# Inhaled Nitric Oxide

> Inhaled nitric oxide for Respiratory Therapy: 5-20 ppm dosing, selective pulmonary vasodilation in PPHN, methaemoglobinaemia monitoring and weaning rebound.

- Canonical URL: https://prepelephant.com/topics/allied/respiratory-therapy/nitric-oxide-inhaled
- Exam / course: Allied Health · Subject: Respiratory Therapy
- Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team
- First published: 2026-10-02
- Last updated: 2026-10-02
- How to cite: "Inhaled Nitric Oxide", PrepElephant, https://prepelephant.com/topics/allied/respiratory-therapy/nitric-oxide-inhaled

## Direct answer

Twenty parts per million is the conventional starting dose of inhaled nitric oxide in term and near-term neonates with hypoxic respiratory failure and pulmonary hypertension — delivered into the inspiratory limb of the ventilator, where it diffuses selectively into ventilated alveoli, relaxes adjacent pulmonary vascular smooth muscle via cyclic GMP, and improves V/Q matching without dropping systemic vascular resistance. It is the one pulmonary vasodilator that goes only where gas goes; intravenous vasodilators dilate everything, including vessels of unventilated lung (worsening shunt). The trade-offs define its management: methaemoglobinaemia (keep below 5%, checked a few hours after initiation and then periodically), nitrogen dioxide formation from NO plus oxygen (monitored, with scavenging of exhaust gas), and rebound pulmonary hypertension if the drug is stopped abruptly.

## What you must remember

- **Mechanism and selectivity:** NO diffuses from ventilated alveoli into adjacent vascular smooth muscle, activates guanylate cyclase, raises cyclic GMP and relaxes the vessel — improving perfusion of ventilated lung (V/Q matching); inactivated almost instantly by haemoglobin, hence no systemic vasodilation.
- **Licensed niche:** persistent pulmonary hypertension of the newborn (PPHN) in term and near-term infants — start conventionally at 20 ppm (range 5-20), weaning to as low as 1-5 ppm once improved; it reduces the need for ECMO in responsive PPHN.
- **Adult ARDS truth:** iNO transiently improves oxygenation in adult ARDS but has not reduced mortality in trials — its adult role is a time-buying bridge (for example, while arranging proning or ECMO), often tested at 20-40 ppm per protocol, not a destination therapy.
- **Monitoring:** methaemoglobin (target below 5%, classically checked about 4-8 hours after starting and then daily), inspired NO2 (kept low per monitor limits), continuous SpO2 and blood pressure, and echocardiographic confirmation of pulmonary hypertension where possible.
- **Delivery engineering:** NO injected into the inspiratory limb with calibrated meters; mixing time with high oxygen concentrations raises NO2 — monitors sample delivered gas, and exhaust gas is scavenged.
- **Weaning:** gradual, in stepwise ppm reductions once the oxygenation index improves; abrupt discontinuation risks rebound pulmonary hypertension and desaturation — a wean is a monitored procedure, not a switch-off.
- **Contraindications and cautions:** ductal-dependent shunt lesions, bleeding diatheses, methaemoglobin reductase deficiency and G6PD deficiency (relative, per specialist judgement).
- **Alternatives in the same niche:** inhaled epoprostenol (prostacyclin) with similar selectivity and no methaemoglobin issue; intravenous sildenafil or milrinone as adjuncts by protocol.

## One newborn, one response, one wean

A term infant with meconium aspiration and right-to-left ductal shunting has an oxygenation index above 25 on conventional ventilation. Nitric oxide starts at 20 ppm; post-ductal saturation climbs from 78% to 92% within the hour and the pre-ductal/post-ductal gradient narrows — a response that both confirms pulmonary hypertension physiologically and buys time while ventilator settings are optimised. At 24 hours the methaemoglobin reads 1.8% (safe), NO2 stays below monitor limits, and the oxygenation index has fallen enough to begin weaning: 20 to 10 to 5 ppm over two days, each step observed, then off. Had there been no response within that first hour, the protocol's honest next steps would be echocardiography to exclude cyanotic structural heart disease and escalation talk — iNO is a diagnostic-therapeutic probe as much as a treatment, and non-response is itself information.

## Where students slip

The examinable distinction is oxygenation versus outcome: candidates who present iNO as an adult ARDS therapy with survival benefit are contradicted by the trials — it improves PaO2 for hours, not mortality, and the mark scheme says so. The second slip is the mechanism sentence: the selectivity is anatomical (delivered by ventilation to vessels it can reach), which is exactly why it cannot vasodilate the circulation of unventilated, shunted lung — the same reason intravenous vasodilators worsen shunt. Third, the safety numbers: methaemoglobin below 5% and NO2 monitoring are the two quoted values, and "stop abruptly" is the wrong wean — rebound pulmonary hypertension is the designed trap of the topic. The Indian-practice angle: neonatal iNO is available in a modest number of tertiary centres, so the realistic exam answer pairs it with the alternatives (inhaled prostacyclin, sildenafil) and the honest timing of referral.

## Frequently asked questions

### Why is inhaled nitric oxide a selective pulmonary vasodilator?

It is delivered only to ventilated alveoli and diffuses into their adjacent vessels, and haemoglobin inactivates it within seconds, so systemic vessels and unventilated lung are spared.

### At what dose is inhaled nitric oxide started in PPHN?

Conventionally 20 ppm in term and near-term neonates (range 5-20), weaned stepwise to as low as 1-5 ppm as the oxygenation index improves.

### What monitoring does inhaled nitric oxide require?

Methaemoglobin (kept below 5%, checked hours after initiation and periodically), inspired nitrogen dioxide levels, and continuous oxygenation and haemodynamics.

### Does inhaled nitric oxide improve survival in adult ARDS?

It improves oxygenation transiently but has not reduced mortality in randomised trials — its adult use is a bridge while other measures are arranged.

### Why must nitric oxide be weaned rather than stopped abruptly?

Sudden withdrawal causes rebound pulmonary hypertension with desaturation, so reductions are stepwise under monitoring.