Which mechanism explains hypoxemia in atelectasis?

• A. Ventilation without perfusion (dead space).
• B. Perfusion without ventilation (shunt).
• C. Increased diffusion distance.
• D. Obstruction of large airways.

Answer: (B)

In atelectasis, some alveoli collapse and are not ventilated, but blood continues to flow through the capillaries in those areas. Gas exchange requires both air reaching the alveoli and blood flowing past them; when the alveoli are not ventilated yet still perfused, the blood passing through those regions does not get oxygenated. This creates a shunt: perfusion without ventilation that dumps deoxygenated blood into the circulation, lowering arterial O2 levels and causing hypoxemia. Supplemental oxygen tends to be less effective for this mechanism because the problem isn’t lack of oxygen in the air but lack of air reaching the blood in those alveoli.

For contrast, a scenario with ventilation without perfusion (dead space) involves air reaching ventilated alveoli that aren’t perfused, which doesn’t cause the same degree of hypoxemia as a shunt. A thicker diffusion barrier or increased diffusion distance would impair gas exchange over time but isn’t the primary mechanism in atelectasis, and obstruction of large airways can lead to collapse but the hypoxemia in atelectasis is best explained by perfusion of unventilated alveoli.