Nitric Oxide, Inhaled

Children: Acute or chronic pulm Htn associated with persistent pulmonary Htn of newborn (PPHN), meconium aspiration, CHD, and congenital diaphragmatic hernia

Adults: Acute or pulm Htn associated with ARDS, pulm embolism, placement of a LVAD, and cardiac surgery

Methemoglobinemia (especially breathing >80 ppm NO)

NO ₂ and peroxynitrite formation

Methemoglobinemia; measure metHb, especially in infants, within 6 h and then every 24 h.

Measure inhaled NO and NO ₂ levels continuously.

Do not give if high NO ₂ levels (>2 ppm).

Do not allow NO to stagnate in ventilator or breathing circuits; it slowly converts to toxic NO ₂ gas.

High inhaled NO levels may inhibit platelet aggregation.

In severe heart failure, reducing PVR with NO may raise left atrial pressure.

Rebound pulm Htn during acute NO withdrawal.

Inhaled NO activates guanylate cyclase in lung vessels and airways and increases levels of cGMP, causing selective pulm vasodilation.

Very rapid and avid binding with RBCs. Hgb inactivates NO and thereby prevents systemic vasodilation.

NO is metabolized to nitrate and excreted in urine.

Supplied as stock gas of ≤1000 ppm by volume of NO in nitrogen or other inert gas.

Inhaled NO is mixed with O ₂ -containing gas immediately before administration via intratracheal cath, ventilator, mask, or nasal prongs.