Cardiovascular changes at birth Flashcards
Three types of mammals
Monotremes, marsupials and placentals.
What is required after birth?
Specific and fully organised neurological reflex pathways.
What changes are required to meet this pathway?
Hormonal function, epidermal function, loss of placenta and cardiovascular changes.
Effect of placenta loss
Heat generation needs to be maintained, intestinal, liver, lung and kindey function starts.
Liver function
Increases after birth and becomes vital for life.
Intestinal function
Movement, digestion and absorption begins.
Renal function
Excretion and increased reabsorption becomes vital.
Why are cardiovascular changes needed?
Loss of placenta, intestinal function, liver function and lung function all increase.
Umbilical cord blood supply
2 arteries and one vein.
What blood enters placenta?
Deoxygenated blood from the mother, maternal venule and arteriole spiral in to deposit into sinuses surrounding villi increasing the pressure.
What is the foetal portion of placenta called?
The chorion.
Placenta structure at birth
12cm in radius, 0.5kg when drained of blood, 2cm thick and 10m^2 exchange surface.
Role of placenta
Transfers respiratory gases, nutrients (not triglycerides), metabolic waste and IgG, acts as a heat sink, as a circulatory reservoir, immune modulator and produces hormones.
How are triglycerides given to foetus?
They are absorbed and broken down by lipase to fatty acids.
Where does NH3 from foetus go?
To maternal kodiney.
Immune modulatory function of placenta
Actively suppresses host vs graft reaction.
Hormones produced by placenta
hCG (maintains CL ), progesterones, CRH/oestrogens, placental lactogen (increases maternal serum glucose) and prostaglandins (auto/paracrine).
Foetal blood distribution
20% lungs (50% in adults), 30% to head and upper limbs and 50% to rest of body.
Three issues with placenta
Before birth need to retain umbilical vessel patent, at birth need to transfer blood from placenta to foetus and need to close placental circulation very rapidly.
How much neonate blood is in the placenta?
33%.
When does the placental blood transfuse to neonate?
30% in the first 15 seconds and the rest in the next 2-3 minutes.
What causes placental blood transfusion to neonate?
Positional differences and contractions of uterus to express placenta immediately after birth, creating a pressure gradient between neonate and placenta.
Blood flow in umbilical cord between weeks 34-39
560ml/min.
Blood pressure in foetal artery
70/45.
Placental blood volume at birth
33%.
Umbilical cord structure
55-60 cm tricanulated tube and an allantoic duct, fairly twisted.
Umbilical arteries
Takes deoxygenated blood away from foetus.
They have no internal elastic membrane with little elastin, no adventitia so have Wharton’s jelly instead.
Umbilical vein
Delivers oxygenated blood from the placenta to the fetus, have an elastic layer but with no valves.
Wharton’s jelly
Gel-like porous ECM with the fibrous scaffold made of collagen and elastin with pores containing proteoglycans and hyaluronic acid that bind water to form a viscous fluid.
Purpose of Wharton’s Jelly
Prevents compression of the umbilical cord and maintains the firmness of it.
Fashion of umbilical arteries
Coil around the vein helically.
Blood flow of placenta and foetus
Pulsatile from the foetus to placenta via arteries and a small palse retained in the passive transfer of blood back.
What does umbilical coiling do?
Appears to confer turgor, producing a strong and flexible cord.
What is low umbilical cord twisting indicative of?
Adverse perinatal outcome.
What if Wharton’s jelly does not develop all throughout the cord?
Foetal vessels are not protected from torsional closure.
Umbilical cord twist
7:1 left (counterclockwise) to right.
What causes degree of twisting?
Intrauterine movement with little twisting suggesting compromised foetus.
Effect of hypertwisting
Intrauterine foetal death by compressing foetal vessels beyond capacity of Wharton’s jelly.
Uterine vessel lining metabolism
Highly metabolically active, forming PGE2 and NO.
What do PGE2 and NO do?
Keep blood vessels open.
What do Bradykinin, ANF, Endothellin and Thrombin do?
Bind endothelial receptors activating PLC causing Ca2+ release and MAPK phosphorylation of cPLA2 cleavining phospholipids in Golgi and ER releasing arachadonic acid for prostaglandin production.
What does shear flow cause?
Calcium release.
PGE synthase expression
In the placenta before birth.
PGE synthase
Produces PGE2.
PGE2 effect
PGE2 binds receptor on vascular smooth muscle causing adenyl cyclase formation producing cAMP that activates PKA, phosphorylating MLCK, inhibiting it causing vasodilation.
Where is nitrous oxide produced?
Endothelial cells in umbilical vessels.
What else does PKA do?
Activates HSA2 producing hyaluronic acid for Wharton’s jelly.
Umbilical circulation maintenance
Maintained through gestation, no nervous input to placental vasculature and little catecholamine effect.
What effects smooth muscle contractility?
Paracrine signals produced by neighbouring epithelia such as PGE2 and NO.
What drives NO expression?
Shear flow, endothelin, bradykinin and ANP.
Order of umbilical circulation closing
Reduction of vessel PGE2 synthase, local mediators induce increased local thromboxane and serotonin (vasoconstrictors), stretching of umbilical cord causes spasm, cooling to 18C causes vessel clamp and high external oxygen tensions.
Effect of increased local thromboxane
Diverts prostaglandin synthesis and is a vasoconstrictor.
What do high external oxygen tensions do?
Close artery not umbilical vein.
Effect of Wharton’s jelly in closing umbilical circulation
It swells and adds pressure to vessels.
NO dependent vasodilation
Releases Ca2+ that activates eNOS converting L-Arg into L-Citralline.
What activates guanylyl cyclase?
NO diffusing into smooth muscle.
Priority for oxygenated blood in embryo
The developing brain, then heart and then the rest of body.
What does umbilical vein fuse with?
Hepatic portal vein.
What does umbilical vein fusion cause?
Oxygenated blood goes to liver first then to the right side of heart and then the lungs.
Issues with umbilical vein fusion
Lung and liver aren’t priority with other tissues needing the nutrients and before birth the lung has high resistance vascular bed so high vascular pressures required to force blood through.
How are issues with umbilical vein fusion overcome?
Development of vascular shunts that can be physiological (catecholamine) or anatomical .
3 embryonic vascular shunts
Ductus venosus, ductus arteriosus and foramen ovale.
Ductus venosus
Shunts 30% of blood directly to inferior vena cava so blood bypasses liver and goes to heart.
Vena cava blood flow
Laminar with oxygenated blood from ductus venosus and deoxygenated blood from inferior vena cava.
Foramen ovale
Transfers 50% blood from right to left atrium, bypassing the lungs and sending it to the aorta, blood is highly oxygenated and nutrient-rich.
Issues with ductus venosus and foramen ovale
50% of blood still would be going to the lungs which has very high resistance and doesn’t need it (only needs 20%) so use another shunt to allow some to go to brain.
Ductus arteriosus
Connects pulmonary artery to proximal descending aorta allowing blood to bypass lungs, blood to arms, head and brain are diverted off before relatively low O2 and nutrient blood are added.
Saturation at foramen ovale
67%.
Saturation at umbilical vein
80%.
Saturation at ductus arteriosus
52%.
Organ of oxygen, nutrients and waste transfer pre-birth
The placenta and maternal liver helps with some functions.
Organ for gas transfer after birth
Lungs, so need to shut shunts.
Closure of ductus arteriosus
Occurs minutes after birth, fully closed by 24-48hrs by birth, reduction in prostaglandins and lower receptor expression causes smooth muscle constriction (2-3 mins after birth) and ductus venosus smooth wall undergoes fibrosis making the duct a ligament.
What causes prostaglandin reductions?
Loss of placenta, increased O2 tension and increased circulation.
What causes fibrosis of ductus venosus smooth wall?
Develop profound ischemic hypoxia that forms Veg-F, TGF beta and imflammatory mediators.
Why may the ductus arteriosus not close?
Prematurity due to low lung function, thin muscle wall in immature DA, expression of PGE2 and NO retained in cell walls keeping muscle relaxed, or limited ischemia stops fibrosis allowing reopening.
Effect of open ductus arteriosus
Join in right and left circulation, overloading lungs with fluid and reduces blood to other tissues.
Signs of open ductus arteriosus
Poor exercise tolerance, cyanosis and weight loss.
What keeps ductus arteriosus open in utero?
High concentrations of vasodilatory prostaglandins formed by the placenta with high levels of EP4 (PG receptor) inhibiting myosin kinase.
Closure of ductus venosus
Sphincter closes in lower oxygen tension, with the smooth muscle weakly responsive to PGE2 vasodilators and is fully closed by 2 weeks.
Why might ductus venosus not close?
Prematurity or congenital disease.
Effects of open ductus venosus
Poor weight gain, hepatic encephalopathy caused by gut derived toxins and ammonia with nervous system effects.
Closure of foramen ovale
At birth the infant takes a breath, decreased resistance in pulmonary vasculature causes increased left atrial pressure against right atrial pressure, forcing it closed.
How many people have a closed foramen ovale?
75%.
Risks of open foramen ovale
Risk of paradoxical emboli such as after deep vein thrombosis or in patent foramen ovale predisposing risk factor for the bends as a portion of venous blood carrying nitrogen doesn’t pass through lungs.
