Acute respiratory distress syndrome pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Acute respiratory distress syndrome primarily results from the diffuse inflammation of lung parenchyma. Loss of aeration can cause fundamental changes in inflammation amplification and progression.

Pathophysiology

A pathohistological image of ARDS.

• ARDS is characterized by a diffuse inflammation of lung parenchyma.
• The triggering insult to the parenchyma usually results in an initial release of cytokines and other inflammatory mediators, secreted by local epithelial and endothelial cells.
• Neutrophils and some T-lymphocytes quickly migrate into the inflamed lung parynchema and contribute in the amplification of the phenomenon.
• Typical histological presentation involves diffuse alveolar damage and hyaline membrane formation in alveolar walls.
• Although the triggering mechanisms are not completely understood, recent research has examined the role of inflammation and mechanical stress.

Inflammation

• Inflammation alone, as in sepsis, causes:

• Endothelial dysfunction
• Fluid extravasation from the capillaries
• Impaired drainage of fluid from the lungs

• Dysfunction of type II pulmonary epithelial cells may also be present, with a concomitant reduction in surfactant production.
• Elevated inspired oxygen concentration often becomes necessary at this stage, and they may facilitate a 'respiratory burst' in immune cells.
• In a secondary phase, endothelial dysfunction causes cells and inflammatory exudate to enter the alveoli
• This pulmonary edema increases the thickness of the alveolo-capillary space, increasing the distance the oxygen must diffuse to reach blood.
• This impairs gas exchange leading to hypoxia, increases the work of breathing, eventually induces fibrosis of the airspace.
• Rdema and decreased surfactant production by type II pneumocytes may cause whole alveoli to collapse, or to completely flood. This loss of aeration contributes further to the right-to-left shunt in ARDS.
• As the alveoli contain progressively less gas, more blood flows through them without being oxygenated resulting in massive intrapulmonary shunting.
• Collapsed alveoli (and small bronchi) do not allow gas exchange. It is not uncommon to see patients with a PaO₂ of 60 mmHg (8.0 kPa) despite mechanical ventilation with 100% inspired oxygen.
• The loss of aeration may follow different patterns according to the nature of the underlying disease, and other factors. In pneumonia-induced ARDS, for example, large, more commonly causes relatively compact areas of alveolar infiltrates.
• Usually distributed to the lower lobes, in their posterior segments, and they roughly correspond to the initial infected area.
• In sepsis or trauma-induced ARDS, infiltrates are usually more patchy and diffuse. The posterior and basal segments are always more affected, but the distribution is even less homogeneous.
• Loss of aeration also causes important changes in lung mechanical properties. These alterations are fundamental in the process of inflammation amplification and progression to ARDS in mechanically ventilated patients.

References

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