2.1 Circulatory System

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  After fertilisation, the human heart starts to beat at a rate of about 65 beats per minute (BPM) during the fourth week of pregnancy. The rate rapidly increases to about 140–170 BPM at 6–7 weeks, and drops to 120–160 BPM in the second and third trimesters.

  
  
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  The placenta acts as the point of gas exchange. The umbilical vein transports oxygenated blood from the placenta away from the high-resistance pulmonary circuit to the low-resistance systemic circuit via the foramen ovale and ductus arteriosus.

  
  
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  The fetal blood is relatively hypoxaemic with a partial pressure of oxygen (pO₂) of 20–30 mmHg and oxyhaemoglobin concentration saturation of 75–85%.

  
  
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  The fetal circulation is a parallel system, while after birth the circulatory system is a series system.

2.2 Formation of Blood Cells

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  Formation of blood cells starts in the yolk sac and mesothelial layers of the placenta at about the third week of fetal development. Thereafter, the fetal mesenchyme and the endothelium of the fetal blood vessels take over, followed by the liver (by six weeks) and then the spleen and other lymphoid tissues (by the third month). Finally, from the third month onward, the bone marrow gradually becomes the principal source of the red blood cells, as well as most of the white blood cells, except for lymphocyte and plasma cell production, which occurs mainly in the lymphoid tissue.

  
  
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  The blood of the human fetus normally contains fetal haemoglobin (haemoglobin F). Its structure is similar to that of haemoglobin A except that the β chains are replaced by γ chains; that is, haemoglobin F is α₂ γ₂.

  
  
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  fetal haemoglobin is normally replaced by adult haemoglobin soon after birth.

  
  
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  The fetal haemoglobin has a higher affinity for oxygen. The oxygen content at a given pO₂ is greater than that of adult haemoglobin because it binds to 2,3-diphosphoglyceric acid (2,3 DPG) less avidly. Haemoglobin F is critical to facilitate movement of oxygen from the maternal to the fetal circulation, particularly at later stages of gestation where fetal oxygen demand increases.

  
  
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  Respiratory system: respiration does not occur during fetal life and the lungs remain almost completely deflated. This prevents the filling of the lungs with fluid and debris from the meconium excreted by the fetus’s gastrointestinal tract into the amniotic fluid.

  
  
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  Nervous system: the reflexes of the fetus involving the spinal cord and even the brain stem are present by the third to fourth months of pregnancy. However, those nervous system functions that involve the cerebral cortex are still only in the early stages of development, even at birth. Indeed, myelinisation of some major tracts of the brain is complete only after about one year of postnatal life.

2.3 The Gastrointestinal Tract

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  By midpregnancy, the fetus begins to ingest and absorb large quantities of amniotic fluid, and during the last two to three months, gastrointestinal function approaches that of the normal neonate. In addition, meconium starts to form from the thirteenth week onwards and is excreted into the amniotic fluid from around 16 weeks.

  
  
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  Meconium is composed of 98% water and 2% residues (mucus, epithelial cells, and other residues of excretory products from the gastrointestinal mucosa and glands) from the fetus. In addition, there are proteins, carbohydrates, lipids, phospholipids and urea; all of which aid in the growth of the fetus.

2.4 Amniotic Fluid

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  Normal pH is 7.0–7.5.

  
  
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  Amniotic fluid index (AFI) is the sum of the deepest vertical pools of amniotic fluid in four quadrants of the abdomen during scanning. The normal value is 5–25 and a median AFI is 14.

  
  
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  Oligohydramnios is when the AFI is <5. This can cause fetal abnormalities such as limb contractures, hypoplastic lungs and other deformities.

  
  
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  Severe oligohydramnios can cause Potter sequence characterised by clubbed feet, low-set ears, parrot-beak nose, cranial abnormalities, pulmonary hypoplasia and adrenal and genital hypoplasia.

2.5 The Renal System

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  fetal kidneys begin to function at about 16 weeks and the fetal urine contributes to the amniotic fluid.

  
  
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  By the second trimester, the fetal kidneys begin to excrete urine, accounting for about 70–80% of the amniotic fluid.

  
  
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  The renal control system for the regulation of blood pressure and other functions of the kidney are almost nonexistent until late fetal life and do not reach full development until a few months after birth.

4.1 Respiratory Readjustments at Birth

One of the most important immediate adjustments required of the infant is to begin breathing as there is a loss of the placental connection with the mother, which is the main source of metabolic support for the fetus.

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  Cause of breathing at birth: the neonate generally begins to breathe within seconds and has a normal respiratory rhythm within less than one minute after birth. Initiation of breathing probably results from the following:

  
  
  
  
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     1. Transient asphyxia, which develops immediately at the time of birth

     
     
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     2. Sensory impulses on the skin, which are triggered with the drop in temperature at birth

     
     
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     3. In a baby who does not breathe immediately at birth, hypoxia and hypercapnia provide additional stimulus to the respiratory centre and usually cause breathing within a minute after birth

  
  
  
  
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  Delayed or abnormal breathing at birth can lead to hypoxia: onset of breathing is likely to be delayed in babies (1) when mothers have been given general anaesthesia during delivery, (2) babies with birth trauma or following prolonged labour/delivery.

  
  
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  Degree of hypoxia that an infant can tolerate: in an adult, failure to breathe for just 4 minutes often causes death, but a neonate can survive a hypoxia of almost 10 minutes. Permanent and serious brain impairment often ensues if breathing is delayed more than 8 to 10 minutes.

  
  
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  Expansion of the lungs at birth: at birth, the walls of the alveoli are at first collapsed because of the surface tension of the viscid fluid that fills them. More than 25 mmHg of negative inspiratory pressure in the lungs is usually required to oppose the effects of this surface tension and to open the alveoli for the first time. Fortunately, the first inspirations of the normal neonate are extremely powerful, usually capable of creating as much as 60 mmHg negative pressure in the intrapleural space. But once the alveoli do open, further respiration can be affected with relatively weak respiratory movements, and surfactant keeps them from collapsing again.

  
  
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  Respiratory distress syndrome (RDS) of the newborn, or infant respiratory distress syndrome (IRDS), is caused when surfactant secretion is deficient: surfactant deficiency is an important cause of IRDS; also known as hyaline membrane disease. It is the serious pulmonary disease that develops in newborns born before their surfactant system is functional. Surface tension in the lungs is high, and the alveoli are collapsed in many areas (atelectasis). An additional factor in IRDS is retention of fluid in the lungs.

  
  
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  Surfactant, a phospholipid-protein complex, which is produced by type II pneumocytes and is deposited along the alveolar surfaces, also helps counteract alveolar surface tension and promote alveolar stability. As a result of the increasing effect of surfactant, less transpulmonary pressure is needed for subsequent breaths, and functional residual capacity is soon established.

  
  
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  Pulmonary blood flow increases as the lungs expand, and pulmonary vascular resistance declines under the influence of oxygen-mediated relaxation of the pulmonary arterioles. This increase in pulmonary blood flow in turn allows the patent foramen ovale and the patent ductus arteriosus to functionally close, thereby allowing further blood flow to the lungs.

  
  
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  The postnatal circulation is then that of a low-resistance pulmonary circuit and high-resistance systemic circuit, and the lungs assume the responsibility of gas exchange and oxygenation.