foetal circulation


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1 : Fetal circulation
2 : FETAL CIRCULATION DEFINITION: the circulation of blood from the placenta to and through the fetus and back to the placenta constitutes the fetal circulation.
3 : FETAL CIRCULATION O2 uptake occurs in the placenta PREFERENTIAL STREAMING : Delivery of highly oxygenated blood to the metabolically active tissues(brain & heart) and of less oxygenated blood to the placenta SHUNTS exists in the venous system, heart & arterial system. PARALLEL CIRCULATION :The fetal circulation is in effect a parallel circulation- various organs receive portions of their blood supply from either ventricles
4 : Preferential pattern of ventricular output. The left ventricle (LV) directs most of its highly saturated blood (red arrow) via the ascending aorta (AAo) to the highly metabolic heart and upper body. The right ventricle (RV) primarily ejects less oxygenated blood (purple arrow) via the main pulmonary artery (MPA) primarily down the ductus arteriosus (PDA) and via the descending aorta (DAo) to the placenta for oxygen uptake.
5 : FETAL CIRCULATION 3 anatomical structures make up for the major difference of the fetal circulation: DUCTUS VENOSUS FORAMEN OVALE DUCTUS ARTERIOSUS
6 :
7 : The left umbilical vein Highly oxygenated,nutrient rich blood comes from the left umbilical vein. Much of this blood is diverted into ductus venosus, which connects the left umbilical vein to IVC in the liver left umbilical vein
8 : Sphincter mechanism in the liver This regulates the flow of remaining blood from umbilical vein into IVC through hepatic veins. It is generally agreed that a physiological sphincter exists and prevents overloading of heart when the venous flow in the left.umb.vein is high(eg.during uterine contractions)
9 : FETAL CIRCULATION Ductus venosus The ductus venosus is a slender trumpet-like shunt connecting the intra-abdominal umbilical vein to the IVC 30-50% of the umbilical blood is shunted through the ductus venosus . O2 saturation in U. Vein is 80%(98%in syst. artery of adult)
10 : FETAL CIRCULATION Ductus venosus blood has… the highest oxygenation the highest kinetic energy in the IVC and predominantly presses open the foramen ovale valve to enter the left atrium, i.e ‘preferential streaming’
11 : FETAL CIRCULATION Ductus venosus The shunt obliterates within 1-3 weeks of birth in term infants takes longer time in : premature births persistent pulmonary hypertension various forms of cardiac malformations. In contrast to the ductus arteriosus where increased oxygen tension triggers the closure, no trigger has been found for the ductus venosus.
12 : Preferential pattern of venous return to the right (RV) and left (LV) ventricles. More highly saturated blood (red arrow) from the umbilical vein (UV) passes via the ductus venosus (DV) and left hepatic vein (LHV) to the left atrium (LA) and LV. Less saturated blood (blue arrows) from the lower body via the inferior vena cava (IVC, not shown), from the main and right portal veins (MPV and RPV) via the right hepatic vein (RHV), from the coronary sinus (CS), and from the superior vena cava (SVC) passes to the right atrium (RA) and RV.
13 : FETAL CIRCULATION FORAMEN OVALE: Formed by the overlapping edge of the septum secundum against the ruptured upper portion of the septum primum. Acts like a flap valve for preferential blood flow from the right atrium to the left atrium.
14 : FETAL CIRCULATION FORAMEN OVALE: the inferior venous inlet to the heart could be viewed as a column of blood that ascends between the two atria from below. This column hits the interatrial ridge, the crista dividens, and is divided into a left and right arm….
15 : FETAL CIRCULATION FORAMEN OVALE: The left arm fills the ‘windsock’, formed between the foramen ovale valve and the atrial septum, to enter the left atrium. The right arm is directed towards the tricuspid valve and joins the flow from the superior vena cava and coronary sinus.
16 : FETAL CIRCULATION DUCTUS ARTERIOSUS: Connects the left branch of the pulmonary trunk to arch of aorta(beyond the origin of left subclavian artery) It protects the lungs from circulatory overloading. The blood that arrives via IVC reaches the LA-LV-Aorta-carotid circulation-brain. The blood that arrives via the SVC reaches the RA-RV-Pulmonary artery-Ductus arteriosus-Aorta- to the lower portion of the body.
17 : FETAL CIRCULATION DUCTUS ARTERIOSUS: 40% or less of the CCO is directed through the ductus arteriosus The lungs receive 13% of the CCO at mid-gestation and 20-25% after 30 weeks
18 : FETAL CIRCULATION DUCTUS ARTERIOSUS: The vessel is under the general influence of circulating substances, particularly prostaglandin E2, which is crucial in maintaining patency. Sensitivity to prostaglandin antagonists is at its highest in the third trimester and is enhanced by glucocorticoids and fetal stress. The increased reactivity of the ductus arteriosus in the third trimester makes it vulnerable to prostaglandin synthase inhibitors, such as indomethacin. Nitric oxide has a relaxing effect prior to the third trimester.
19 : FETAL CIRCULATION DUCTUS ARTERIOSUS(of fetal rats) After indomethacin Before indomethacin
20 : Umbilical arteries About 65%of blood in the descending aorta Passes into umbilical arteries(right and left) Which are direct branches of fetal internal iliac arteries(hypo gastric arteries) Remaining 35% of blood supplies the lower half of the body and viscera
21 : FETAL CIRCULATION Blood volume The blood volume in the human fetus is estimated to be 10-12% of the body weight, compared with 7-8% in adults. The estimated volume of 80 ml/kg contained within the fetal body is marginally more than that in adults.
22 : FETAL CIRCULATION Arterial and venous blood pressure mean arterial pressure - 15 mmHg during cordocentesis at gestational weeks 19-21. systemic systolic pressure increases from 15-20 mmHg at 16 weeks to 30-40 mmHg at 28 weeks. There is no obvious difference between the left and right ventricles.
23 : FETAL CIRCULATION Arterial and venous blood pressure This increase is also seen for diastolic pressure, which is <5 mmHg at 16-18 weeks and 5-15 mmHg at 19-26 weeks. Umbilical venous pressure, increased from 4.5 mmHg at 18 weeks to 6 mmHg at term.
24 : The fetal heart Fetal and neonatal myocardial cells are smaller in diameter contain relatively more non-contractile mass (primarily mitocondria, nuclei & surface membrane). force generation and the extent and velocity of shortening are low stiffness and water content of ventricular myocardium are high The fetal heart is surrounded by fluid-filled rather than air-filled lungs. Hence the fetal and neonatal heart has limited ability to increase CO in the presence of either a volume load or a lesion that increases resistance to emptying. CO is more dependent on changes in heart rate : bradycardia is poorly tolerated by the fetus.
25 : FETAL CIRCULATION Cardiac performance The myocardium grows by cell division until birth, and growth beyond birth is due to cell enlargement. The density of myofibrils increases particularly in early pregnancy and the contractility continues to improve during the second half of pregnancy.
26 : FETAL CIRCULATION Cardiac performance The fetal heart has limited capacity to increase stroke volume by increasing diastolic filling pressure, the right ventricle even less than the left, as they are already operating at the top of their function curves. increased heart rate may be the single most prominent means of increasing cardiac output in the fetus.
27 : FETAL CIRCULATION Cardiac performance The two ventricles pump in parallel and the pressure difference between them is minimal compared with postnatal life. Fetal myocardium is more stiff attributed to the constraint of the pericardium, lungs and chest wall, all of which have low compliance before air is introduced.
28 : FETAL CIRCULATION Cardiac output & distribution: The right ventricular output is slightly larger than that of the left ventricle, and pulmonary flow in the human fetus is 13-25%, at 28-32 weeks when the pulmonary blood flow reaches a maximum.
29 : FETAL CIRCULATION Cardiac output & distribution: The lowest saturation is found in the abdominal IVC, and the highest saturation is found in the umbilical vein.The difference between the left and right ventricles is only 10%
30 : Postnatal changes The changes in the central circulation at birth are primarily caused by the rapid and large decrease in pulmonary vascular resistance and the disruption of the umbilical-placental circulation.
31 : Postnatal changes Placenta is cutoff Peripheral resistance suddenly rises Aortic pressure exceeds PA pressure Fetal asphyxia Infant gasps- lungs expand Suction effect of first breath & U. Vein constriction – 100 ml of blood Enters the fetus: placental transfusion.
32 : Postnatal changes Lungs expand Pulmonary resistance falls PBF increases Blood returning to LA increases PFO closes
33 : Postnatal changes Once the child takes the first respiration,pulmonary circulation begins and the right and left hearts become completely independent of each other. All the by-pass channels having served their purpose,obliterate. Foramen ovale is closed and becomes fossa ovalis in the right atrium closure of the foramen ovale at birth is entirely passive, secondary to alterations in the relative return of blood to the right and left atria.
34 : Postnatal changes Ductus arteriosus constricts in a few minutes Functional closure begins by 10-15 hrs. Anatomical closure complete by 2 weeks(by probe patency). Ligamentum arteriosum by 3 weeks. Arterial o2, bradykinin play a critical role in the closure after birth.
35 : Postnatal closure of the ductus arteriosus is effected in two phases: Immediately after birth: contraction and cellular migration of the medial smooth muscle in the wall of the ductus arteriosus intimal cushions or mounds functional closure within 12 hours after birth in full-term human infants. The second stage : completed by 2 to 3 weeks in human infants produced by infolding of the endothelium, disruption and fragmentation of the internal elastic lamina proliferation of the subintimal layers hemorrhage and necrosis in the subintimal region.
36 : Patency or closure of the ductus arteriosus represents a balance between the constricting effects of oxygen, and perhaps certain vasoconstrictive substances, and the relaxing effects of several prostaglandins
37 : Ligamentum venosum Ductus venosus becomes a fibrous band called ligamentum venosum which is seen in continuation with ligamentum teres(obliterated left umbilical vein) The functional closure of the ductus venosus is probably a passive phenomenon, although it has been demonstrated that the isolated ductus venosus can respond to adrenergic stimulation and prostanoids
38 : Other changes and clinical aspects The umbilical arteries become umbilical ligaments attached to the internal iliac arteries upto superior vesical arteries. The left umbilical vein remains patent for considerable time and can be used for exchange transfusions.
39 : Fetal pulmonary circulation Pulmonary blood flow is low despite the dominance of the right ventricle, which in the fetus ejects 55% to 60% of total cardiac output Most of the right ventricular output is diverted away from the lungs through the widely patent ductus arteriosus to the descending thoracic aorta and the placenta for oxygenation At about 0.5 gestation, 3% to 4% of total cardiac output perfuses the lungs; increase thereafter to 8% to 10% near term.
40 : Fetal pulmonary circulation Fetal pulmonary arterial mean blood pressure increases progressively with gestation and at term is about 50 mm Hg, exceeding mean aortic blood pressure by 1 to 2 mm Hg.
41 : Fetal pulmonary circulation Total pulmonary vascular resistance early in gestation is extremely high ,owing to the small number of small arteries present. Total pulmonary vascular resistance decreases progressively over the last half of gestation, with growth of new arteries and an overall increase in cross section.
42 : Transitional Circulation with initiation of pulmonary ventilation: pulmonary vascular resistance decreases rapidly eightfold to tenfold increase in pulmonary blood flow. by 24 hours of age, mean pulmonary arterial blood pressure is half systemic. adult levels reached after 2 to 6 weeks This is due to vascular remodeling, muscular involution, and rheologic changes.
43 : Regulation of Pulmonary Vascular Resistance state of oxygenation the production of vasoactive substances: oxygen modulates the production of both prostacyclin and endothelium-derived nitric oxide (EDNO)
44 : Control of the perinatal pulmonary circulation balance between factors producing active pulmonary vasoconstriction (leukotrienes, low oxygen, and possibly even ET-1 acting through the ETA receptor) and those leading to pulmonary vasodilation (EDNO, ET-1 acting through the ETB receptor, bradykinin, and prostaglandins). The dramatic increase in pulmonary blood flow after birth most likely reflects a shift from active pulmonary vasoconstriction to active pulmonary vasodilation.
45 : Persistent fetal circulation Also called Persistent Pulmonary Hypertension of the Newborn (PPHN) Most commonly occurs in full term infants. Causes : Meconium aspiration Severe respiratory distress syndrome Pneumonia caused by Group B beta streptococci Episodes of asphyxia Progressive increase in RV afterload ? RV dysfunction. results in right to left shunting through the PFO and / or PDA.
46 : tachypnoea & acidosis a parasternal heave, loud S2 and a systolic murmur. chest X-ray shows decreased vascular flow but no evidence of pulmonary parenchymal disease. A higher O2 level in the right radial artery than in the umbilical artery Echo and Doppler evaluation to rule out TAPVC. 3 forms are described Hypertrophic type Hypoplastic type Reactive type
47 : Treatment increase in the inspired O2 level and correction of acidosis with NaHCo3. artificial ventilation inhaled NO to reduce pulmonary vascular resistance IV Prostaglandins Treatment of severe disease with an extra corporeal membrane oxygenator
48 : Response of fetal circulation to stress A hypoxic insult in late pregnancy activates a chemoreflex mediated by the carotid bodies causing an immediate vagal effect with reduced heart rate and a sympathetic vasoconstriction endocrine responses (e.g. adrenaline and noradrenaline) maintaining vasoconstriction (a-adrenergic), increasing heart rate (b-adrenergic) and reducing blood volume with renin release and increased angiotensin II concentration
49 : Response of fetal circulation to stress Orchestrate circulatory redistributional pattern that maintains placental circulation and gives priority to the adrenal glands, myocardium and brain
50 : Response of fetal circulation to stress Sustained hypoxia forces an adaptational shift to less oxygen demand, reduced DNA synthesis and growth a gradual return towards normal concentrations of blood gases and endocrine status Even subtle differences in the development of autocrine, paracrine, endocrine and metabolic functions induced by circulatory variations during pregnancy could have lasting effects with increased risks of cardiovascular and endocrine diseases in adult life..
51 : Summary In the fetal state, oxygen uptake occurs in the placenta, which is perfused in parallel with the systemic vascular beds. To deliver relatively highly oxygenated blood to the metabolically active tissues (such as the heart and brain) and to deliver less oxygenated blood to the placenta for oxygen uptake, central shunts and preferential blood flow patterns exist. At birth, these shunts are abolished over a very short period of time, and the mature postnatal central circulation is established within the first few days of life.

 

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