What is the pathophysiology of pulmonary irritation from smoke inhalation?

Updated: Oct 15, 2021
  • Author: Keith A Lafferty, MD; Chief Editor: Joe Alcock, MD, MS  more...
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Pulmonary injury from smoke inhalation is characterized by both hyperinflation and atelectasis. Debris from cellular necrosis, inflammatory exudate, and shed epithelium combine with carbonaceous material to narrow airways that are already compromised by edema. Reflex bronchoconstriction further exacerbates the obstruction.

Both inspiratory and expiratory resistance are increased, and the premature closure of small airways occurs, producing hyperinflation and air trapping. Surfactant production and activity are both impaired, leading to alveolar collapse and segmental atelectasis.

Low-pressure pulmonary edema plays an important role in the development of lung injury from smoke inhalation. Damage to the alveolar capillary membrane increases its permeability, and intravascular leakage into the pulmonary interstitium ensues. Eventually, increased lymphatic flow may be overwhelmed, resulting in alveolar edema. Alveoli fill with thick, bloody fluid. Loss of compliance, further atelectasis, and increasing edema can result in severe ventilation-perfusion mismatch and hypoxia.

Pulmonary injury may also occur as a direct result of hypoxia. The decrease in ambient oxygen tension that occurs during fires in closed spaces depends on the substances that are burned. Gasoline self-extinguishes when oxygen concentrations fall below 15%. Other substances may continue to undergo thermal decomposition, further decreasing ambient oxygen tension. Even small decrements in oxygen tension have a potentiating effect on inhaled asphyxiant gases, such as CO and HCN, resulting in severe lactic acidosis and a high fatality rate.

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