w6

• embryonic period (0-7w)

  First stage of lung development

  • Major organs beginning to form

  • A lung bud develops from a tube of cells called the foregut (which will itself later go on to form

  the gut)

  • This bud separates into two

  • Two buds become a baby’s right and left lungs

  • Pulmonary vasculature (arteries and veins) develops and divides with lung in a caudal direction
• pseudoglandular period (5-17w)

  Airway multiplication – bronchial branching and

  formation completed

  • 3 buds right side – upper, middle and lower lobes of

  right lung

  • 2 buds on left side - upper and lower lobes of left

  lung

  • By 16 weeks lungs - bronchi and terminal

  bronchioles ↑ in length and size

  • Formation of muscle fibres, elastic, early cartilage

  within the bronchi, and mucous glands

  • Vascular system and diaphragm start to develop
• cannallcular period ( 13-27 w)

  Development of and vascularisation of

  respiratory portion of the lung

  • Differentiation of type I pneumocyte,

  primary structural cell of alveolus

  • Gas exchange occur across thin,

  membrane-like cells

  • Capillaries grow in close proximity to

  distal surface of alveolar cells

  • By 13 weeks cilia appear in trachea and

  main bronchi

  • Alveolar buds and sacculi form

  • Surfactant and lecithin production may

  begin

  • May be able to survive in NICU towards the

  end of this stage
• canalicular period

  
• saccular period (24-40w)

  The primary phase of cilia, surfactant and alveoli development

  • Terminal sacs appear as outpouchings of terminal bronchioles

  • Over the next few weeks these multiply forming multiple pouches

  off the alveolar chamber (alveolar duct)

  • Pores of Kohn connect adjacent alveoli
• Recognizable differentiation of Type I and Type II cells

  • Type 1 cells (95%): the surface epithelium thins as vascular

  proliferation increases. Creation of the future blood- gas barrier

  • Type II (5%) – surfactant production

  • Further development of pulmonary arterial system

  • At term 150 million primitive alveoli called ‘saccules’ are present

  • Alveoli develop at 2 months old

  • Full complement (3-400 million) by 8 years old

  
• surfactant

  decreases surface tension within alveoli and prevents collapse of alveoli during exhalation.

  present from 18-24 weeks gestation
• Absence of surfactant = alveolus would be unstable and collapse at the end of each breath

  —> would require significant work to require the alveolus to open in each breath.

  preterm babies often suffer surfactant insufficiency
• surfactant reduces surface tension.

  its molecules repel each other more as they get closer and therefore splint the aveoli open
• lung development continues after birth

  aveoli continue to form until 8-11yrs

  increase in growth and development of airways
• development of heart

  day 22: heart tube formed

  day 24:heart tube folding completed -->primitive common ventricle and common atrium.

  day 28-37 :atrial septum forms with interatrial shunt (foramen ovale) right to left ( to bypass the lungs) .

  -intramembranous ventricular septum forms creating left and right ventricles

  day 35-42:truncus arteriosis and conus cordis develop a spirarling septum -->pulmonary trunk and aorta
• foetal heart anatomy:

  • oxygenated blood from placenta enters inferior vena cava via umbilical vein.

  • most blood is SHUNTED from RIGHT atrium to LEFT atrium via foramen ovals then passes through left ventricle into the aorta

  • blood which flows from the right atrium into the right ventricle and into the pulmonary arteries is redirected into the aorta via the ductus arterious.

  • shunts bypass the pulmonary circulation and close soon after birth,

  • deoxygenated blood is sent to the placenta via umbilical arteries.
• congenital heart defects :

  PATENT FORAMEN OVALE (PFO)

  -shunt (connection) between left and right atria

  naturally occurs in about 35% of the pop , usually asymptomatic
• patent ductus arteriosus (PDA)

  — shunt (connection ) between pulmonary artery and aorta remains open after birth

  — increases pulmonary arterial volume and can damage vessels over time.

  — small PDA may close on its own over months

  — large PDA can be closed via catheter or surgery.
• Coarctation of the aorta:

  — narrowing of the aorta after the arch , where the ductus arteriosis closes

  — causes increased blood pressure to left side of the heart , arms , and head

  — left ventricular hypertrophy can develop if left untreated

  — repaired via surgery or catheter
• coarctation of the aorta

  
• patent ductus arteriosus (PDS)

  
• patent foramen ovale (PFO)

  
• ventricular septal defect (VSD)

  — Common cardiac defect with one or more defects (holes/openings) in the intraventricular septum

  — Shunts from left ventricle into right ventricle and into the pulmonary system

  — Can lead to increased pulmonary artery pressure

  — Symptoms: ‘failure to thrive’, increased RR

  — Small VSD may close on their own

  — Large VSD may need a ‘staged’ repair
• ventricular septal defect

  
• tetrology of fallor (TOF)

  — severe cyanotic congenital cardiac condition combining four defects

  • pulmonary valve stenosis

  • ventricular septal defect (VSD)

  • right ventricular hypertrophy

  • overriding aorta - inferior and centrally located aorta that emerges from both ventricles (above VSD)

  • usually corrected over 2 procedures — a temp repair soon after birth, and a complete repair around 6 months old

  • does not return cardiac fn back to normal
• Tetrology of fallor

  
• ANATOMICAL DIFFERENCES in infants

  airway diameter and length

  -small change in airway diameter will increase resistance significantly , this will lead to airway collapse and marked increase in work of breathing.

  -smaller in diameter

  -nasal passages 30-50% airway resistance

  -infants-high resistance to flow

  -increase in airway as child grows
• effect of airway oedema :

  
• comparative heart size

  adult 1/3 of rib cage

  infant 1/2 of rib cage -less space for lungs
• thorax differences:

  cross-sectional : infant is cylindrical, adult is elliptical

  chest wall:

  ribs of newborn infant :soft ,cartilaginous

  older children and adult chest walls more rigid

  bucket handle movement NOT possible in infants
• diaphragm differences:

  horizontal angle of insertion in infants compared to older children

  combined with compliant ribs results in:

  -less efficient ventilation

  -distortion of chest wall shape on inspiration

  -piston pattern not bucket

  infant diaphragm has lower relative muscle mass and lower content of high-endurance muscle fibres

  susceptibility to respiratory compromise
• diaphragm difference

  
• intercostals:

  infants :weak , poorly developed

  increased ventilatory requirements by increasing respiratory rate rather than depth

  chest wall compliance decreases rapidly for first 2 years of life-becomes approximately equal to lung compliance as in the adult

  -intercostal muscles develop

  -bucket and pump handle of chest wall achieved by 2 yr
• breathing differences:

  infants are preferential nasal breathers

  prone to obstruction

  -airway due to shape and orientation of head and neck

  -small nasal passages

  issue with feeding:

  nutritive suck-swallow-breathe control

  minute ventilation decreased, exhalation is prolonged, inhalation is shortened during feeding
• upper airway structures:

  infants trachea is short,narrow,more compliant than older children and adults.

  due to presence of immature/thinner cartilages

  airways prone to collapse with neck hyperflexioon,extension or rotation

  higher resistance to airflow due to small diameters
• difference in aveoli

  -decreased SA for gas exchange

  -full term infant has no aveoli but 150 million saccules

  -aveoli develop @ 2 months old
• collateral ventilation:

  -poorly developed until 2yo,fully at 8

  pores of kohn:intra-aveloar (1-2 yrs)

  canals of lambert : bronchiole-aveolar (6 yrs)

  late development

  high incidence, of lower obstructive airways disease

  atelectasis
• collateral ventilation:

  
• physiological differences:

  measure of pressure required to increase volume of air in lungs and reflects combination of lung and chest wall compliance

  child-adult : lung compliance is comparable

  
  

  BUT infant lung compliance is decreased due to amount of cartilage in airways.

  chest wall compliance is high (calcifies with age)

  intercostals unable to stabilise rib cage during diaphragm contraction

  respiratory compromise = increased respiratory rate instead of depth of diaphragmatic excursion
• respiratory muscle fatigue

  
• lung volume adaption:

  small VT

  closing volume (CV) -volumes small airways close

  CV +RV = CC

  adult :CC occurs within FRC

  <8yrs CC> frc and occurs during tidal volume

  -due to greater chest compliances and reduced elastic recoil of lungs

  -causes air trapping in alveoli because of early closure of terminal airways
• ventilation and perfusion:

  -different body positions change the orientation of the lungs, in healthy subjects , with respect to gravity thereby affecting the distribution of ventilation.

  distribution of ventilation in response to different body positions in adults - greater ventilation occurring in the dependent (lower lung)
• ventilation in children

  distribution of V is more complex

  pattern of V is not uniform

  some better ventilate the non-dependent lung, others may not

  variability may also be due to differences in development

  size of chest wall : changes in respiratory muscle strength and function and chest wall compliance ages 2 yo
• metabolic rate

  infants and children have higher metabolic rate and higher oxygen consumption than adults

  -growth and to maintain body temperature e.g. newborn 2x O2 consumption compared to adult

  work of breathing also accounts for 15% of total body oxygen consumption in neonates , 5% in adults

  infants will progress to hypoxemia more rapidly