1. Acute Respiratory Distress Syndrome Module G5 Chapter 27 (pp. 369-378)

2. Compliance Compliance =  Volume  Pressure Normal Values Lung 0.2 L/cm H 2 0 Thorax 0.2 L/cm H 2 0 Total 0.1 L/cm H 2 0 Measurement of how easy or hard it is to inflate the lungs. COMPLIANCE IS RECIPROCAL OF ELASTANCE.

3. Increased Lung Compliance Easier to inflate the lung Lower inflation pressures Decreased Elastance Causes Emphysema

4. Decreased Compliance Higher inflation pressures Higher airway pressures on the ventilator Increased complications (barotrauma, decreased CO) Harder to inflate the lung “Stiff lung” Increased Elastance Causes Atelectasis Fibrosis Pneumothorax ARDS

5. Lung Injury Acute Lung Injury (ALI) Normal barriers to fluid movement within the lungs is disrupted. If it is severe enough to cause acute hypoxemic respiratory failure it is termed: Acute respiratory distress syndrome (ARDS) Most severe gas exchange abnormalities Multiple Organ Dysfunction Syndrome (MODS)

6. Lung Injury Normal  ALI  ARDS Clinical Spectrum

7. Historical Look ARDS was referred to as “Shock Lung Syndrome”. Disease first identified in WWII. Many different names in the literature: Da Nang Lung Shock Lung Syndrome Wet lung/White lung/Capillary Leak Syndrome Non-cardiogenic pulmonary edema Adult Hyaline Membrane Disease

8. Diagnosis of ARDS Acute Process Bilateral Infiltrates PCWP less than 18 mm Hg Non-Cardiogenic PaO 2 /F i O 2 ratio less than or equal to 200

9. Criteria Differentiating ALI and ARDS PaO 2 /F i O 2 ratio Example 100 mm Hg/.21 = 476 As the number decreases, oxygenation is getting worse ALI is when the ratio is LESS THAN 300 ARDS the ratio LESS THAN 200

10. Clinical Course in ARDS Initial Injury Apparent Respiratory Stability X-rays and BS normal Tachypnea, tachycardia, cough Respiratory Deterioration Begins around 24 hours after initial insult Peaks at 48-72 hours Recovery Process

11. Etiology DIRECT INJURY Gastric Aspiration Near Drowning Fat or air emboli Smoke Inhalation Pneumonia O 2 Toxicity INDIRECT INJURY Sepsis Cardiopulmonary bypass Burns Thoracic trauma Massive blood transfusion Pancreatitis

12. Acute Respiratory Distress Syndrome Injury of the lung Destruction of the alveolar-capillary membrane Engorged capillaries Interstitial and alveolar edema Hemorrhage Decreased surfactant with atelectasis Hyaline Membrane formation Fibrosis

14. Pathological Abnormalities Exudative phase (3 - 7 days) Edema, hyaline membrane formation, damage to type I cells, capillary damage Fibroproliferative phase (7 days - ?) Regeneration of alveolar epithelium. Fibroblasts mediate the formation of alveolar and interstitial fibrosis develops. The extent of fibrosis determines the degree of pulmonary disability in patients who survive.

15. Anatomic Alterations On examine, lungs appear: “red”, “beefy”, or “liver-like” in appearance & heavy and hemorrhagic. Restrictive lung disease “Baby Lungs” Low lung compliance – difficult to ventilate Stiff lungs High ventilator pressures needed. Refractory hypoxemia Shunting

19. Lapinsky & Mehta, Critical Care 2005 9:1 (60-65)

20. Clinical Findings Tachypnea Decreased lung volumes Cyanosis Increased shunting Retractions Dull percussion note & bronchial BS

21. Chest X-ray Radiopaque – white The more severe the ARDS, the whiter the lungs appear Often described as “White Out” or diffuse “fluffy” infiltrates Non-homogenous “Baby Lungs” Heart size is normal Air Bronchograms Honeycombing or Ground Glass

22. Complications of ARDS Nosocomial Infections Pulmonary emboli Oxygen Toxicity GI hemorrhage/gastric distension Sepsis, microemboli, Disseminated Intravascular Coagulation (DIC), anemia Pulmonary fibrosis – permanent disability Cardiovascular Problems

23. Multiorgan Failure in ARDS

24. Management Reversal of underlying associated disorder Oxygen & Diuretics (keep on dry side) Steroids (after 7 days if no infection) Antibiotics Mechanical Ventilation Proning Nutritional support

25. Management Minimize O 2 demand by reducing metabolic rate Control fevers Control anxiety and pain Altered Style of Ventilation Bi-Level Ventilation (APRV) High frequency ventilation Recruitment Maneuvers Proning Experimental Treatments: Nitric Oxide Extracorporeal membrane oxygenation (ECMO) Exogenous Surfactant Administration

26. Proning Should see improvement in 1 hour Response should be significant PaO 2 improves from 60 – 100 mm Hg Works better in indirect ARDS Pancreatitis May improve oxygenation but does not improve mortality Facial Edema can be severe

27. Recovery Extent of recovery depends on: Severity of the initial lung injury Influence of secondary forms of injury Oxygen toxicity Nosocomial infections DIC Barotrauma with mechanical ventilation Normal lung function after 1 year Residual effects may result in decreased flowrates and D L CO

28. Mortality Rate Mortality rates have declined over the past two decades from 90% to 30 – 40%

29. Indications for Mechanical Ventilation Acute Hypercapnic Respiratory Failure Respiratory Acidosis Acute Hypoxemic Respiratory Failure PaO 2 less than normal F i O 2 greater than 60% oxygen

30. PEEP Set PEEP at lower infection point to recruit alveoli and keep them open Shunting will improve with improved PaO 2 PEEP may decrease blood pressure and cardiac output so monitor both closely Do not allow oxygen delivery to decrease

31. Ventilation Strategies Use higher PEEP levels (10 – 15 cm H 2 0) Set low tidal volumes at 5-7 mL/kg KEEP ALVEOLAR (PLATEAU) PRESSURE LESS THAN 30 – 35 cm H 2 0 This may result in permissive hypercapnia.