FOETAL CIRCULATION

• The fetal circulation is the circulatory system

of a human fetus, encompassing the entire
fetoplacental circulation which includes the
umbilical cord and the blood vessels within the
placenta that carry fetal blood.
 Umbilical Cord
• 2 umbilical arteries: return deoxygenated
blood, wastes, CO2 to placenta.
• 1 umbilical vein: brings oxygenated blood and
nutrients to the fetus.
 Placenta
• Organ that connects the developing fetus to
the uterine wall.
• Functions as respiratory centre,as a site of
filtration for plasma nutrients and wastes.
• Two components:
- the fetal placenta(Chorion frondosum),which
develops from the fetus
- the maternal placenta(Decidua basalis), which
develops from the maternal uterine tissue
• Foetal hemoglobin has higher affinity for
oxygen than adult hb,
which allows diffusion of oxygen from the
mother's circulatory system to the foetus.
• Water, glucose, amino acids, vitamins,
and inorganic salts freely diffuse across
the placenta along with oxygen.
• Foetal circulation differs from the adult one by the
presence of 3 major vascular shunts :

- Ductus venosus: between the umbilical vein and IVC

- Foramen ovale: between the right and left atrium
- Ductus arteriosus: between the pulmonary trunk
and descending aorta
4 unique FETAL CVS structures : FOUR SHUNTS
• Placenta  Oxygenated blood  Umbilical vein

Hepatic circulation Bypasses liver & joins IVC

via ductus venosus

Partially mixes with poorly oxygenated IVC

blood derived from lower part of fetal body

• Combined lower body blood + umbilical venous blood flow passes through IVC to
the right atrium
• Part of IVC blood with high O2 concentration
goes into LA via Foramen Ovale.
• Remaining IVC blood enters RV.
• Most of SVC blood goes to the RV traversing the
tricuspid valve and into the pulmonary trunk.
Because the pulmonary arterial circulation is
vasoconstricted, only about 10% of right
ventricular outflow enters the pulmonary
arteries. The rest 90% blood bypasses the lungs
and flows through the ductus arteriosus into the
descending aorta to perfuse the lower part of
the fetal body.
• The left atrium receives blood from :
- Pulmonary veins
- Right atrium through the foramen ovale
• This blood passes into left ventricle then into the
aorta supplying head,neck,brain and upper
extremities through carotid and subclavians,
then mixes with poorly oxygenated blood from
the ductus arteriosus and perfuses the rest of the
body through branches of descending aorta.
 Overview of fetal circulatory
dynamics
• Parallel arrangement of two main arterial
systems and their respective ventricles.
• Mixing of venous return and preferential
streaming.
• High resistance and low flow of pulmonary
circulation.
• Low resistance and high flow of systemic
circulation.
• Presence of shunts.
 Perinatal circulatory transition
At birth

Mechanical expansion of lungs Increase in arterial PO2

Rapid DECREASE in pulmonary vascular resistance

Removal of the low-resistance placental circulation

INCREASE in systemic vascular resistance.

 1. High arterial PO2

Constriction of ductus arteriosus

It closes, becoming the ligamentum arteriosum.

• Right ventricle output now flows entirely into the
pulmonary circulation.

• Pulmonary vascular resistance becomes lower than

systemic vascular resistance

Shunt through ductus arteriosus reverses &

becomes left to right.
2. Increased volume of pulmonary blood flow
returning to left atrium

Increases left atrial volume and pressure

Closure of foramen ovale (functionally)

Becomes Fossa Ovalis.

• CLOSURE of :

- Foramen ovale :
Functional Closure: 3rd month of life.
Anatomical closure of septum primum & septum
secundum by 1 year of age.

- Ductus arteriosus :
Functional Closure: By 10–15 hr in a normal neonate.
Anatomic closure: May take several weeks.
In a full-term neonate, oxygen is the most important
factor controlling ductal closure.
When the PO2 in the blood passing through the ductus
reaches about 50 mm Hg , the ductal wall constricts.
 3. Removal of the placenta from the circulation

Also results in closure of the ductus venosus.

• The left ventricle is now coupled to the high-resistance

systemic circulation  its wall thickness begins to
increase.

• In contrast, the right ventricle is now coupled to the low-

resistance pulmonary circulation  its wall thickness
decreases slightly.
 FETAL NEWBORN
Gas exchange Placenta Lungs

RV,LV circuit Parallel Series

Pulmonary circulation Vasoconstricted Dilated

Fetal myocardium
Contractility,Compliance Less Good

Dominant ventricle Right Left

Change in Structure Umbilical vein Ligamentum teres

Umbilical artery Medial umb ligament
Ductus venosus Ligamentum venosum
Ductus arteriosus Ligamentum arteriosum
Foramen ovale Fossa ovalis
Persistent Pulmonary Hypertension of
the Newborn (PPHN)
• Disruption of normal transition of fetal
circulation to neonatal circulation
• “Persistent fetal circulation”
• Suprasystemic resistance in the pulmonary
vasculature

PVR > SVR

• Leading to perpetuation of R->L shunt through
foramen ovale and/or ductus arteriosus
• Resulting in diminished pulmonary perfusion
and systemic hypoxemia
• Incidence is 1-2 /1000 live births
• More common among full term and post term
neonates
• In preterm neonates,RDS may be complicated
by PPHN
 RISK FACTORS
• Maternal : fever,anemia,pulmonary
disease,UTI,DM,drugs like
aspirin/NSAID’s/SSRI’s,smoking(antenatally)
• Foetal :
1.Birth asphyxia – prolonged hypoxemia leads to
release of humoral factors which cause
vasoconstriction and remodelling of pulmonary
vasculature
(abnormal muscularization of arterial wall with >>
medial thickness)
 decreased cross sectional area of the vessels
>> PVR.

2.Parenchymal lung diseases like

pneumonia,surfactant deficiency,meconium
aspiration – reversible,due to vasospasm.
3.Pulmonary developmental abnormalities like
CDH,Potter syndrome (parenchymal hypoplasia)
Alveolar capillary dysplasia (malalignment of
pulmonary veins and arteries).

4. Congenital heart disease (left and right sided

obstructive lesions),myocardial
dysfunction,myocarditis,intrauterine constriction of
DA.
5.Infections- viral/bacterial pneumonias,sepsis cause
vasospasm by release of thromboxanes,by
suppressing endogenous NO production and by
direct endotoxin mediated myocardial depression.

6. Genetic predisposition – low levels of NO

metabolites,arginine,diminished endothelial NOS
expression.

7. Mechanical factors like low cardiac

output,hyperviscosity,polycythemia.
 PATHOPHYSIOLOGY
Pulmonary vasospasm
Vascular remodelling with smooth muscle hyperplasia
 TYPES

• PRIMARY PPHN

• SECONDARY PPHN
 DIAGNOSIS
• Presents within 18 hours of birth
• Respiratory distress
• Marked cyanosis
• Differential cyanosis between regions
perfused by preductal and postductal
vasculature
• Prominent precordial impulse
• Loud,single or narrowly split S2
• Systolic murmur
• A gradient of 10% or more in oxygen
saturation between preductal and postductal
areas
• CXR appears normal or shows associated
parenchymal lung disease
• ECG shows RV strain or hypertrophy
• ECHO shows hemodynamic shunting,helps to
evaluate ventricular function,tricuspid
insufficiency and to exclude congenital heart
disease
• Color doppler shows presence of
intracardiac/ductal shunting
 MANAGEMENT
• Case fatality rate of 30-60%
• Requires immediate intervention to reverse
hypoxemia,improve pulmonary and systemic
perfusion,preserve end organ function
• Supplemental oxygen
(postductal SaO2 is > 90% and < 98%)
• Intubation,mechanical ventilation
(persisting hypoxemia,hypercapnea,acidosis)
o In the absence of pulmonary disease -> mechanical
ventilation with rapid,low pressure and short
inspiratory time
o PPHN + parenchymal lung disease ->
High frequency oscillatory ventilation/High
frequency jet ventilation (MAS,air leak)
 • Sildenafil
o PDE-5 inhibitor
o Inhibits metabolism of NO
o >> available NO
o Dose : 0.4mg/kg/dose IV over 3hrs
followed by a continuous infusion of
1.6mg/kg/24hrs
for upto 7days
• iNO

diffuses into smooth muscle cells

>>cGMP

relaxes vascular smooth muscle

pulmonary vasodilation
o Started at a dose of 20ppm.
o Delivered via the ventilator circuit.
o Most effective when administered after adequate
alveolar recruitment(by use of HFOV / surfactant).
o When the condition improves,dose is slowly
tapered by halving.
o Stopped when SaO2 is adequate on FiO2 of < 50%
and i NO dose of 1ppm.
o High doses lead to methemoglobinemia.
o Abruptly stopping iNO leads to rebound hypoxemia.
 • ECMO
o Extra Corporeal Membrane Oxygenation
o Used when conventional therapy and iNO
treatment fails
o Criteria to start ECMO : oxygenation index of
>30 in 2 ABG’s taken 30 minutes apart
&
alveolar-arterial oxygen difference > 600
• Intravascular volume support
• Dobutamine and vasopressors
• Correct hypoglycemia,hypocalcemia
(to provide adequate substrates to the myocardium)
• Neutral/alkalotic pH reduces PVR
(by sodium bicarbonate boluses)
• Sedation and analgesia with fentanyl/morphine
(prevents release of catecolamines which activate
pulmonary adrenergic receptors)
• Muscle relaxants like pancuronium
• Correct polycythemia,hyperviscosity
(partial exchange transfusion with normal saline to
maintain HCT between 50-55%)
• Other therapies : Magnesium sulfate , adenosine ,
tolazoline , calcium channel blockers , inhaled
prostacyclin , inhaled ethyl nitrite
 PROGNOSIS
• Neurodevelopmental sequelae in 15-20%
• Hyperventilation reduces cerebral perfusion,
leads to sensorineural hearing loss
• Prolonged ventilation leads to development of
chronic lung disease
• 20% risk of rehospitalization within 1 year of
discharge