein-rich edema fluid into the alveolar spaceInjury of Type I cells results loss of epithelial integrity and fluid extravasation (edema)Injury of Type II cells then impairs the removal of the edema fluid (loss of surfactant)
  • 15. Exudative Phase
  • 16. Proliferative Phase With intervention (mechanical ventilation) there is clearance of alveolar fluid Soluble proteins are removed by diffusion between alveolar epithelial cells Insoluble proteins are removed by endocytosis and transcytosis through epithelial cells and phagocytosis through macrophages
  • 17. Proliferative Phase Type II cells begin to differentiate into Type I cells and reepithelialize denuded alveolar epithelium Further epithelialization leads to increased alveolar clearance
  • 18. Proliferative phase
  • 19. ARDS - OutcomesMost studies - mortality 40% to 60%; similar for children/adultsDeath is usually due to sepsis/MODS rather than primary respiratory
  • 20. Management of ARDSTreat underlying illness  Sepsis, etcNutritionSupportive careDVT prophylaxisGI prophylaxisMedications
  • 21. Fluid management“Dry lungs are happy lungs”Conservative fluids:  Improved oxygenation  More ventilator-free days  More days outside ICU  No increase in shock or dialysis  No mortality effects
  • 22. Pulmonary supportKEYS  Low tidal volumes – 6-8mL/kg ideal body weight  Maintain plateau (end-inspiratory) pressures <30cm H20  Permissive hypercapnia and acidosisDecreased mortality by 22%
  • 23. Positive End-Expiratory Pressure(PEEP)Titrate PEEP to decrease FiO2  Goal sat 88% with FiO2 <60% Minimize oxygen toxicity  PEEP can improve lung recruitment and decrease end-expiratory alveolar collapse (and therefore right-to-left shunt)  Can also decrease venous return, cause hemodynamic compromise, worsen pulmonary edema
  • 24. Other Ideas in VentilatorManagement Prone positioning  May be beneficial in certain subgroup, but complications including pressure sores  RCT of 304 patients showed no mortality benefit High-frequency oscillatory ventilation  In RCT, improved oxygenation initially, but results not sustained after 24 hours, no mortality benefit ECMO  RCT of 40 adults showed no benefit
  • 25. Complications of mechanicalventilationMechanical ventilation causes:  Overdistention of lungs (volutrauma)  Further damaging epithelium  Increased fluid leak, indistinguishable from ARDS damage  Barotrauma  Rupture alveolar membranes  Pneuomothorax, pneumomediastinum  Sheer stress  Opening/closing alveoli  Inflammatory reaction, cytokine releaseOxygen toxicity  Free radical formation
  • 26. Drug therapy Agents studied:  Corticosteroids  Ketoconazole  Inhaled nitric oxide  Surfactant No benefit demonstrated

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