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Anaesthetic FRCA Primary - eLFH Obstetrics > eLFH - The Foetal Circulation > Flashcards

eLFH - The Foetal Circulation Flashcards

1
Q

Where does gas exchange occur in foetal circulation

A

Placenta

Placenta receives deoxygenated blood via umbilical arteries and returns oxygenated blood via umbilical vein

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2
Q

Why is foetal circulation “shunt dependent”

A

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

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3
Q

Describe foetal circulation

A

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

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4
Q

Venous blood which forms SVC deoxygenated blood

A

Jugular venous blood
Coronary sinus

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5
Q

Venous blood which forms deoxygenated anterior IVC blood

A

Venous blood from extremities
Hepatic venous flow

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6
Q

Partial pressure O2 of blood in umbilical vein

A

~4.7 kPa

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7
Q

O2 saturations of blood in umbilical vein

A

~80%

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8
Q

O2 saturations of blood in left atrium

A

~65%

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9
Q

Partial pressure of blood in descending aorta which supplies lower half of the body (distal to ductus arteriosus)

A

~2.7 kPa

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10
Q

Oxygen saturations as different points within the foetal circulation - in picture form

A
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11
Q

Combined ventricular output definition

A

Combined cardiac output of both ventricles in one minute

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12
Q

Use of combined ventricular output

A

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

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13
Q

Percentage of venous return received by RV

A

65%

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14
Q

Percentage of venous return received by LV

A

35%

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15
Q

Cause of high Pulmonary vascular resistance in foetus

A

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

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16
Q

Mechanisms of maintaining patent ductus arteriosus in utero

A

Low oxygen tension

Vasodilation effect of prostaglandin E2

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17
Q

Reasons gas exchange in the placenta is less efficient than gas exchange in the lung

A

Larger minimum diffusion distance in placenta

Blood-blood permeability lower in placenta

18
Q

How is less efficient gas exchange in placenta offset

A

Large surface area of gas exchange compared to the size of the foetus

19
Q

Maternal and foetal blood flow to placenta

A
20
Q

Haemoglobin oxygen dissociation curve of adult Hb compared to foetal Hb

A

HbF has lower content of 2,3-DPG shifting O2 dissociation curve to left

21
Q

2,3 DPG

A

2, 3 diphosphoglycerate

22
Q

Foetal Hb concentration at term and why

A

160 - 180 g/L

Increase oxygen content of blood

23
Q

Bohr effect definition

A

As level of CO2 in tissue rises, affinity of Hb for O2 decreases

24
Q

Double Bohr effect

A

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

25
Q

Rate of increased uterine blood flow during pregnancy

A

Increases 20 fold during pregnancy

26
Q

Foetal percentage of HbF vs HbA

A

75% HbF
25% HbA

27
Q

When does high HbF in foetus become disadvantage

A

After birth

28
Q

Adaptations that need to be made as foetus transitions to post natal life

A

Gas exchange transfers from placenta to lungs

Foetal circulatory shunts must close

Left ventricle output must increase

29
Q

How does pulmonary vascular resistance decrease at birth

A

Expansion of lungs

Dramatic fall in PVR

8-10x increase in pulmonary blood flow

Improved oxygenation of neonatal blood reverses hypoxic pulmonary vasoconstriction

30
Q

Effect of drop in pulmonary vascular resistance on circulatory system at birth

A

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

31
Q

How long does it take for foreman ovale to close

A

Initially closes in minutes to hours after birth

Anatomic closure occurs later by tissue proliferation

32
Q

Closure of ductus arteriosus

A

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

33
Q

Closure of ductus arteriosus timing

A

Functional closure of DA by 96 hours

Anatomical closure later by endothelial and fibrous tissue proliferation

34
Q

Closure of ductus venosus

A

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

35
Q

Persistent foetal circulation

A

Circumstances can occur which revert neonate back to foetal circulation - pathophysiological state termed persistent foetal circulation

36
Q

Patent ductus arteriosus

A

Failure of DA to close

Left to right shunt

Increased volume and workload of LV

Eventually leads to left heart failure

37
Q

Ventricular septal defect

A

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

38
Q

Tetralogy of Fallot features (two most important features first)

A

Pulmonary stenosis resulting in RV outflow obstruction

Ventricular septal defect

Right ventricular hypertrophy

Overriding aorta

39
Q

Consequences of tetralogy of Fallot after birth

A

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

40
Q

Transposition of the great arteries origin and initial presentation

A

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

41
Q

Management of Transposition of the Great Arteries

A

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

Anaesthetic FRCA Primary - eLFH Obstetrics (6 decks)

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