Atelectasis II: Pathophysiology

Atelectasis develops when alveoli lose their air and collapse inward. Because lung tissue is naturally elastic, these air sacs shrink rather than remaining open. Collapsed alveoli are no longer ventilated, reducing their role in gas exchange. Blood flow may continue in these regions, creating a ventilation–perfusion mismatch. Clinical findings include decreased breath sounds, dullness to percussion, reduced chest expansion, and decreased tactile fremitus as sound transmission through collapsed lung tissue is impaired.

Ventilation–Perfusion Consequences

In affected areas, airflow is reduced or absent while perfusion persists, impairing oxygen transfer and causing hypoxemia. Carbon dioxide levels may initially remain normal due to its high diffusibility and compensatory increased ventilation in unaffected lung regions. Small areas of involvement often maintain normal arterial CO₂ levels. The body supports this compensation by increasing breathing rate and depth to help remove carbon dioxide.

Effects on Gas Exchange and Blood Flow

Low oxygen in collapsed alveoli causes local vasoconstriction, redirecting blood to better-ventilated areas. In extensive atelectasis, this mechanism becomes insufficient, leading to impaired gas exchange. Reduced oxygen delivery may affect cellular function and increase susceptibility to infection and lung dysfunction.

Systemic Effects

Widespread atelectasis decreases functional alveolar surface area, leading to sustained hypoxemia and increased strain on the respiratory and cardiovascular systems, potentially worsening underlying conditions. Early treatment helps re-expand alveoli and improve ventilation.

Clinical Manifestations

Symptoms include dyspnea, tachypnea, and hypoxemia, which may present as cyanosis in severe cases. Patients may also have a dry cough and signs of respiratory distress, including use of accessory muscles.