L18 RDA Transition at birth

Overview

Birth requires the newborn to switch, within minutes, from placental gas exchange to air breathing. The lecture follows that sequence: endocrine priming before labour, clearance of foetal lung fluid, the first breath and surfactant, the switch from foetal to postnatal circulation, oxygen carriage and haemoglobin, and thermoregulation. It then covers how transition is assessed and supported (Apgar, Newborn Life Support), what goes wrong (poor respiratory effort, birth hypoxia, airway obstruction, impaired lung function, persistent pulmonary hypertension, congenital heart disease) and the common postnatal complications: sepsis, jaundice, hypoglycaemia and prematurity.

Neonatal transition: what has to change

Newborns adapt across five domains: pulmonary function and lung mechanics, cardiovascular circulation, respiratory control, energy metabolism, and thermoregulation.

Most infants transition without help:

• about 10% require some form of medical intervention
• about 1% need advanced resuscitative support

Key requirements for successful transition:

• endocrine priming beginning before birth
• effective clearance of foetal lung fluid to allow air entry
• initiation of spontaneous breathing to establish functional residual capacity
• lung expansion and establishment of pulmonary gas exchange
• cardiovascular transition from foetal to postnatal circulation, including closure of shunts
• adjustment of oxygen tension, saturation and haemoglobin oxygen affinity

Endocrine priming

Physiological preparation begins as early as 35 weeks’ gestation. Cortisol rises by about 50% between 35 weeks and term, driving organ maturation, and rapid hormonal and physiological changes during labour and delivery prime the fetus for extrauterine life.

Cortisol surge: levels increase fourfold during labour and peak in the hours after delivery. It promotes:

• lung maturation and surfactant production
• gastrointestinal development and readiness for enteral feeding
• regulation of energy metabolism, particularly glucose homeostasis
• thyroid hormone activation, supporting thermoregulation and metabolism
• activation of epithelial sodium channels in the lung, facilitating alveolar fluid clearance

Catecholamine surge: adrenaline and noradrenaline are released from the adrenal during labour and delivery, and act to:

• increase systemic vascular resistance, supporting the shift to postnatal circulation
• raise plasma glucose, ensuring energy availability
• initiate thermogenesis, enabling independent temperature regulation

Lung fluid: production, then clearance

Production and swallowing of amniotic fluid are essential for normal lung growth; inadequate production or swallowing causes pulmonary hypoplasia. Foetal lungs are filled with fluid derived from swallowed amniotic fluid and from active secretion by the airway epithelium driven by chloride ion transport. This fluid maintains lung expansion and supports structural maturation in utero.

As labour approaches, cortisol switches the epithelium from fluid production to active resorption:

1. Airway epithelium reabsorbs fluid by active sodium transport, with water following sodium passively into the interstitium.
2. Because this starts before birth, substantial clearance has already occurred by delivery.
3. At birth, rising oxygen tension enhances epithelial capacity for fluid reabsorption.
4. Inspiratory pressure from the first breaths drives further fluid out of the alveoli, aiding aeration.

The lecture diagram makes the same point as a two-state shift: a “lung growth” state (interstitial fluid movement via active chloride transport) becomes an “alveolar fluid clearance” state (alveolar fluid into the interstitium via active sodium transport, water following), with increased cortisol as the arrow between them.

Failure of clearance: rapid deliveries allow less time for reabsorption, which can cause transient tachypnoea of the newborn.

• most common respiratory disorder of newborns
• caused by retained foetal lung fluid
• symptoms: tachypnoea, increased work of breathing, grunting, retractions, oxygen requirement
• self-resolving, but may require respiratory support

Initiation of breathing and surfactant

Initiation of breathing is the most crucial step in transition. The switch from intermittent foetal breathing movements to continuous postnatal respiration happens almost instantaneously, triggered by:

• umbilical cord clamping
• tactile stimulation
• rapid changes in pO2 and pCO2

Most infants breathe spontaneously, signalled by a vigorous cry, and need no intervention. In the delivery room the cry guides immediate decisions: a crying baby is likely stable; a silent baby may need prompt resuscitative support.

Mechanics of the first breaths:

1. Baby cries, chest wall expands, intrathoracic pressure becomes more negative, air enters the lungs.
2. Increased inspiratory pressure expands alveoli, increasing surface area for gas exchange and improving oxygenation.
3. Lung expansion stimulates surfactant production, which reduces alveolar surface tension, improves compliance and enhances oxygenation efficiency.

Surfactant reduces surface tension at the alveolar air-fluid interface and prevents alveolar collapse during breathing cycles. At birth, alveoli stretch as they fill with air, which triggers surfactant secretion. Regulation: labour onset stimulates production, and catecholamine release enhances secretion.

Lack of surfactant: preterm infants may have immature lungs producing insufficient surfactant, leading to respiratory distress syndrome (RDS), a significant cause of preterm mortality and morbidity. Artificial surfactant (1989) increased preterm survival.

Hypoxia suppresses respiratory drive. Common causes of perinatal hypoxia: maternal haemorrhage, birth asphyxia, nuchal cord (cord wrapped around the neck), meconium aspiration, placental abruption. Severe hypoxia can cause complete apnoea and severe bradycardia, and without rapid intervention can result in neonatal death.

Foetal circulation and the circulatory switch

In the fetus the placenta is the primary site of oxygen and carbon dioxide exchange: it has the lowest vascular resistance and receives about 40% of foetal cardiac output. The lungs contribute nothing to gas exchange: they have the highest vascular resistance and receive about 10% of cardiac output.

	Foetal	Postnatal
Pulmonary vascular resistance	High	Low
Systemic vascular resistance	Low	High
Venous return	Majority bypasses lungs	All directed to lungs

Foetal circulation as drawn: oxygenated blood from the placenta travels via the umbilical vein and ductus venosus into the IVC and the heart, streams through the foramen ovale and is preferentially directed via the ascending aorta to the brain (26%) and coronary arteries (3%). Deoxygenated blood returns via the SVC. With high PVR only about 8% of output reaches the lungs; with low SVR most flow passes through the ductus arteriosus to the placenta (41%) and lower body (22%), returning via the umbilical arteries. Postnatally the same schematic shows low PVR, pulmonary flow of 100% and high SVR.

Warning

On the postnatal version of the circulation schematic the PVR, SVR and lung-flow labels appear superimposed on the previous slide’s values (struck-through text), so the exact final wording of those labels is ambiguous in the transcript.

Sequence of the circulatory transition:

1. Umbilical cord clamping removes the placenta from the circulation.
2. Lung expansion reduces pulmonary vascular resistance.
3. Pulmonary blood flow increases significantly.
4. Catecholamine surge raises systemic vascular resistance and blood pressure.
5. Closure of the foetal shunts begins: ductus arteriosus (PDA) and foramen ovale (PFO).
6. Transition to postnatal (adult-type) circulation is complete.

Oxygenation and haemoglobin

The fetus needs less oxygen because of lower metabolic demands, and the organs with the highest oxygen demand preferentially receive the highest-oxygen-content blood:

• liver: supplied directly from the umbilical vein without mixing with deoxygenated blood
• brain and heart: supplied by blood streaming through the foramen ovale into the ascending aorta

Foetal haemoglobin (HbF) must extract oxygen from maternal haemoglobin and deliver it to tissue:

• high oxygen affinity, promoting transfer from maternal to foetal haemoglobin and allowing effective extraction across the placental barrier
• low affinity for 2,3-bisphosphoglycerate (2,3-BPG), increasing oxygen-binding capacity
• low foetal oxygen tension, promoting unloading at tissue level and stimulating angiogenesis
• high foetal haematocrit, enhancing overall oxygen-carrying capacity

After birth production switches from HbF to adult haemoglobin (HbA), which must extract oxygen from alveoli and deliver it to tissue:

• low oxygen affinity, promoting transfer from haemoglobin to tissues
• high affinity for 2,3-BPG, decreasing oxygen-binding capacity at tissue level
• high oxygen tension, promoting loading at the alveoli

Thermoregulation

The infant is at high risk of hypothermia, which increases the risk of hypoglycaemia. Mechanisms:

• large surface area to body mass ratio
• decreased subcutaneous fat
• inability to shiver
• immature skin, causing increased evaporative water and heat loss

The aim is to minimise energy consumption and maximise metabolic efficiency, which decreases oxygen use and conserves energy for growth and basic functions. Practical measures: check temperature after birth, skin to skin with mother or father, keep dry, keep wrapped, use a hat. Where an infant cannot be kept warm this way, an artificial heat source (incubator) is used.

Transition is complete when: the baby is breathing spontaneously, the lungs are clear of fluid, the lungs are expanded and air filled, blood flow to the lungs has increased, oxygen saturations have normalised, and the baby is thermoregulated and skin to skin with the mother.

Assessing and supporting transition

The clinician’s role after birth is to support the infant through a difficult transition. Neonatal Life Support (NLS) is a standardised newborn resuscitation pathway, followed at every birth attended by perinatal staff; all deliveries should have an NLS-certified person in attendance.

Apgar score: developed by Virginia Apgar in 1952, it objectively scores infants on 5 criteria at 1, 5 and 10 minutes to determine whether further resuscitation is needed. Normal >7, concerning 4-6, critical 3 or less.

Acronym	Sign	0	1	2
Appearance	Colour	Blue, pale	Body pink, extremities blue (acrocyanosis)	Body completely pink
Pulse	Heart rate	Absent	Below 100 bpm	At or above 100 bpm
Grimace	Reflex irritability	No response	Grimace, some response	Cough, sneeze, cry
Attitude	Muscle tone	Flaccid, limp	Some flexion of extremities	Well flexed extremities
Respirations	Respiratory effort	Apnoea	Weak cry, hypoventilates	Good strong cry and spontaneous breathing

A worked example from the lecture: heart rate 150 bpm scores 2, colour 1, respirations 2, tone 2, reflex 2, giving an Apgar of 9.

First step of NLS, three questions:

• Is the infant full term?
• Does the infant have good muscle tone?
• Is the infant breathing or crying?

Yes to all three means no further support: infant skin to skin with mother. No to any question means proceeding down the NLS pathway.

NLS pathway, with interventions determined by heart rate:

1. At all stages ask: do you need help?
2. If not vigorous: maintain temperature, ensure an open airway, stimulate; assess heart rate and breathing at 1 minute.
3. Heart rate <100 bpm, gasping or apnoeic: positive pressure ventilation with SpO2 monitoring.
4. Heart rate still <100 bpm: ensure open airway, consider intubation or laryngeal mask, increase pressure and oxygen.
5. Heart rate <60 bpm on PPV: chest compressions, three compressions to each breath, 100% oxygen, consider intubation or laryngeal mask, obtain venous access.
6. Heart rate still <60 bpm: IV adrenaline, consider volume expansion, then post-resuscitation care.

Targeted pre-ductal SpO2 after birth: 1 min 60-70%, 2 min 65-85%, 3 min 70-90%, 4 min 75-90%, 5 min 80-90%, 10 min 85-90%.

IV adrenaline 1:10,000 by gestation: 23-26 weeks 0.1 mL; 27-37 weeks 0.25 mL; 38-43 weeks 0.5 mL. Dose range 10-30 microg/kg (0.1-0.3 mL/kg).

Important

Positive pressure ventilation is the most effective intervention: it generates tidal volume, provides a respiratory rate during apnoea, increases alveolar surface area and improves oxygenation, allowing re-initiation of spontaneous breathing. Improvement is almost always seen with effective PPV, and effective PPV means visible chest movement.

Difficulties in transition and their risk factors

Causes of difficult transition: poor or absent respiratory effort, delayed clearance of foetal lung fluid, airway obstruction, impaired lung function, persistently increased pulmonary vascular resistance, abnormal cardiac function or anatomy, congenital anomalies, prematurity.

Risk factors, by category:

• Maternal conditions: diabetes, hypertension, history of substance use, previous stillbirth, foetal loss or early neonatal death
• Foetal conditions: prematurity (<37 0/7 weeks), post maturity (>41 weeks), congenital anomalies, multiple gestations
• Pregnancy complications: placenta praevia, oligohydramnios, polyhydramnios, pregnancy induced hypertension, gestational diabetes
• Birth complications: breech presentation, chorioamnionitis, meconium at birth, birth asphyxia, caesarean section, instrumental delivery (forceps, vacuum)

Decreased respiratory effort and birth hypoxia

Causes of impaired respiratory effort:

• mild: exposure to maternal opioids, exposure to general anaesthesia via the mother
• severe: severe and prolonged hypoxia, congenital neuromuscular disorder

Consequences: decreased alveolar fluid clearance, poor lung inflation, and a decreased fall in pulmonary vascular resistance.

Birth hypoxia proceeds in three phases:

1. Primary apnoea: foetal hypoxia stops the respiratory centres functioning and breathing stops. Intervention: tactile stimulation (“dry and stimulate”).
2. Gasping: primitive spinal centres initiate gasping, slow, exaggerated, irregular breaths at 10-12 per minute. Gasping can provide just enough oxygen to raise heart rate and improve oxygen delivery, and spontaneous breathing may resume at this stage without further intervention. An infant may already be gasping at birth. Intervention: tactile stimulation, positive pressure ventilation.
3. Secondary (terminal) apnoea: gasping can no longer provide enough oxygen to improve circulation and oxygenation. Without immediate positive pressure ventilation, death occurs. PPV is usually adequate to deliver oxygen, improve circulation and resume spontaneous breathing; tactile stimulation will not be effective.

Airway obstruction and impaired lung function

Airway obstruction prevents adequate initial breaths, interferes with alveolar fluid clearance and lung inflation, and interferes with the fall in pulmonary vascular resistance. Causes: meconium aspiration, congenital airway malformation, anatomical airway obstruction (laryngeal webs, cystic hygroma, congenital goitre).

Impaired lung function, external or mechanical: any collection between lung and chest wall prevents lung expansion. Air gives pneumothorax, fluid gives pleural effusion, lymph gives chylothorax.

Impaired lung function, intrinsic lung disease:

• excessive fluid in the lungs, giving transient tachypnoea of the newborn (most common)
• surfactant deficiency due to prematurity, giving respiratory distress syndrome
• neonatal pneumonia

Persistent pulmonary hypertension of the newborn

In PPHN, pulmonary vascular resistance remains abnormally elevated after birth: pulmonary blood flow is reduced or restricted and shunted right to left, causing severe hypoxaemia from inadequate oxygenation. The persistent-foetal-circulation schematic shows PVR greater than SVR, flow into the lungs blocked, and blood shunted through the ductus arteriosus into the systemic circulation.

Mechanisms of raised pulmonary vascular resistance, understood through Poiseuille’s law:

$R=\frac{8\eta l}{\pi r^4}$

• pulmonary vascular vasoconstriction (smaller lumens)
• pulmonary vascular inflammation (thickened vessels)
• pulmonary vasculature hypoplasia (fewer vessels)

compared with normal pulmonary vasculature. Because radius is raised to the fourth power, small reductions in vessel calibre have large effects on resistance.

Meconium aspiration syndrome: foetal distress leads to in utero passage of meconium, and aspiration causes the syndrome. Consequences of meconium in the lungs:

• chemical pneumonitis and narrowing of pulmonary vessels, developing into pulmonary hypertension
• localised areas of collapse and hyperinflation
• high risk of pneumothorax

Chest X-ray shows bilateral patchy, diffuse opacities and consolidation through both lung fields.

Pulmonary hypoplasia: underdevelopment of the lung with decreased cross-sectional area of lung tissue, leading to PPHN. Causes: congenital diaphragmatic hernia (abdominal contents herniate through a diaphragmatic defect into the chest), decreased amniotic fluid production (anhydramnios), and renal or urinary tract anomalies (also via decreased amniotic fluid production).

Treatment of PPHN:

• inhaled nitric oxide, the gold standard, a selective pulmonary vasodilator relaxing pulmonary vascular smooth muscle
• oxygen, a pulmonary vasodilator that also improves oxygenation
• assisted ventilation
• sildenafil, which inhibits reuptake of inhaled nitric oxide
• extracorporeal membrane oxygenation (ECMO)

Congenital cardiac disease

Congenital heart disease is the most common congenital disorder in newborns, prevalence 6-13 per 1000 live births (UpToDate).

• Non-critical (75%): will not need surgery or another invasive procedure in the first year. Examples: bicuspid aortic valve, atrial septal defects, small ventricular septal defects.
• Critical (25%): will need surgery or an invasive procedure in the first year. Includes cyanotic defects, ductal dependent defects, and symptomatic non-cyanotic defects such as large VSDs.

Cyanotic heart defects involve mixing of oxygenated and deoxygenated blood. Ductal dependent defects rely on a patent ductus arteriosus for adequate pulmonary and/or systemic blood flow; when the duct closes the infant rapidly decompensates, with no pulmonary or systemic blood flow and no oxygenated blood reaching the systemic circulation.

Classification of cyanotic defects:

• Left sided lesions: hypoplastic left heart syndrome, critical coarctation of the aorta, critical aortic stenosis
• Right sided lesions: tetralogy of Fallot, critical pulmonary valve stenosis, tricuspid atresia, Ebstein anomaly
• Parallel circulations: transposition of the great arteries
• Other (not ductal dependent): total anomalous pulmonary venous return, truncus arteriosus

Warning

The lecture includes a box diagram of parallel circulation (SVC and IVC feeding a grid of boxes, pulmonary venous flow and several inter-box connections marked blocked, the two lower boxes joined by a bidirectional “ductus arteriosus” arrow that is also blocked at both ends, with outputs labelled “Lungs / Systemic” and “Systemic / Lungs”). The slide carries no title and does not state which chamber or vessel each box represents, so the diagram cannot be resolved further than this.

Neonatal infection

Risk factors: male sex, maternal fever, chorioamnionitis, preterm labour, prolonged rupture of membranes (>18 hours), GBS positive mother (risk decreased by appropriate antenatal treatment).

Clinical features are non-specific, and an infant may be critically ill at birth or develop symptoms over time: respiratory distress, tachycardia, temperature instability (hyperthermia, or hypothermia), poor feeding, lethargy, poor tone, irritability, seizures.

Early onset (<7 days) versus late onset (>7 days):

Presentation	Early (<7 days)	Late (>7 days)
Sepsis	80-85%	65%
Pneumonia	10%	5-10%
Meningitis	5-7%	25-30%
Urinary tract infection	not listed	7-15%

Management, early onset sepsis: respiratory support (respiratory distress is very common in all types of infection) with chest X-ray, blood culture, and IV antibiotics with gram positive and gram negative cover, since group B streptococcus and E. coli are the most common organisms.

Management, late onset sepsis: respiratory support with chest X-ray, blood culture, CSF culture, urine culture, and IV antibiotics with gram positive and gram negative cover for group B streptococcus and E. coli, additionally considering staphylococcal cover.

Neonatal jaundice

Half of infants become visibly jaundiced in the newborn period. Causes of physiological jaundice:

• rapid turnover of red blood cells
• increased volume of red blood cells relative to body mass
• immature uridine-diphosphoryl-glucuronosyltransferase (UDP-GT) activity, the enzyme converting unconjugated to conjugated bilirubin in the liver

Bilirubin metabolism as drawn: red blood cells give heme, which becomes biliverdin, then bilirubin, existing as free bilirubin and bilirubin bound to albumin; from there one route goes to the CNS and the other to the liver, where bilirubin plus UDP-GT forms conjugated bilirubin, which becomes stercobilinogen. Haemolysis increases production upstream. Increased enterohepatic circulation feeds back into this pathway: delayed gastric motility leads to reabsorption and deconjugation of bilirubin.

Causes of significant unconjugated hyperbilirubinaemia:

• Increased production: isoimmune-mediated haemolysis (ABO incompatibility, common; RH incompatibility), inherited RBC membrane defects, sepsis (mechanism unknown)
• Decreased clearance: syndromes (Gilbert, Crigler-Najjar and others), increased enterohepatic circulation from breastfeeding jaundice (most common cause overall) and breastmilk jaundice

Consequences, acute bilirubin encephalopathy by phase:

• early: sleepy, hypotonia, high pitched cry
• intermediate: lethargic, shrill cry and difficult to console, mild to moderate hypertonia
• late: apnoea, inability to feed, seizures, progression into coma, severe hypertonia

Chronic bilirubin encephalopathy (kernicterus) is permanent: choreoathetoid cerebral palsy, sensorineural hearing loss, gaze palsies, dental enamel hypoplasia, with cognitive function usually spared.

Treatment is determined by plotting the level on a nomogram (serum bilirubin against postnatal age in hours, with low risk, low intermediate risk, high intermediate risk and high risk zones, the high risk zone being the 95th percentile; the curves rise then plateau after roughly 72-96 hours). Management: ensure good hydration; phototherapy, which converts bilirubin into lumirubin, which is not neurotoxic and is more easily absorbed; and double volume exchange transfusion, now very rare because of phototherapy and anti-D immunoglobulin.

Hypoglycaemia

Very common in neonates. Risk factors: infant of the diabetic mother, macrosomia (very large baby), perinatal stress, prematurity, growth restricted infants, preterm infants.

Mechanism in the infant of a diabetic mother:

1. Maternal hyperglycaemia.
2. The infant increases endogenous insulin to compensate.
3. At delivery the high maternal glucose source is removed rapidly.
4. The infant’s insulin remains high.
5. The infant’s blood glucose drops.

Symptoms: asymptomatic (most common), jitteriness, tremors, abnormal high-pitched cry, lethargy, hypotonia, hypothermia, tachypnoea, apnoea, cyanosis, convulsions, cardiac arrest.

Treatment: screen infants with risk factors; prompt recognition and treatment minimises neurologic damage; optimise the thermal environment; early feedings; IV dextrose or oral dextrose gel.

Prematurity

Prematurity is birth before 37 0/7 weeks gestation. The edge of viability in New Zealand is 23 0/7 weeks. Most premature infants need a higher level of resuscitation after birth, and the more preterm the infant the more interventions are required: oxygen, positive pressure ventilation, intubation and mechanical ventilation, surfactant administration, placement of umbilical catheters, total parenteral nutrition.

Classification by birthweight:

• low birth weight (LBW): <2500 g
• very low birth weight (VLBW): <1500 g
• extremely low birth weight (ELBW): <1000 g

Classification by gestational age:

• late preterm: 34 weeks to 36 weeks and 6 days
• moderately preterm: 32 weeks to 33 weeks and 6 days
• very preterm (VPT): <32 weeks
• extremely preterm (EPT): <28 weeks

Incidence: worldwide about 10% of births. In 2019, 7001 infants (1.9% of live births) were born at or before 36 weeks in Australia and New Zealand. Incidence varies by race and ethnicity, likely due to disparity and inequity within the health care systems: Caucasian mothers 44.8% (70.2% of total population), Māori mothers 21.5% (17.1%), Pasifika mothers 14.4% (7.4%), Asian mothers 16% (11.8%).

Risk factors for prematurity:

• OB/GYN history: previous preterm birth, previous cervical surgeries, uterine anomalies
• Maternal demographics: age <17 or >35 years, Māori or Pasifika ethnicity, lower educational level, single marital status, lower socioeconomic status, short interpregnancy interval (<18 months), poor access to health care, physical abuse
• Nutritional status: low BMI or pre-pregnancy weight, poor nutritional status, long working hours, hard physical labour
• Maternal and pregnancy characteristics: assisted reproduction, multiple gestations, foetal disorders, vaginal bleeding, poly- or oligohydramnios, maternal medical conditions, abdominal surgery during pregnancy, stress and depression, substance use, infections, short cervical length, uterine contractions, premature rupture of membranes

Growth by gestation: from roughly 500 g at 24 weeks to roughly 2000-2100 g at 36 weeks, with males slightly heavier than females throughout. The lecture illustrates the extreme end with a twin born at 23 weeks weighing 515 g.

Risks and outcomes: risk of morbidity and mortality increases with decreasing gestational age. Antenatal steroids and surfactant given after birth have improved outcomes over the last 20 years; antenatal steroids improve lung maturation, reduce intraventricular haemorrhage and decrease mortality. In the lecture’s 23-25 week outcome data, average survival is the highest bar (roughly 62-77%, highest at 25 weeks), while impairment and complication rates are mostly low (0-35%), near 0% for blindness and deafness, with cognitive developmental delay around 20-35%. These figures assume a female singleton who received steroids, and every percentage is the best case of the range.

Complications of extreme prematurity: respiratory distress syndrome, chronic lung disease, infection or pneumonia, intracranial haemorrhage, necrotizing enterocolitis, cerebral palsy, neurocognitive deficits, deafness, blindness.

Viability guidelines:

• active resuscitation can be started at 23 0/7 weeks
• between 23 0/7 and 24 6/7 weeks, parents may choose active resuscitation or comfort care
• at 25 0/7 weeks and beyond, full resuscitation is the only option

Self-test

1. List the five physiological domains in which the newborn must adapt at birth, and state what proportion of infants need some medical intervention and what proportion need advanced resuscitation.
2. Describe the effects of the cortisol surge on the fetus preparing for birth.
3. Distinguish the effects of the catecholamine surge from those of the cortisol surge during labour.
4. Explain how lung fluid handling changes from mid-gestation to the moments after birth, naming the ion transported at each stage.
5. Predict what happens to alveolar fluid clearance after a very rapid delivery, and name the resulting condition and its features.
6. Describe the sequence from the first cry to improved oxygenation, including the role of surfactant.
7. Explain why preterm infants develop respiratory distress syndrome, and what intervention changed their survival.
8. State the proportion of foetal cardiac output going to the placenta and to the lungs, and the vascular resistance of each.
9. Describe the six steps of the neonatal circulatory transition in order.
10. Explain how a fetus preferentially delivers the highest-oxygen blood to the liver, brain and heart.
11. Distinguish HbF from HbA in terms of oxygen affinity, 2,3-BPG affinity, and the oxygen tension each operates at.
12. List the four mechanisms that put a newborn at risk of hypothermia, and five practical measures to prevent it.
13. List the five Apgar criteria and state the score bands for normal, concerning and critical.
14. A newborn has a heart rate of 90 bpm and is gasping at 1 minute despite drying and stimulation. What is the next intervention, and what would you escalate to if the heart rate fell below 60 bpm?
15. What are the targeted pre-ductal SpO2 values at 1, 5 and 10 minutes after birth?
16. What is the IV adrenaline dose range in neonatal resuscitation, and the 1:10,000 volume for a 38-43 week infant?
17. Describe the three phases of birth hypoxia and state which intervention works in each.
18. A baby is deeply apnoeic and does not respond to vigorous drying and stimulation. Explain the physiological reason tactile stimulation has failed and what must be done instead.
19. Distinguish external or mechanical causes of impaired lung function from intrinsic lung disease, giving examples of each.
20. Define persistent pulmonary hypertension of the newborn, and explain how it causes hypoxaemia.
21. List the four vascular states depicted as causes of raised pulmonary vascular resistance, and explain why vessel radius matters so much.
22. Describe the consequences of meconium in the lungs.
23. List the causes of pulmonary hypoplasia and the common mechanism linking two of them.
24. List the treatments for PPHN, naming the gold standard and its mechanism.
25. Distinguish critical from non-critical congenital heart disease, with examples and their relative frequencies.
26. Explain what happens when the ductus closes in a ductal dependent lesion, and classify tetralogy of Fallot, hypoplastic left heart syndrome and transposition of the great arteries within the lecture’s scheme.
27. List the risk factors for neonatal infection.
28. Distinguish early onset from late onset neonatal infection by timing, the relative frequency of meningitis, and the investigations and antibiotic cover required.
29. Explain the three causes of physiological neonatal jaundice.
30. Distinguish increased production from decreased clearance as causes of significant unconjugated hyperbilirubinaemia, and name the single most common cause.
31. Describe the features of acute bilirubin encephalopathy by phase, and the permanent features of kernicterus.
32. Explain how phototherapy works and how the decision to treat jaundice is made.
33. Describe the mechanism of hypoglycaemia in the infant of a diabetic mother.
34. List the treatment measures for neonatal hypoglycaemia.
35. State the birthweight and gestational-age classifications of prematurity.
36. State the New Zealand viability guidelines for resuscitation at 23 0/7, 23 0/7 to 24 6/7, and 25 0/7 weeks and beyond.
37. Explain what antenatal steroids achieve for a preterm infant.
38. List the complications of extreme prematurity.
39. Integrative: a term infant is delivered by rapid caesarean section after meconium-stained liquor and is tachypnoeic and cyanosed with poor response to oxygen. Trace, using the transition physiology from this lecture, how these features connect from lung fluid through to pulmonary vascular resistance and shunting.

Answers

Reveal answers

1. Pulmonary function and lung mechanics, cardiovascular circulation, respiratory control, energy metabolism, thermoregulation. About 10% need some medical intervention and about 1% need advanced resuscitative support.
2. Cortisol rises about 50% between 35 weeks and term and fourfold during labour, peaking in the hours after delivery. It promotes lung maturation and surfactant production, gastrointestinal development and readiness for enteral feeding, regulation of energy metabolism (particularly glucose homeostasis), thyroid hormone activation supporting thermoregulation and metabolism, and activation of epithelial sodium channels facilitating alveolar fluid clearance.
3. Catecholamines (adrenaline and noradrenaline, from adrenal release during labour and delivery) increase systemic vascular resistance to support the shift to postnatal circulation, raise plasma glucose, and initiate thermogenesis. Cortisol instead prepares organs in advance: lung maturation and surfactant, gut readiness, glucose homeostasis, thyroid activation and epithelial sodium channels. Catecholamines also enhance surfactant secretion.
4. In utero the airway epithelium actively secretes fluid via chloride transport (with swallowed amniotic fluid also contributing), maintaining lung expansion and structural maturation. As labour approaches cortisol switches this to resorption: fluid is reabsorbed by active sodium transport with water following passively into the interstitium. At birth rising oxygen tension enhances reabsorptive capacity and inspiratory pressure from the first breaths drives remaining fluid out of the alveoli.
5. There is less time for reabsorption, so foetal lung fluid is retained, causing transient tachypnoea of the newborn, the most common respiratory disorder of newborns: tachypnoea, increased work of breathing, grunting, retractions and oxygen needs. It is self-resolving but may require respiratory support.
6. The baby cries, the chest wall expands, intrathoracic pressure becomes more negative and air enters the lungs; increased inspiratory pressure expands the alveoli, increasing surface area for gas exchange and improving oxygenation; alveolar stretch as they fill with air triggers surfactant secretion, which reduces surface tension, improves compliance and enhances oxygenation efficiency.
7. Preterm lungs may be immature and produce insufficient surfactant, and decreased surfactant leads to respiratory distress syndrome, a significant cause of preterm mortality and morbidity. Artificial surfactant, introduced in 1989, increased survival rates.
8. The placenta receives about 40% of foetal cardiac output and has the lowest vascular resistance; the lungs receive about 10% and have the highest vascular resistance, and do not contribute to gas exchange.
9. (1) Umbilical cord clamping removes the placenta from circulation; (2) lung expansion reduces pulmonary vascular resistance; (3) pulmonary blood flow increases significantly; (4) the catecholamine surge raises systemic vascular resistance and blood pressure; (5) closure of the foetal shunts begins, ductus arteriosus and foramen ovale; (6) transition to postnatal adult-type circulation is complete.
10. The liver receives blood directly from the umbilical vein without mixing with deoxygenated blood; the brain and heart receive blood streaming through the foramen ovale and supplying the ascending aorta. The fetus also needs less oxygen overall because of lower metabolic demands.
11. HbF has high oxygen affinity (promoting transfer from maternal haemoglobin across the placenta), low affinity for 2,3-BPG (increasing oxygen-binding capacity), and operates at low foetal oxygen tension, which promotes unloading at tissue level and stimulates angiogenesis; high foetal haematocrit adds carrying capacity. HbA has low oxygen affinity (promoting transfer to tissues), high affinity for 2,3-BPG (decreasing oxygen-binding capacity at tissue level), and operates at high oxygen tension, promoting loading at the alveoli.
12. Large surface area to body mass ratio, decreased subcutaneous fat, inability to shiver, and immature skin causing increased evaporative water and heat loss. Measures: check temperature after birth, skin to skin with mother or father, keep dry, keep wrapped, use a hat (with an artificial heat source such as an incubator where needed).
13. Appearance (colour), Pulse (heart rate), Grimace (reflex irritability), Attitude (muscle tone), Respirations (respiratory effort), scored 0-2 each at 1, 5 and 10 minutes. Normal >7, concerning 4-6, critical 3 or less.
14. Positive pressure ventilation with SpO2 monitoring, since the heart rate is below 100 with gasping. If the heart rate falls below 60 bpm: chest compressions at three compressions to each breath with 100% oxygen, considering intubation or laryngeal mask and obtaining venous access; if still below 60, IV adrenaline and consider volume expansion.
15. 1 minute 60-70%, 5 minutes 80-90%, 10 minutes 85-90%.
16. 10-30 microg/kg (0.1-0.3 mL/kg). For a 38-43 week infant the 1:10,000 volume is 0.5 mL.
17. Primary apnoea: hypoxia stops the respiratory centres functioning and breathing stops, treated with tactile stimulation (dry and stimulate). Gasping: primitive spinal centres drive slow, exaggerated, irregular breaths at 10-12 per minute, which may provide just enough oxygen to raise heart rate and improve delivery, so spontaneous breathing may resume; treated with tactile stimulation and positive pressure ventilation. Secondary (terminal) apnoea: gasping is inadequate, and without immediate positive pressure ventilation death occurs.
18. The infant is in secondary (terminal) apnoea, where gasping has failed to provide enough oxygen to improve circulation and oxygenation; tactile stimulation will not be effective at this stage. Positive pressure ventilation is required and is usually adequate to deliver oxygen, improve circulation and resume spontaneous breathing; without it death will occur.
19. External or mechanical: any collection between lung and chest wall prevents expansion, air giving pneumothorax, fluid giving pleural effusion, lymph giving chylothorax. Intrinsic lung disease: excessive lung fluid giving transient tachypnoea of the newborn (most common), surfactant deficiency from prematurity giving respiratory distress syndrome, and neonatal pneumonia.
20. PPHN is persistently abnormally elevated pulmonary vascular resistance after birth. Pulmonary blood flow is reduced or restricted and blood is shunted right to left (through the ductus arteriosus into the systemic circulation), so blood bypasses the lungs and is inadequately oxygenated, giving severe hypoxaemia.
21. Normal pulmonary vasculature, pulmonary vascular vasoconstriction, pulmonary vascular inflammation, and pulmonary vasculature hypoplasia. By Poiseuille’s law resistance is proportional to $8\eta l/\pi r^4$, so resistance varies with the fourth power of the radius and small reductions in calibre raise resistance sharply.
22. Chemical pneumonitis and narrowing of pulmonary vessels, leading to pulmonary hypertension; localised areas of collapse and hyperinflation; and a high risk of pneumothorax. The chest X-ray shows bilateral patchy, diffuse opacities and consolidation.
23. Congenital diaphragmatic hernia (abdominal contents herniating through a diaphragmatic defect into the chest), decreased amniotic fluid production (anhydramnios), and renal or urinary tract anomalies. The last two share the mechanism of decreased amniotic fluid production, since production and swallowing of amniotic fluid are required for normal lung growth.
24. Inhaled nitric oxide (gold standard), a selective pulmonary vasodilator relaxing pulmonary vascular smooth muscle; oxygen, a pulmonary vasodilator that also improves oxygenation; assisted ventilation; sildenafil, which inhibits reuptake of inhaled nitric oxide; and ECMO.
25. Non-critical (75%) will not require surgery or another invasive procedure in the first year: bicuspid aortic valve, atrial septal defects, small ventricular septal defects. Critical (25%) will require surgery or an invasive procedure in the first year: cyanotic defects, ductal dependent defects, and symptomatic non-cyanotic defects such as large VSDs.
26. Ductal dependent lesions rely on a patent ductus arteriosus for adequate pulmonary and/or systemic blood flow, so when the duct closes the infant rapidly decompensates with no pulmonary or systemic blood flow and no oxygenated blood to the systemic circulation. Tetralogy of Fallot is a right sided lesion, hypoplastic left heart syndrome a left sided lesion, and transposition of the great arteries a parallel circulation.
27. Male sex, maternal fever, chorioamnionitis, preterm labour, prolonged rupture of membranes over 18 hours, and a GBS positive mother (with decreased risk if appropriately treated antenatally).
28. Early onset is under 7 days: sepsis 80-85%, pneumonia 10%, meningitis 5-7%; investigated with chest X-ray and blood culture and treated with respiratory support and IV antibiotics covering gram positives and negatives (group B streptococcus and E. coli). Late onset is over 7 days, with much more meningitis (25-30%), sepsis 65%, pneumonia 5-10% and urinary tract infection 7-15%; it additionally requires CSF and urine culture, and staphylococcal cover should be considered.
29. Rapid turnover of red blood cells, increased volume of red blood cells relative to body mass, and immature UDP-glucuronosyltransferase activity, the enzyme that converts unconjugated to conjugated bilirubin in the liver.
30. Increased production: isoimmune-mediated haemolysis (ABO incompatibility, common, and RH incompatibility), inherited red cell membrane defects, and sepsis by an unknown mechanism. Decreased clearance: syndromes such as Gilbert and Crigler-Najjar, and increased enterohepatic circulation from breastfeeding jaundice and breastmilk jaundice. Breastfeeding jaundice is the most common cause.
31. Early phase: sleepy, hypotonia, high pitched cry. Intermediate: lethargic, shrill cry and difficult to console, mild to moderate hypertonia. Late: apnoea, inability to feed, seizures, progression into coma, severe hypertonia. Kernicterus is permanent: choreoathetoid cerebral palsy, sensorineural hearing loss, gaze palsies and dental enamel hypoplasia, with cognitive function usually spared.
32. Phototherapy converts bilirubin into lumirubin, which is not neurotoxic and is more easily absorbed. Treatment is determined by plotting the serum bilirubin level against postnatal age on a nomogram with low, low intermediate, high intermediate and high risk zones (the high risk zone being the 95th percentile), alongside ensuring good hydration; double volume exchange transfusion is now very rare because of phototherapy and anti-D immunoglobulin.
33. Maternal hyperglycaemia causes the infant to raise endogenous insulin to compensate. At delivery the high maternal glucose source is removed rapidly while the infant’s insulin remains high, so the infant’s blood glucose drops.
34. Screen infants with risk factors, recognise and treat promptly to minimise neurologic damage, optimise the thermal environment, give early feedings, and give IV dextrose or oral dextrose gel.
35. By birthweight: low birth weight <2500 g, very low birth weight <1500 g, extremely low birth weight <1000 g. By gestational age: late preterm 34 weeks to 36 weeks and 6 days, moderately preterm 32 weeks to 33 weeks and 6 days, very preterm <32 weeks, extremely preterm <28 weeks.
36. Active resuscitation can be started at 23 0/7 weeks; between 23 0/7 and 24 6/7 weeks parents may choose active resuscitation or comfort care; at 25 0/7 weeks and beyond full resuscitation is the only option.
37. Antenatal steroids improve lung maturation, reduce intraventricular haemorrhage and decrease mortality; with post-birth surfactant they have improved outcomes over the last 20 years.
38. Respiratory distress syndrome, chronic lung disease, infection or pneumonia, intracranial haemorrhage, necrotizing enterocolitis, cerebral palsy, neurocognitive deficits, deafness and blindness.
39. A rapid caesarean delivery gives less time for cortisol-driven sodium-dependent reabsorption of alveolar fluid, so retained lung fluid causes tachypnoea and impairs lung inflation. Meconium aspiration adds airway obstruction, preventing adequate initial breaths, plus chemical pneumonitis with narrowing of pulmonary vessels and areas of collapse and hyperinflation. Poor lung inflation and pulmonary vasoconstriction both prevent the normal fall in pulmonary vascular resistance, so PVR stays above systemic vascular resistance; blood is then shunted right to left through the ductus arteriosus (persistent pulmonary hypertension), bypassing the lungs, which explains the cyanosis that responds poorly to oxygen.