The hypoxic pulmonary vasoconstriction (HPV) response serves to improve ventilation-perfusion matching. Which of the following clinical scenarios represents the OPPOSITE of the expected HPV response, potentially worsening V/Q mismatch?
- A During pneumonia lobar consolidation, HPV diverts blood away from the affected lobe
- B At high altitude, global alveolar hypoxia causes generalized HPV, increasing pulmonary artery pressure uniformly
- C Administration of vasodilators (sildenafil, prostacyclin) in primary pulmonary hypertension may abolish HPV in poorly ventilated areas, worsening V/Q mismatch and arterial hypoxemia ✓
- D In ARDS, HPV is maximally activated in diffuse lung injury areas, completely preventing shunt
Explanation
In pulmonary arterial hypertension, pulmonary vasodilators (sildenafil/PDE5 inhibitors, prostacyclin analogs) lower PAP by dilating pulmonary vasculature. However, if they dilate vessels in poorly ventilated lung regions (where HPV was appropriately diverting blood away), the vasodilator abolishes this protective HPV, increasing perfusion to non-ventilated alveoli and worsening V/Q mismatch and arterial hypoxemia. This is the mechanism of 'pulmonary vasodilator paradox' — systemic oxygen saturation may paradoxically fall when pulmonary vasodilators are given to patients with underlying V/Q mismatch. Option D is incorrect: HPV in ARDS is overwhelmed by cytokine-mediated vasodilation and cannot prevent shunt.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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