A 55-year-old man with COPD has PaO2 60 mmHg and PaCO2 52 mmHg on ABG. His pulmonary vascular resistance is increased. The primary mechanism driving pulmonary vasoconstriction in this patient is:
- A Hypercapnia-induced acidosis activating adrenal catecholamines
- B Alveolar hypoxia causing local pulmonary vasoconstriction via inhibition of Kv channels in PASMC ✓
- C Systemic sympathetic activation increasing pulmonary vascular tone
- D Elevated PaCO2 directly constricting pulmonary smooth muscle
Explanation
Hypoxic pulmonary vasoconstriction (HPV) is a unique local reflex of the pulmonary circulation. Alveolar hypoxia inhibits voltage-gated potassium channels (Kv) in pulmonary artery smooth muscle cells, causing membrane depolarization, calcium influx via L-type channels, and vasoconstriction. This mechanism is intrinsic to the pulmonary vasculature and does not require systemic catecholamines. HPV is initially adaptive (redirecting blood from poorly ventilated alveoli) but chronic HPV leads to pulmonary hypertension. CO2 itself is not the primary vasoconstrictor; systemic vasculature responds oppositely (vasoconstriction to hypoxia occurs in pulmonary, vasodilation elsewhere).
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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