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Acute Respiratory Distress Syndrome (ARDS)


Pathophysiology

Physician-developed and -monitored.

Original Date of Publication: 05 Dec 2000
Reviewed by: Stanley J. Swierzewski, III, M.D.
Last Reviewed: 04 Dec 2007

Original Source: http://www.pulmonologychannel.com/ards/pathophysiology.shtml

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Pathophysiology



The respiratory system resembles an upside-down, hollow tree. Indeed, the passageways leading from the mouth to the interior of the lungs are referred to as the tracheobronchial tree. The parts of the body through which air enters and exits the body (i.e., the mouth, nose, larynx, and trachea) make up the "trunk" of the tree. The tubes that lead to the lungs (bronchi) and the tiny tubes inside the lungs (bronchioles) are the tree's "branches" and "twigs."

Air moves through the respiratory system from the base of the trunk to the tips of the twigs. Clustered at the tips of the trachiobronchial twigs are tiny air sacs called alveoli, where inhaled oxygen passes into the blood stream. This is where acute respiratory distress syndrome (ARDS) occurs.

Injury to the alveoli
About 90% of the cells that make up the alveoli are very thin "type I epithelial cells" across which actual gas exchange takes place. Oxygen normally diffuses very easily through this layer of cells into the capillaries where it binds with the hemoglobin in the red blood cells.

The alveolar epithelial cells normally form a very tight barrier around the alveolar space, preventing any fluid from entering and disrupting gas exchange. In ARDS, the alveolar epithelial barrier breaks, allowing flooding of the alveolar space and making it difficult or impossible for oxygen to diffuse into the capillaries.



ARDS also can affect the "type II alveolar cells". Type II cells are thicker, square-shaped cells and the main function of these cells is to produce surfactant. Surfactant plays an essential role in preventing the alveoli from collapsing. The flooding through the broken type I cell barrier and the diminished production of surfactant by the type II cells collapse the alveoli.

Alveolar damage is increased by the activity of immune system cells (neutrophils) that rush to the site of injury, ironically, to help out. The activity of these cells and the inflammation they cause create a cascade of further injury that may extend into the capillaries as well.

Injury to the alveolar capillaries
If the original injury is in the alveolar capillaries that lie just beneath the alveoli, chemical mediators (usually cytokines) that the immune system releases in response, rush to the site of the injury, damaging and causing inflammation to the cells that line the capillaries (i.e., the capillary endothelium).

As a result, cells and fluid leak through the capillaries and into the alveolar spaces; the capillaries become blocked with cellular debris and fibrin (i.e., protein that makes up blood clots); surfactant production ceases; and the alveoli collapse.


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