Fetal circulation.. Dr.Padmesh

Dr_Padmesh 49,188 views 40 slides Nov 27, 2011
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About This Presentation

Presentation on Fetal Circulation


Slide Content

THE WONDERS OF FETAL, TRANSITIONAL & NEONATAL CIRCULATION Dept of Pediatrics, Dr.SMCSI Medical College & Hospital

The Fetal Circulation

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, 2 nd Century

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

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%) Placenta

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%).

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.

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)

FETAL CIRCULATION: The pathway: Placenta  Oxygenated blood  U mbilical vein Hepatic circulation Bypasses liver & joins IVC via ductus venosus Partially mixes with poorly oxygenated IVC blood derived from lower part of fetal body Umbilical vein Hepatic portal vein Ductus venosus

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.

FETAL CIRCULATION: From the right ventricle  P ulmonary 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.

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.

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.

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 Pulm artery  Lungs

Aorta Deoxygenated blood Descending aorta Abdominal aorta Common iliac artery Umbilical arteries PLACENTA Oxygenation Umbilical Vein

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.

The Transitional Circulation

TRANSITIONAL CIRCULATION: At birth Mechanical expansion of lungs Increase in arterial PO 2 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 PO 2 (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) Therapeutic agents may either : Maintain fetal pathways o pen - P GE 1 Promote their c losure - I ndomethacin PO L IC E – P GE1 O pens, I ndomethacin C loses

The Neonatal Circulation

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

Neonatal Circulation: Decrease in PVR: 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.

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.

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.

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 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.

Summary

Reference: Nelson Textbook of Pediatrics Park – Pediatric Cardiology for Practitioners Kulkarni – Pediatric Cardiology IB Singh – Embryology O.P Ghai – Essential Pediatrics

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