Anatomy of foetal circulation

Foetal circulation, Anaesthesthetic implications.

1. Anatomy of Foetal Circulation Dr Leena Tayshete ( Jr Reg ) Dr Anil K Sharma (Moderator) 28-10-2014 Indraprastha Apollo Hospital 1

2. Objectives Review of Fetal Circulation Changes at Birth Postnatal circulation Defects 28-10-2014 Indraprastha Apollo Hospital 2

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6. Begins to develop toward the end of 3 rd wk Heart starts to beat at the beginning of 4 th wk Critical period of heart development- day 20 to day 50 aft fertilization. 28-10-2014 Indraprastha Apollo Hospital 6

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9. ‘Shunt-Dependent’ Circulation PaO2 in the umbilical vein around 4.7 kPa & foetal blood saturation 80–90%. 50–60% of this placental venous flow bypasses the hepatic circulation via the ductus venosus (DV) to enter the inferior vena cava (IVC). Venous blood, which is returning from the lower portions of the body SVO2 of around 25–40%. Eustachian valve -flap tends to direct the more highly oxygenated blood, streaming along the dorsal aspect of the IVC, across the foramen ovale (FO). 28-10-2014 Indraprastha Apollo Hospital 9

10. In LA, O2 saturation of foetal blood is 65%. Majority of the LV blood is delivered to the brain and coronary circulation. Desaturated blood(SO2 25–40%),from SVC & coronary sinus, in addition to the IVC’s anteriorly streamed flow (comprised mainly of venous return from lower body and hepatic circulation)  directed across tricuspid valve. Due to high pulmonary vascular resistance (PVR) about 12% of the RV output  pulmonary circulation; remaining 88% crossing the ductus arteriosus (DA)  descending aorta Lower half of the body supplied with relatively desaturated blood (PaO2 2.7 kPa ). 28-10-2014 Indraprastha Apollo Hospital 10

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12. Three shunts in foetal circulation Ductus arteriosus   � protects lungs against circulatory overload � allows the right ventricle to strengthen  � hi pulmonary vascular resistance, low pulmonary blood flow � carries mostly medium oxygen saturated blood. Ductus venosus   � connecting the umbilical vein to IVC � blood flow regulated via sphincter � carries mostly highly oxygenated blood. Foramen ovale � shunts highly oxygenated blood from RA  LA. 28-10-2014 Indraprastha Apollo Hospital 12

13. Foetal circulation is characterized by High PVR (fluid filled lungs and a hypoxic environment). Low systemic vascular resistance (SVR) (large surface area of low resistance utero -placental bed). Most oxygenated blood from the umbilical vein perfuses the brain and heart preferentially by shunting across Ductus Venosus & Foramen Ovale . Lesser oxygenated blood perfuses the lower body by shunting across the Ductus Arteriosus . 28-10-2014 Indraprastha Apollo Hospital 13

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15. Physiology of Foetal Hb Umbilical vein PaO2 30-35 mmHg. Approximately 80% of foetal haemoglobin is Hb F Hb F (P50 19mmHg) is left shifted in comparison to Hb A (P50 26mmHg), which improves oxygen uptake at the placenta. Foetal pH (normal values 7.25-7.35) is lower than in adults. L ow foetal pH improves oxygen unloading at tissue level. Foetal Hb is high compared to adult levels (raises oxygen carrying capacity). 28-10-2014 Indraprastha Apollo Hospital 15

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17. CaO2 (ml O2/dl blood) = (SaO2 x Hgb x 1.34) + (PaO2 x 0.003) Umbilical vein PaO2 30-35 mmHg. Foetal Hb 70%-80% saturated at this PaO2 in (comparison adult Hb SaO2 50-60%). CaO2 for foetus - Hb 18 grams/dl & SaO2 75% in the umbilical vein yields: CaO2 = 0.75 x 18 x 1.34 = 18.1 ml O2/ dl blood 28-10-2014 Indraprastha Apollo Hospital 17

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19. Foetal Hb conc. - 16 g dl/1 at term, with high % of haemoglobin F ( HbF ), which has a lower content of 2,3-DPG (shifting the oxygen dissociation curve to the left)  f avours oxygen uptake in placenta. After birth, presence of HbF becomes a disadvantage. The P50 fetal blood-3.6 kPa compared with adult blood-4.8 kPa . When PO2 is 5.3 kPa (approximates to normal neonatal venous value), the oxygen content of fetal blood is much higher than that of adult blood. Thus, in the neonate, HbF impairs oxygen extraction at tissue level. 28-10-2014 Indraprastha Apollo Hospital 19

20. Combined ventricular output (CVO) SV of foetal LV ≠ SV of RV. The RV receives about 65% of the venous return and the LV about 35%. In the shunt dependent circulation of the foetus, the situation is much more complex. The cardiac output of the foetus determined as  combined ventricular output (CVO)₂. About 45% of the CVO is directed to the placental circulation with only 8- 12% of CVO entering the pulmonary circulation. 28-10-2014 Indraprastha Apollo Hospital 20

21. Review of changes at birth Overview - As soon as the baby is born Increasing uptake of oxygen by lungs (first and subsequent breaths)  vasoconstriction of ductus venosus and ductus arteriosus . The sphincter in ductus venosus constricts  blood entering liver diverts to the hepatic sinusoids). � Occlusion of placental circulation  BP fall in the IVC & RA. 28-10-2014 Indraprastha Apollo Hospital 21

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23. Aeration of the lungs at birth 1. ↓ in PVR due to lung expansion. 2. ↑ in pulmonary blood flow (thus raising LA pr > IVC pr) 3. progressive thinning of walls of the pulmonary arteries (due to stretching). 28-10-2014 Indraprastha Apollo Hospital 23

24. Factors affecting Pulmonary Vasculature 28-10-2014 Indraprastha Apollo Hospital 24

25. The first breath: Pulmonary alveoli open up: pressure in pulmonary tissues decrease. Blood from right heart rushes to fill the alveolar capillaries. Pressure in right side of heart ↓ . Pressure in the left side of the heart ↑ (as more blood is returned from pulmonary tissue via pulmonary veins to the LA). 28-10-2014 Indraprastha Apollo Hospital 25

26. Resulting circulatory changes: blood pressure is now high in the aorta and systemic circulation is well established Control of circulation is a reflex function regulated: Peripheral baroreceptors in aortic arch & carotid sinus. Central baroreceptors in cardiovascular center of medulla (close proximity to chemoreceptors that regulate respiration). Respiratory and circulatory reflexes are usually strong in the healthy full-term newborn, but efficiency in controlling cardiovascular function is susceptible to environmental factors . Parasympathetic > sympathetic activity. 28-10-2014 Indraprastha Apollo Hospital 26

27. Foramen ovale - Closes at birth Decreased flow from placenta & IVC to hold open foramen and; Increased pulmonary blood flow & pulmonary venous return to left heart causing pressure in the LA > RA. Other changes in the heart - The RV wall is thicker than LV wall in foetus and newborn infants. By the end of the first month the left ventricular wall is thicker than the right. 28-10-2014 Indraprastha Apollo Hospital 27

28. Ductus Arteriosus - DA constricts at birth, often a small shunt from the aorta to the left pulmonary artery for a few days in a healthy, full-term infant. In premature infants and in those with persistent hypoxia the DA may remain open longer.  Oxygen, most important factor in controlling closure of DA in full-term infants. Closure of DA appears to be mediated by bradykinin . PO2 of blood passing through DA reaches about 50 mm Hg, the wall of the DA constricts. (May be mediated directly or by Oxygen effect on decreasing PG E2 & prostacyclin secretion. Implication - Coarctation of aorta requires PGE2 infusion to reopen the DA for blood flow. 28-10-2014 Indraprastha Apollo Hospital 28

29. Umbilical Arteries constrict at birth To prevent loss of infant’s blood. Umbilical cord is not tied for 30-60s; transferring blood from placenta to infant. The closure of the foetal vessels and foramen ovale is initially a functional change; later anatomic closure (from proliferation of endothelial and fibrous tissues). 28-10-2014 Indraprastha Apollo Hospital 29

30. UMBILICAL CORD CLAMPING EXPOSURE TO ROOM AIR TRANSITIONAL CIRCULATION ↓↓PVR ↑ SVR ↑ PULMONARY BLOOD FLOW ↑ OXYGENATION RESPONDS TO CHANGES IN PaO2, PaCO2, pH & CIRCULATING FACTORS SVR – systemic vascular resistance PVR – pulmonary vascular resistance ↑ SVR ↓PVR MECHANICAL INFLATION OF LUNGS ( ↑ alveolar O2 tension,↑PaO2,↓PaCO2) EDRF & PGs ↑ LT. ATRIAL FLOW ↓FORAMEN OVALE SHUNT F.O. CLOSURE DUCTUS ARTERIOSUS CONSTRICTION

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32. Adult Derivatives of Fetal Vascular Structures Fetal Structure Adult Structure Foramen Ovale Fossa Ovalis Umbilical Vein (intra-abdominal part) Ligamentum Teres Ductus Venosus Ligamentum Venosum Umbilical Arteries and Abdominal Ligaments Medial Umbilical Ligaments, Superior Vesicular Artery (supplies bladder) Ductus Arteriosum Ligamentum Arteriosum 28-10-2014 Indraprastha Apollo Hospital 32

33. P ersistent Foetal Circulation Neonate to revert back to foetal type circulation, pathophysiological state - PFC. Causes- Hypothermia, hypercarbia , acidosis, hypoxia and sepsis. One major difference—NO PLACENTA for oxygenation  vicious cycle of worsening hypoxia and acidosis. 28-10-2014 Indraprastha Apollo Hospital 33

34.  Patent Ductus Arteriosus Female: Male, 2-3:1. Aortic blood shunted into Pulmonary Artery(shunt in opposite direction to that in foetus). The magnitude of the shunt increases as PVR continues to fall. Increased volume and workload  left heart failure. Associated with maternal rubella infection during early pregnancy. Premature infants usually have a PDA due to hypoxia and immaturity. Surgical closure of PDA is achieved by ligation and division of the DA. 28-10-2014 Indraprastha Apollo Hospital 34

35. Patent Foramen Ovale Most common form of an ASDs Small isolated patent foramen ovale (no hemodynamic significance); but if other defects present (e.g. pulmonary stenosis or atresia ), blood is shunted through the foramen ovale into LV  cyanosis. Probe patent foramen ovale , in up to 25% of people (superior part of the floor of the fossa ovalis ). Though not clinically significant, may be forced open because of other cardiac defects. 28-10-2014 Indraprastha Apollo Hospital 35

36. Ventricular Septal Defects Ventricular septal defects (VSD) are one of the most common forms of CHD. Well-tolerated in the fetus , as LV and RV pressures are equal. After birth, circulatory effects are dependent on size of the defect and balance between PVR & SVR. In neonates with large VSD, as SVR rises and PVR falls, L  R shunt through VSD develops. As PVR continues to fall during the first weeks of life, this shunt increases  CCF . 28-10-2014 Indraprastha Apollo Hospital 36

37. Tetralogy of Fallot TOF, one of the most common congenital heart malformations. Most important features- RV outflow obstruction, with hypoplastic pulmonary artery; large subaortic VSD with malalignment of conal septum. In foetus, depending on severity of the obstruction to pulmonary blood flow, the aorta will carry percentage of CVO. If obstruction to pulmonary blood flow is very severe, blood flow to the lungs will be supplied via the DA from descending aorta (i.e. the reverse of normal). After birth- If pulmonary obstruction is severe, the neonatal circulation is ‘duct-dependent’ and duct closure  severe cyanosis. Re-establishment of ductal flow- prostaglandin infusion. 28-10-2014 Indraprastha Apollo Hospital 37

38. Transposition of Great Arteries Abnormal rotation & septation of the arterial truncus during embryogenesis. The aorta arises from the RV and the pulmonary artery from the LV (pulmonary and systemic circulations are arranged in parallel ). The FO and DA develop as normal(no major circulatory consequences of this lesion in utero ). After birth, survival depends on presence of ASD, VSD or PDA between the two circulations. Newborns with TGA & intact ventricular septum (IVS) who have small PFO or ASD will be severely cyanosed after closure of the DA. Immediate management- establishing ductal patency (PGE1 infusion) and, if necessary, balloon atrial septostomy . Complete surgical repair- electively later. 28-10-2014 Indraprastha Apollo Hospital 38

39. Anaesthetic Agents 28-10-2014 Indraprastha Apollo Hospital 39

40. Propofol For induction/ procedural sedation. In healthy children without CHD , decrease in blood pressure of 30% due to decreases in SVR (15%) and heart rate (10-20 %). C hildren with CHD - primary effect is drop in BP through decrease in SVR. Systemic cardiac output increased without a change in heart rate or PVR. In children without shunt there was a small decrease in Pa02 (decreased respiratory drive), but no increase in PVR. In children with shunts the decrease in SVR  L-to-R shunting decreased and R-to-L shunting increased. Used with caution as the sole agent in R-to-L shunts and in those for whom a decrease in systemic afterload is dangerous (aortic stenosis , hypertrophic cardiomyopathy , severe ventricular dysfunction). 28-10-2014 Indraprastha Apollo Hospital 40

41. Ketamine A nesthesia , analgesia, cardiovascular stability and lack of respiratory depression with maintenance of airway reflexes. Drawbacks- prolonged action, emergence and dissociative anesthetic state. Anesthetic dose 50-75 mcg/kg/min, analgesic dose 5-10 mcg/kg/min. In children with CHD, ketamine (50-75 mcg/kg/min) maintenance of the relationship between SVR and PVR. Systemic blood pressure increased through an increase in cardiac output with little change in heart rate . Increased inotropy - beneficial for children with significant ventricular dysfunction. Sympathomimetic  increased PVR??? In the setting of normocarbia with supplemental oxygen , PVR is not increased. Combined with 0.5 minimal alveolar concentration (MAC) sevoflurane in spontaneously breathing children with severe PHTN, ketamine did not raise PVR. 28-10-2014 Indraprastha Apollo Hospital 41

42. Etomidate Few studies. Bolus dosing of 0.3 mg/kg well tolerated- maintenance of systemic BP & preservation of balance between SVR and PVR. Drawbacks- Transient adrenal suppression, pain on injection, vomitting . 28-10-2014 Indraprastha Apollo Hospital 42

43. Volatile Agents Halothane- equivalent MAC to isoflurane and sevoflurane , greater myocardial depression and suppression of baroreceptor mediated increase in heart rate. The Qp:Qs ratio is unchanged with halothane, sevoflurane or isoflurane if ventilation is controlled even with high Fi02. Isoflurane - CO was maintained even at 1.5 MAC (decrease in SVR and increase in HR counters reduced inotropy ). Sevoflurane - similar, but overall decrease in CO (lack of compensatory increase in HR with reduced inotropy ). Children with significant ventricular dysfunction may not hemodynamically tolerate MAC levels of volatile anesthesia . 28-10-2014 Indraprastha Apollo Hospital 43

44. Fentanyl / Midazolam Limited to sick children who will remain intubated at the end of procedure. The ratio of Qp:Qs is unchanged in controlled ventilation. Fentanyl 25 mcg/kg maintains SVR, PVR and systemic blood pressure. Caution- Avoid bradycardia . T he general tone of the sympathetic nervous system influences BP. Sympatholytic - combination of synthetic opioids with volatile anesthetics , midazolam or propofol . 28-10-2014 Indraprastha Apollo Hospital 44

45. Dexmedetomidine Selective α-2 agonist. Analgesic and sedative with minimal respiratory depression . S imilar to natural sleep state. Decreased sympathetic outflow  relative bradycardia and stable blood pressure. S ide effects detrimental to children with CHD - hypertension (peripheral α-2 agonist effect), bradycardia and hypotension. P oorly tolerated in heart rate dependent neonates and infants. L ack of respiratory depression  ICU sedation in children at risk for OSA such as Down syndrome. 28-10-2014 Indraprastha Apollo Hospital 45

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