Fetal circulation

Fetal Circulation

1. 1.FETAL & NEONATAL CIRCULATION 2.PERSISTENT FETAL CIRCULATION Dr Robin Thomas Resident in Pediatrics JJMMC, Davangere

2. FETAL CIRCULATION By Dr Robin Thomas

3. Fetal circulation

4. Before birth-blood from placenta -80% saturated with O2 –returns to fetus – umbilical vein . PO2 30-35 mmHg Liver -most of this blood flows through Ductus venosus directly into inferior vena cava (IVC) , short-circuiting liver. Smaller amount enters liver sinusoids & mixes with blood from portal circulation. Sphincter mechanism in ductus venosus –regulates flow of umbilical blood tru liver sinusoids.

5. IVC-placental blood mixes with deoxygenated blood returning from lower limbs- enters right atrium.PO2 26-28mmHg Guided towards Foramen ovale by valve of IVC & blood passes directly into left atrium. Small amount of blood remains in right atrium-lower edge of septum secundum – crista dividens - mixes with desaturated blood returning from head & arms-superior vena cava.

6. Left atrium -mixing of desaturated blood returning from lungs tru pulmonary vein-blood enters left ventricle ejected - Ascending aorta . Some Oxygen rich blood –coronary & carotid arteries –supplies heart musculature & brain. Desaturated blood from superior vena cava (SVC) –( PO2 12-14 mmHg ) right atrium- right ventricle ejected - Pulmonary trunk .

7. Fetal pulmonary arterial circulation is vasoconstricted-10% right ventricular outflow enters lungs. Fetal life-resistance in pulmonary vessels high-blood passes directly through Ductus arteriosus ( PO2 18-22mmHg) into Descending aorta - mixes with blood from proximal aorta-lower part of fetal body. Descending aorta- 2 umbilical arteries -placenta. O2 saturation umbilical arteries -58%

8. During course from placenta –organs of fetus –blood in umbilical vein (PO2 30-35 mmHg) loses its high oxygen content, as it mixes with desaturated blood. Theoretically ,mixing of blood occurs in 5 places. 1. Liver -mixes with blood from portal circulation. 2. IVC -mixes with deoxygenated blood returning from lower extremities,pelvis , kidneys.

9. 3 .Right atrium -mixes with desaturated blood returning from head & arms via SVC.(PO2 12-14 mmHg) 4. Left atrium -mixes with desaturated blood returning from lungs-pulmonary vein. 5.Entrance of Ductus arteriosus (PO2 18-22mmHg ) into descending aorta -mixes with blood from proximal aorta.

10. Changes in vascular system at birth-caused by cessation of placental blood flow & beginning of respiration. Closure of Umbilical arteries –contraction of smooth musculature of wall-thermal & mechanical stimuli & change in O2 tension. Functionally umbilical arteries close a few minutes after birth. Actual obliteration by fibrous proliferation –takes 2-3 months. Circulatory changes at Birth

11. Distal part of umbilical arteries form median- umbilical ligaments , proximal portion remain open as superior vesical arteries . Closure of umbilical vein & ductus venosus occurs shortly after that of umbilical arteries. Blood from placenta may enter newborn for sometime after birth. Umbilical vein form ligamentum teres - hepatis , in lower margin of falciform - ligament.

12. Ductus venosus forms ligamentum venosum . Closure of ductus arteriosus occurs by contraction of muscular wall-immediately after birth-mediated by bradykinin -substance released from lungs during initial inflation. Functional closure-10-15 hr. Complete anatomical obliteration –proliferation of intima -takes 1-3 months. Ductus arteriosus forms ligamentum arteriosum .

13. Closure of foramen ovale –caused by increased pressure in left atrium combined with decrease in pressure on right atrium. flap valve of foramen ovale close against edge of crista dividens . functional closure-3 rd month of life. Closure of ductus arteriosus –amount of blood flowing tru lung vessels increases rapidly-raises pressure in left atrium. Pressure in right atrium decreases –result of interruption of placental blood flow.

14. First breath presses septum primum against septum secundum -functionally foramen- ovale closes. First days of life-closure is reversible. Crying by baby creates shunt from right to left-cyanotic periods in newborn. Constant apposition leads to fusion of 2 septa by 1year.

15. 20% -perfect anatomical closure never obtained- Probe patent foramen ovale .

16. At birth, fetal circulation must immediately adapt extrauterine life –gas exchange is transferred from placenta to lung. Soon after onset of spontaneous respiration-placenta is removed from circulation –by clamping umbilical cord or constriction of umbilical arteries –increases Systemic - vascular resistance . Neonatal circulation

17. Onset of spontaneous respiration expands the lung & brings O2 to pulmonary alveoli. Heart rate slowes as a result of baroreceptor response to increase in systemic vascular resistance –when placental circulation is eliminated. Average central aortic pressure in term neonate-75/50 mmHg.

18. Sudden increase in systemic vascular resistance & drop in pulmonary vascular resistance –cause reversal of flow through ductus arteriosus & increase in pulmonary blood flow. Before birth pulmonary & systemic resistances cause 90% blood to go through ductus arteriosus into descending aorta.

19. After birth, 90% blood goes to pulmonary arteries with pulmonary blood flow increasing from 35 ml/kg/min to 160-200 ml/kg/min. Normal neonate-closure of ductus arteriosus & fall in PVR results in decrease in pulmonary arterial & right ventricular pressure. Major decline in PVR occurs within 1 st 2-3 days –may be prolonged for 7 days.

20. 1 st weeks of life-remodeling of pulmonary vasculature-thinning of vascular smooth muscle & recruitment of new vessels. Decrease in PVR influences the timing of clinical appearance of many congenital heart lesions. Left to right shunt through a VSD may be minimal in 1 st week after birth, when PVR is still high.

21. Differences between neonatal circulation & that of older infants. 1.R-L or L-R to shunt may persist across foramen ovale . 2.Cardiopulmonary disease-patency of ductus arteriosus allow L-R ,R-L or bidirectional shunting. 3.Neonatal pulmonary vasculature constricts more vigorously in response to hypoxemia, hypercapnea & acidosis.

22. 4.Wall thickness & muscle mass of neonatal left & right ventricles are almost equal. 5.New born infants at rest have high O2 consumption assoc. with high cardiac output. New born cardiac output 350 ml/kg/min falls in 1 st two month of life to 150 ml/kg/min & more gradually to normal adult cardiac output of 75 ml/kg/min.

23. Foramen ovale is functionally closed by 3 rd month of life. Functional closure of ductus arteriosus is by 10-15 hr in normal neonate. Remains patent in congenital heart disease. Premature new born infant with evanescent systolic murmur or continuous murmur –PDA should be suspected.

24. Fetal life-patency of ductus arteriosus maintained by low O2 tension & endogenously produced prostaglandins PGE2. Full term neonate-O2 major factor controlling ductal closure. PO2 of blood passing through ductus reaches 50 mmHg – ductal wall constricts.

25. Gestational age play a important role. Ductus of a premature infant –less responsive to O2 , eventhough its musculature is developed.

26. Fetus-placenta provides for gas & metabolite exchange. 3 cardiovascular structures unique to fetus for maintaining parallel circulation : ductus venosus , foramen ovale , ductus arteriosus . After birth –mechanical expansion of lungs causes increase in PO2, decrease in PVR & increase in systemic vascular resistance. Closure of umbilical arteries,umbilical vein, ductus venosus , ductus arteriosus . Summary

27. Umbilical arteries-median umbilical ligament. Left umbilical vein- ligamentum teres of liver. Ductus venosus-ligamentum venosum . Ductus arteriosus-ligamentum arteriosum . Functional closure of foramen ovale by 3 rd month of life & ductus arteriosus by 10-15 hr in a normal neonate.

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