Atelectasis II: Pathophysiology

During atelectasis, 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 and impairing oxygen transfer to the bloodstream.

Atelectasis creates a ventilation-perfusion mismatch where airflow is reduced or absent in collapsed alveoli while blood flow continues. This prevents oxygen from being effectively transported into the bloodstream, resulting in hypoxemia. The body cannot adequately oxygenate blood in these non-ventilated regions.

Carbon dioxide levels may initially remain normal because it diffuses more readily than oxygen. The body compensates by increasing breathing rate and depth in unaffected lung regions to help remove carbon dioxide. This hyperventilation in healthy alveoli maintains normal arterial CO₂ levels during small areas of involvement.

Clinical findings include decreased breath sounds, dullness to percussion, reduced chest expansion, and decreased tactile fremitus. These signs occur because sound transmission through collapsed lung tissue is impaired. Physical examination reveals characteristic changes reflecting the loss of aeration in affected regions.

If atelectasis is extensive or prolonged, the body's compensatory mechanisms fail, and hypercapnia can develop. Widespread atelectasis decreases functional alveolar surface area, leading to sustained hypoxemia and increased strain on the respiratory and cardiovascular systems. This may worsen underlying conditions and increase susceptibility to infection.

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.

Patients may develop shortness of breath, rapid breathing, coughing, chest pain, and cyanosis. Symptoms include dyspnea, tachypnea, and signs of respiratory distress, including use of accessory muscles. Early treatment helps re-expand alveoli and improve ventilation to resolve these clinical manifestations.