Neonatal cardiorespiratory physiology Flashcards

1
Q

What do the umbilical arteries and veins carry?

A

de-oxgenated blood from the foetus to the placenta

veins carry oxygenated blood to the foetus

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2
Q

Oxygen exchange in the uterine and umbilical artery

A

The uterine artery carries PO2 at 12.7kPA and leaving the placenta in the vein is 5.6kPA.
Loss of O2 across the placenta

Umbilical artery has a low O2 of 3.2kPA from the foetus and then back to the foetus is 4.2kPA.

Quite low compared to usual arteries.

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3
Q

Carbon dioxide exchange in the uterine and umbilical artery

A

Uterine artery has a low pCO2 of 5.3kPA, increasing in the vein to 6.4kPA

Umbilical artery coming from the foetus has pCO2 of 6.6kPA and in the vein, 5.8kPA

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4
Q

Composition of foetal haemoglobin

A

2 alpha and 2 gamma chains

Has a higher affinity for oxygen as it has a lower concentration of 2-3, DPG

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5
Q

Describe the foetal haemoglobin curve compared to that of an adult

A

Foetal haemoglobin curve is shifted to the left
It has a lower p50 so oxygen can easily diffuse from the maternal blood
The bohr shift pushes the adult curve to the right but the foetal curve to the left, so more oxygen can be saturated in the haemoglobin

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6
Q

How is foetal circulation arranged to optimise oxygen delivery esp. to the brain?

A

3 shunts:
1. ductus venosus -allows blood from umbilical vein to short circuit through the liver to join the IVC

  1. foramen ovale -natural hole between right and left atrium
  2. ductus arteriosus -junction that joins the output of right ventricle to the aorta stopping the blood from passing through the lungs

All dependant on pressure gradients.

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7
Q

Differences between foetal and adult cardiac output?

A

In adult circulation there are no shunts so right SV = left SV

In foetus, there is shunts so the SV is not equal. RV receives 65% of venous return and LV only receives 35%.
Therefore foetal cardiac output = combined ventricular output (CVO)

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8
Q

Control of foetal circulation

A

Adrenal glands produce circulating catecholamines and other hormones and locally released vasoactive substances that all play a part

Circulating catecholamines act on alpha and beta adrenoreceptors

The receptors mature during early gestation to become active but develop independently of the autonomic innervation process

Peripheral circulation of the foetus is under a tonic adrenergic vasoconstrictor influence mainly due to circulating noradrenaline

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9
Q

What is the HR at 11 weeks

A

160bpm

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10
Q

What is the HR from week 28

A

autonomic control develops thus reduces the HR to 140bpm

The vagus nerve develops and slows it down

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11
Q

Describe the development of the systemic ABP

A

By 11th week the systemic ABP is 70/45mmHg but gradually rises as sympathetic tone develops so peripheral resistance increases to 80/55mmHg at birth

Over the same time baroreceptor reflex develops to regulate ABP and the peripheral chemoreceptors/reflex (carotid and aortic bodies) start to function

This means the foetus starts to respond to changes in pressure and PO2

Therefore, hypoxia evokes primary chemoreceptor reflex causing foetal bradycardia and peripheral vasoconstriction

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12
Q

Foetal breathing movements

A

Start to develop from 11 weeks

Both irregular and regular breathing can occur often in REM (rapid eye movement) sleep

Importance is that foetus is trying out the respiratory mechanism and starting to use the breathing muscles (diaphragm and intercostal)

Time spent in foetal breathing movements is pulsatile – higher in the morning At 34 weeks the foetal breathing movements become more rhythmic (50 breaths/min)

Present around 30% of the time especially during the night and after meals had by the mother

They play a role in development of respiratory muscles and aspiration of amniotic fluid

Incidence of FBMs decreases prior to delivery – can be used as a predictor that delivery is going to happen

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13
Q

Respiratory events at birth

A

Fluid taken into the lungs is squeeze out during the birth as it moves through the birth canal meaning this is not so effective during Caesarean birth

The first breath is triggered by change in stimuli – cooling, sensory stimulation and chemoreceptor stimulation both central and peripheral

Breathing is made possible by surfactant secreted by type II cells at weeks 28-30 under the influence of foetal cortisol

It reduces surface tension force that opposes the lung inflation

This may be inadequate in pre-term babies

As air moves in it forces the lung fluid across alveoli and surfactant is adsorbed onto the alveoli surfaces

Fluid is sucked into alveoli and across the alveolar walls into the interstitial space so it can be taken away by lymphatics

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14
Q

Changes in compliance and functional residual capacity

A

First breath generates large drop in intrapleural pressure in order to open the lungs which is made harder by them being fluid filled

Open up the lungs and increase the FRC as lungs become more expanded in resting state

Increases the compliance of the lungs with successive breaths so breathing is easier

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15
Q

Cardiovascular events at birth

A

First breath = decrease in pulmonary vascular resistance as it expands the lungs which pulls and opens up the blood vessels

Increases pulmonary perfusion causing a greater volume per minute is returning from the lungs to the left atrium

Increases the pressure in the left atrium and becomes greater than right atrial pressure causing pressure gradient to reverse and foramen ovale to close

Umbilical cord clamped causing total peripheral resistance to increase as there is no longer blood passing through placental circulation

Systemic ABP increases above pulmonary ABP causing reverse flow through the ductus arteriosus before it then closes

Reduced flow in the umbilical vein due to umbilical cord being clamped

Ductus venosus constricts and collapses before closing therefore losing that shunt across the liver

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16
Q

Changes in the neonatal period

A
  1. foramen ovale fuses within few days
  2. ductus arteriosus closes within 2 days and thought to be initiated by high PO2 of the blood
    - Due to reduction in local synthesis of prostaglandins that are synthesised in the lungs due to low PO2 to act as a vasodilator for ductus arteriosus
    - When PO2 increases the lungs decreases prostaglandin synthesis so lose vasodilatory influence so the ductus arteriosus constricts
    - NSAIDS can be used to promote closure of ductus arteriosus by blocking the COX pathway
    - Local bradykinins may also be responsible for closure

3.thickness of RV decreases and LV increases

  1. peripheral chemoreceptors reset
    - sensitivity has to shift to adult range (foetal below 4.2, adult below 12.5)
    - baby is vulnerable to hypoxia during this period (cot death)
17
Q

What is Eisenmengers syndrome?

A

Foramen ovale between right and left atrium may not close

This causes a left-right shunt so more blood than should be is in the right side of the heart

Causes pulmonary circulation to remodel leading to pulmonary hypertension and in turn causes right ventricular overload and hypertrophy

Due to high resistance and right ventricular hypertrophy can cause the right ventricular pressure to increase above left ventricular pressure to reverse the shunt

This is known as Eisenmenger’s syndrome where oxygenation is then compromised as deoxygenated blood is being pumped around the body

18
Q

What is blue baby

A

If foramen ovale doesn’t close but remains as a right-left shunt then there is mixing of oxygenated and deoxygenated blood causing blue baby

19
Q

What happens if the ductus arterious remains open after birth?

A

Causes left ventricular output to be diverted into pulmonary circulation from aorta

This in turn causes pulmonary hypertension and right ventricular overload leading to heart failure