Birth and First Breath

• hCG during pregnancy

  • produced by trophoblast (syntrophoblast)
  • supports corpus luteum - oestrogen and progesterone up to 12 weeks
• oestrogen during pregnancy

  • complex synthesis involving placenta and fetus
  • declines sharply after birth
  • promotes connexin insertion between myometrial cells (strong, unified contractions)
  • stimulates oxytocin receptor insertion into myometrium (strong, unified contractions)
  • increase’s prostaglandin (PGE2) production (softens cervix)
• progesterone during pregnancy

  • from placenta after 12 weeks
  • concentration falls in last few days of pregnancy
  • inhibits uterine contractility (prevents foetal expulsion)
  • promotes cervical plug development (provides microbial barrier)
• oestrogen synthesis in pregnancy - complex pathway involving corticotropin-releasing hormone (CRH) from the placenta and the fetal adrenal
• relaxin

  • peptide produced by placenta (and corpus luteum)
  • increased greatly in last trimester
  • softens cervix (preparation for labour)
  • softens pelvic ligament (preparation for delivery)
• Triggering of labour is variable and unpredictable. Progesterone and CRH lead to membrane rupture and uterine contractions. Whichever starts first triggers the other in due course.
• LABOUR - 1st stage

  • cervix stretched to full dilaaction (10cm)
  • contractions are painful
  • Release of oxytocin in posterior pituitary by positive feedback
  • oxytocin stimulates further uterine contraction both directly and indirectly via PGF2a
  • Uterine contractions
  • Fetal head dilates cervix
• Prostaglandins G2 and H2 are produced from arachidonic acid by COX-1 and COX-2 enzymes. These become tissue-specific synthases PGE2, PGI2, PGD2, PGF2 and TXA2
• Prostaglandins are part of the eicosanoid system - local hormones for cell signalling derived from arachidonic acid. They are short-lived - synthesised and released almost immediately. They have a range of functions in labour/delivery, for example PGE2 relaxes cervix and PGF2a contracts the uterus.
• Synthetic oxytocin is used therapeutically to enhance uterine contractility thereby augmenting labour.
• Foetal oxygenation may be compromised during contractions. Uterine contractions produce extrinsic compression of the uteroplacental blood vessels, reducing flow and O2 delivery to the foetus.
• LABOUR - 2nd stage

  • Delivery of the foetus
  • Combination of uterine contraction (oxytocin-enhanced) and maternal effort
• LABOUR - 3rd stage

  • Delivery of the placenta after shearing off
  • uterine contraction compresses vessels to produce haemostasis (enhanced by oxytocin)
  • synthetic oxytocin or PGF2a used to enhance uterine contractility to treat post-partum bleeding
• Fetal respiration

  • In utero the fetal lungs are filled with amniotic fluid
  • after birth this must be eliminated and replaced with ventilation
  • The stimulus for the first breath is not certain, but involves mechanical stimulation and temperature change
• Immediately after birth new born takes first breath but needs to generate 40-100 cm negative pressure to draw in the air to inflate the lungs.

  First breath causes surfactant secretion to form a mononuclear layer and reduce the surface tension and improve complianc
• Fetal lung fluid

  • At the onset of labour, hormones decrease fetal lung production and initiate active reabsorption
  • Some lung fluid is forced out of the trachea as fetus passes through birth canal.
• Compliance

  • the ease with which something can be stretched
  • lungs are poorly compliant for initial inflation in a manner similar to a balloon
  • starting and sustaining initial lung inflation is therefore a challenge
• Surface tension

  • the tendency of liquid surface to pull together by molecular forces
  • responsible for creating a meniscus or droplets
  • surface tension in the fluid lining the alveoli reduces lung compliance and makes alveolar collapse more likely
• Pressure in alveolus is inversely proportional to the radius.
• Pulmonary surfactant

  • In normal neonate a lipoprotein surfactant is interspersed between the water molecules in the liquid lining the alveoli
  • this reduces surface tension, increases compliance and contributes to lung stability
  • also reduces risk of pulmonary oedema
  • secreted by type II alveolar cells
  • production increases markedly after 34 weeks
  • several hormones stimulate surfactant production: cortisol, thyroxine, prolactin
• Late surge of corticotropin-releasing hormone may trigger labour.
• Without surfactant: because pressure is inversely related to radius, the pressure in small alveoli is higher than in large ones, encouraging small alveoli to empty into large ones, leading to collapse at low lung volumes.

  With surfactant: as alveoli become smaller, the surfactant concentration increases. This lowers surface tension more in small alveoli than large ones. Pressure in all alveoli is equal creating lung stability.
• An hour after delivery, an infant born at 33 weeks gestation is noted to have an increasing respiratory rate, with a grunting pattern during expiration. A pulse oximeter is applied, which shows an oxygen saturation of only 84% (normal > 97%). What is the likely cause of this?

  Infant respiratory distress syndrome secondary to surfactant deficiency
• Surfactant deficiency - lung fields have a hazy ground glass appearance on x-ray
• Prevention of surfactant deficiency:

  • corticosteroid treatment to mother (ideally >24 hours pre-delivery reduces its incidence in prematurity
• Treatment for surfactant deficiency

  • oxygen
  • supportive continuous positive airway pressure (CPAP)
  • artificial ventilation, instillation of artificial surfactant
• Pneumothorax is a risk of ventilation requiring chest drain insertion and can be bilateral.
• If a baby is born prior to the development of type II pneumocytes, they will be unable to produce surfactant. As a result, they will have difficulty expanding their lungs to take their first breath.

  If a pre-term delivery is unavoidable or inevitable, the mother can be given glucocorticoids to stimulate surfactant production in the fetus.
• Labour (also known as parturition) is the physiological process by which a foetus is expelled from the uterus to the outside world. There are three separate stages, characterised by specific physiological changes in the uterus which eventually result in expulsion of the foetus. At this point, the foetus becomes known as a neonate.
• The exact process by which labour is initiated in humans is not fully understood. Throughout the third trimester, involuntary contractions of the uterine smooth muscle begin to occur - these are known as Braxton Hicks contractions. they occur irregularly and are thought to be a form of 'practice contraction' but they are not regarded as a part of labour.
• For labour to commence, cervical ripening needs to occur. Furthermore, the uterine myometrium needs to become more excitable. A woman is typically said to be in labour when regular, painful contractions lead to effacement and dilation of the cervix.
• Cervical ripening refers to the softening of the cervix that occurs before labour. Without these changes, the cervix cannot dilate.
• Cervical ripening occurs in response to oestrogen, relaxin and prostaglandins breaking down cervical connective tissue; prostaglandins are of particular importance. Prostaglandins are produced by the placenta, the uterine decidua, the myometrium and the membranes. Their synthesis increases throughout the third trimester as a result of an increase in the oestrogen:progesterone ratio.
• Cervical ripening involves:

  • a reduction in collagen
  • an increase in glycosaminoglycans
  • an increase in hyaluronic acid
  • reduced aggregation of collagen fibres

  The cervix offers less resistance to the presenting part of the foetus during labour.
• The relative decrease in progesterone in relation to oestrogen that occurs towards the end of pregnancy helps to facilitate an increase in the excitability of the uterine musculature. This is because progesterone typically inhibits contractions and oestrogen increases the number of gap junctions between smooth muscle cells, increasing contractility. Mechanical stretching of the uterus also helps to increase contractility - this means as the foetus grows, the contractility of the muscle increases.
• Oxytocin is responsible for initiating uterine contractions. Throughout pregnancy it has limited action as there are a low number of oxytocin receptors and it is inhibited by relaxin and progesterone.
• At around 36 weeks gestation, under the influence of oestrogen there is an increase in the number of oxytocin receptors present within the myometrium. This means the uterus begins to respond to the pulsatile release of oxytocin from the posterior pituitary gland.
• Oxytocin production is increased by afferent impulses from the cervix and vagina. This means that contractions result in a positive feedback loop to the posterior pituitary gland to release more oxytocin, leading to stronger contractions which then drives the process of labour. This is known as the Ferguson reflex.
• The first stage of labour results in the creation of the birth canal and lasts from the beginning of labour until the cervix is fully dilated. The maximum size of the birth canal is determined by the pelvix - the pelvic inlet is typically around 11cm but this may increase slightly during pregnancy as ligaments soften under the influence of hormones.
• Throughout the first stage contractions will occur every 2-3 minutes. If foetal membranes have not already ruptured, they do during this stage. It consists of two phases:

  • latent phase - slow cervical dilation over several hours which lasts until the cervix has reached 4cm dilation
  • active phase - faster rate of cervical dilation until 10cm reached, typical rate around 1cm/hr in nulliparous women and 2cm/hr in multiparous women. Should not normally last longer than 16 hours

  once the cervix is dilated the foetal head is able to descend, remaining flexed to maintain smallest diameter possible