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8 – Fetal and Perinatal Circulation

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8 – Fetal and Perinatal Circulation 8 Fetal and Perinatal Circulation OUTLINE Fetal Circulation, 92 Changes in Circulation After Birth, 92 Course of Fetal Circulation, 92 Pulmonary Vascular Resistance, 93 Dimensions of Cardiac Chambers, 92 Closure of the Ductus Arteriosus, 94 Fetal Cardiac Output, 92 Premature Newborns, 95 Knowledge of fetal and perinatal circulation is an integral part with higher oxygen saturation (Po2 of 28 mm Hg) than of understanding the pathophysiology, clinical manifesta- the lower half of the body (Po2 of 24 mm Hg) (see Fig. 8.1). tions, and natural history of congenital heart disease (CHD), 4. Less oxygenated blood in the PA flows through the widely especially anomalies seen in the newborn period. Only a brief open ductus arteriosus to the descending aorta and then to discussion of clinically important aspects of fetal and perina- the placenta for oxygenation. tal circulation is presented. Dimensions of Cardiac Chambers FETAL CIRCULATION The proportions of the combined ventricular output tra- versing the heart chambers and the major blood vessels are Fetal circulation differs from adult circulation in several ways. reflected in the relative dimensions of these chambers and Almost all differences are attributable to the fundamental dif- vessels (see Fig. 8.1). ference in the site of gas exchange. In adults, gas exchange 1. Because the lungs receive only 15% of combined ven- occurs in the lungs. In fetuses, the placenta provides the tricular output, the branches of the PA are small. This is exchange of gases and nutrients. important in the genesis of the pulmonary flow murmur of newborns (see Chapter 2). Course of Fetal Circulation 2. The RV is larger and more dominant than the left ventri- There are four shunts in fetal circulation: placenta, ductus cle (LV). The RV handles 55% of the combined ventricular venosus, foramen ovale, and ductus arteriosus (Fig. 8.1). The output, and the LV handles 45% of the combined ventric- following summarizes some important aspects of fetal circu- ular output. In addition, the pressure in the RV is identical lation: to that in the LV (unlike in adults). This fact is reflected 1. The placenta receives the largest amount of combined (i.e., in electrocardiograms (ECGs) of newborns, which show right and left) ventricular output (55%) and has the lowest more RV force than adult ECGs. vascular resistance in fetuses. 2. The superior vena cava (SVC) drains the upper part of the Fetal Cardiac Output body, including the brain (15% of combined ventricular Unlike the adult heart, which increases its stroke volume output), and the inferior vena cava (IVC) drains the lower when the heart rate decreases, the fetal heart is unable to part of the body and the placenta (70% of combined ven- increase stroke volume when the heart rate falls because it has tricular output). Because the blood is oxygenated in the a low compliance. Therefore, the fetal cardiac output depends placenta, the oxygen saturation in the IVC (70%) is higher on the heart rate; when the heart rate drops, as in fetal dis- than that in the SVC (40%). The highest PO2 is found in tress, a serious fall in cardiac output results. the umbilical vein (32 mm Hg) (see Fig. 8.1). 3. Most of the SVC blood goes to the right ventricle (RV). CHANGES IN CIRCULATION AFTER BIRTH About one third of the IVC blood with higher oxygen sat- uration is directed by the crista dividens to the left atrium The primary change in circulation after birth is a shift of (LA) through the foramen ovale, and the remaining two blood flow for gas exchange from the placenta to the lungs. thirds enters the RV and pulmonary artery (PA). The result The placental circulation disappears, and the pulmonary cir- is that the brain and coronary circulation receive blood culation is established. 92 CHAPTER 8 Fetal and Perinatal Circulation 93 Ductus 60 arteriosus 50 15% Pulmonary 40 Ascending aorta arterial 45% mean pressure 30 20 SVC (mm Hg) 10 PV 160 28 15% 19 Pulmonary 120 Lung 18 blood flow 80 (mL/min/kg) RA LA 40 Foramen ovale 1.8 Pulmonary v. 1.6 RV LV 55% 1.4 Pulmonary a. 1.2 IVC 70% Ductus Pulmonary venosus vascular 1.0 and resistance .8 sphincter (mm Hg/mL/min/kg) .6 .4 24 70% Descending Liver .2 aorta Birth -7 -5 -3 -1 135 7 Portal v. Weeks Umbilical v. Fig. 8.2 Changes in pulmonary artery pressure, pulmonary blood flow, and pulmonary vascular resistance during the 7 weeks preced- 32 ing birth, at birth, and in the 7 weeks after birth. The prenatal data Umbilical a. were derived from lambs and the postnatal data from other species. 55% (From Rudolph AM: Congenital Diseases of the Heart, 1974, Chicago, Mosby.) Placenta the right atrium (RA). The RA pressure falls as a result of closure of the ductus venosus c. Closure of patent ductus arteriosus (PDA) as a result of Fig. 8.1 Diagram of the fetal circulation showing the four sites of increased arterial oxygen saturation shunts: placenta, ductus venosus, foramen ovale, and ductus arte- Changes in the PVR and closure of the PDA are so import- riosus. Intravascular shading is in proportion to oxygen saturation, ant in understanding many CHDs that further discussion is with the lightest shading representing the highest PO2. The numer- ical value inside the chamber or vessel is the PO2 for that site in necessary. mm Hg. The percentages outside the vascular structures represent the relative flows in major tributaries and outlets for the two ventri- Pulmonary Vascular Resistance cles. The combined output of the two ventricles represents 100%. a, The PVR is as high as the SVR near or at term. The high PVR Artery; IVC, inferior vena cava; LA, left atrium; LV, left ventricle; PV, pulmonary vein; RA, right atrium; RV, right ventricle; SVC, superior is maintained by an increased amount of smooth muscle in vena cava; v, vein. (From Guntheroth WG, Kawabori I, Stevenson JG: the walls of the pulmonary arterioles and alveolar hypoxia Physiology of the circulation: fetus, neonate and child. In Kelley VC resulting from collapsed lungs. (The role of alveolar hypoxia [ed]: Practice of Pediatrics, vol 8, Philadelphia, 1983, Harper & Row.) in increasing PVR is further discussed in Chapter 29.) With expansion of the lungs and the resulting increase in the alveolar oxygen tension, there is an initial, rapid fall in the 1. The removal of the placenta results in the following: PVR (Fig. 8.3). This rapid fall is secondary to the vasodilat- a. An increase in systemic vascular resistance (SVR) ing effect of oxygen on the pulmonary vasculature. Between results (because the placenta has the lowest vascular 6 and 8 weeks after birth, there is a slower fall in the PVR and resistance in the fetus) the PA pressure. This fall is associated with thinning of the b. Cessation of blood flow in the umbilical vein results in medial layer of the pulmonary arterioles. A further decline in closure of the ductus venosus the PVR occurs after the first 2 years. This may be related to c. Fall of prostaglandin (PGE2), which is produced by pla- the increase in the number of alveolar units and their associ- centa and promotes ductus arteriosus patency in utero ated vessels. 2. Lung expansion results in the following: Several neonatal conditions may interfere with normal a. A reduction of the pulmonary vascular resistance maturation (i.e., thinning) of pulmonary arterioles, resulting (PVR), an increase in pulmonary blood flow, and a fall in the delay in normal decline of PVR and PA pressure: (1) in PA pressure (Fig. 8.2) hypoxia (resulting from lung diseases or high altitudes), (2) b. Functional closure of the foramen ovale as a result of acidosis, (3) increased pulmonary artery pressure (resulting increased pressure in the LA in excess of the pressure in from large left-to-right shunt lesions), or (4) high pulmonary 94 PART 3 Pathophysiology ) 3560 -5 ductal tissue of a premature infant responds less intensely to oxygen than that of a full-term infant. This decreased respon- 2400 siveness of the immature ductus to oxygen is because of its 2000 decreased sensitivity to oxygen-induced contraction; it is not the result of a lack of smooth muscle development because 1600 the immature ductus constricts well in response to acetylcho- line. It may also be caused by persistently high levels of PGE2 1200 y resistance (dyne sec cm in preterm infants (see later section). 800 Prostaglandin E and the Ductus 400 A few clinical situations are worth mentioning to show the otal pulmonar T 0 importance of the PG series in maintaining the patency of the 246810 12 14 16 ductus arteriosus in fetuses. Age (yr) 1. A decrease in PGE2 levels after birth results in constriction Fig. 8.3 Postnatal changes in pulmonary vascular resistance. (From of the ductus. This decrease results from removal of the Moller JH, et al: Congenital Heart Disease, Kalamazoo, MI, 1974, placental source of PGE production at birth and from the Upjohn Company.) 2 marked increase in pulmonary blood flow, which allows effective removal of circulating PGE2 by the lungs. venous pressure (resulting from such condition as mitral ste- 2. Constricting effects of indomethacin or ibuprofen and the nosis). A few examples of clinical situations follow. dilator effects of PGE2 and PGI2 are greater in the ductal 1. Infants with a large ventricular septal defect (VSD) may tissues of an immature fetus than of a near-term fetus. not develop congestive heart failure (CHF) while living at 3. Prolonged patency of the ductus can be maintained by a high altitude, but they may develop CHF if they move intravenous (IV) infusion of a synthetic PGE2, in newborn to sea level.
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