The majority of neonates successfully transition from intrauterine to extrauterine life without or with only limited assistance


The majority of neonates successfully transition from intrauterine to extrauterine life without or with only limited assistance (Michel & Lowe, 2017). Nevertheless, a small percentage of neonates experience disturbances and display signs of hypotension, hypoxia, hypercarbia, hypoglycaemia and hypothermia.This assessment reviews normal fetal and neonatal circulation, and issues preterm infants may experience during the transition period.

Fetal circulation
In utero, the placenta is the principal site of gas and metabolic exchange for foetus (Hillman, Kallapur, & Jobe, 2012). Oxygenated blood flows to the fetus through the umbilical vein, via the ductus venosus (DV) and enters the inferior vena cava and into the right atrium and ventricle (Askin, 2009; Assali, 2013). The majority of blood flows directly through the foramen ovale (FO) to the left atrium and ventricle, and from there into the ascending aorta (Askin, 2009; Assali, 2013). It is then primarily directed to the fetal heart and brain (Gupta & Paria, 2016). Deoxygenated blood from the head and upper extremities comes back to the right atrium through the superior vena cava, where it blends with oxygenated blood in right atrium and right ventricle (Assali, 2013). Blood then is pumped into the pulmonary artery where 90% of blood is then shunted across the ductus arteriosus (DA) into the descending aorta, providing oxygen to the lower half of the fetal body (Assali, 2013). Blood then eventually drains back to the placenta through the two umbilical arteries (Assali, 2013). The remaining 10% of the blood coming from the right ventricle perfuses lung tissue to meet metabolic needs (Yigit, Kowalski, Hutchon, & Pekkan, 2015).

Neonatal Circulation
At birth, the clamping of the umbilical cord eliminates the placenta to provide blood and nutrition to the foetus (Evans, 2016). It also trigers an increase in systemic vascular resistance (SVR), and leads to an increase in pressure in the left side of the heart (Michel & Lowe, 2017). Blood from high pressure in left trium into left ventricle pumped into aorta and continue to the low pressure system circulation (Evans, 2016; Hillman et al., 2012) .The deoxygenated blood from the Superior Vena Cava comes into right artrium and right ventricle and to low pressure pulmonary vasculary resistance (PVR) lung (Michel & Lowe, 2017). The infant’s first breath after birth fills the air sacs, and the capillary network surrounding air sacs dilate. The rise in the partial pressure of arterial oxygen decreases PVR (Graves ; Haley, 2013). Clamping of the corld and the subsequent increase SVR also cause the constricton of the DA (Evans, 2016). Oxygenated blood comes via the pulmonary vein to the left atrium and left ventricle , and through to the aorta and into systemic circulation (Evans, 2016). The clamping of the placenta also removes the need for blood flow through the DV. Systemic venous blood flow is directed through the portal system for hepatic circulation (Michel ; Lowe, 2017).

For some preterm babies, the failure of success of this transition can be life threatening. If immediate cord clamping after birth is used, occlusion of the umbilical vein causes an abrupt drop in right ventricular venous return; decreasing preload by 40 to 50% (Michel ; Lowe, 2017). Further more, occlusion of the umbilical arteries results in the elimination of blood flow to the low resistance placental circulation, which in turn leads to an immediate increase in left ventricular afterload (Hooper et al., 2016). Both the decrease in preload and the increase in afterload negatively affect cardiac contractility (Wu, Azhibekov, ; Seri, 2016; Yigit et al., 2015). Due to the immaturity of the myocardium of preterm baby, the myocardium is forced to generate significantly higher cardiac output with limited cardiac reserve. This sets the stage for a hypoperfusion-reperfusion cycle. Cardiac function is depressed, with decreased stroke volume and cardiac output, leading to cardiogenic shock (Wu et al., 2016)

Hypercarbia – the retention of carbon dioxide (CO2) is due to abnormally elevated carbon dioxide levels in the blood (Wu et al., 2016). In a normal healthy neonate, adequate blood supply and high oxygen saturation through effective ventilation post birth, enable healthy neonates to successfully eliminate CO2 through well developed and ventilated lungs soon after birth occurs (Su, Lin, Huang, Tsai, ; Huang, 2016). The increased left atrial pressure and blood return, as well as high oxygen level in the blood, cause the FO and ductus arteriosus (DA) to close (Schwaberger et al., 2015). Preterm newborns often exhibit immature lungs, surfactant deficiency, an unstable thoracic cage, and weak respiratory muscles, and are, therefore, unable to effectively ventilate (Evans, 2016). Further, infants’ ductal closure is often significantly delayed, resulting in spontaneous shunting of blood between the systemic and pulmonary circulations (Evans, 2016). Decreased oxygen supply results in hypoxaemia, and less well oxygenated tissues become more hypoxic (Schwaberger et al., 2015).

Compared to term infants, preterm babies have relatively thin skin, lack brown fat deposition, and higher body-surface ratio increases their heat loss (Rajani, Chitkara, & Halamek, 2009). They therefore have limited ability to maintain normal body temperature and become hypothermic (Rajani et al., 2009). Due to cold stimulation, the brain sends out norepinephrine. Norepinephrine causes peripheral vasoconstriction, and the blood is shunted to the core of the body (Rajani et al., 2009). Vasoconstriction of the peripheral circulation also causes vasoconstriction of the pulmonary system. Decreased oxygen supply cause hypoxaemia and tissues become hypoxic (Hillman et al., 2012). Therefore, the body urgently needs to resort to anaerobic metabolism and utilize glycogen to keep warm. This leads to lactic acid accumulation, and pH drops. The neonate becomes acidotic (Hillman et al., 2012). In addition, most of preterm babies only have minimal glycogen and fat stores (Assali, 2013). After delivery and cord clamping, the plasma glucose levels fall without tranfer plasma glucose from placenta. The preterm baby has a tendency to be hypoglycaemic, which is exacerbated by hypothermia (Hillman et al., 2012).

Cardiovascular changes in premature infants during the transitional period are dynamic and complex. Premature infants are born with limited capacity to adjust to the haemodynamic challenges in the immediate postnatal period. Compromised systemic circulation is associated with the development of a number of short- and long-term complications. Further research may be needed to increase understanding and further improve care.