Serial cardiac ultrasound has given us a window on circulatory transition, both normal and abnormal. Preterm birth is not physiological so physiology has to be assessed in well term babies. Pulmonary blood flow increases with the first breath as resistance falls and these balance each other so that the fall in pulmonary artery pressure (PAP) over the first 4–6 h of life is modest. So, early on, well babies will have PAPs close to systemic pressures confounding early assessment for pulmonary hypertension.
The ‘pulmonary ischaemia’ model of RDS originated from early studies when RDS was a different disease. PAP will fall more slowly in preterm babies ventilated with RDS but, in most preterm babies, PAP is below systemic BP even in the early hours after birth. Thus the impact is too much blood in the pulmonary circulation due, not pulmonary ischaemia from high vascular resistance and blood bypassing the lungs.
There are exceptions to the above, particularly babies with severe RDS, congenital pneumonia or those born after prolonged oligohydramnios, in whom raised PAP is a consistent finding. Oligohydramnios babies are not common, so have been a difficult group to study systematically but several case series have described this as well as the responsiveness of this group to iNO.
There seems to be sub-clinical persistent raised pulmonary vascular resistance in many babies with chronic lung disease. The significance of this is uncertain but in the most severe cases, pulmonary hypertension can be an important component of the disease.
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