Question

Because of the inflammatory cytokine “cloud” released from macrophages and neutrophils, what damage can occur to the type-2 pneumocytes?  

Answer 1

Pathophysiology of Acute Lung Injury/ Acute Respiratory Distress Syndrome

The exact cause to the damage of alveolar- capillary interface is not known, but it is thought to be caused by the stimulation of the inflammatory and immune system, which cause an attraction of neutrophils to the pulmonary interstitium. The neutrophils release biochemical,humoral and cellular mediators that produe changes in the lung. These include increased capillary permeability, destruction of elastin and collagen, formation of pulmonary micro emboli and plmonary artey vasoconstriciton

Alveolar Type I and Type II cells (which produce surfactant) are damged by the changes caused by the ARDS. This damage, in addition to further fluid and protein accumulation, results in surfactant dyfunction. The function of surfactant is to maintain alveolar stability by decreasing alveolar surface tension and preventing alveolar collapse. Decreased synthesis of surfactant and presence of inactivation of existing surfactant cause alveoli to become unstable and collapse (atelectasis). Widespread atlectasis further decreases lung compliance , decreases gas exchange,and contributes to hypoxemia

Also during this stage, necrotic cells,fibrin and protein form hyaline membranes that line the alveoli. Hyaline membranes contribute to the development of fibrosis and atlectasis leading to decrease in gas exchange and lung compliance

The primary pathophysiologic changes that describe the injury/exudative phase of ARDS are

• Interstitial and alveolar edema (non-cardiogenic pulmonary edema)
• Atlectasis

Severe ventillation perfusion mismatch and shunting of pulmomary capillary blood result in hypoxemia unresponsive to increased concentration of oxygen (termed as refractory hypoxemia)