FETAL, TRANSITION AND

NEONATAL CIRCULATION

Divya Mishra
Dept of Pediatrics
 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
4 unique FETAL CVS structures : FOUR SHUNTS
 1.Placenta:
 Has the lowest vascular resistance in the fetus.
 Receives the largest amount of combined (Rt +
Lt) Ventricular Output (55%)

COURSE OF FETAL
CIRCULATION:
 2. Superior Vena Cava:
 Drains the upper part of the body,including the brain (15% of
combined ventricular output).
 Most of SVC blood goes to the Right Ventricle.
 3. Inferior Vena Cava:
 Drains lower part of body
and placenta (70% of combined
ventricular output)

 Part of IVC blood with high O2

goes into LA via Foramen Ovale.

 Remaining IVC blood enter

RV and Pulmonary artery.

 Since blood is
oxygenated in the
placenta, Oxygen
saturation in IVC
(PO2 = 26-28%) is higher
than that in SVC (12-14%).
 Most of SVC blood (less oxygenated blood) goes into RV.
 Most of IVC blood (high O2 concentration) is directed by the Crista
Dividens to the LA through Foramen ovale.
 Rest of IVC blood enters RV & pulmonary artery.
 Less oxygenated blood in Pulmonary artery flows through Ductus
Arteriosus to descending aorta and then to placenta for oxygenation.

COURSE OF FETAL
CIRCULATION:
 The Result is:
 Brain and coronary circulation receive blood with higher
concentration (PO2 = 28 mm Hg) than the lower part of the
body (PO2 = 24 mm Hg)

COURSE OF FETAL
CIRCULATION:
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 plus umbilical venous blood
flow (PO2 of ≈26–28 mm Hg) passes through IVC to the
Right atrium and is preferentially directed across the
foramen ovale to the left atrium.
 The blood then flows into the left ventricle and is ejected
into the ascending aorta.

 Fetal SVC blood, which is considerably less oxygenated

(PO2 of 12–14 mm Hg), enters the Right atrium and
preferentially traverses the tricuspid valve, rather than the
foramen ovale, and flows primarily to the right ventricle.
 From the right ventricle  Pulmonary artery.

 Because the pulmonary arterial circulation is

vasoconstricted, only about 10% of right ventricular outflow
enters the lungs.

 The rest 90% blood (which has a PO2 of ≈18–22 mm Hg)

bypasses the lungs and flows through the ductus arteriosus
into the descending aorta to perfuse the lower part of the
fetal body.

 It the returns to the placenta via the two umbilical

arteries.
 Thus, upper part of fetal body (including coronary & cerebral arteries
and those to upper extremities) is perfused exclusively from the Left
ventricle with blood that has a slightly higher PO2 , than the blood
perfusing the lower part of the fetal body, which is derived mostly
from the Right ventricle.

 Only a small volume of blood from the ascending aorta (10% of fetal
cardiac output) flows across the aortic isthmus to the descending aorta.
 LA  LV  Aorta  Ductus arteriosus

Foramen ovale RV
SVC

 upper body
IVC
50% through 50% to
ductus venosus Portal circulation

Umbilical Vein
Oxy.blood

PLACENTA
 Aorta
Deoxygenated blood

Descending aorta

Abdominal aorta

Common iliac artery

Umbilical arteries

PLACENTA
Oxygenation
Umbilical Vein
 The total fetal cardiac output—the combined output of both
the left and right ventricles—is ≈ 450 mL/kg/min.

 Descending aortic blood flow :

-65%  returns to placenta;
-Remaining 35%  perfuses the fetal organs & tissues.

 Right ventricular output is about 1.3 times the left

ventricular flow.

 Thus, during fetal life the right ventricle

-is pumping against systemic blood pressure
-is performing greater volume of work than
LV.
  TRANSITIONAL CIRCULATION:
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.
 TRANSITIONAL CIRCULATION:

 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.
 TRANSITIONAL CIRCULATION:

High arterial PO2 (In several days)

Constriction of ductus arteriosus

 It closes, becoming the ligamentum arteriosum.

 TRANSITIONAL CIRCULATION:
Increased volume of pulmonary blood flow
returning to left atrium

Increases left atrial volume and pressure

Closure of foramen ovale (functionally)

(Although the foramen may remain probe
patent)
Becomes Fossa Ovalis
 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 and mass begin
to increase.

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

resistance pulmonary circulation its wall thickness and
mass decrease slightly.
 The left ventricle in the fetus pumped blood only to the
upper part of the body and brain

 After birth, LV must deliver the entire systemic cardiac

output (≈350 mL/kg/min). (almost 200% increase in output)

 This marked increase in left ventricular performance is

achieved through a combination of hormonal and metabolic
signals, including an INCREASE IN :
-The level of circulating catecholamines and
-The myocardial receptors (β-adrenergic)
(through which catecholamines have their effect)
 When congenital structural cardiac defects are
superimposed on these dramatic physiologic changes, they
often impede this smooth transition and markedly
increase the burden on the newborn myocardium.

 In addition, because the ductus arteriosus and foramen

ovale do not close completely at birth, they may remain
patent in certain congenital cardiac lesions.
 Patency of these fetal pathways may either :
 Provide a lifesaving pathway for blood to bypass a
congenital defect
(eg: -Patent ductus in Pulmonary atresia or
COA.
-Foramen ovale in Transposition of the great
vessels)
or
 Present an additional stress to the circulation
(eg: -Patent ductus arteriosus in a premature
infant,
-RtLt shunt in infants with pulmonary
hypertension)
 Neonatal Circulation:
 Adaptation to extrauterine life: Some of these changes are
instantaneous with the 1st breath, whereas others develop
over a period of hours or days.

 Gas exchange: Transferred from the placenta to the lungs.

 Systemic blood pressure: After an initial slight fall in

systemic BP, progressive rise occurs with increasing age.

 Heart rate: Elimination of Placental

circulation Increase in systemic

vascular resistance
  Decrease in PVR:

 With the onset of ventilation, pulmonary vascular resistance

is markedly decreased, as a consequence of both
active (PO2 related) and passive (mechanical related)
pulmonary vasodilation.

 In a normal neonate, closure of the ductus arteriosus and the

fall in pulmonary vascular resistance result in a decrease in
pulmonary arterial and right ventricular pressures.
 Decrease in PVR:

 The major decline in pulmonary resistance from the high

fetal levels to the low ―adult‖ levels in the human infant at
sea level usually occurs within the 1st 2–3 days but may be
prolonged for 7 days or more.

 Over the 1st several weeks of life, pulmonary vascular

resistance decreases even further, secondary to remodeling
of the pulmonary vasculature, including thinning of the
vascular smooth muscle and recruitment of new vessels.
 Decrease in pulmonary vascular resistance influences the
timing of clinical appearance of many congenital heart
lesions that are dependent on the relative systemic and
pulmonary vascular resistance.

 Eg: Left-to-right shunt through VSD may be minimal in 1st

wk after birth when pulmonary vascular resistance is still
high.

As pulmonary resistance decreases in the next 1-2 weeks, the

volume of the left-to-right shunt through an unrestrictive
ventricular septal defect increases and eventually leads to
symptoms of heart failure.
 Differences between neonatal circulation and that of older
infants:
 (1) Right-to-left or left-to-right shunting may persist across
patent foramen ovale;

 (2) In the presence of cardiopulmonary disease, continued

patency of ductus arteriosus may allow left-to-right, right-
to-left, or bidirectional shunting;

 (3) The neonatal pulmonary vasculature constricts more

vigorously in response to hypoxemia, hypercapnia, and
acidosis;

 (4) The wall thickness and muscle mass of the neonatal left
and right ventricles are almost equal;
 Differences between neonatal circulation and that of older
infants: contd…

 (5) Newborn infants at rest have relatively high oxygen

consumption, which is associated with relatively high
cardiac output.

 (6) Newborn cardiac output (about 350 mL/kg/min) falls in

the 1st 2 mo of life to about 150 mL/kg/min and then more
gradually to normal adult C.O of about 75 mL/kg/min.

 (7) High percentage of fetal hemoglobin present in the

newborn may interfere with delivery of oxygen to tissues in
neonate, so increased cardiac output is needed for adequate
delivery of oxygen
 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.
 CLOSURE OF DUCTUS ARTERIOSUS:

 In a full-term neonate, oxygen is the most important factor

controlling ductal closure.

 When the PO2 of the blood passing through the ductus

reaches about 50 mm Hg, the ductal wall constricts.

 The effects of oxygen on ductal smooth muscle may be

direct or mediated by its effects on prostaglandin synthesis.

 Gestational age also appears to play an important role;

The ductus of a premature infant is less responsive to oxygen,
even though its musculature is developed.
 Nelson Textbook of Pediatrics
 Park – Pediatric Cardiology for Practitioners
 Kulkarni – Pediatric Cardiology
 IB Singh – Embryology
 O.P Ghai – Essential Pediatrics