Pulmonary hypertension

Published on 03/06/2015 by admin

Filed under Neonatal - Perinatal Medicine

Last modified 22/04/2025

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CHAPTER 6 Pulmonary hypertension

Description

Whilst pulmonary artery pressures are increased in this condition, the main pathophysiological problem is the restriction of pulmonary blood flow due to increased pulmonary vascular resistance.

Some degree of pulmonary hypertension will be present with any significant lung disease (such as hyaline membrane disease, HMD); we usually use the term when there is significant pulmonary blood flow restriction and hypoxia due to:

1. pulmonary hypoplasia (e.g. diaphragmatic hernia, oligohydramnios)

2. increased pulmonary arteriolar muscle constriction (which may be sensitive to hypoxaemia and acidaemia)

— primary (i.e. no apparent cause) — once known as persistent fetal circulation

— secondary to lung disease, such as meconium aspiration syndrome or infection.

Management

• Cover for bacterial infection — give antibiotics.

• Hyper-oxygenation, paralysis and forced alkalosis are no longer routinely recommended.

• Optimise lung volume. Lung disease and ventilation-perfusion (V/Q) mismatch are important — get the lungs expanded first.

• Optimise circulation — correct any hypovolaemia, use inotropes.

• Pulmonary vasodilation — nitric oxide (NO) is the best agent (see below).

• With ventilation:

— make sure you have adequate PEEP (positive end expiratory pressure)

— aim for pre-ductal oxygen saturation SpO₂ of 90–94%

— PaCO₂ of 45–55 mmHg is adequate (PaCO₂ = partial pressure of carbon dioxide in arterial blood)

— high-frequency ventilation (HFV) may be needed to achieve adequate lung expansion.

• Confirm raised pulmonary artery pressures with echocardiography — this will also exclude congenital cyanotic heart disease.

Some neonatologists still chase hyperoxia and aim for SpO₂ (pre- or post-ductal) of 99–100% or high PaO₂ values.

Inhaled nitric oxide (iNO)

• Nitric oxide (NO) is a potent vasodilator and it can be added to the inspiratory line of the ventilator. Thus the NO in the inspired gases will get to the pulmonary arterioles and dilate them.

• It has an ultrashort half-life, so it does not get into the systemic circulation.

• There is a theoretical risk of platelet dysfunction, and you must monitor for methaemoglobinaemia (metHb is available on some gas machines; >5% is bad).

• Dose: use 10–20 ppm.

• Wean slowly when able, e.g. when FiO₂ is <0.4.

• Inhaled NO will be next to useless if there is significant atelectasis, V/Q mismatch and/or poor circulation.

Related

Pocket Notes on Neonatology 2e