Neonatal cardiorespiratory physiology Flashcards
What do the umbilical arteries and veins carry?
de-oxgenated blood from the foetus to the placenta
veins carry oxygenated blood to the foetus
Oxygen exchange in the uterine and umbilical artery
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.
Carbon dioxide exchange in the uterine and umbilical artery
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
Composition of foetal haemoglobin
2 alpha and 2 gamma chains
Has a higher affinity for oxygen as it has a lower concentration of 2-3, DPG
Describe the foetal haemoglobin curve compared to that of an adult
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
How is foetal circulation arranged to optimise oxygen delivery esp. to the brain?
3 shunts:
1. ductus venosus -allows blood from umbilical vein to short circuit through the liver to join the IVC
- foramen ovale -natural hole between right and left atrium
- 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.
Differences between foetal and adult cardiac output?
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)
Control of foetal circulation
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
What is the HR at 11 weeks
160bpm
What is the HR from week 28
autonomic control develops thus reduces the HR to 140bpm
The vagus nerve develops and slows it down
Describe the development of the systemic ABP
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
Foetal breathing movements
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
Respiratory events at birth
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
Changes in compliance and functional residual capacity
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
Cardiovascular events at birth
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