Fetal circulation.pptx

FETAL CIRCULATION

1. The fetal circulation is the circulatory system of a human fetus, often encompassing the entire fetoplacental circulation which includes the umbilical cord and the blood vessels within the placenta that carry fetal blood.

2. - Begins to develop toward the end of the third week. - Heart starts to beat at the beginning of the fourth week. The critical period of heart development is from 20 day to 50 day after fertilization. Many critical events occur during cardiac development, and any deviation from this normal pattern can cause congenital heart defects, if development of heart doesn't occur properly.

3. Foetal circulation consequently differs from the adult one predominantly due to 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 artery and descending aorta

4. 4 unique FETAL CVS structures : FOUR SHUNTS

5. Umbilical Cord 2 umbilical arteries : return non-oxygenated blood, waste product, CO2 to placenta 1 umbilical vein: brings oxygenated blood and nutrients to the fetus

6. Pair of umbilical arteries carry deoxygenated blood & wastes to placenta. Umbilical vein carries oxygenated blood and nutrients from the placenta.

7. organ that connects the developing fetus to the uterine wall to allow nutrient uptake, waste elimination, and gas exchange via the mother's blood s two components: the fetal placenta , or (Chorion frondosum), which develops from the fetus; and the maternal placenta , or (Decidua basalis), which develops from the maternal uterine tissue

8. Facilitates gas and nutrient exchange between maternal and fetal blood. The blood itself does not mix.

9. The core concept behind foetal circulation is that foetal hemoglobin has a higher affinity for oxygen than does adult hemoglobin, which allows a diffusion of oxygen from the mother's circulatory system to the foetus. The circulatory system of the mother is not directly connected to that of the fetus, so the placenta functions as the respiratory center for the fetus as well as a site of filtration for plasma nutrients and wastes. Water, glucose, amino acids, vitamins, and inorganic salts freely diffuse across the placenta along with oxygen. The umbilical arteries carry blood to the placenta , and the blood permeates the sponge-like material there. Oxygen then diffuses from the placenta to the chorionic villus, an alveolus-like structure, where it is then carried to the umbilical vein.

10. Um b i l ic a l V e i n Placenta Umbilical Arteries Foramen Ovale Right Atrium Inferior Venacava Ductus Venosus Liver Arch of Aoarta Right Lung Ductus Arteriosus Left Atrium Left Ventricle Right Ventricle Portal Vein

11. 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%)

12. 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.

13. 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%).

14. 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.

15. 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)

16. FETAL CIRCULATION: The pathway: Placenta  Oxygenated blood  Umbilical vein Hepatic circulation Bypasses liver & joins IVC via ductus venosus Partially mixes with poorly oxygenated I V C blood derived from lower part of fetal body

17. FETAL CIRCULATION: Combined lower body blood plus umbilical venous blood flow (PO 2 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 (PO 2 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.

18. 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 PO 2 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.

19. 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 PO 2 , 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.

20. 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 PO 2 , 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.

21. SVC  upper LA  LV  Aorta  Ductus arteriosus Foramen ovale RV body IVC 50% through ductus venosus 50% to Portal circulation Umbilical Vein Oxy.blood PLACENTA

22. A o rta Deoxygenated blood Descending aorta Abdominal aorta Common iliac artery Umbilical arteries PLACENTA Oxygenation Umbilical Vein

23. FETAL CIRCULATION: The total fetal cardiac output—the combined output of both the left and right ventricles—is ≈ 350 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.

24. During fetal life 350ml per kg per min Cardiac Output Heart Rate Following birth 500ml per min 120-140per min

25. It is the fetal heart and not the mother's heart that builds up the fetal blood pressure to drive its blood through the fetal circulation. Intracardiac pressure remains identical between the right and left ventricles of the human fetus. The blood pressure in the fetal aorta is approximately 30 mmHg at 20 weeks of gestation , and increases to ca 45 mmHg at 40 weeks of gestation .The fetal pulse pressure is ca 20 mmHg at 20 weeks of gestation , increasing to ca 30 mmHg at 40 weeks of gestation. The blood pressure decreases when passing through the placenta. In the arteria umbilicalis, it is ca 50 mmHg . It falls to 30 mmHg in the capillaries in the villi . Subsequently, the pressure is 20 mm Hg in the umbilical vein , returning to the heart

26. Pulmonary circulation is reduced in the human fetus because the baby gets its oxygen from its mother and does not breath on its own.

27. The change from fetal to postnatal circulation happens very quickly. Changes are initiated by baby’s first breath.

28. TRANSITIONAL CIRCULATION: At birth Increase in arterial Mechanical expansion of lungs PO 2 Rapid DECREASE in pulmonary vascular resistance Removal of the low-resistance placental circulation

29. 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.

30. TRANSITIONAL CIRCULATION: High arterial PO 2 (In several days) Constriction of ductus arteriosus It closes, becoming the ligamentum arteriosum.

31. 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

32. 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.

33. Foetal circulation : 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 (≈450 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)

34. 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.

35. 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) Therapeutic agents may either : Maintain fetal pathways o pen - P GE 1 Promote their c losure - I ndomethacin

36. Umbilical arteries → Umbilical ligaments Umbilical vein → Ligamentum teres Shunt Fu n ction a l closure A n atomical closure Remnant Ductus arte r i o sus 10 – 96 hrs after birth 2 – 3 wks after birth L i gamentum arteriosum Formamen ovale Within several mins after birth One year after birth Fossa ovalis Ductus venos u s Within several mins after birth 3 – 7 days after birth L i gamentum venosum

37. 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

38. Neonatal Circulation: Decrease in PVR (pulmonary vascular resistance): With the onset of ventilation, pulmonary vascular resistance is markedly decreased, as a consequence of both active (PO 2 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.

39. 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.

40. 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.

41. FE T AL N E WBO R N Gas exchange P l acenta Lungs RV,LV circuit P a ral l el S e ries Pulmonary circulation Vasoconstricted D i l a ted Fetal myocardium Contra c ti l it y ,Complian c e Less Good Dominant ventricle R i ght Left Change in Structure Umbilical vein Umbilical artery Ductus venosus Ligamentum teres Medial umb ligament Ligamentum venos u m Ductus arteriosus Ligamen t um

42. Differences between neonatal circulation and that of older infants: Right-to-left or left-to-right shunting may persist across patent foramen ovale; In the presence of cardiopulmonary disease, continued patency of ductus arteriosus may allow left-to- right, right-to-left, or bidirectional shunting; The neonatal pulmonary vasculature constricts more vigorously in response to hypoxemia, hypercapnia, and acidosis; The wall thickness and muscle mass of the neonatal left and right ventricles are almost equal;

43. Differences between neonatal circulation and that of older infants: contd… Newborn infants at rest have relatively high oxygen consumption, which is associated with relatively high cardiac output. 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. 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

44. 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.

45. CLOSURE OF DUCTUS ARTERIOSUS: In a full-term neonate, oxygen is the most important factor controlling ductal closure. When the PO 2 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.

46. Patent ductus arteriosus: Failure of a child's DA to close after birth generation of a left-to-right shunt as blood flows form hogh pressure aorta to low pressure pulmonary artery. If left uncorrected, patency leads to pulmonary hypertension and possibly congenital heart disease and cardiac arrythmia Prostaglandins are responsible for maintaining the ductus arteriosus by dilatation of the vascular smooth muscles. Closure may be induced with NSAIDs because these drugs inhibit prostaglandin

47. Patent foramen ovale: is an incomplete closure of the atrial septum that results in the creation of a flap or a valve-like opening in the atrial septal wall is present in everyone before birth but seals in about 80% of people. With each heartbeat, blood can flow in either direction directly between the right and left atrium. When blood moves directly from the right atrium to the left atrium, this blood bypasses the filtering system of the lungs

48. Patent (open) ductus arteriosus and patent foramen ovale each characterize about 8% of congenital heart defects. Both cause a mixing of oxygen-rich and oxygen- poor blood; blood reaching tissues not fully oxygenated. Can cause cyanosis Surgical correction now available, ideally completed around age two. Many of these defects go undetected until child is at least school age.