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Acute respiratory distress syndrome pathogenesis

What is the pathogenesis of Acute respiratory distress syndrome?
Pathogenesis and clinical course of Acute respiratory distress syndrome is the alveolar - capillary acute injury. Lung injury may be direct, such as gastric acid or the inhalation of toxic gases or on endothelial cells lead to physical and chemical injury. And more to see is the indirect lung injury. Although the mechanism of lung injury has not been completely clarified so far, but has confirmed that it is a systemic inflammatory response syndrome part. In the level of alveolar capillaries by cellular and humoral-mediated acute inflammatory response, which involves two main processes of the migration of inflammatory cells and aggregation, as well as the release of inflammatory mediators, and they complement each other, the role of the alveolar capillary membrane specific components, resulting in increased permeability.

1. the migration and aggregation of inflammatory cells: almost all the lung cells to varying degrees are involved in the pathogenesis of ARDS, ARDS acute inflammation as the most important one of the effector cells are polymorphonuclear leukocytes (PMNs). Separation of people and only a small amount of interstitial PMNs, about 1.6%. In trauma, sepsis, acute pancreatitis, such as physical and chemical stimulation, or cardiopulmonary bypass, as a result of lipopolysaccharide (LPS), C5a, Interleukin -8 (IL-8) the role of such factors, PMNs in the pulmonary capillary together with a large number of blood vessels, the first wall is attached to the flow and adhesion to endothelial cells, and then by inter-endothelial migration to the pulmonary, and then by desquamative alveolar epithelial and alveolar space to move. This process has the participation of a wide range of adhesion molecules and regulation. PMNs respiratory outbreak and the release of its product is an important part of lung injury. Alveolar macrophages (Ams) not only as phagocytic cells and immune response of antigen-presenting cells, the inflammatory response is an important effector cell involved in the pathogenesis of ARDS by stimulating the release of the AMS-activated IL-1, tumor necrosis factor-α (TNF-α) and IL-87, such as in lung PMNs to chemotactic and aggregation is likely to be the initiation factor ALI. Platelet aggregation and micro-embolism is a common pathological changes of ARDS, presumably platelet aggregation and micro-embolism is a common pathological changes of ARDS, presumably a product of platelets and its mechanism in ARDS, such as disease also plays an important role.

2. the release of inflammatory mediators: activation of inflammatory cells and release of medium is associated with the inflammatory response exist, and are inseparable. To bacterial LPS stimulation for example, the surface of macrophages and the receptor-binding, causing cell loss and cell release of many media, including:

  • lipid media: such as arachidonic acid metabolites, platelet-activating factor (PAF);
  • reactive oxygen metabolites: A superoxide anion (O2-), hydrogen peroxide (H2O2), hydroxyl root (OH) and single oxygen (IO2).
  • peptides: as PMNs / Ams protease, complement substrate to participate in the process of coagulation and fibrinolytic components, cell factor.

    3. alveolar capillary damage and increased permeability: to maintain and regulate the structural integrity of capillary permeability and extracellular matrix components include, inter-connected cells, the cytoskeleton, as well as pinocytosis substrate transport and cell interactions. ARDS injury direct and indirect links to each of the above can have an impact. Base their own oxygen, proteases, cytokines, arachidonic acid metabolites, as well as a product of high-charge (for example, the major neutrophil cationic protein), etc. can be changed by the following means of membrane permeability barriers:

  • lysis of basement membrane proteins and cell adhesion molecule;
  • change in fiber extracellular matrix network structure;
  • filament cytoskeleton affected system, leading to cell deformation and connection tear.

    What is effects on pulmonary respiration with Acute respiratory distress syndrome?
    ARDS due to respiratory dysfunction outside to alveolar ventilation - perfusion imbalance mainly with diffuse dysfunction, manifested as hypoxemia and respiratory failure. Very serious cases of a total reduction of alveolar ventilation can occur when the hypercapnic respiratory failure.

    1. alveolar ventilation - perfusion imbalance: as a result of type Ⅱ alveolar epithelial cell damage caused by the generation of surfactant reduced the surface activity of alveolar edema and destruction of substances diluted and hyperventilation-induced alveolar surfactant consumption, resulting in increased alveolar surface tension, lung compliance decreased, leading to atelectasis, which form a functional streaming and true streaming. Neutrophils such as leukotriene release and other media so that contraction of bronchial and small airway plugging tissue fluid, gas can cause lung ventilation and the formation of functional barriers to diversion. ARDS patients flow of pulmonary blood flow of up to 30%. Pulmonary intravascular micro thrombosis, caused by vasoactive substances uneven pulmonary vasoconstriction and pulmonary vascular pressure edema, increased pulmonary vascular resistance is not only so that pulmonary arterial hypertension. Kind of dead space can increase the ventilation. Therefore, alveolar ventilation - perfusion imbalance is the occurrence of respiratory failure patients with the most important reason.

    2. diffusion dysfunction: pulmonary interstitial and alveolar edema and hyaline membrane formation and chronic stages of cell proliferation and pulmonary fibrosis, may increase the diffusion film thickness, resulting in diffuse dysfunction.

    3. decreased alveolar ventilation: Lung disease is the uneven distribution in ARDS. Reduced lung compliance caused by restrictive ventilation barriers and small airway obstruction caused by obstructive pulmonary ventilation barriers, resulting in some reduction in alveolar ventilation, is not affected or less disease compensatory alveolar ventilation rather than enhanced, excessive carbon dioxide emissions, so patients would reduce Paco2. When the alveolar - capillary membrane injury is more serious when more extensive, the total lung volume of the alveolar ventilation will be reduced, CO2 will be retention and hypercapnia occurred at this time will be a further decline in Pao2.

    • Submitted by Health Studies on Fri, 04/24/2009 - 22:14
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