• Acute Respiratory Distress Syndrome
    • Non-Cardiogenic form of pulmonary edema.
    • Acute persistent diffuse lung inflammation that injures the alveolar epithelial cells and pulmonary capillary endothelial cells.
      • --> increased vascular permeability and cytokine release --> leakage of protein, fluid, neutrophils into the interstitium and alveoli --> creates oncotic gradient to move further fluid into the lung airspace. 
      • Decreased surfactant function causes atelectasis --> further impairs gas exchange. 
      • Alveolar flodding reduces lung compliance and therefore increase work of breathing.
    • This creates hypoxemic respiratory failure from shunt, but eventually can cause hypercapnic failure (work of breathing).
    • Bottom Line: Physiologic hallmark of ARDS is hypoxemia
      • Can be corrected via mechanical ventilation combined with supplemental O2 and PEEP.


    • Diffuse alveolar damage. (diagnosis is clinical!)



    • Historically: classified by arterial pO2:FiO2 ratio
      • P:F ratio < 300 = Acute Lung Injury.
      • P:F ratio < 200 = ARDS
      • Also involved PA catheters for wedge pressure
    • NEWER: 2012 Berlin Definition of ARDS
      (consensus statement by European Society of Intensive Care Medicine, American Thoracic Society, Society of Critical Care Medicine).
      • Changes:
        • Removed PA catherers from criteria (studies show their use does not improve outcomes in lung injury, so they are removed from new guidelines).
        • Heart failure and volume overload can coexist in ARDS (exclusion of cardiogenic edema does not require objective assessment with echo or PCWP) unless no risk factors for ARDS.
        • Can now use CT or CXR for bilateral opacity criteria.
      • Classify ARDS into mild/mod/severe by level of oxygenation, eliminating "Acute Lung Injury".
      • 2012 Berlin Definition of ARDS 

            1. Acute onset within 1 week of an apparent clinical insult or development and

                progression of respiratory symptoms


            2. Bilateral opacities on chest imaging not explained by other pulmonary pathology

                (such as pleural effusions, lung collapse, nodules, etc..)


            3. Respiratory failure not explained by heart failure or volume overload 


        • Severity Arterial pO2 / FiO2 Ratio (P:F Ratio)
          MILD 201 to 300 mmHg (26.7-39.9 kPa)
          MODERATE 101 - 200 mmHg (13.4-26.6 kPa)
          SEVERE < 100 mmHg (<13.3 kPa)

        • NOTE: All 3 categories require P:F ratio measured with a PEEP of at least 5cm
          of H2O (Can be non-invasively w/ CPAP in mild ARDS).



    • More than 60 disorders can precipitate ARDS (direct or indirect lung injury).
      • Severe sepsis from pneumonia or non-pulmonary lung sources are majority of cases.
    • Common Causes of Acute Respiratory Distress Syndrome

      Direct Pulmonary Injury



      Near drowning

      Inhalational injury

      Trauma or lung contusion

      Indirect Pulmonary Injury


      Severe trauma

      Multiple blood transfusions



    • Mortality rate is 40%, varies by cause:
      • Best prognosis: trauma.
      • Worst prognosis: Severe sepsis from pulmonary source.
    • Deaths are caused by underlying precipitant of lung injury or subsequent nosocomial infections
      • Not by direct lung injury.



    (Based on the ARDS Clinical Network Trial & MKSAP 16)

    • Mechanical ventilation / POSITIVE PRESSURE is primary supportive treatment. (less applicable in focal disease)
      • Physiologic hallmark of ARDS is hypoxemia, corrected with mechanical ventilation + FiO2 and PEEP
        • Atelectrauma (lung injury from repetitive opening and closing of alveoli) and barotrauma can cause "Ventilator Associated Lung Injury".  Limit this by:
          • Limit tidal volumes  (10-12 mL/kg traditionally used, now suggest 6 mL/kg and lower)
            • use predicted ideal body weight (aka IBW)!!!
            • Decrease tidal volumes below 6mL/kg by 1mL/kg to achieve plateau pressure < 30 cmH2O (to prevent vent-ass'd lung injury)  (can allow some hypercapnea, and may need to increase FiO2)
          • Minimize plateau pressure (ideally < 30 cmH2O)
          • Reduce FiO2 level <0.6
          • Optimize PEEP (recruits alveoli, prevents atelectrauma)
            • Barotrauma/pneumothorax risk higher >15ncmH2O, but RCT studies show no difference in survival with 15 vs. 8 cmH2O.
            • Higher PEEP is likely OK.  
            • Current guidelines titrate PEEP to keep FiO2<0.6 and not cause hypotension.
        • Reducing tidal volumes can cause hypercapnia, called "permissive hypercapnia", and is NOT HARMFUL (reduces VALI).
        • ARMA landmark trial:
          • Decreasing tidal volume 12 mL/kg of IDW to 6 mL/kg, while keeping plateau pressure <30 cmH2O reduced mortality from 40-->30%.  (USE Ideal body weight).
        • ProningPROSEVA RCT: better oxygenation, but no mortality difference, increase in complication (ET obstruction, accidental extubation, pressure ulcers).
          • Proning is recommended only in experienced centers in severe ARDS, if oxygenation is unsuccessful.
      • NOTE: key pathologic change: flooding of alveoli by membrane disruption.
      • NOTE: Latest trial: NIPPV did not improve survival or need for intubation in ARDS pts.
        (May be beneficial in select pts with pneumonia).
    • Limit intravascular volume to level enough to maintain perfusion.
      • Additional volume will cause leaky capillaries to be more leaky.
      • Multi-Center Study: relatively complex fluid strategy improved lung function, shortened duration of mechanical ventilation and ICU stay, but did not change mortality.
        • Conservative strategy: lower CVP pressures. (less boluses, more furosemide)
        • vs. Liberal strategy.
    • Many therapies trialed:
      • Most shown to improve oxygenation, but not survival.
    • Nonventilator Management of Acute Respiratory Distress Syndrome (Source:MKSAP16)



      Inhaled vasodilators

      ↑ O2 saturation; no proven survival benefit

      Systemic corticosteroids

      ↑ O2 saturation; may reduce duration of invasive ventilation; no survival benefit; optimal patient selection, timing, dose, and duration uncertain

      Neuromuscular blockade

      Used in early severe ARDS; may improve mortality but limited published experience and not widely used in North America

      Conservative fluid strategy

      ↑ O2 saturation and reduced duration of invasive mechanical ventilation in single large National Institutes of Health study

      Prone positioning

      ↑ O2 saturation; no survival benefit in individual trials (signal towards mortality improvement)

      Extracorporeal membrane oxygenation

      (After H1N1, limited expr)

      May improve mortality in severe ARDS but limited published experience, limited availability

      ARDS = acute respiratory distress syndrome.


    Guideline Summaries

    • Surviving Sepsis Guidelines Summary (2012): ARDS component:
      • Surviving Sepsis Guidelines 2012: Ventilators  (ARDS)

        • low tidal volume (1A) and limitation of inspiratory plateau pressure (1B) for (ARDS)
        • Application of at least a minimal amount of PEEP in ARDS (1B)
        • Higher rather than lower level of PEEP for patients with sepsis-induced moderate or severe ARDS (2C)
        • Recruitment maneuvers in sepsis patients with severe refractory hypoxemia due to ARDS (2C)
        • Prone positioning in sepsis-induced ARDS patients with a PaO2/FiO2 ratio of B100 mm Hg in facilities that have experience with such practices (2C)
        • Head-of-bed elevation in mechanically ventilated patients unless contraindicated (1B)
        • conservative fluid strategy for patients with established ARDS with no evidence of tissue hypoperfusion (1C);
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