Fetal physiology and the CTG Flashcards
What does normal variability demonstrate and why is this reassuring?
Sympathetic NS - adrenalin and noradrenalin act on SA node to increase HR and blood pressure
Parasympathetic NS - acetylcholine act on SA node to reduce HR and BP
Variability demonstrates normal development and good oxygenation of the CNS and ability to self-regulate HR and BP to respond and compensate for external pressures
What is the fetal response to a gradual fall in available oxygen?
The chemoreceptors in carotid sinus, aortic arch and brainstem detect low partial pressure of oxygen, and stimulate the cardioregulatory centre in the medulla oblongata. Increased sympathetic nerve firing stimulates the adrenals to release adrenalin (80%) and noradrenalin (20%). Adrenalin acts of beta-adrenergic receptors, and noradrenalin acts as neurotransmitter for sympathetic neurones.
They act to increase HR and increase peripheral vasoconstriction - both increasing BP (and O2 delivery) and directing blood flow away from peripheries in favour of perfusion key organs (heart, brain, adrenals).
This causes a high baseline rate and reduced variability as the sympathetic drive outweighs the parasympathetic.
What is the fetal response to a significant fall in available oxygen?
The chemoreceptors in carotid sinus, aortic arch and brainstem detect low partial pressure of oxygen, and stimulate the cardioregulatory centre in the medulla oblongata. This triggers the vagus nerve and ACH is secreted to act on the SA node to reduce HR, thus causing a deceleration.
Where are the baroreceptors located and what is their function?
Carotid sinus, aortic arch and brainstem.
They detect hypertension and hypotension.
Their mode of action is to increase vagal stimulation and ACH release (causing drop in HR and BP), or switch off vagal firing and ACH release (causing rise in HR and BP).
What happens during cord compression?
Chemoreceptors detect sudden and significant drop on O2 concentration of fetal blood. They stimulate vagus nerve and increase ACH release, which acts on SA node to cause a deceleration in HR.
As cord is released after contraction, the relative hypotension from low cardiac output and removal of downstream obstruction is detected by baroreceptors, and causes reduced vagal firing and ACH release, thus causing increase in HR and BP.
Overshoot is caused by increased sympathetic drive in response to hypoxia, as it is unopposed by parasympathetic innervation.
How does the fetus compensate for acute versus chronic hypoxia?
Acute
- sympathetic and parasympathetic effects on fetal HR to increase/reduce HR
- redirecting blood flow from gut/peripheries in order to maintain constant perfusion to essential organs (brain/adrenals/heart)
- minimising movements to reduce oxygen requirement
Chronic - (in addition to above) increase fetal Hb concentration to maximise oxygen carrying capacity.
Fetal response to hypoxia
Aim of fetus: decrease myocardial workload by slowing FHR—–> Deceleration
If this is insufficient to maintain adequate oxygenation —> conserves non essential activity therefore stops moving —-> lack of accelerations
If intrapartum hypoxia continues:
—> Release of catecholamines to increase HR which increase oxygenation from placental bed and results in peripheral vasoconstriction to divert non essential blood flow from periphery to central organs. Also causes breakdown of glycogen to glucose for use in myocardium
Compensated response **–> Rise in baseline HR but normal variability
Still hypoxic:
DECOMPENSATION*
loss of variability due to myocardial hypoxia and acidosis —-> unstable baseline and a progressive stepwise reduction of the HR (preterminal)
How is the parasympathetic nervous system mediated?
Baroreceptors
- Stretch receptors in carotid sinus and arch of aorta
Chemoreceptors
- Found on aortic and carotid bodies and in brain
How does the fetal response to head/cord compression manifest?
Baroreceptor driven
- Stretch receptors in carotid sinus and arch of aorta
- In labour, both fetal heart and umbilical cord may undergo compression
- Compression = Increased peripheral resistance => increased blood pressure => stimulation of baroreceptors => parasympathetic NS triggered => vagus nerve triggers AV node to slow down HR
- Baroreceptors also decrease sympathetic stimulation
- Seen as a sudden decrease and rapid return when compression finishes- variable decels
- In the absence of other abnormalities on CTG (e.g. rising BR) this shows mechanical stress and no further intervention other than observation is needed
Describe fetal response if chemoreceptors triggered?
- On aortic and carotid bodies + in brain
- Respond to changes blood- acidaemia and hypoxia
- Stimulation of these chemoreceptors leads to PS stimulation and therefore drop in FHR
- When stimulated, take longer to return to BR as oxygenated blood needs to return to maternal venous sinuses to remove the stimulus to chemoreceptors
- Late onset and late recovery —> LATE decelerations
- Often associated with fetal acidosis
What is the sympathetic response to hypoxia?
Release of catecholamines from adrenals
Purpose:
- Increase HR to increase oxygemation from placental bed
- Peripheral vasoconstriction to achieve effective redistribution of blood centrally
What causes normal variability?
interaction between sympathetic and parasympathetic systems- normal variability means the fetus is unlikely to be hypoxic
Cause of a fetal tachycardia?
- maternal pyrexia / dehydration
- infection
- prematurity
- hypoxia
How does a rise in temperature affect a fetus’ ability to deal with hypoxia?
Can predispose fetus to neurological injury from hypoxia
Cause of accelerations?
Fetal movement and somatic NS
Sign of fetal well being
