acute respiratory distress syndrome

1. Acute Respiratory Distress Syndrome (ARDS) Yuan Zhiming Department of Emergency Medicine The General Hospital Tianjin Medical University

4. Respiration ventilation diffusion circulation oxygen extraction and utilization (1) (2) (3) (4)

6. ARDS denotes acute hypoxemic respiratory failure following a systemic or pulmonary insult without evidence of heart failure. It is the most severe form of acute lung injury(ALI) and is characterized by bilateral, widespread radiographic pulmonary infiltrates, normal pulmonary capillary wedge pressure (PCWP) (<18 mmHg) and Pa0 2 /Fi0 2 < 200 mmHg . Definitions

7. ALI is a syndrome of inflammation and increased permeability that is associated with a constellation of clinical, radiologic, and physiologic abnormalities that cannot be explained by, but may coexist with, left atrial or pulmonary capillary hypertension. Exclusion of left atrial hypertension as the primary cause of hypoxemia is critical to this definition

8. The distinction between ALI and ARDS is the degree of hypoxemia ALI: Pa0 2 /Fi0 2 < 300 mmHg ARDS: Pa0 2 /Fi0 2 < 200 mmHg

12. Pathogenesis The pathogenesis of ARDS is not well known inflammatory cells stimulated damage of capillary endothelial cells and alveolar epithelial cells vascular permeability surfactant interstitial and alveolar pulmonary edema risk factors pro-inflammatory cytokines and mediators released hypoxemia alveolar collapse

13. Pathophysiology

14. Pathology In ARDS, the injured lung go through three phases: exudative , proliferative , and fibrotic , but the course of each phase and the overall disease progression is variable, and the three phases don’t have a definite borderline, they overlap partly.

15. damage to the alveolar epithelium (type I alveolar cells mainly) and vascular endothelium Exudative phase(<7d): leakage of water, protein, and inflammatory and red blood cells into the interstitium and alveolar lumen; producing hyaline membranes

18. Nondescript very heavy and poorly aerated lungs. Each lung in ARDS usually weighs over 1000 grams. (A normal lung weighs 200-300 grams)

19. Heavy, red lungs showing congestion and edema.

20. 3-4 weeks after onset of ARDS, extensive interstitial fibrosis developed.

21. Photomicrograph shows ARDS in the exudative stage. Note the hyaline membranes and loss of alveolar epithelium in this early stage.

22. Photomicrograph shows ARDS in the early proliferative stage. Note the type 2 pneumocytic proliferation, with widening of the septa and interstitial fibroblast proliferation.

23. Photomicrograph shows ARDS in the late proliferative stage. Note the extensive fibroblast proliferation, with incorporation of the hyaline membranes.

24. Diffuse Alveolar Damage Hyaline membranes are lining the alveolar ducts and alveolar septa.

27. Chest radiograph shows an endotracheal tube, left subclavian central venous catheter into the superior vena cava, and bilateral patchy opacities in mostly the middle and lower lung zones. The patient had been in respiratory failure for 1 week with the diagnosis of ARDS.

28. chest radiographic findings in a patient with ARDS that evolved over approximately 1 week

29. chest radiographic findings in a patient with ARDS that evolved over approximately 1 week

30. CXR shows bilateral opacities suggestive of ARDS.

31. Typical patterns of ARDS with diffuse internal infiltrates

32. Early phase of ARDS showing interstitial changes and patchy infiltrates

33. Late stage of ARDS showing bilateral and diffuse alveolar and reticular opacification

34. CT scan of the chest showing diffuse infiltrates, ground glass appearance, and air bronchograms. ARDS

35. a small right pleural effusion, consolidation with air-bronchograms, and some ground-glass appearing opacities. The findings indicate an alveolar process, in this case, alveolar damage. High-resolution computed tomographic (HRCT) image in a patient with ARDS

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