eLFH - The Foetal Circulation Flashcards
Where does gas exchange occur in foetal circulation
Placenta
Placenta receives deoxygenated blood via umbilical arteries and returns oxygenated blood via umbilical vein
Why is foetal circulation “shunt dependent”
Foetal circulatory system has preferential streaming of oxygenated blood and intracardiac and extracardiac shunts to ensure most highly oxygenated blood is received by brain and myocardium
Describe foetal circulation
Deoxygenated blood to placenta via umbilical arteries
Oxygenated blood from placenta via umbilical vein
50-60% umbilical venous blood bypasses hepatic circulation via ductus venosus to enter IVC
Eustachian valve in IVC directs more oxygenated blood along dorsal IVC and across foramen ovale into LA
Highly oxygenated blood ejected via LV to ascending aorta, to brain and coronary circulation
Deoxygenated blood from SVC + anterior IVC flow directed across tricuspid into RV
RV ejected into pulmonary arteries
High pulmonary vascular resistance so only 12% of RV output enters pulmonary circulation
Remaining 88% RV output crosses ductus arteriosus into descending aorta
Descending aorta supplies lower half of body
Umbilical arteries arise from iliac arteries
Venous blood which forms SVC deoxygenated blood
Jugular venous blood
Coronary sinus
Venous blood which forms deoxygenated anterior IVC blood
Venous blood from extremities
Hepatic venous flow
Partial pressure O2 of blood in umbilical vein
~4.7 kPa
O2 saturations of blood in umbilical vein
~80%
O2 saturations of blood in left atrium
~65%
Partial pressure of blood in descending aorta which supplies lower half of the body (distal to ductus arteriosus)
~2.7 kPa
Oxygen saturations as different points within the foetal circulation - in picture form
Combined ventricular output definition
Combined cardiac output of both ventricles in one minute
Use of combined ventricular output
Used to define and measure foetal cardiac output
In adults there are no shunts so RV and LV stroke volumes are equal. Therefore CO defined as volume of blood ejected by one ventricle in one minute
However intracardiac and extracardiac shunts in foetal circulation mean RV and LV stroke volumes are not equal
Percentage of venous return received by RV
65%
Percentage of venous return received by LV
35%
Cause of high Pulmonary vascular resistance in foetus
Foetal pulmonary arterioles have high muscle mass and high resting tone
Foetal lungs are collapsed with low resting oxygen tension
Ductus arteriosus contains muscle that is sensitive to oxygen tension and vasoactive substances
Mechanisms of maintaining patent ductus arteriosus in utero
Low oxygen tension
Vasodilation effect of prostaglandin E2
Reasons gas exchange in the placenta is less efficient than gas exchange in the lung
Larger minimum diffusion distance in placenta
Blood-blood permeability lower in placenta
How is less efficient gas exchange in placenta offset
Large surface area of gas exchange compared to the size of the foetus
Maternal and foetal blood flow to placenta
Haemoglobin oxygen dissociation curve of adult Hb compared to foetal Hb
HbF has lower content of 2,3-DPG shifting O2 dissociation curve to left
2,3 DPG
2, 3 diphosphoglycerate
Foetal Hb concentration at term and why
160 - 180 g/L
Increase oxygen content of blood
Bohr effect definition
As level of CO2 in tissue rises, affinity of Hb for O2 decreases
Double Bohr effect
CO2 excreted by foetus is removed in placenta into maternal intervillous sinuses
Higher PCO2 in maternal side increases O2 unloading of maternal Hb
Lower PCO2 in foetal side (as removed in placenta) leads to better oxygen loading of foetal Hb
Rate of increased uterine blood flow during pregnancy
Increases 20 fold during pregnancy
Foetal percentage of HbF vs HbA
75% HbF
25% HbA
When does high HbF in foetus become disadvantage
After birth
Adaptations that need to be made as foetus transitions to post natal life
Gas exchange transfers from placenta to lungs
Foetal circulatory shunts must close
Left ventricle output must increase
How does pulmonary vascular resistance decrease at birth
Expansion of lungs
Dramatic fall in PVR
8-10x increase in pulmonary blood flow
Improved oxygenation of neonatal blood reverses hypoxic pulmonary vasoconstriction
Effect of drop in pulmonary vascular resistance on circulatory system at birth
Increased pulmonary blood flow causes massive rise in venous return to LA
Decrease in IVC flow reduces venous return to RA
Therefore LA and RA pressures equalise
Foreman ovale flap pushed against atrial septum and closes atrial shunt
How long does it take for foreman ovale to close
Initially closes in minutes to hours after birth
Anatomic closure occurs later by tissue proliferation
Closure of ductus arteriosus
Simultaneous with drop in pulmonary vascular resistance, DA becomes bi-directional
Increased PO2 in neonatal blood causes direct constriction of DA smooth muscle (exact mechanism not known)
PGE2 produced by placenta also drops adding to constriction of duct
Closure of ductus arteriosus timing
Functional closure of DA by 96 hours
Anatomical closure later by endothelial and fibrous tissue proliferation
Closure of ductus venosus
Placental circulation removed causing drop in flow through ductus venosus and fall in venous return through IVC
DV closes passively 3-10 days after birth
Persistent foetal circulation
Circumstances can occur which revert neonate back to foetal circulation - pathophysiological state termed persistent foetal circulation
Patent ductus arteriosus
Failure of DA to close
Left to right shunt
Increased volume and workload of LV
Eventually leads to left heart failure
Ventricular septal defect
Well tolerated in foetus as LV and RV pressures are equal
After birth, SVR increases and PVR decreases
Causes left to right shunt
Leads to congestive heart failure
Tetralogy of Fallot features (two most important features first)
Pulmonary stenosis resulting in RV outflow obstruction
Ventricular septal defect
Right ventricular hypertrophy
Overriding aorta
Consequences of tetralogy of Fallot after birth
As foetus, depending on severity of pulmonary obstruction, pulmonary blood flow is dependent on ductus arteriosus
After birth as DA closes, develop right to left shunt
Severe cyanosis
Prostaglandin infusion to re-establish DA flow is vital to stabilise these neonates
Transposition of the great arteries origin and initial presentation
Abnormal rotation and separation of arterial truncus during embryogenesis
Aorta arises from RV and pulmonary artery from LV
To maintain arterial O2 sats compatible with life relies on PFO, VSD or PDA
Management of Transposition of the Great Arteries
Re-establish ductus arteriosus patency with prostaglandin infusion
Balloon atrial septoplasty under echo guidance on PICU
Complete surgical repair electively at later date once neonate has been stabilised
