special situation- petal exchange Flashcards
what happens to the mother during pregnancy?
- big increase in cardiac output
- increased blood volume and peripheral vasodilatation
- normal ABP but a large pulse pressure
- ## increased production of relaxin, oestrogen and progesterone
outline some further systemic cardiovascular changes which occur during pregnancy
- CO increases progressively by up to 45%
- ABP declines in proportion to increased CO
- increased BRR reflex (due to the excessive vasodilatation preventing a large drop in ABP)
- increased RAA activity, raising plasma volume
- increased erythropoiesis to match the increased plasma volume
- structural changes such as hypertrophy of the LV wall
what are the peripheral effects of the hormone relaxin?
- important in inducing systemic vasodilatation and renal vasodilatation in pregnancy (via NO)
- stimulates ADH release promoting drinking and water retention in kidneys
why is oestrogen important?
- stimulates RAA system increasing synthesis of angiotensinogen promoting sodium absorption at the DCT
what happens during 02 and co2 exchange at the foetus?
- the fatal umbilical vein blood does not achieve equilibrium with maternal blood for 02 of the uterine artery
- fetal umbilical vein does almost achieve EQ with maternal blood for CO2
- however the foetus is still supplied with adequate oxygen
how does the structure of fetal Hb differ with adult Hb?
- is comprised as 2 alpha and 2 gamma polypeptide chains
- whereas adult Hb is composed of 2 a and 2 b chains
- gradually disappears after birth from 6 months
why does fetal Hb have a higher affinity for 02?
- is explained by its lack of interaction with 2,3-DPG (due to gamma side chains)
- fetal Hb curve is left shifted
- has a much lower P50 than adult Hb (higher saturation at a lower P02)
- therefore at P02 of 4.2kpa, HbF is 75% saturated
- the Bohr shift also further separates the 2 curves even further apart
how does the metal arterial Hb content differ to an adults?
- fetal HB has a higher concentration compared with maternal blood
- 18g/dl vs 15 g/dl in mother
- therefore at any given P02 fatal blood carries more 02
list the locations of the 3 shunts of which develop in fetal circulation
- the ductus venosus –> short circuits straight through liver into vena cava
- foramen ovale –> hole in the heart allowing blood to pass right to left atria
- ductus arteriosus–> flow between pulmonary artery and aorta
how is flow ensured through these shunts?
Flow through each shunt is dependent on intravascular pressure gradient across the shunt keeping blood moving in particular direction
1) Umbilical vein P > IVC P, blood movement always into fetal circulation 2) RatrP > LatrP (blood flows from R --> L atria of heart) --> small atrial pressure low due to less blood flow in fetal lungs 3) Pulm ABP > aortic ABP (due to high resistance in pulm due to less blood flow and less expansion of vessels)
how do the fatal and adult cardiac outputs differ?
- adult circulation there are no shunts so RSV= LSV
- shunting in the foetus means LSV does not equal RSV
- LV receives only a modest amount which comes back from the lungs
how is control of fetal circulation exhibited ?
- circulating catecholamines and other locally released vasoactive substances play a part
- these act on a/b ADRs
- receptors mature early in gestation independently of ANS innervation
- circulation is under tonic adrenergic vasoconstriction influence mainly via serum NA
when does the baroreceptor reflex develop and what are the effects of chemoreceptor activation?
- develops 28 weeks onwards
- hypoxia evokes primary chemoreceptor reflex (peripheral) –> fetal bradycardia and peripheral VC (all reducing heart 02 consumption and protecting it)
- also preserves blood flow to the brain
in regards to fetal breathing movements what happens at 11 weeks?
- FBMs begin –> they are shallow and irregular
- at 34 weeks they become more rhythmic (50b/min)
- are present 30% of time during night and after maternal meals
- ## related to calorie intake
why do FBMs occur?
- allows strengthening and pattern gaining of respiratory muscles
- play a developmental role in respiratory muscle
- allows aspiration of amniotic fluid from fatal lungs
- the first breathe requires enormous ventilatory effort so it is Important the foetus has been training these respiratory muscles in utero
why do FBMs decrease during fatal hypoxia?
- due to local effect of hypoxia on central inspiratory neurones
- peripheral chemoreceptor reflex on respiration is not yet apparent
- incidences decrease prior to delivery
what triggers the first fatal breath?
- cooling, sensory stimulation and chemoreceptor activation (C + P)
- declining 02 and hypercapnia once the fatal connection via the umbilical cord is lost (during clamping)
what makes the first fatal breath possible ?
- release of surfactant by type 2 pneumocytes
- under influence of cortisol
- reduces surface tension -> force that opposes lung inflation
- · As air moves in forces kung fluid across alveoli wall and surfactant is absorbed on alveolar surface and fluid is forced out into interstitial space into P capillaries
what are the cardiovascular events at birth?
- 1) 1st breathe the pulmVR decreases as lungs expand and there is a greater volume return to L.ATr
- L.atrial > R.atrial P
- this closes the foramen ovale
2) umbilical cord is clamped therefore TPR increases so systemic ABP> pulp ABP
this closes the ductus arteriosus reversing flow and then closing it
3) there is reduced flow in the umbilical vein because the UC is clamped
therefore the ductus venosus constricts and then closes
what happens to the atria during the neonatal period ?
- septal leaflets of foramen ovale fuse along wall of atrium (2 chambers)
- ductus A closes within 2 days initiated by higher P02 leading to reduced production of local PGs (which usually dilate)
- NSADS can be given to induce closure
what happens to wall thickness during the neonatal period ?
- Wall thickness of pulmonary arteries and right ventricles decreases relative to left side (resistance of P circulation has decreased) –> no longer needed to be as big
- Wall thickness of LV increases –> due to increasing TPR
ABP gradually increases –> until 7 yrs
- Wall thickness of LV increases –> due to increasing TPR
what happens to peripheral chemoreceptors during the neonatal period ?
- Peripheral chemoreceptors are ‘re-set’ over 2 weeks after birth from fetal p02 range (when firing at p02 4.2kpa)
- Shifted to the adult p02 range –> so activated when p02 drops below 12.5kpa
- Threshold shifts rightwards
