The fetal circulation differs from adult circulation through the presence of shunts that direct blood flow away from the lungs. The ductus venosus directs oxygenated blood from the umbilical vein and liver to the heart and brain. The foramen ovale allows blood to bypass the lungs. The ductus arteriosus directs blood from the right ventricle away from the lungs. This pattern preferentially delivers oxygenated blood to vital organs and less oxygenated blood to the placenta. After birth, closure of the ductus venosus, foramen ovale and changes in blood flow cause transition to adult circulation with increased pulmonary blood flow. Pulmonary vascular resistance is high in fetuses due to

1. Fetal circulation

3. How is it different?
Shunts
• Venous system ( Ductus venosus )
• Heart ( Foramen ovale )
• Arterial system ( Ductus arteriosus )
Preferential blood flow pattern

4. Purpose
1. To deliver highly oxygenated to the metabolically active tissues ( Heart and brain )
2. To deliver less oxygenated blood to placenta

5. The RV supplies most of its blood via the ductus arteriosus and descending aorta to
the placenta for oxygenation.
The LV supplies most of its blood via the ascending aorta to the heart and brain for
oxygen delivery

6. 5 components of the central venous
circulation
Venous return from
1. The upper body
2. The myocardium
3. The lungs
4. The lower body
5. The placenta
Among these, the least saturated blood is from the upper body and the myocardium

7. Preferential blood flow pattern
 The course of the IVC ( Eustacian ) valve is positioned in such a way that >95% of
the blood entering the RA from the SVC is directed towards the tricuspid valve to the
RV preventing it from going through the Foramen ovale

9.  The location coronary sinus cauded to the Foramen ovale assists venous blood
coming from the myocardium to flow through the tricuspid valve to the RV

10.  The relatively desaturated blood from the lower body and the placenta ascends the
distal IVC and enters the lateral margin of the RA and is directed primarily through the
tricuspid valve
 Exception in the central venous blood flow pattern is that the pulmonary veins from
the lungs doesn’t drain into the RA. It flows into the LA like it normally does in
adults.But it doesn’t matter much because
- it has only an intermediate saturation
- it amounts to only about 5 % of the combined ventricular output
(maximum 25%)
Therefore it doesn’t have a significant effect on the oxygen delivery

11. Placental (umbilical venous) and liver
venous return
 Majority (≈55%) of the umbilical venous blood passes through the ductus venosus
to reach the RA
 ≈45% enters the left lobe of liver – joins left hepatic vein – which joins the ductus
venosus near the IVC and eventually pours into the RA
 Well oxygenated blood from these two sources on entering the RA preferentially
crosses the Foramen ovale to enter the LA thereby supplying the systemic circulation.
 The remainder of the umbilical venous blood along with >95% of the poorly
saturated portal venous blood enters the right lobe of liver and from there through
the right hepatic vein joins the distal IVC and empties into the RV finally

13. Other dynamic changes in fetal
circulation
 Pulmonary blood flow is low despite the dominance of the RV which in fetus ejects
55% to 60% of the total cardiac output.
 Most of the RV output is diverted away from the lungs through the widely patent
ductus arteriosus.
 Fetal pulmonary arterial mean pressure increases progressively with gestation and
at at term it is about 50 mmHg exceeding the mean aortic blood pressure by 1 to 2
mmHg

14. Transitional circulation (After birth)
 Rapid decrease in the pulmonary vascular resistance
 8 to 10 fold increase in pulmonary blood flow
 Mean pulmonary arterial pressure rapidly drops, and by 24 hours of age mean PAP
may be half systemic
 After the initial rapid fall, there is slow progressive decrease, with adult levels
reached after 2 to 6 weeks

15. Postnatal circulatory changes
 Rapid and large decrease in the pulmonary vascular resistance and the disruption of
the umbilical-placental circulation.
 The ductus arteriosus changes from a right – to – left conduit of blood to the
descending aorta, to a right – to – left conduit of blood to the lungs until it closes in
the first hours or days of life
 Closure of ductus venosus
 Closure of the foramen ovale due to increase in the proportion of combined venous
return that directly enters the LA via the pulmonary veins (>50%)

16. Physiologic regulation of pulmonary
vascular resistance
• Pulmonary vessels produce and actively metabolise many vasoactive substances
• The three main factors influencing the regulation of the fetal pulmonary circulation
are
mechanical effects
state of oxygenation and
production of vaso active substances
The most prominent among these is the normally low blood and alveolar oxygen tension that is
responsible for the high fetal pulmonary vascular resistance

17. Other factors that increase pulmonary
vascular resistance
Apart from the low oxygen tension, the other factors responsible for constriction in pulmonary fetal
circulation are
alpha agonists
thromboxane
leuokotrienes ( present in fetal tracheal fluid )

18. EDRF – Endothelium Derived Relaxing
Factor
• NO – nitric oxide / Endothelium Derived NO (EDNO)
• Produced by endothelial cells in response to various stimuli , generally involving
specific receptors and the activation of endothelial NO synthase (eNOS)
• Subsequent smooth muscle relaxation is produced by a NO/guanylyl cyclase/cGMP
mediated mechanism

19. Effect of EDNO on fetal circulation
• After certain stimuli such as shear stress or receptor binding of specific vasodilator
NO is synthesized by the activation of NO synthase
• NO released from endothelial cell
• NO diffuses into smooth muscle cell
• Activates guanylate cyclase
• Increase concentration of cGMP
•This causes smooth muscle relaxation

21. • Inhibition of EDNO synthesis produces marked increase in resting fetal pulmonary
vascular resistance
• Studies of intra pulmonary arterial and isolated lung preparation of sheep show
maturative increase in NO mediated relaxation during the late fetal and early
postnatal period
• Therefore basal EDNO production is an important mediator of both normal fetal
Pulmonary vascular tone and dramatic decrease in resistance that occurs with O2
ventilation at birth

22. Prostacyclins
•Prostaglandins ( arachidonic acid metabolite ) are not the central factor in the
regulation of resting fetal pulmonary circulation
• But they ( PGI2) act in modulating the tone and there by maintaining the pulmonary
vascular resistance relatively constant

23. •PC – primarily synthesized in vascular endothelial cells
• Produce vasodilation by activating adenylate cyclase and producing increased
concentration of cAMP
• Causes smooth muscle relaxation

24. Endothelin
• ET1 – endothelially derived vasoactive factor
• Has both vasoconstrictive and vasodilatory effect
• Acts on two receptors – ETa , ETb
• ETa – vascular smooth muscle – Vasoconstriction
• ETb – endothelial cell - Vasodilatation
• Predominant action of ET1 is VD by acting on ETb and EDNO release

25. Role of oxygen in pulmonary
vasodilation
• Increase in alveolar or arterial O2 tension may decrease the pulmonary vascular
resistance either directly via K+ channel activation or indirecty by stimulating the
production of vasodilator substances like PGI2, bradykynin, adenosine, adenosine 5’ –
triphosphate, or EDNO
• EDNO is the most important mediator for casusing decreasing in PVR at birth
associated with increased oxygenation

26. Exogenous prostaglandins
• Particularly PGI2, lowers the PVR in the fetus
• Indomethacin acts by inhibiting the PG production when given before the fetal lung
starts ventilating – thereby attenuating the subsequent decrease in the pulmonary
vascular resistance that occurs after the initial rapid decrease in resistance

27. Other vasoactive substances
Adenosine
Adenosine triphosphate
Bradykynin

28. Immediate and late vasodilatory effects
after birth
• Atleast two components appear to determine the decrease in PVR with the initiation
of ventilation and oxygenation
• First ( independent of fetal oxygenation ) – physical expansion and production of
prostaglandins ( PGI2 and PGD2)
• Second – EDNO ( associated with the fetal oxygenation )
• Both components are necessary for the successful extrauterine life.

29. PULMONARY VASOCONSTRICTORS PULMONARY VASODILATORS
1. Leukotrienes 1. EDNO
2. Low oxygen 2. ET1 – acting through ETb
3. ET1 – acting through ETa 3. Bradykynin
4. Prostaglandins