A patient with obstructive sleep apnea (OSA) has repeated nocturnal episodes of hypoxia (SaO2 drops to 75%) and hypercapnia. Which long-term physiological consequence most directly follows from repetitive pulmonary arterial hypoxic vasoconstriction?

• A Pulmonary hypertension and RV hypertrophy (cor pulmonale) due to sustained hypoxic pulmonary vasoconstriction causing structural remodeling ✓
• B Systemic hypertension due to baroreceptor resetting from chronic nocturnal hypoxia
• C Left ventricular diastolic dysfunction only, due to increased afterload from systemic vasoconstriction during apneic episodes
• D Secondary polycythemia only, with no vascular remodeling because vasoconstriction is fully reversible

Explanation

Hypoxic pulmonary vasoconstriction (HPV) is a local reflex mediated by inhibition of K+ channels in pulmonary artery smooth muscle cells, causing depolarization and Ca2+ influx-mediated constriction. While HPV is initially reversible, chronic/repetitive hypoxia (as in OSA) causes structural vascular remodeling — medial hypertrophy and intimal proliferation — resulting in sustained pulmonary hypertension. This increases RV afterload progressively, leading to RV hypertrophy and eventually cor pulmonale. Secondary polycythemia also occurs (EPO-driven) but does not prevent vascular remodeling. Systemic hypertension also occurs in OSA but via a different mechanism (sympathetic activation, not HPV).

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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