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intrauterine environment
why do babies not need to generate their own heat
how is their metabolic demand/energy kept low
why do they not need to defecate
why do they not need lungs or an active GIT
Warm environment, dont need to generate own heat
Long nap times, no need to wake or move
Automatic waste filtration, no need to defecate
Ready oxygen supply, no need to use lungs
Ready food source, no need to eat
respiration
where is the site of gas exchange in foetus
how do they ‘practice‘ breathing in the uterus, what pressure does this create
why do they do this 2
Placenta is the site for gas exchange in foetus
Foetal lungs undergo structural changes throughout pregnancy
Spend 1-4 hours each day making rapid respiratory movements
Creates negative pressure in chest
Diaphragmic
Moves amniotic fluid in and out of lungs
‘practice’
Promotion of lung growth
why does the first breath need to happen
what mechanisms can also encourage this
Upon birth, the neonate needs to clear its airways of fluid
Cold exposure
Environmental stimulation
Tactile
Gravitational
Auditory
Noxious
what are the difficulties a neonate has to overcome on the first breath
compliance
fluids
ST
Low compliance of uninflated lungs
The viscosity of any remaining fluids in the airway
The surface tension created by the establishment of the air-water interface in the lungs
which cells secrete surfactant
what does this help do
Type II pneumocytes
Secrete pulmonary surfactant
Helps reduce surface tension at newly formed air-water interface
name a condition that is caused by a lack of surfactant (IRDS)
why is this an issue
symptoms
treatment
what does CPAP stand for
Infant respiratory distress syndrome
Risk increases with reduced gestational age
Failure to produce sufficient surfactant
Struggle to overcome increased surface tension
Main airways closed due to atelectasis
Symptoms
Cyanosis, tachypnoea, tachycardia, nasal flaring, chest retractions and expiratory grunting
Treatment
Injecting mother with glucocorticoids
Prior to pre-term birth
Provision of oxygen
CPAP – continuous positive airway pressure
Endotracheal tube
Introduction of exogenous surfactant
Breathing tube
foetal circulation adaptations
how do the ventricles pump
what are the 3 vascular shunts
what is the purpose of these shunts
Two ventricles pump in parallel, rather than in series in the foetus
Three vascular shunts (ductus venosus, foramen ovale, and ductus arteriosus), divert blood away from the lungs and liver towards the placenta
explain the 3 vascular shunts
ductus venosus- bypasses the liver (U cord - ivc/heart)
foramen ovale - bypasses lungs (from r-l atrium to pump round the body)
ductus arteriosus - bypasses lungs (pulmonary artery - aorta)
haemodynamics: pre-birth
why does the lungs have high vascular resistance
what does a low systemic vascular resistance allow blood to travel to
where does oxygenated blood travel to
where does blood that travels into the RV travel to
High pulmonary vascular resistance
needed to ensure that blood bypasses the fluid filled, non functioning lungs
Collapsed, fluid filled lungs
Hypoxic pulmonary vasoconstriction
Low systemic vascular resistance
Placenta
Highest O2
Umbilical vein -> ductus venosus -> IVC -> foramen ovale -> LV -> ascending aorta
Lower O2
SVC -> RV -> ductus arteriosus -> descending aorta
haemodynamics: birth
what does cord clamping increase 3
contributes to the closure of which shunt
first breath decreases what pressure (pvp)
Cord clamping increases SVR
Aortic pressure increases
Left ventricle afterload increases
Left atrium pressure increases
Contributes to foramen ovale closure
First breaths decreases PVP
Lung fluid absorbed and alveoli expand
Increased alveolar O2 reverses hypoxic pulmonary vasoconstriction
Pulmonary blood flow increases
Right atrial and ventricular pressure falls
rise in PaO2
inhibits what channel
polarisation effect on sm
what type of Ca2+ channels open
causing what shunt to constrict
Inhibition of voltage-gated K+ channels
Smooth muscle depolarisation
Opening of L-type Ca2+ channels
Increased intracellular Ca2+
Ductal constriction (ductus arteriosus)
thermoregulation
name 3 ways to increase bosy temperature
4 ways of decreasing it
basal metabolic rate, shivering/muscle contraction, non shivering thermogenesis
conduction, convection, radiation, evaporation
what is BAT
where is it significantly distributed round and why
Brown adipose tissue and non-shivering thermogenesis
Significant distribution of BAT
Interscapular region
Clavicles
Heart and aorta
Trachea
Kidney
Pancreas
Central blood vessels to ensure core body temperature stays high
non shivering thermogenesis
what 2 things does it have an increased consumption of
what is the result of cold stress
this can lead to a risk of
Non shivering thermogenesis
Increase O2 consumption by 2-3x
Increased glucose utilisation
Consequences of cold stress
Increased metabolic rate -> increased O2 consumption -> increased O2 production
Risk of:
Hypoxaemia
Anaerobic metabolism
Lactic acidosis
Pulmonary vasoconstriction ->^ PVR
Risk of persistent pulmonary hypertension of the newborn
WHO warm chain examples
warm delivery room
immediate drying
skin to skin
breast feeding
clothing
warm transportation
energy stores
what is usual gestation duration
why does the placenta have a high amount of glycogen storage
36-40 week gestation
Insulin and high placental glucose delivery drive hepatic glycogen storage - Glycogenesis
Preparation for a rapid release glucose reserve for the first hours after birth
GI maturation
what digestive enzyme is very high at birth
what DE is low, why
what 2 will increase after birth
what proteins can GIT absorb
why are bile and pancreatic lipase low 2
Lactase relatively high at birth – cortisol
Amylase low (pancreatic and salivary)
Limited starch digestion
Pepsin and trypsin activity increases postnatally
Neonatal gut can absorb intact proteins (important for IgA, growth factors)
Bile acids and pancreatic lipase low
Human milk lipase compensates
Efficient fat absorption
pre-term babies - GIT
what is an issue with the GIT
symptoms
Underdeveloped GIT
Poorly coordinated motility > gastric reflux
Slowed gastric emptying
Slowed transit through the GIT
Feeding intolerance
Necrotising enterocolitis (GIT dies and leaves hole, bacteria can enter abdomen)
renal system - foetus
what concentration of urine do babies produce
GFR rate
Foetal kidneys mainly produce hypotonic urine – amniotic fluid
Low GFR, low concentrating ability, limited sodium reabsorption
Renal blood flow is due to high pulmonary vascular resistance
Foetal aldosterone rises in late pregnancy
at birth: renal
what can low GFR and immature tubules lead to
what 3 substances are released (adrenal G, liver, kidney) for homeostasis of BP, and salt conc
Low GFR and immature tubules
Vulnerability to dehydration, overload, hyponatraemia, acidosis
The neonate most maintain blood pressure, circulating volume and electrolyte balance alone
This triggers:
^^ renin release
> ^ angiotensin II
> ^ aldosterone secretion
Aldosterone becomes a primary stabiliser of neonatal homeostasis
how does kidney function mature (DCT)
Distal tubules become more responsive to aldosterone