The blood volume model of neonatal transition. 

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Context 1

... the mus- cular-walled, high-pressure arteries may continue to move blood from the fetus to the placenta, whereas return flow to the fetus in the thin-walled vein is impeded. The loss of fetal blood volume may be particularly severe when the recovery time between contractions is short. Neonatal status may be compromised by the uncorrected physiologic effects of hypoxia as well as reduced blood volume. The fetal heart rate variable decelerations commonly attributed to cord compression can occur as a result of umbilical vessel occlusion. According to Weiss et al., 17 Doppler studies have demonstrated that, for many variable decelerations, a sharp decrease in umbilical vessel perfusion precedes the drop in the fetal heart rate by a few seconds. The interruption of umbilical perfusion stimulates dis- charge of the parasympathetic nervous system via the vagus nerve and results in fetal bradycardia. Factors, such as amniotic fluid volume, the number of encirclements, presence of knots, and tightness of the cord may influence the impact of nuchal cords on fetuses and newborns. Strong et al. 18 found that oligohydramnios worsened the effect of nuchal cords on fetal status during labor. The same appears to be true of multiple nuchal cord encirclements. 4 To protect the physiologic processes at birth, one must understand the role that blood volume plays in the success of the fetus-to-neonate transition. The following model explains how an adequate blood volume promotes a normal physiologic neonatal transition and helps to protect the infant from harm. A shift is needed in thinking about the fetus-to-neonate transition, from the current focus on immediate respiration only to the role that blood volume plays in a successful transition. 19 The blood volume model states that the limit- ing factor at birth may be the availability of adequate red blood cells and volume for tissue oxygen delivery. 19 During fetal life, only 8% to 12% of the fetal cardiac output goes to the fetal lungs, whereas 45% to 50% circulates through the placenta. 20 The alveoli during fetal life are filled with lung fluid. Immediately after birth, the lung must structurally change from a fluid-filled organ to one filled with air. Functionally, it must change from an organ of fluid production to an organ of gas exchange. Immediately after birth, 50% of the neonate’s cardiac output must flow to and through the lungs to effect appropriate gas exchange. A volume of blood (at least 40 mL) must be available to expand the pulmonary capillary bed. 21 However, the volume of blood available to the baby for this purpose is limited to the amount that was in the neonate at the time the cord was clamped. If the blood volume needed to expand the lung does not come from the placenta through an intact umbilical cord, it must be forfeited from other organ systems and the general circulation in the neonate’s body. 22 A full-term fetus has approximately 110 to 115 mL/kg of blood that is distributed in the fetal and placental compart- ments. Prior to birth, about two-thirds volume perfuses the fetal body, whereas one third flows through the placenta. A 3000 g fetus will have approximately 330 to 345 mL of blood in the fetal-placental circulation. The average blood volume of infants after immediate cord clamping is 70 mL/kg versus 90 mL/kg in infants after delayed cord clamping. For the 3000 g infant, this difference is 210 mL versus 270 mL for the circulating blood volume. 23 Delayed cord clamping will provide an extra 60 mL of blood to the infant for circulatory adjustments. This 60 mL of blood is needed for lung volume expansion as the neonatal cardiac output to the lung increases from 40% to 50% of the cardiac output, in contrast to the fetal flow of 8% to 12%. 20 The millions of capillaries covering the alveoli are actually cemented to the alveoli by an intracellular matrix. 24 At birth, these capillaries fill with blood for the first time, causing the capillary plexuses to expand with blood and become erect. This process of capillary “erection” opens the alveoli and provides the “scaffolding” structure to keep them open. 25 Air pressure does not keep lungs open, because lungs have only atmospheric pressure. It is the hydrostatic exoskeleton generated by the capillary network that maintains alveolar expansion and prevents the alveoli from closing or collapsing on expiration. Surfactant helps keep the alveoli open due to reduction in the surface tension, but surfactant does not directly support the alveolar structure. Adequate blood flow to the lung clears the lung fluid during the initial breaths because higher colloidal osmotic pressure of the blood in the capillaries draws the fluid from the alveoli. As respiration continues, a higher level of systemic oxygen stimulates the respiratory centers of the brain and causes the oxygen-sensitive umbilical arteries and ductus arteriosus to close. 26 Normal neonatal respiration and circulation is then established (Figure 1). Stembera and colleagues documented that blood flow in the umbilical vein continues at an average of 75 mL/min for an average of 100 to 120 seconds after birth. 27 Anatomic sections of the cord after birth show the arteries are open when the cord is clamped immediately and constricted when clamping is delayed for a few minutes. This postnatal placental circulation continues to support the infant during the transition to breathing. Even in compromised infants, Stembera found a flow of about 50 mL/kg per minute. 28 Symptomatic polycythemia and hyperbilirubinemia are the two concerns most commonly associated with delayed cord clamping. The idea that delayed cord clamping causes either problem is based on two reports from a study from the 1960s, which did not randomly allocate subjects and has not been replicated. 29,30 Systematic reviews of the literature reveal that neither risk has been validated in randomized controlled trials of delayed cord clamping involving preterm or term infants. 31–33 Further discussion can be found in a comprehensive review of the literature on cord clamping. 31 Immediate cord clamping after birth has been shown to result in a 25% to 40% reduction in blood volume at birth. 23 Clamping the cord before birth removes the infant from the placental life support system before the infant is born and increases blood volume loss. The basic cause of hypoxia is interruption of the normal blood flow between the fetus and the placenta. The practice of clamping the cord before birth places the infant at high risk of hypoxia, hypovolemia, and related problems. If there is a delay in delivery of the shoulders, this practice can lead to morbidity and mortality. It also necessitates an abrupt, rather than gradual, adapta- tion to extrauterine breathing. 19,34 Potential adverse effects from premature ligation of nuchal cords and the resulting blood loss include hypovolemia, hypotension and shock, 6,35 anemia, 7 and cerebral palsy. 1,8,9 An infant who presents with a nuchal cord may already be compromised because of compression of the umbilical cord during contractions, which prevents normal blood flow and correction of acid-base imbalance. If the cord is not cut before or immediately after birth, the infant may be able to equalize these imbalances after birth when the nuchal cord is reduced. In 1973, Cashore and Usher reported that tight nuchal cords at birth resulted in neonatal hypovolemia in a case series of 11 infants. 6 Infants requiring cord ligation prior to delivery of the shoulders had a 20% reduction of red blood cell volume after birth. The diminished blood flow to the fetus accounted for a decrease in body iron content, resulting in anemic, pale, and hypotensive infants after birth. 6 In a case report, Vanhaesebrouck described two term infants who suffered from acute hypovolemic shock resulting from a tight nuchal cord, despite unremarkable pregnancies and labors. 35 Early clamping and cutting of the cords was deemed necessary for delivery because the nuchal cords were too tight to slip over the infants’ heads. These infants exhibited pallor, irregular respirations, low Apgar scores, gasping, tachycardia, weak peripheral pulses, hypotension, and acidemia. Resuscitation efforts included intubation and ventilation as well as blood transfusions to restore blood volume. The authors suggested “fetoplacental hemorrhage” due to tight nuchal cord was the cause of the infants’ condition. An observational study by Shepherd examined tight or loose nuchal cord as a potential cause of neonatal anemia in 437 newborns consecutively admitted to the nursery. 7 Anemia was defined as any venous hemoglobin level less than 13.2 g/dL or hematocrit of less than 39.2%. She found that 16% of 57 neonates with a nuchal cord were anemic within the first 24 hours after birth. Three infants in the nuchal cord group developed hypotension requiring blood transfusions, but no anemia was found in the group without a nuchal cord. Shoulder dystocia occurs in 1.7% of births and is most often an unanticipated event. A few case reports suggest that clamping and cutting the nuchal cord before delivery of the infant’s shoulders can influence outcomes after shoulder dystocia. Iffy described several cases of cerebral palsy after nuchal cords were cut, and subsequent shoulder dystocia delayed birth by as little as 3 minutes. 8 All of the fetuses were considered healthy prior to the onset of labor. The infants were all born with low Apgar scores and developed signs of hypoxic-ischemic encephalopathy. The authors highly advise avoiding nuchal cord ligation prior to full delivery whenever possible. Iffy remarked that, in Europe, it is routine to deliver the infant’s head and then wait for the next contraction to effect restitution and deliver the shoulders. 1 The diagnosis of shoulder dystocia is not made until after this second contraction. This is in contrast to the practice in the United States of attempting delivery ...

Context 2

... respiration continues, a higher level of systemic oxygen stimulates the respiratory centers of the brain and causes the oxygen-sensitive umbilical arteries and ductus arteriosus to close. 26 Normal neonatal respiration and circulation is then established (Figure 1). ...