Injury or Exudative Phase
Occurs approximately 1 to 7 days (usually 24 to 48 hours) after the direct lung injury or host insult.
The primary pathophysiological changes that characterize this phase are interstitial and alveolar edema (noncardiogenic pulmonary edema) and atelectasis.
Severe V/Q mismatch and shunting of pulmonary capillary blood result in hypoxemia unresponsive to increasing concentrations of O2 termed refractory hypoxemia.
Hypoxemia and the stimulation of juxtacapillary receptors in the stiff lung parenchyma (J reflex) initially cause an increase in respiratory rate, decrease in tidal volume, respiratory alkalosis and an increase in cardiac output.
Reparative or Proliferative Phase
Begins 1 to 2 weeks after the initial lung injury.
During this phase there is an influx of neutrophils, monocytes, lymphocytes and fibroblast proliferation as part of the inflammatory response.
The proliferative phase is complete when the diseased lung becomes characterized by dense, fibrous tissue.
Increased pulmonary vascular resistance and pulmonary hypertension may occur in this stage because fibroblasts and inflammatory cells destroy the pulmonary vasculature.
Lung compliance continues to decrease as a result of interstitial fibrosis and hypoxemia.
Hypoxemia worsens because of the thickened alveolar membrane causing diffusion limitation and shunting.
If the reparative phase persists widespread fibrosis results, if it is arrested the lesions resolve.
Fibrotic or Chronic Phase
Occurs approximately 2 to 3 weeks after the initial lung injury.
By this time the lung is completely molded by sparsely collagenous and fibrous tissues.
There is diffuse scarring and fibrosis resulting in decreased lung compliance.
The surface area for gas exchange is significantly reduced because the interstitium is fibrotic and therefore hypoxemia continues.
Pulmonary hypertension results from pulmonary vascular destruction and fibrosis.
(Lewis, et. al 2007 pg 1812)