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Ards starks


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Ards starks

  1. 1. Acute Respiratory Distress Syndrome Holly Starks, MS4 March 2007
  2. 2. Outline  Definitions and Diagnosis  Pathophysiology  Cardiogenic vs Non-cardiogenic Edema  Management of ARDS  Pulmonary Artery Catheters
  3. 3. Definition  A diffuse inflammatory injury of the lungs which is an EXPRESSION of a host of various diseases and is not a specific disease entity in and of itself. It is often—but not always— accompanied by inflammatory injury of other organ systems.  Inflammatory cells and proteinaceous fluid accumulate in the alveolar spaces leading to a decrease in diffusing capacity and hypoxemia.
  4. 4. Acute Lung Injury (ALI) vs. ARDS  ALI is the term used for patients with significant hypoxemia (PaO2/FiO2 ratio of <300)  ARDS is the term used for a subset of ALI patients with severe hypoxemia (PaO2/FiO2 ratio of <200) Fan, E. et al. Ventilatory Management of Acute Lung Injury and Acute Respiratory Distress Syndrome. 2005. JAMA. 294 (22). pp. 2889-96.
  5. 5. ARDS Diagnostic Criteria From the American-European Consensus Conference on ARDS 1. Acute Onset 2. Predisposing Condition 3. Bilateral Infiltrates 4. PaO2/FiO2 < 200 mm Hg 5. Wedge Pressure ≤ 18 mm Hg or no clinical evidence of LA HTN. Note: According to The ICU Book, wedge pressure should be excluded from the diagnostic criteria because it underestimates capillary hydrostatic pressure (p 435).
  6. 6. Predisposing Conditions  Sepsis (#1 cause)  Severe Trauma  Severe PNA  DIC  Aspiration  Drug overdose:  Near Drowning Heroin, methamphetami  Smoke inhalation ne, cocaine  Multiple blood product  Acute pancreatitis transfusions  Severe Burn Look for the + Tube Sign!!!!
  7. 7. Positive Tube Sign The majority of patients with ARDS require intubation and mechanical ventilation
  8. 8. An Interesting Note  All of the predisposing conditions share the ability to trigger a systemic inflammatory response. Hum….  The majority of ARDS deaths are NOT due to respiratory failure, but multiple organ failure secondary to systemic inflammatory processes.
  9. 9. Pathology of ARDS  A diffuse inflammatory process  Circulating neutrophils are activated and become ―sticky.‖ They adhere to the vascular endothelium and spill their cytoplasmic granules which then damage the endothelium leading to leaky capillaries. The result: An exudative fluid accumulates in the lung parenchyma, which leads to further damage locally (i.e. alveolar cell damage) decreasing oxygenation and lung compliance.  Fibrin Deposition. Fibrin release is triggered by tissue factor. Over time the fibrin can later remodel to form fibrosis. Marino, P.L. The ICU Book. 3rd Ed. Lippincott Williams & Wilkins. Philadelphia. 2007.
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  11. 11. Again…  ARDS is a diffuse inflammatory process involving both lungs, in which the overall lung volume increases secondary to inflammatory and proteinaceous materials accumulating in the lung parenchyma. This results in a loss of compliance and severe loss of gas exchange.  The overall lung volume increases, but the there is a decreased volume of lung available for gas exchange.
  12. 12. Histologic Findings Hyaline Protein in air spaces Cellular Congestion  Typical histological findings in ARDS  alveolar inflammation, thickened septal from protein leak (pink), congestion and decreased alveolar volume ←Normal Lung Histology—large alveolar volumes, septal spaces very thin, no cellular congestion.
  13. 13. Determining ARDS Radiographically  Can be difficult to do. Should always try to make the diagnosis in light of the clinical picture.  Need to determine Cardiogenic vs. Non- cardiogenic edema.
  14. 14. Cardiogenic vs. Non-Cardiogenic Edema Cardiogenic Non-Cardiogenic  Patchy infiltrates  Infiltrates are more appearing in the lung homogeneous bases first  No pleural effusions  Effusions may be present  No Kerley B’s  Clinical signs and  Radiographic evidence symptoms lag behind lags behind clinical signs radiographic evidence (i.e. and symptoms (i.e. the CXR is more impressive CXR is unimpressive given than the degree of the degree of hypoxemia) hypoxemia)
  15. 15. Cardiogenic vs. Non-Cardiogenic Edema Cardiogenic Non-Cardiogenic  Excess fluid in alveoli  Protein, inflammatory  Due to high cells, and fluid pulmonary capillary accumulation in the pressure (estimated by alveoli measuring pulmonary  Due to “other” artery wedge pressure) systemic factors NOT elevated pulmonary capillary pressure
  16. 16. Cardiogenic vs. Non-Cardiogenic Edema via CXR Cardiogenic Non-Cardiogenic Bilateral infiltrates predominately in Diffuse Bilateral patchy infiltrates lung bases. Kerley B’s. Cardiomegaly. homogenously distributed throughout the lungs. Positive tube sign. No Kerley B’s.
  17. 17. Cardiogenic vs. Non-Cardiogenic Edema via CT Cardiogenic 16078&quiz=no&comebackto=mode=caption_list Non-Cardiogenic No septal thickening. Diffuse alveolar infiltrates. Atelectasis of dependent Septal thickening. More severe in lung lobes usually seen (not well shown bases. here)
  18. 18. Cardiogenic Edema: Weenie Man ENDOthelium  Vascular Endothelium breaks under stress easily, however it also repairs itself quickly  Cardiogenic edema often develops quickly and can resolve quickly because vascular endothelium is able to repair itself quickly
  19. 19. Non-Cardiogenic Edema: Muscle Man EPIthelium  Alveolar epithelium is quite resistant to damage. It withstands greater force before becoming damaged. However, once ―broken‖ it takes much longer to heal than weenie man endothelium.  Cellular damage in Non- Cardiogenic edema runs along a spectrum from predominately vascular endothelial damage to predominately alveolar epithelial damage
  20. 20. Management for ARDS  There is no definitive treatment for ARDS
  21. 21. Management: Reducing Ventilator- Induced Lung Injury  Low tidal volume mechanical ventilation  In ARDS there is a large amount of poorly compliant (i.e. non-ventilating) lung and a small amount of healthy, compliant lung tissue. Large tidal volume ventilation can lead to over-inflation of the healthy lung tissue resulting in ventilator-induced lung injury of that healthy tissue.  PEEP  Setting a PEEP prevents further lung injury due to shear forces by keeping airways patent during expiration
  22. 22. The Flip Side  Is there such thing as too low a TV?  Tidal Volume must be sufficient for gas exchange to take place. Permissive hypercapnia is the term used to state that a certain degree of hypercapnia and its resulting acidemia can be allowed in order to maintain lung-protective TVs.  Absolute limits is unclear, but a pH of 7.2-7.25 and a PCO2 of 60-70 mm Hg is a good cut off range.  Is there such thing as too much PEEP?  PEEP serves to help open less compliant alveoli and keep alveolar open during expiration, but it too can lead to overinflation of alveoli that are already maintaining aeration.  Setting PEEP too high also increases intrathoracic pressure leading to decreased venous return.  Start patients at a PEEP trial of 5 – 12 cm H2O and increase if needed.
  23. 23. Diuretics—A Good or Bad Therapy in ARDS? Yes No  Diuretics have been shown  Diuretics are not anti- to decrease any pulmonary inflammatory agents: lung edema that is infiltrates in ARDS are neutrophils and present, increase lung proteins, NOT edema compliance, and improve gas  Hemodynamic compromise: exchange. However they tissue oxygenation = #1 have shown no survival concern. Aggressive diuretics benefit. decrease venous pressures leading to decrease CO and increased tissue ischemia
  24. 24. FACTT Study: New Evidence for the Benefits of Diuretic Use in ARDS  Large prospective trial addressed the use of conservative (higher, more frequent lasix doses) verse liberal fluid management (more frequent fluid boluses).  Outcomes: NO significant difference in 60-day mortality between the two groups, however the conservative fluid group had improved lung function, shorter durations of mechanical ventilation, and shorter ICU stays, SUPPORTING THE USE OF DIURETICS. ARDS Clinical Trial Network. 2006. Comparison of Two Fluid-Management Strategies in Acute Lung Injury. N Engl J Med. 354 (24). pp 2564-75.
  25. 25. Management: Fluid Status  Remember, the #1 goal in therapy is to decrease tissue ischemia. We must maintain ARDS patient’s CO to insure tissue profusion.  In the FACTT study, conservative fluid therapy was not followed if a patient was deemed to be in shock, in the presence of oliguria, or if a patient’s circulation was deemed inadequate.
  26. 26. Use of Pulmonary Arterial Catheters in ARDS Swan-Ganz Catheter
  27. 27. History of Pulmonary Arterial Catheters  1945: Dexter used PAC under fluoro to diagnose congenital heart disease, mitral valve disease, and left ventricular failure.  1975: Swan developed a technique that enabled the use of PAC at the bedside. Initially used to guide therapy following acute MI.  By inflating a small balloon at the end of the catheter he was able to float the tip of the catheter through the right heart into the pulmonary arteries.
  28. 28. Uses of the PAC  Guide therapy, aid in determining diagnoses, help determine prognosis  Measures  Central venous and pulmonary artery pressures  Pulmonary capillary wedge pressure (PCWP) → left- arterial pressure  Mixed venous blood gases  Cardiac output  Can also determine systemic and pulmonary vascular resistances from the above measurements
  29. 29. Uses of the PAC in ARDS  Used to aid in diagnosis  Traditionally placed to confirm non-cardiogenic edema verses cardiogenic edema in cases of uncertainty  If PCWP is elevated > 18 mm Hg then by diagnostic criteria—as set by the American-European Consensus— the edema is NOT noncardiogenic.  Used to guide treatment
  30. 30. Should PCWP Be Used to Confirm the Diagnosis of ARDS?  PCWP is an estimate of left atrium pressure  When the PAC balloon is inflated it occludes blood flow through the lungs. The pressure measured in this closed circuit is equal to the pressure in the left-atrium.  In ARDS, PCWP is used to estimate pulmonary capillary pressure. PCWP CANNOT be equal to pulmonary capillary pressure and left atrial pressure. If this were true there would be no pressure gradient making forward blood flow through the pulmonary arteries possible. Therefore PCWP underestimates pulmonary capillary pressure.  Suggests wedge pressure should not be part of the diagnostic criterion for ARDS.
  31. 31. Further Reason Why PCWP Should Not Be Used to Diagnose ARDS  In ARDS, arterial and venous thrombosis in the pulmonary vasculature is very common (i.e. destruction of the weenie man endothelium). This means there is a disruption in the arterial-venous circuit within the lung. But wait; don’t we need a complete circuit to measure the left atrium pressure from a catheter sitting in the pulmonary artery?  It is conceivable that a PAC may in fact be measuring VENTILATORY PRESSURES not left atrial pressure.
  32. 32. Should PCWP Be Used to Dictate the Treatment of ARDS?  The Fluid and Catheter Treatment Trial (FACTT)  A randomized, multi-center trial comparing outcomes of ARDS patients with use of PACs vs. CVCs (central venous catheters).
  33. 33. FACTT  Result: No difference in mortality, number of days on the ventilator or in the ICU, lung or kidney function, rates of hypotension, ventilator settings or use of dialysis between two groups. The PAC group had ≈ twice as many catheter- related complications (mainly arrhythmias). ARDS Clinical Trial Network. 2006. Pulmonary-Artery versus Central Venous Catheter to Guide Treatment of Acute Lung Injury. N Engl J Med. 354 (21). pp 2213-24.
  34. 34. FACTT Conclusions in Regards to PACs  PAC-guided therapy for ARDS does not improve survival or organ-function, reduce ventilator time or decrease ICU-stays. Although associated with more complications, major harm did not occur from PAC use. The evidence does not favor the routine use of the PAC.
  35. 35. Other Evidence For or Against PAC  There have been multiple studies designed to determine the effect of mortality and morbidity of PAC use in ICU patients.  No randomized trials that I could find suggested that PAC use either increased or decreased mortality.  Their use may provide useful information in limited settings, but their use should be pursued with though towards how the information gathered will aid patient management.
  36. 36. References • ARDS Clinical Trial Network. 2006. Comparison of Two Fluid-Management Strategies in Acute Lung Injury. N Engl J Med. 354 (24). pp 2564-75. • ARDS Clinical Trial Network. 2006. Pulmonary-Artery versus Central Venous Catheter to Guide Treatment of Acute Lung Injury. N Engl J Med. 354 (21). pp 2213-24. • Fan, E., Needham, D.M., Stewart, T.E. Ventilatory Management of Acute Lung Injury and Acute Respiratory Distress Syndrome. 2005. JAMA. 294 (22). pp. 2889-96. • Hansen-Flaschen, J., Siegel, M.D. Acute Respiratory Distress Syndrome: Definition; Epidemiology; Diagnosis; and Etiology. 2006. • Heresi, G.A., Arroligo, A.C., Weidemann, H.P., Matthay, M.A. 2006. Pulmonary Artery Catheter and Fluid Management in Acute Lung Injury and the Acute Respiratory Distress Syndrome. Clin Chest Med. 27. pp 627-628. • Marino, P.L. The ICU Book. 3rd Ed. Lippincott Williams & Wilkins. Philadelphia. pp. 419-35. • Petty, T.L. Acute Respiratory Distress Syndrome: Consensus, Definitions, and Future Directions. 1996. Crit Care Med. 24(4). pp 555-556. • Rouby, J-J., Puybasset, L., Nieszkowska, A., Lu, Q. Acute Respiratory Distress Syndrome: Lessons form Computed Tomography of the Whole Lung. 2003. Crit Care Med. 31(4S). pp. S285-95. • Weinhouse, G.L., Manaker, S. Swan-Ganz Catheterization: Indications and Complications. 2006.