Which therapy in persistent pulmonary hypertension of the newborn acts as a pulmonary vasodilator?

Prepare for the Neonatal/Pediatric Specialist Test. Use flashcards and multiple-choice questions with hints and explanations. Ready yourself for the exam!

Multiple Choice

Which therapy in persistent pulmonary hypertension of the newborn acts as a pulmonary vasodilator?

Explanation:
In persistent pulmonary hypertension of the newborn, the key issue is elevated pulmonary vascular resistance that keeps blood flow away from the lungs and through fetal circulatory routes. The therapy that acts as a pulmonary vasodilator is inhaled nitric oxide. When inhaled, nitric oxide reaches the lungs and relaxes the smooth muscle in the pulmonary vasculature, lowering pulmonary vascular resistance and improving perfusion to ventilated lung areas. This targeted effect helps reduce the right-to-left shunt across the foramen ovale and ductus arteriosus, improving oxygenation while largely sparing systemic blood pressure because the gas has a short half-life and acts locally in the lungs. Mechanistically, NO activates soluble guanylate cyclase in smooth muscle, increasing cGMP and causing relaxation. In practice, NO is used at low concentrations (often around 5–20 ppm) with monitoring for methemoglobinemia and potential rebound hypertension if stopped abruptly. Other options either don’t directly dilate the pulmonary vessels (vasoconstrictors would worsen PPHN), are only supportive (ECMO for severe cases), or affect ventilation rather than directly lowering PVR, so inhaled NO is the most specific pulmonary vasodilator among these therapies.

In persistent pulmonary hypertension of the newborn, the key issue is elevated pulmonary vascular resistance that keeps blood flow away from the lungs and through fetal circulatory routes. The therapy that acts as a pulmonary vasodilator is inhaled nitric oxide. When inhaled, nitric oxide reaches the lungs and relaxes the smooth muscle in the pulmonary vasculature, lowering pulmonary vascular resistance and improving perfusion to ventilated lung areas. This targeted effect helps reduce the right-to-left shunt across the foramen ovale and ductus arteriosus, improving oxygenation while largely sparing systemic blood pressure because the gas has a short half-life and acts locally in the lungs. Mechanistically, NO activates soluble guanylate cyclase in smooth muscle, increasing cGMP and causing relaxation. In practice, NO is used at low concentrations (often around 5–20 ppm) with monitoring for methemoglobinemia and potential rebound hypertension if stopped abruptly. Other options either don’t directly dilate the pulmonary vessels (vasoconstrictors would worsen PPHN), are only supportive (ECMO for severe cases), or affect ventilation rather than directly lowering PVR, so inhaled NO is the most specific pulmonary vasodilator among these therapies.

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