ARDS

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ARDS

  1. 1. ACUTE RESPIRATORY DISTRESS SYNDROME Michael L. Fiore, MD – Fellow in Critical Care Medicine Mary W. Lieh-Lai, MD, Director, ICU and Fellowship Program Division of Critical Care Medicine Children’s Hospital of Michigan/Wayne State UniversityCil e’s op ao M h a h d n H sit f icign r l
  2. 2. A.K.A.  Adult Respiratory Distress Syndrome  Da Nang Lung  Transfusion Lung  Post Perfusion Lung  Shock Lung  Traumatic Wet LungCil e’s op ao M h a h d n H sit f icign r l
  3. 3. HISTORICAL PERSPECTIVES  Described by William Osler in the 1800’s  Ashbaugh, Bigelow and Petty, Lancet – 1967 12 patients   pathology similar to hyaline membrane disease in neonates  ARDS is also observed in children  New criteria and definitionCil e’s op ao M h a h d n H sit f icign r l
  4. 4. ORIGINAL DEFINITION  Acute respiratory distress  Cyanosis refractory to oxygen therapy  Decreased lung compliance  Diffuse infiltrates on chest radiograph  Difficulties:  lacks specific criteria  controversy over incidence and mortalityCil e’s op ao M h a h d n H sit f icign r l
  5. 5. REVISION OF DEFINITIONS  1988: four-point lung injury score  Level of PEEP  PaO2 / FiO2 ratio Static lung compliance   Degree of chest infiltrates  1994: consensus conference simplified the definitionCil e’s op ao M h a h d n H sit f icign r l
  6. 6. 1994 CONSENSUS Acute onset  may follow catastrophic event Bilateral infiltrates on chest radiograph PAWP < 18 mm Hg Two categories:  Acute Lung Injury - PaO /FiO ratio < 300 2 2  ARDS - PaO2/FiO2 ratio < 200Cil e’s op ao M h a h d n H sit f icign r l
  7. 7. EPIDEMIOLOGY  Earlier numbers inadequate (vague definition)  Using 1994 criteria:  17.9/100,000 for acute lung injury  13.5/100,000 for ARDS  Current epidemiologic study underway  In children: approximately 1% of all PICU admissionsCil e’s op ao M h a h d n H sit f icign r l
  8. 8. INCITING FACTORS  Shock  Aspiration of gastric contents  Trauma  Infections  Inhalation of toxic gases and fumes  Drugs and poisons  MiscellaneousCil e’s op ao M h a h d n H sit f icign r l
  9. 9. STAGES  Acute, exudative phase  rapid onset of respiratory failure after trigger  diffuse alveolar damage with inflammatory cell infiltration  hyaline membrane formation  capillary injury  protein-rich edema fluid in alveoli  disruption of alveolar epitheliumCil e’s op ao M h a h d n H sit f icign r l
  10. 10. STAGES  Subacute, Proliferative phase:  persistent hypoxemia  development of hypercarbia  fibrosing alveolitis  further decrease in pulmonary compliance  pulmonary hypertensionCil e’s op ao M h a h d n H sit f icign r l
  11. 11. STAGES  Chronic phase  obliteration of alveolar and bronchiolar spaces and pulmonary capillaries  Recovery phase  gradual resolution of hypoxemia  improved lung compliance  resolution of radiographic abnormalitiesCil e’s op ao M h a h d n H sit f icign r l
  12. 12. MORTALITY  40-60%  Deaths due to: multi-organ failure   sepsis  Mortality may be decreasing in recent years  better ventilatory strategies  earlier diagnosis and treatmentCil e’s op ao M h a h d n H sit f icign r l
  13. 13. PATHOGENESIS  Inciting event  Inflammatory mediators  Damage to microvascular endothelium  Damage to alveolar epithelium  Increased alveolar permeability results in alveolar edema fluid accumulationCil e’s op ao M h a h d n H sit f icign r l
  14. 14. NORMAL ALVEOLUS Type I cell Alveolar macrophageEndothelialCell RBC’s Type II cell CapillaryCil e’s op ao M h a h d n H sit f icign r l
  15. 15. ACUTE PHASE OF ARDS Type I cell Alveolar macrophage Endothelial Cell RBC’s Type II cell Capillary NeutrophilsCil e’s op ao M h a h d n H sit f icign r l
  16. 16. PATHOGENESIS  Target organ injury from host’s inflammatory response and uncontrolled liberation of inflammatory mediators  Localized manifestation of SIRS  Neutrophils and macrophages play major roles  Complement activation  Cytokines: TNF-α, IL-1β, IL-6  Platelet activation factor  Eicosanoids: prostacyclin, leukotrienes, thromboxane  Free radicals  Nitric oxideCil e’s op ao M h a h d n H sit f icign r l
  17. 17. PATHOPHYSIOLOGY  Abnormalities of gas exchange  Oxygen delivery and consumption  Cardiopulmonary interactions  Multiple organ involvementCil e’s op ao M h a h d n H sit f icign r l
  18. 18. ABNORMALITIES OF GAS EXCHANGE  Hypoxemia: HALLMARK of ARDS  Increased capillary permeability  Interstitial and alveolar exudate  Surfactant damage  Decreased FRC  Diffusion defect and right to left shuntCil e’s op ao M h a h d n H sit f icign r l
  19. 19. OXYGEN EXTRACTION Cell O2Arterial O2 O2 Venous O2Inflow Outflow O2 O2 O2 O2 (Q) capillary (Q) VO2 = Q x Hb X 13.4 X (SaO2 - SvO2) (Adapted from the ICU Book by P. Marino)Cil e’s op ao M h a h d n H sit f icign r l
  20. 20. OXYGEN DELIVERY DO2 = Q X CaO2 DO2 = Q X (1.34 X Hb X SaO2) X 10 Q = cardiac output CaO2 = arterial oxygen content Normal DO2: 520-570 ml/min/m2 Oxygen extraction ratio = (SaO2-SvO2/SaO2) X 100 Normal O2ER = 20-30%Cil e’s op ao M h a h d n H sit f icign r l
  21. 21. HEMODYNAMIC SUPPORT Max O2 Max O2 extraction extraction VO2 VO2 Critical DO2 Critical DO2 DO2 DO2 Normal Septic Shock/ARDS VO2 = DO2 X O2ER Abnormal Flow DependencyCil e’s op ao M h a h d n H sit f icign r l
  22. 22. OXYGEN DELIVERY & CONSUMPTION  Pathologic flow dependency  Uncoupling of oxidative dependency  Oxygen utilization by non-ATP producing oxidase systems  Increased diffusion distance for O2 between capillary and alveolusCil e’s op ao M h a h d n H sit f icign r l
  23. 23. CARDIOPULMONARY INTERACTIONS  A = Pulmonary hypertension resulting in increased RV afterload  B = Application of high PEEP resulting in decreased preload  A+B = Decreased cardiac outputCil e’s op ao M h a h d n H sit f icign r l
  24. 24. RESPIRATORY SUPPORT  Conventional mechanical ventilation  Newer modalities: High frequency ventilation   ECMO  Innovative strategies  Nitric oxide  Liquid ventilation  Exogenous surfactantCil e’s op ao M h a h d n H sit f icign r l
  25. 25. MANAGEMENT  Monitoring:  Respiratory  Hemodynamic  Metabolic  Infections  Fluids/electrolytesCil e’s op ao M h a h d n H sit f icign r l
  26. 26. MANAGEMENT  Optimize VO2/DO2 relationship  DO2  hemoglobin  mechanical ventilation  oxygen/PEEP  VO2  preload  afterload  contractilityCil e’s op ao M h a h d n H sit f icign r l
  27. 27. CONVENTIONAL VENTILATION  Oxygen  PEEP  Inverse I:E ratio  Lower tidal volume  Ventilation in prone positionCil e’s op ao M h a h d n H sit f icign r l
  28. 28. RESPIRATORY SUPPORT  Goal: maintain sufficient oxygenation and ventilation, minimize complications of ventilatory management  Improve oxygenation: PEEP, MAP, Ti, O2  Improve ventilation: change in pressureCil e’s op ao M h a h d n H sit f icign r l
  29. 29. Mechanical Ventilation Guidelines  American College of Chest Physicians’ Consensus Conference 1993  Guidelines for Mechanical Ventilation in ARDS  When possible, plateau pressures < 35 cm H O 2  Tidal volume should be decreased if necessary to achieve this, permitting increased pCO2Cil e’s op ao M h a h d n H sit f icign r l
  30. 30. PEEP - Benefits  Increases transpulmonary distending pressure  Displaces edema fluid into interstitium  Decreases atelectasis  Decrease in right to left shunt  Improved compliance  Improved oxygenationCil e’s op ao M h a h d n H sit f icign r l
  31. 31. No Benefit to Early Application of PEEP  Pepe PE et al. NEJM 1984;311:281-6.  Prospective randomization of intubated patients at risk for ARDS  Ventilated with no PEEP vs. PEEP 8+ for 72 hours  No differences in development of ARDS, complications, duration of ventilation, time in hospital, duration of ICU stay, morbidity or mortalityCil e’s op ao M h a h d n H sit f icign r l
  32. 32. Everything hinges on the matter of evidence Carl SaganCil e’s op ao M h a h d n H sit f icign r l
  33. 33. Pressure-controlled Ventilation (PCV)  Time-cycled mode  Approximate square waves of a preset pressure are applied and released by means of a decelerating flow  More laminar flow at the end of inspiration  More even distribution of ventilation in patients with marked different resistance values from one region of the lung to anotherCil e’s op ao M h a h d n H sit f icign r l
  34. 34. Pressure-controlled Inverse-ratio Ventilation  Conventional inspiratory-expiratory ratio is reversed  (I:E 2:1 to 3:1)  Longer time constant  Breath starts before expiratory flow from prior breath reaches baseline → auto-PEEP with recruitment of alveoli  Lower inflating pressures  Potential for decrease in cardiac output due to increase in MAPCil e’s op ao M h a h d n H sit f icign r l
  35. 35. Extracorporeal Membrane Oxygenation (ECMO)  Zapol WM et al. JAMA 1979;242(20):2193-6  Prospectively randomized 90 adult patients  Multicenter trial – Conventional mechanical ventilation vs. mechanical ventilation supplemented with partial venoarterial bypass – No benefitCil e’s op ao M h a h d n H sit f icign r l
  36. 36. Partial Liquid Ventilation (PLV)  Ventilating the lung with conventional ventilation after filling with perfluorocarbon  Perflubron  20 times O and 3 times the CO solubility 2 2  Heavier than water  Higher spreading coefficient  Studies in animal models suggest improved compliance and gas exchangeCil e’s op ao M h a h d n H sit f icign r l
  37. 37. Partial Liquid Ventilation (PLV)  CL Leach, et al. NEJM 1996;335:761-7. The LiquiVent Study Group  13 premature infants with severe RDS refractory to conventional treatment  No adverse events  Increased oxygenation and improved pulmonary compliance  8 of 10 survivorsCil e’s op ao M h a h d n H sit f icign r l
  38. 38. Partial Liquid Ventilation (PLV)  Hirschl et al  JAMA 1996;275:383-389 • 10 adult patients on ECMO with ARDS  Ann Surg 1998;228(5):692-700 • 9 adult patients with ARDS on conventional mechanical ventilation  Improvements in gas exchange with few complications  No randomized or case controlled trialsCil e’s op ao M h a h d n H sit f icign r l
  39. 39. High-Frequency Jet Ventilation  Carlon GC et al. Chest 1983;84:551-59  Prospective randomization of 309 adult patients with ARDS to receive HFJV vs. Volume Cycled Ventilation  VCV provided a higher PaO 2  HFJV had slightly improved alveolar ventilation  No difference in survival, ICU stay, or complicationsCil e’s op ao M h a h d n H sit f icign r l
  40. 40. High Frequency Oscillating Ventilator (HFOV)  Raise MAP  Recruit lung volume  Small changes in tidal volume  Impedes venous return necessitating intravascular volume expansion and/or pressorsCil e’s op ao M h a h d n H sit f icign r l
  41. 41. Predicting outcome in children with severe acuterespiratory failure treated with high-frequencyventilation Sarnaik AP, Meert KL, Pappas MD, Simpson PM, Lieh-Lai MW, Heidemann SM Crit Care Med 1996; 24:1396-1402Cil e’s op ao M h a h d n H sit f icign r l
  42. 42. SUMMARY OF RESULTS Significant improvement in pH, PaCO2, PaO2 and PaO2/FiO2 occurred within 6 hours after institution of HFV The improvement in gas exchange was sustained Survivors showed a decrease in OI and increase in PaO2/FiO2 twenty four hours after instituting HFV while non-survivors did not Pre-HFV OI > 20 and failure to decrease OI by > 20% at six hours predicted death with 88% (7/8) sensitivity and 83% (19/23) specificity, with an odds ratio of 33 (p= .0036, 95% confidence interval 3-365)Cil e’s op ao M h a h d n H sit f icign r l
  43. 43. STUDY CONCLUSIONS  In patients with potentially reversible underlying diseases resulting in severe acute respiratory failure that is unresponsive to conventional ventilation, high frequency ventilation improves gas exchange in a rapid and sustained fashion.  The magnitude of impaired oxygenation and its improvement after high frequency ventilation can predict outcome within 6 hours.Cil e’s op ao M h a h d n H sit f icign r l
  44. 44. High Frequency Oscillating Ventilation (HFOV) – Pediatric ARDS  Arnold JH et al. Crit Care Med 1994; 22:1530-1539.  Prospective, randomized clinical study with crossover of 70 patients  HFOV had fewer patients requiring O at 30 days 2  HFOV patients had increase survivor  Survivors had less chronic lung diseaseCil e’s op ao M h a h d n H sit f icign r l
  45. 45. New England Journal of Medicine 2000;342:1301-8Cil e’s op ao M h a h d n H sit f icign r l
  46. 46. STUDY CONCLUSION  In patients with acute lung injury and the acute respiratory distress syndrome, mechanical ventilation with a lower tidal volume than is traditionally used results in decreased mortality and increases the number of days without ventilator useCil e’s op ao M h a h d n H sit f icign r l
  47. 47. Prone Position  Improved gas exchange  More uniform alveolar ventilation  Recruitment of atelectasis in dorsal regions  Improved postural drainage  Redistribution of perfusion away from edematous, dependent regionsCil e’s op ao M h a h d n H sit f icign r l
  48. 48. Prone Position  Nakos G et al. Am J Respir Crit Care Med 2000;161:360-68  Observational study of 39 patients with ARDS in different stages  Improved oxygenation in prone (PaO /FiO 189±34 2 2 prone vs. 83±14 supine) after 6 hours  No improvement in patients with late ARDS or pulmonary fibrosisCil e’s op ao M h a h d n H sit f icign r l
  49. 49. Prone Position  NEJM 2001;345:568-73  Prone-Supine Study Group  Multicenter randomized clinical trial  304 adult patients prospectively randomized to 10 days of supine vs. prone ventilation 6 hours/day  Improved oxygenation in prone position  No improvement in survivalCil e’s op ao M h a h d n H sit f icign r l
  50. 50. Exogenous Surfactant  Success with infants with neonatal RDS  Exosurf ARDS Sepsis Study. Anzueto et al. NEJM 1996;334:1417-21  Randomized control trial  Multicenter study of 725 patients with sepsis induced ARDS  No significant difference in oxygenation, duration of mechanical ventilation, hospital stay, or survivalCil e’s op ao M h a h d n H sit f icign r l
  51. 51. Exogenous Surfactant  Aerosol delivery system – only 4.5% of radiolabeled surfactant reached lungs  Only reaches well ventilated, less severe areas  New approaches to delivery are under study, including tracheal instillation and bronchoalveolar lavageCil e’s op ao M h a h d n H sit f icign r l
  52. 52. Inhaled Nitric Oxide (iNO)  Pulmonary vasodilator  Selectively improves perfusion of ventilated areas  Reduces intrapulmonary shunting  Improves arterial oxygenation  T1/2 111 to 130 msec  No systemic hemodynamic effectsCil e’s op ao M h a h d n H sit f icign r l
  53. 53. Inhaled Nitric Oxide (iNO)  Inhaled Nitric Oxide Study Group  Dellinger RP et al. Crit Care Med 1998; 26:15-23  Prospective, randomized, placebo controlled, double blinded, multi-center study  177 adults with ARDS  Improvement in oxygenation index  No significant differences in mortality or days off ventilatorCil e’s op ao M h a h d n H sit f icign r l
  54. 54. Inhaled Aerosolized Prostacyclin (IAP)  Potent selective pulmonary vasodilator  Effective for pulmonary hypertension  Short half-life (2-3 min) with rapid clearance  Little or no hemodynamic effect  Randomized clinical trials have not been doneCil e’s op ao M h a h d n H sit f icign r l
  55. 55. Corticosteroids Acute Phase Trials  Bernard GR et al. NEJM 1987;317:1565-70  99 patients prospectively randomized  Methylprednisolone (30mg/kg q6h x 4) vs. placebo  No differences in oxygenation, chest radiograph, infectious complications, or mortalityCil e’s op ao M h a h d n H sit f icign r l
  56. 56. Corticosteroids Fibroproliferative Stage  Meduri GU et al. JAMA 1998;280:159-65  24 patients with severe ARDS and failure to improve by day 7 of treatment  Placebo vs. methylprednisolone 2mg/kg/day for 32 days  Steroid group showed improvement in lung injury score, improved oxygenation, reduced mortality  No significant difference in infection rateCil e’s op ao M h a h d n H sit f icign r l
  57. 57. PROGNOSIS  Underlying medical condition  Presence of multiorgan failure  Severity of illnessCil e’s op ao M h a h d n H sit f icign r l
  58. 58. We are constantly misled by the ease with which our minds fall into the ruts of one or two experiences. Sir William OslerCil e’s op ao M h a h d n H sit f icign r l

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