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4/ RED > Neonatal Physiology > Flashcards

Neonatal Physiology Flashcards

1
Q

Describe the feto-placental unit
What is it made up of?
Which structures are foetal and which are maternal?
What are the vessels and what do they carry?

A

O2, CO2 and nutrients move by diffusion between the material intervillous space and fetal capillaries
Villi = fetal
Intervillous space = maternal
2 x umbilical arteries = carrying deoygenated blood to the placenta
1 x umbilical vein = carrying oxygenated blood away from the placenta

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2
Q

What are the partial pressures of oxygen in the following structures:

  • uterine artery
  • uterine vein
  • umbilical artery
  • umbilical vein
A
  • uterine artery = 12.7kPa
  • uterine vein = 5.6kPa
  • umbilical artery = 3.2kPa from foetus
  • umbilical vein = 4.2kPa to foetus
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3
Q

What are the partial pressures of CO2 in the following structures:

  • uterine artery
  • uterine vein
  • umbilical artery
  • umbilical vein
A
  • uterine artery = 5.3kPa
  • uterine vein = 6.1kPa
  • umbilical artery = 6.6kPa from foetus
  • umbilical vein = 5.8kPa to foetus
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4
Q

Does foetal umbilical vein blood achieve equilibrium with O2 and CO2?
Why?

A
  • -> Foetal umbilical vein blood does not achieve equilibrium with maternal blood fro O2
  • -> Foetal umbilical vein blood almost achieves equilibrium with maternal blood for CO2
  • the placental barrier is more permeable to CO2 than to O2
  • not all the maternal blood comes in contact with the villi
  • the placental tissue is highly active and consumes O2 (20%)
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5
Q

Describe the properties of foetal haemoglobin
How does its levels change during gestation?
Why does it have a higher affinity for O2?

A

HbF comprises 2 alpha and 2 gamma polypeptide chains
Reaches peak level at 10 weeks:
- maintained until 30 weeks
- declines to 80% of total at term
- gradually disappears after birth from 6 months
HbF has higher affinity for O2 - explained by lack of interaction with 2,3DPG, adult Hb-O2 is right shifted by 2,3DPG

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6
Q

Describe feotal Hb-O2 saturation

A
  • P50 of HbF is rich lower the adult Hb
  • O2 diffuses from maternal to foetal Hb
  • at PO2 4.2kPa, HbF is 75% saturated
  • Bohr shift separates curve even further
  • foetal curve to left, maternal curve to right
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7
Q

Describe foetal arterial O2 content

A
  • foetal blood has higher Hb concentration than maternal blood: 18 vs 15
  • Therefore at any PO2, foetal blood carries more O2
  • even at PO2 4.2kPA, foetal blood has O2 content similar to maternal arterial blood
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8
Q

What are the 3 shunts in the foetal circulation, what are they between?

A

ductus venous = left umbilical vein to IVC
foramen ovale = right and left atria
ductus arteriosus = pulmonary artery and aorta

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9
Q

What is flow through each shunt dependent on?

Describes the pressure in areas

A

dependent on intravascular pressure gradient

  • umbilical vein P > IVC P
  • Ratria P > Latria P
  • Pulm ABP > Aortic ABP
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10
Q

Where does blood with the highest saturation go to?

How?

A

the brain
streaming affect of blood through the right atrium, little mixing so blood retains saturation as it reaches aorta
- blood going to rest of body is less saturated as it has mixed with blood coming through ductus arteriosus from the lungs

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11
Q

What are the differences between foetal and adult cardiac outputs?

How is CO defined in the foetus?
Where is this CO directed?

A
  • in adult circulation, there are no shots, R stroke volume = L stroke volume
  • CO is defined as volume ejected by one ventricle/min
  • In foetus, shunting means, foetal left SV does not equal right SV
    RV receives 65% of venous return
    LV receives 35%
  • Thus, foetal cardiac output must be defined as total output of ventricles (combined ventricular output, CVO)
  • 45% of the CVO is directed to placental circulation
  • 8% of CVO enters the pulmonary circulation
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12
Q

What controls foetal circulation?

A
  • circulating chatecholamines, other hormones and locally released vasoactive substances all play a part
  • circulating catecholamines act on alpha and beta adrenoreceptors
  • receptors mature during early gestation, independently of autonomic innervation process
  • peripheral circulation of foetus is under a tonic adrenergic vasoconstrictor influence, mainly circulating noradrenaline
  • other factors such as arginine vasopressin (AVP) and renin-angiotensin system may also have a role
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13
Q

Describe the neural control of foetal circulation:
What is foetal heart rate at 11wks and 28wks, what does this change reflect?
What is systemic ABP at 11wks and at term, what does this change reflect?

What else develops that influences the foetal circulation?

A
  • By 11 of gestation, HR is 160bpm
  • From 28 weeks, autonomic control developed, HR slows to 140bpm
  • by 11th week, systemic ABP is 70/25mmHG, it rises very gradually as sympathetic tone develops and peripheral resistance increases: 80/50mmHg at term

Over same time

  • baroreceptor reflex develops, regulates ABP
  • peripheral chemoreceptors and reflex begin to function: therefore hypoxia evokes primary chemoreceptor reflex
  • foetal bradycardia and peripheral vasoconstriction
  • blood flow to brain is preserved
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14
Q

When do foetal breathing movements (FBM) first appear?
How does FBM change with sleep?
What is the pattern of time spent in FBM?
Describe the coupling seen between FBM and HR

A
  • 11wks
  • irregular breathing pattern in REM sleep, regular breathing at other times
  • exhibits a circadian rhythm, can reflect what the mother is doing
  • this develop in-utero, inspiration –> inhibition of vagus –> tachycardia, stopping breathing –> bradycardia. Coupling in CNS between breathing and heart rate, as seen in the adult
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15
Q

How does FBM change throughout gestation?

Why are FBMs important? x2

A

11 wks –> foetal breathing movements begin - shallow and irregular
34 wks –> become more rhythmic, present 30% of the time, during night and after mother eats.
Play role in development of respiratory muscles, aspiration of amniotic fluid

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16
Q

How do FBMs change during foetal hypoxia? Why?

A

Foetal hypoxia –> decreased FBMs

  • due to local direct effect of hypoxia on central respiratory neurones
  • peripheral chemoreceptor effect on respiration is not yet developed
17
Q

How does FBMs change prior to delivery?

A

incidence of FBMs decreases prior to delivery - predictor of delivery in healthy foetus

18
Q

Describe the respiratory events at birth
What triggers first breath?
How is the first breath made possible?

A
  • fluid that has been in lungs is squeezed out during birth
    First breath
  • triggered by cooling, sensory stimulation and chemoreceptor stimulation - central and peripheral
    Made possible by surfactant
  • secreted by Type II alveolar cells - 28/30 wks
  • under influence of foetal cortisol
  • reduces surface tension force that oppose lung inflation
  • may be inadequate in pre-term baby
    As air move in, forces fluid across alveoli, and surfactant is adsorbed onto alveoli surface
19
Q

Describe the changes in compliance curves after birth

A
  • First breath requires generation of large negative intraplural pressure in order to open the lungs for the first time
  • all subsequent breaths up to two weeks, have gradually increasing FRC and compliance
20
Q

Describe the cardiovascular events at birth

A 
1 = 1st breath --> pulmonary vascular resistance decrease (lungs expand), therefore pulmonary purfusion increases. Greater volume/min return to LA, LA pressure > RA pressure --> FORAMEN OVALE closes 
2 = umbilical cord is clamped --> TPR increases, systemic ABP > pulmonary ABP, flow in DUCTUS ARTERIOSUS reverses, then closes 
3 = reduced flow in umbilical vein because umbilical cord is clamped, therefore DUCTUS VENOSUS constricts and then closes
21
Q

What changes occur in the neonatal period? x5

A
  1. Septal leaflets of foramen ovale fuse within a few days 2. Ductus arteriosus closes within 2 days
    - removal of tonic dilator effect of prostaglandins
    - prostaglandins normally produced in lungs due to low PO2 –> vasodilatory so DA is open
    - after birth, high PO2 in lungs –> decrease prostaglandin synthesis –> DA closes
    - NAIDs can be used to promote closure, bradykinin may also be responsible for closure
  2. Wall thickness of pulmonary arteries and right ventricle decreases - due to decreased pulmonary resistance
  3. Wall thickness of left ventricle increases - ABP gradually increases to 7 years old
  4. Peripheral chemoreceptors ‘reset’ over 2 weeks after birth from foetal PO2 <4.2kPa, rightwards to adult range <12.5kPa
    - baby may be vulnerable to hypoxia during this period - ‘cot death’
22
Q

Describe the problems associated with patient foramen ovale

A

Foramen ovale between L and R atrium may not close

  1. If left-right shunt
    - causes R ventricualar overload –> hypertrophy –> pulmonary HT
    - Eisenmenger syndrome
    - not hypoxic but exercise intolerance
  2. If right-left shunt
    - mixing of oxygenated and deoxygenated blood
    - ‘blue baby’ or Tetrology of Fallot
    - surgery required
23
Q

Describe the problems associated with patient ductus arteriosus

A
  • L ventricular output diverted into pulmonary circulation from aorta
  • leads to pulmonary hypertension
  • right ventricular overload
  • eventually heart failure
  • surgery required
24
Q

Describe pre-eclampsia

A
  • high ABP, proteinuria in the mother –> convulsions?
  • delivery urgent - only cure
  • inflammatory mediators release by hypoxic placenta?
25
Q

Describe IGUR

A
  • associated with high blood pressure, advanced diabetes, malnutrition, substance abuse, smoking
  • poor placental perfusion in mother –> low birth weight
26
Q

Descobre foetal programming

A
  • adverse conditions in-utero including poor nutrition, poor O2 supply, IUGR, lead to adverse effects (e.g. cortisol, oxidative stress, epigenetic processes)
  • thereby to increased risk of CVD, diabetes, obesity, metabolic syndrome in adult life

4/ RED (19 decks)

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