During sleep apnea, episodic hypoxia and hypercapnia lead to an increase in pulmonary artery pressure via which vascular mechanism?

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Multiple Choice

During sleep apnea, episodic hypoxia and hypercapnia lead to an increase in pulmonary artery pressure via which vascular mechanism?

Explanation:
Intermittent low oxygen in sleep apnea triggers hypoxic pulmonary vasoconstriction, a response where small pulmonary arteries constrict in reaction to alveolar hypoxia. This increases pulmonary vascular resistance, raising the pressure in the pulmonary artery. Mechanistically, hypoxia causes depolarization of pulmonary artery smooth muscle cells, opening voltage-gated calcium channels, increasing intracellular calcium, and leading to contraction. Endothelin production can rise and nitric oxide may fall, amplifying the constriction. This pulmonary-specific response elevates mean pulmonary artery pressure, especially with repeated nocturnal hypoxemia. The other options don’t fit because systemic vasodilation would lower systemic, not pulmonary, pressures; right atrial dilation alone doesn’t explain a rise in pulmonary artery pressure; and decreased venous return isn’t the primary driver of increased pulmonary vascular pressure.

Intermittent low oxygen in sleep apnea triggers hypoxic pulmonary vasoconstriction, a response where small pulmonary arteries constrict in reaction to alveolar hypoxia. This increases pulmonary vascular resistance, raising the pressure in the pulmonary artery. Mechanistically, hypoxia causes depolarization of pulmonary artery smooth muscle cells, opening voltage-gated calcium channels, increasing intracellular calcium, and leading to contraction. Endothelin production can rise and nitric oxide may fall, amplifying the constriction. This pulmonary-specific response elevates mean pulmonary artery pressure, especially with repeated nocturnal hypoxemia. The other options don’t fit because systemic vasodilation would lower systemic, not pulmonary, pressures; right atrial dilation alone doesn’t explain a rise in pulmonary artery pressure; and decreased venous return isn’t the primary driver of increased pulmonary vascular pressure.

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