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Constrictive and restrictive pulmonary hypertension in the newborn and infant
1Department of Pathology, Children's Hospital, Harvard Medical School, Boston, Massachusetts.
Insights
The newborn pulmonary circulation adapts rapidly after birth, but developmental issues can lead to persistent pulmonary hypertension in newborns. Understanding these adaptations is key to managing this condition.
Area of Science:
- Neonatal physiology
- Pulmonary vascular development
- Cardiopulmonary adaptation
Background:
- The pulmonary circulation in newborns is constricted and less dense than in older children.
- Pulmonary arterial dilatation and increased arterial compliance occur during adaptation to air breathing.
- The resistance segment of the pulmonary vasculature is located proximally in fetuses and newborns.
Purpose of the Study:
- To describe the normal development and adaptation of the pulmonary circulation in newborns.
- To identify the causes of persistent pulmonary hypertension in the newborn (PPHN).
- To characterize the role of vascular hyperreactivity in PPHN.
Main Methods:
- The study reviews the physiological changes in the pulmonary circulation from fetal to neonatal stages.
- It analyzes factors contributing to PPHN, including lung and vascular hypoplasia, abnormal muscularization, and adaptation failures.
- It discusses the concept of vascular hyperreactivity or "twitchiness" in immature pulmonary circulation.
Main Results:
- Pulmonary vascular bed expansion occurs through lumen growth and new artery formation, but alveolar and arterial multiplication can be dissociated.
- Persistent pulmonary hypertension in the newborn is linked to lung hypoplasia, abnormal arterial muscularization, failed adaptation, and hyperreactivity.
- Vascular hyperreactivity can lead to labile or fixed pulmonary hypertension unresponsive to dilators.
Conclusions:
- Normal pulmonary circulation undergoes rapid adaptation post-birth, involving arterial dilatation and compliance changes.
- Persistent pulmonary hypertension in the newborn arises from a combination of structural and functional abnormalities.
- Immature pulmonary vascular beds exhibit hyperreactivity, contributing to difficult-to-treat hypertension.
Abstract:
The normal pulmonary circulation is constricted at birth and, as judged by its low arterial density, is relatively more restricted than in the older infant and child. During adaptation to air breathing, pulmonary arterial dilatation occurs rapidly, but also the compliance of the resistance arterial segment increases. In the fetus and newborn, the resistance segment is proximal to the respiratory or alveolar surface. Further expansion of the pulmonary vascular bed occurs by growth in size of lumen diameter of existing arteries and growth of new ones. Multiplication of alveoli and arteries is relatively dissociated--alveolar density can increase normally without normal vascular multiplication. Persistent pulmonary hypertension of the newborn occurs because of (1) lung hypoplasia associated with hypoplasia of the vascular bed, usually affecting both size and number of units, (2) abnormal muscularization of intraacinar arteries before birth, causing restriction of vascular volume, (3) failure of the adaptation programs, and (4) hyperreactivity. Immaturity of the circulation is apparent as hyperreactivity or "twitchiness": this can be superimposed on each of the other types. A hyperirritable vascular bed can cause a labile and then a fixed pulmonary hypertension that does not respond to dilators.