Aetiology

In the fetus, the ductus arteriosus diverts cardiac output away from the lungs towards the placenta to support systemic oxygenation.[10]​ The fetal ductus has intrinsic tone and its patency is maintained by a low-oxygen environment and dilating factors (circulating prostaglandins produced by the placenta [PGE2 and PG12], nitric oxide, adenosine, atrial natriuretic peptide, carbon monoxide, and potassium channels).[10][11]​​​​ After birth, systemic oxygen saturation increases with the onset of breathing, contributing to the constriction of the ductus through potassium-mediated channels.[12][13]​​​ Postnatally, the level of circulating prostaglandins falls as the placenta is removed from the circulation. In addition, pulmonary blood flow increases, resulting in increased metabolism of prostaglandins. There may be several other unknown factors that contribute to ductal closure.[11][14]​​​ Haemodynamic constriction is later followed by complete structural closure mediated by histological changes that obliterate the ductal lumen.[15]

While the process of ductal closure is fairly well understood, the factors that result in persistence of the ductus are less clear. Emerging research reveals that genetic predisposition and intrauterine inflammation play critical roles in affecting the neurodevelopmental of children with congenital heart disease, indicating a significant interplay between genetic and environmental factors in brain development.[9] ​The incidence of patent ductus arteriosus (i.e., an open ductus beyond the first 3 postnatal days) exceeds 50% in preterm infants ≤28 weeks’ gestational age.[10] In preterm infants, there may be a decreased response to oxygen and a continued sensitivity to prostaglandins compared with full-term infants, in addition to generalised immaturity of the smooth muscle.[10][16][17]​​​​​ On histological examination, differences between the tissue of a persistent ductus versus a physiological ductus have been noted and suggest an anatomic reason for persistence.[15]

Pathophysiology

The pathophysiology occurs as a result of shunting of blood from the aorta to the pulmonary artery across this persistent vascular connection. After birth, pulmonary vascular resistance falls, while systemic resistance remains unchanged, leading to left-to-right shunting through the patent ductus arteriosus (PDA). The degree of shunting, and thus the clinical presentation, depends on both the systemic-to-pulmonary artery pressure ratio and the size of the ductus.[18]​ A small ductus in the setting of near systemic pulmonary pressures will have limited flow. However, a larger ductus will have less resistance to flow and will initially be associated with a greater degree of shunting as pulmonary resistance falls in the newborn period. This will result in an increase in left ventricular volume, increased left ventricular output, and pulmonary over-circulation.[19] Increased blood flow to the lungs leads to decreased pulmonary compliance and increased work of breathing. With the increased pre-load, the left ventricle dilates and left ventricular end diastolic pressures and left atrial pressures increase. The increase in left-sided cardiac pressure inhibits pulmonary venous return, furthering pulmonary congestion.

The effects of pulmonary over-circulation and systemic steal are most pronounced in preterm infants. Increased pulmonary blood flow not only leads to pulmonary oedema, but also to pulmonary haemorrhage, respiratory distress syndrome, and bronchopulmonary dysplasia.[20][21][22][23]​ Decreased systemic perfusion may be responsible for the increased incidence of necrotising enterocolitis and interventricular haemorrhage seen in preterm infants with PDA.[24]​​[25]​​ Additionally, a large PDA can impact myocardial perfusion by decreasing diastolic blood pressure. This, along with the shorter diastolic time caused by compensatory tachycardia, can reduce coronary artery blood flow.[26]

Classification

Small, moderate, or large

  • If the ductus is widely patent, such that the vessel itself provides no resistance to flow, then it is considered large. The amount of shunting across a large PDA will be dependent upon the relative pulmonary and systemic vascular resistance. A large ductus is usually of equal or greater diameter than one of the proximal branch pulmonary arteries.

  • A moderate-sized ductus will provide some resistance to flow. However, the amount of shunting will be great enough to result in some degree of left atrial dilation.

  • A small ductus will significantly restrict flow such that there will be no dilation of the left atrium or left ventricle.

Overt or silent

While some patients with patent ductus arteriosus (PDA) may present with overt clinical features, others may present with no signs or symptoms; this is referred to as a silent PDA. A murmur is absent. The ductus becomes evident as an incidental finding when an echocardiogram is performed for another purpose. There has been some controversy over the treatment of a silent PDA.

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