1.4. The transition from intra-uterine to extra-uterine life
To appreciate the reasons why a newly born infant may require more than routine care following birth it is imperative to have at least a basic understanding of the physiological changes that need to occur in order for an infant to undergo a successful transition from intra-uterine to extra-uterine life. The boxes below compare fetal life in utero, where the fetus is entirely dependent upon its mother and the function of the placenta for survival, to extra-uterine life, where the newborn must take over the role of oxygenation in order to survive.
Features of intra-uterine (fetal) life
- Oxygen diffuses across the placental membrane from the mother’s blood to the fetus.
- The fetal alveoli are expanded, but are liquid filled.
- Blood flow to the fetal lungs is minimal (~8%) as the lungs do not act as a source of oxygenation or carbon dioxide removal.
- The blood vessels perfusing the fetal lungs are constricted.
- Due to the increased resistance to flow in the constricted vessels in the fetal lungs, blood from the right side of the heart (~ 92%) takes the path of lower resistance across the ductus arteriosus into the aorta and to the systemic circulation.
- Fetal SpO2 is approximately 50 – 60%, dropping to an intrapartum mean of 40 – 50%, (East, Colditz, Begg & Brennecke, 2002; East, 2008) hence it is normal for a healthy newborn infant to appear cyanotic in the first few minutes after birth.
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TRANSITION TO EXTRA-UTERINE LIFE |
Features of transition to extra-uterine (post-natal) life
- The umbilical arteries and umbilical vein constrict and are then clamped.
- The placental circulation ceases (thus no longer provides oxygen) and systemic vascular resistance rises as a result.
- To survive, the newborn must take his/her first breath to initiate the complex series of events that switch gas exchange from the placenta to the lungs.
- The normal newborn will make vigorous efforts to inhale air into the lungs.
- The hydrostatic pressure created during inspiration causes fetal lung liquid to move out of the alveoli and into the surrounding lung tissue. This can occur rapidly: within 5 to 10 breaths.
- The liquid is cleared from the tissue via the blood vessels and lymphatics but this occurs much more slowly (1 to 4 hours) and may impede ventilation during this time.
- An osmotic gradient induced by sodium re-absorption is also thought to assist in liquid movement into the lung tissue (this mechanism is immature in premature infants).With the onset of effective ventilation there is an eight to tenfold increase in blood flow to the lungs due to a very large decrease in pulmonary vascular resistance.
- Pulmonary capillary recruitment and relaxation of blood vessels caused by lung aeration and increased blood oxygen content are mostly responsible for the decrease in pulmonary vascular resistance.
- The decrease in pulmonary vascular resistance and increase in systemic vascular resistance reverses the pressure gradient across the ductus arteriosus, resulting in shunting of blood from the aorta into the pulmonary circulation which contributes to pulmonary blood flow (Crossley et al., 2009).
- These combined changes, along with biochemical factors that control constriction of the smooth muscle of the ductus, eventually leads to closure of the fetal cardiovascular shunts.
- In healthy, full term infants, functional closure of the ductus begins within hours of birth, with 20% of ducts closed by 24 hours, 82% by 48 hours and 100% by 96 hours (Briton, 1998).
- The transition from fetal to extra-uterine life is then complete.
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Table 1: Comparison of fetal and postnatal circulation
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Vascular resistance |
Shunts |
PO2 |
SpO2 |
FETAL |
High pulmonary
Low systemic |
Ductus arteriosus |
15-25 (Umbilical artery)
32-35 (Umbilical vein) |
~50 – 60%
Falling to an intrapartum mean of 40 – 50% |
Ductus venosus |
Foramen ovale |
POSTNATAL |
Low pulmonary
High systemic |
No shunts |
50-80 mmHg |
>90% by 10 minutes of postnatal age
(pre-ductal) |
Adapted from Sansoucie & Cavaliere, 1997, p. 6 |
Oxygen saturations after birth
With the rise in blood oxygen content over the first few minutes of life, arterial oxygen saturation (SaO2) will rise. Recent studies have demonstrated that in healthy, uncompromised newborns, oxygen saturation rises from intrapartum levels of 40- 50%, increasing to a mean of 60% by one minute of age and reaching a mean of 90% by seven to ten minutes of post natal age when measured via pulse oximetry (SpO2). (Dawson, et al., 2007).
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Newborn infants who are breathing effectively and have a heart rate above 100 bpm do not require supplemental oxygen to “pink them up” during the first ten minutes after birth.
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