Fetal circulation
The mixed IVC blood, with a saturation of 65%, enters the right atrium, but only one-third passes into the right ventricle. The majority is directed through the foramen ovale to the left atrium and left ventricle to supply the heart, brain and upper body with relatively oxygenated blood. Venous blood from the superior vena cava, with low saturation (25%), is directed preferentially to the right ventricle and pulmonary artery. In the fetus, pulmonary vascular resistance (PVR) is high, and less than 10% of cardiac output passes through the lungs. This is achieved by intense vasoconstriction in the pulmonary arterioles and patency of the ductus arteriosus, which allows the majority of blood passing into the pulmonary artery to join the aorta. This mixed aortic and ductal blood flow supplies the lower body with blood with a saturation of approximately 55%. Blood returns to the placenta via two umbilical arteries arising from the internal iliac arteries. Placental blood flow is large, comprising 60% of the fetal cardiac output.
Newborn circulation
At birth, with onset of spontaneous ventilation in the lungs and loss of the placenta, the circulation changes dramatically. The first breath generates a negative pressure of approximately 50 cmH2O, drawing in about 80 mL of air and expanding the functional residual capacity. Pulmonary vascular resistance (PVR) falls rapidly, allowing blood to flow from the right ventricle through the lungs. As placental flow ceases with clamping of the umbilical cord, systemic vascular resistance (SVR) rises. The result is a reversal of right-to-left flow through the ductus arteriosus. Exposure to oxygenated blood and reduced prostaglandin-E2 production stimulates ductal constriction, with functional closure in the majority of newborns by 24 hours. A shunt murmur may be audible prior to closure. Histological obliteration occurs by 3 weeks in most normal term infants. Preterm babies have a higher incidence of patent ductus arteriosus, and may require medical treatment with indomethacin, or surgical ligation. The ductus venosus closes passively, due to absent blood flow.
After the first breath, pulmonary venous blood returns to the left atrium, causing pressure in the left atrium to exceed that in the right. This effect on raised left atrial pressure is enhanced by the sudden rise in SVR from loss of the placental blood flow. The valve-like foramen ovale closes, thus preventing deoxygenated blood from the right atrium crossing to the left.
Although the PVR is reduced after birth, it continues to fall for several days after birth, and the pulmonary arteriolar medial walls remain very muscular. This muscle layer reduces considerably over the first few months and becomes thin-walled and elastic with little muscle by 6 months. However, immediately after birth, resistance in the pulmonary circuit is higher than in adults and the pulmonary arterioles remain very reactive. If the neonate becomes hypoxic, hypercapnic or acidotic, pulmonary vasoconstriction can lead to raised right-sided pressures and significant shunting through the foramen ovale, and reversion to a fetal-type circulation. This condition is called persistent pulmonary hypertension of the newborn (PPHN). Oxygen, hyperventilation or nitric oxide may be needed to reverse the condition, and extracorporeal membrane oxygenation (ECMO) has been successfully used in severe and persistent cases.
Fetal and newborn circulation
The placenta supplies oxygen and nutrients to the fetus via an umbilical vein, and removes carbon dioxide and waste via two umbilical arteries.
Fetal circulation depends on three shunts to direct the best oxygenated blood to the upper body (foramen ovale), to bypass the underdeveloped liver (ductus venosus), and to bypass underdeveloped lungs (ductus arteriosus and foramen ovale).
Following delivery and the first breath, PVR decreases rapidly, allowing blood to flow through the lungs, from the RV to LA. This reverses the pressure gradient across the foramen ovale and closes it.
SVR increases after delivery, reversing the pressure gradient and flow in the ductus arteriosus.
Blood flow through the liver increases, and the flow is decreased through the ductus venosus, which closes spontaneously.
The heart
The newborn heart consists of cardiac myofibrils that are poorly organised and lack the structured architecture of the mature heart. The increased ratio of connective tissue to contractile tissue compared to adults results in limitation in myocyte contractility and ventricular compliance. In addition, calcium metabolism is immature in neonatal myocytes. Consequently there is a relatively flat Starling curve, and while inadequate preload is poorly tolerated, overloading results in early cardiac failure.
Ventricular end-diastolic volume increases from 40 mL m–2 body surface area at birth to 70 mL m–2 in children over 2 years of age. Normal heart rate at birth ranges from 100 to 170 beats per minute, decreasing with age and reaching adult values by puberty (Figure 24.2). The preterm neonate has significantly lower blood pressure than the term infant, and adult levels are not reached until adolescence.
| Age | Systolic BP (mmHg) | Diastolic BP (mmHg) | Heart rate (beats min–1) |
|---|---|---|---|
| Preterm 750 ga | 45 | 25 | > 120 |
| Birth | 60 | 35 | > 120 |
| Neonate | 70–80 | 40–50 | 120–150 |
| 3–6 months | 80–90 | 50–60 | 120–140 |
| 1 year | 90–100 | 60–80 | 110–130 |
| 5 years | 95–100 | 50–80 | 90–100 |
| 12 years | 110–120 | 60–70 | 80–100 |
a Mean arterial BP ≤ gestational age in weeks is a good rule of thumb for preterm infants.
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