Fetal Circulation Flashcards

1
Q

Describe the fetal circulation

A

Oxygenated blood from placenta –> umbilical vein to IVC via portal system or venous duct. High oxygenated IVC blood enters RA and goes to either PFO into LA –> LV to developing brain. SVC - RA - RV - arterial duct into systemic circulation.

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2
Q

Proportion of pulmonary blood flow changes with gestation. When does it increase?

A

Increases during 3rd trimester

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3
Q

How can fetal pulmonary blood flow be increased?

A

By pulmonary vasodilator agents (such as o2) administered to mother

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4
Q

What is the maximum cardiac output at term?

A

250ml/kg/min

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5
Q

How much of the fetal cardiac output does the RV and lV contribute?

A

RV 55%

LV 45%

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6
Q

Of the combined output (RV + LV) how much returns to the placenta and how much goes to the fetal organs and tissues?

A

65% returns to the placenta

35% to fetal organs and tissues

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7
Q

Characteristics of the immature fetal heart

A

Less compliant

Less able to generate contractile force for the same degree of stretch

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8
Q

Effects of advancing gestation on fetal heart

A

Allow maturation of excitation-contraction coupling as well as increasing autonomic innervation

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9
Q

What happens to the circulatory system at birth?

A

Shifts from parallel circulation to ‘series’ circulation
Increase in CO from both ventricles
With inspiration –> rapid fall in PVR (due to lung expansion allows new vessels to open and existing vessels to enlarge)
Reduced resistance and decreased PA pressures –> increase Pulmonary blood flow
Lower-resistance placental circulation is removed from systemic circulation (cut cord)
Sudden Increase in O2 tension produced by breathing - alters local PG synthesis –> constriction of arterial and venous ducts

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10
Q

When does functional closure of PDA occur?

A

Within 24-72 hrs

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11
Q

When does anatomical closure of PDA occur?

A

1-2 weeks

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12
Q

When does PFO functionally close?

A

In most cases by 3rd month of life

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13
Q

What could mask signs of underlying structural congenital CV malformations?

A

PFO and venous duct which can potentially allow shunting after birth.

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14
Q

Three principle mechanisms of cyanosis

A

1) Obstruction to PBF, associated with a right-to-left shunt
2) Discordant VA connections with adverse streaming of blood through the heart
3) Mixing of blood which may occur at atrial, ventricular or great artery level (miseducating systemic and Pulmonary venous return is distributed to both PA and aorta)

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15
Q

Where does obstruction occur in patients with cyanosis and reduced pulmonary blood flow (PBF)?

A

May occur at TV, RV, PV or PA level with obligatory communication within the heart, allowing shunting of the blood returning via the systemic veins from the right to the left side of the heart

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16
Q

What are examples of ACHD in patients with cyanosis and reduced PBF?

A

ToF
Pulmonary atresia (with or without VSD)
Tricuspid atresia

17
Q

What causes cyanosis with normal/increased PBF?

A

Complete transposition or complete mixing.

18
Q

At what levels can mixed blood occur?

A
Atrial (Total anomalous PV connection)
Ventricular (functionally single ventricle)
Great arteries (Common arterial trunk)
19
Q

What are some complications of long term cyanosis?

A

Impaired growth
Developmental delay
Chronic hyperaemia –> finger clubbing and polycythaemia, renal dysfunction, hyperuricaemia and acne