3. Introduction:
"Nature is neither lazy nor devoid of foresight.
Having given the matter thought, she knows in
advance that the lung of the fetus does not require
the same arrangements of a perfected lung. She has
therefore anastomosed the pulmonary artery with
the aorta, and the left and right atria. . . .“
-Galen, 2nd Century
4. 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
6. COURSE OF FETAL CIRCULATION:
1.Placenta:
Has the lowest vascular resistance in the fetus.
Receives the largest amount of combined (Rt + Lt)
Ventricular Output (55%)
7. 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.
8. 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%).
9. COURSE OF FETAL CIRCULATION:
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.
10. 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)
11. FETAL CIRCULATION: The pathway:
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
12. FETAL CIRCULATION:
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.
13. FETAL CIRCULATION:
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.
14. 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.
15. 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.
16. 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
18. FETAL CIRCULATION:
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.
19.
20. 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.
21. 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.
22. TRANSITIONAL CIRCULATION:
High arterial PO2 (In several days)
Constriction of ductus arteriosus
It closes, becoming the ligamentum arteriosum.
23. 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
24. 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.
25. 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)
26. 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.
27. 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,
-RtLt shunt in infants with pulmonary hypertension)
Therapeutic agents may either :
Maintain fetal pathways open - PGE1
Promote their closure - Indomethacin
28.
29. 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
Baroreceptor response Slowing of HR
30. Neonatal Circulation:
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.
31. Neonatal Circulation:
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.
32. Neonatal Circulation:
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.
33. 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;
34. 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
35. 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.
36. 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.
37.
38. Nelson Textbook of Pediatrics
Park – Pediatric Cardiology for Practitioners
Kulkarni – Pediatric Cardiology
IB Singh – Embryology
O.P Ghai – Essential Pediatrics