Electronic fetal monitoring to assess adequate oxygen delivery to the fetus occurs in approximately 89% of births in the United States.¹ Data obtained from monitoring allows clinicians to potentially identify interruptions in the transfer of oxygenated blood from the environment to the fetus. The focus of monitoring is to identify fetal heart rate (FHR) characteristics that reflect an inadequate oxygen supply so that interventions may be carried out. Interruptions in oxygen delivery can occur at several levels of a pathway, with uterine activity being most common. Most fetuses tolerate brief interruptions, so long as episodes are brief and respond to corrective measures. Over time, if oxygen delivery continues to be interrupted or occurs for longer periods, insufficient oxygen levels could potentially result in fetal hypoxia, and ultimately neurologic injury or death.

Inaccurate interpretation and management decisions concerning FHR and uterine activity patterns may affect fetal oxygenation, specifically acid-base values and metabolic condition at birth. Unfortunately, an insufficient number of prospective electronic fetal monitoring studies validates an association between specific FHR patterns and fetal acidemia. As a result, electronic fetal monitoring’s ability to decrease adverse perinatal and neonatal outcomes remains unsupported. Apgar scores, which guide neonatal resuscitation, may not correlate with acid-base status or predict adverse neurologic development because other circumstances, such as prematurity or intra-amniotic infection, may influence acid-base values. Therefore a direct, objective, and sensitive measurement of fetal acid-base status may become necessary at birth to assess the level of fetal oxygenation or provide validation that an intrapartum event was not the source of neurological injury. This chapter will review the fundamental principles of fetal oxygenation and focus on umbilical cord blood gas measurement for determining acid-base status at birth. See Chapter 27 for more information about FHR monitoring.

The placenta is the foundation for fetal acid-base and respiratory blood gas homeostasis.² Acting as a low-resistance structure, the placenta adapts to considerable increases in uterine perfusion during pregnancy and functions as an interface between maternal-fetal circulation. Approximately 20% to 25% of maternal cardiac output targets the uterus and placenta.^3,4

MATERNAL-FETAL GAS EXCHANGE

On the maternal side of the placenta, arterial pressure circulates oxygenated blood through the uterine arteries and spiral arteries leading into the placenta’s intervillous space. At term, maternal blood flow into the intervillous space is reported to be between 500 and 750 mL/min.^3,4 Chorionic villi protruding into the intervillous space are bathed in oxygenated blood, which results in oxygen binding to fetal hemoglobin. In cases such as preeclampsia with severe features, an adequate amount of oxygenated blood flow may not be present in the intervillous space due to decreased utero-placental perfusion from hypertension. After oxygen attaches to fetal hemoglobin, oxygenated blood is directed to the fetus by way of villous veins, which merge to form placental veins, which in turn connect to create a single umbilical vein within the umbilical cord. The umbilical vein then delivers oxygenated blood into the fetal circulation for fetal consumption. The physiology of maternal-fetal gas exchange is shown in Figure 51-1.

Deoxygenated blood flows back through two umbilical arteries into the intervillous space to dispose of carbon dioxide and fetal waste products. This is one of only two situations in human physiology when an artery carries deoxygenated blood. Several other independent physiologic functions occur in the placenta, including nutrient uptake and secretion of hormones to sustain pregnancy.⁵

OXYGENATION PATHWAY IN LABOR

Sufficient oxygen delivery through the intricate maternal-fetal circulatory system is critical for fetal growth, development, and survival. A number of extrinsic sources, including an oxygenation pathway incorporating the maternal lungs, heart, vasculature, uterus, placenta, and umbilical cord, allow adequate oxygen to be delivered (Fig. 51-2). Any interruption at one or more points along this pathway can influence fetal capacity to maintain homeostasis, organ perfusion, and acid-base balance, leading to progressive deterioration through hypoxemia, hypoxia, metabolic acidosis, and metabolic acidemia, and eventually neurologic injury if left uncorrected.^6,7 For example, prolonged periods of uterine tachysystole in the first or second stage can affect the transfer of oxygen to the fetus and disrupt the exchange of carbon dioxide from the fetus. This may result in a progressive accumulation of carbon dioxide and decreased oxygen content. Consequences of this pathway interruption may include an increased incidence of fetal acidemia in umbilical artery cord blood gas values.^8,9

FETAL METABOLISM OF ENERGY

In human physiology, cells require oxygen and glucose for energy production. This occurs through the process of aerobic metabolism, which is necessary for basic cellular function and fetal homeostasis. The amount of oxygen necessary is determined by basic metabolic requirements, fetal size, and fetal activity.¹⁰ So long as oxygen supply and demand are balanced, oxygen will support metabolism of glucose aerobically to produce energy, known as adenosine triphosphate (ATP). By-products of aerobic metabolism are water and carbon dioxide.

COMPENSATORY MECHANISMS FOR INTERRUPTED OXYGEN SUPPLY

Hypoxemia occurs as a result of decreased oxygen content and uptake by fetal hemoglobin, resulting in lower PaO₂ values. Cell and organ functions are usually not affected at this level. Hypoxia follows if mechanisms are not in place to correct this problem, as there are inadequate tissue oxygenation and reduced tissue oxygen content. Stored glycogen and glucose are converted anaerobically to produce enough energy to meet basic fetal metabolic needs. Lactic acid, a type of noncarbonic acid, is created as a by-product. Normally, to overcome lactic acid buildup, base buffers such as bicarbonate and hemoglobin resist pH changes by adding acid or alkali and help to stabilize tissue pH within the fetal circulatory system. This is reflected as a base deficit, which measures the total amount of base buffer reserves that are below normal.

Base excess is the total amount of base buffer reserves that are above normal. If adequate oxygenation is not reestablished, lactic acid continues to accumulate in the fetal tissues, and bicarbonate is consumed.¹¹ The fetus responds with a physiologic compensatory mechanism that increases cardiac output to redistribute blood flow. This allows preferential circulatory streaming to essential organs (brain, myocardium, and adrenal glands) and reduced blood flow to less vital organs such as kidneys, gastrointestinal tract, extremities, and muscles).^12,13 Trunk, limb, and eye movement, as well as breathing, may also be suppressed.¹²

An FHR tracing may reflect these alterations via an elevated baseline rate, minimal variability, and the absence of accelerations. Once buffering capacity is surpassed, metabolic acidosis occurs when lactic acid buildup continues to decrease tissue pH. Eventually, blood pH lowers, leading to metabolic acidemia in arterial cord blood, with the potential end result of neurologic injury.^6,7,10 Acidosis may not always develop into metabolic acidemia if corrective measures, such as lateral positioning and administration of intravenous (IV) fluids, are implemented because the fetus may retain compensatory mechanisms. These mechanisms respond to surrounding extrinsic maternal influences that assist with preserving tissue oxygenation and lowering energy consumption.

Specific terminology related to fetal acid-base balance is defined in Table 51-2. Language such as fetal distress and birth asphyxia historically has been used in clinical practice and has been associated inappropriately with abnormal fetal acid-base status and used in clinical diagnosis. These terms are vague, imprecise, and inaccurate because the newborn may be in satisfactory condition at birth based on Apgar scores or umbilical cord gas analysis.⁷ Reassuring and nonreassuring are also terms that are ill defined and are not included in standardized terminology when referring to acid-base status.^6,14 This language should not be used in communication or documentation.

Fetal scalp sampling and umbilical cord blood gas sampling are the only direct methods of assessing fetal acid-base status. Intrapartum fetal scalp sampling was first reported in the literature as a way to identify fetuses with acidemia. While still used in several countries, this assessment technique is no longer utilized in the United States. The need for fetal scalp sampling also has been downplayed because fetal scalp stimulation, a less invasive assessment method used to elicit FHR acceleration, has been demonstrated to be a reliable indicator of absent acidemia. Furthermore, two consensus-based principles have recognized moderate FHR variability, accelerations, or both to reliably predict the absence of metabolic acidemia at the time that the pattern is observed.¹⁴

UMBILICAL CORD BLOOD GAS SAMPLING

Umbilical cord blood gas sampling is an independent method of clarifying fetal acid-base status. It can support clinical management when neonatal resuscitation or neuroprotective cooling for suspected neonatal hypoxic-ischemic encephalopathy becomes necessary.¹⁵ Blood pH, PCO₂, PO_2, CO_2, hemoglobin, and oxygen content is measured and calculated in the cord blood sample. Once analyzed, HCO₃, oxygen saturation, and base excess or base deficit can be established. Normal umbilical blood gas measurements exclude the presence of acidemia at or immediately before birth,² and this method is more impartial than the Apgar scoring system, especially in the preterm fetus.^16–18

INDICATIONS FOR UMBILICAL CORD BLOOD GAS SAMPLING

There is a lack of agreement among professional organizations and obstetric experts about when to perform umbilical cord blood gas sampling. Historically, suggested indications for sampling have included the following:¹⁶

• 
  

  Cesarean birth for fetal compromise

  
  
• 
  

  Low 5-minute Apgar score

  
  
• 
  

  Severe intrauterine growth restriction

  
  
• 
  

  Abnormal FHR tracing

  
  
• 
  

  Maternal thyroid disease

  
  
• 
  

  Intrapartum fever

  
  
• 
  

  Multiple gestations

More recently, recommendations suggest that samples be obtained in situations where fetal metabolic status is questioned.⁷ This may include cesarean or operative vaginal deliveries performed for FHR tracing indications, or situations of fetal compromise such as shoulder dystocia or umbilical cord prolapse. In addition, umbilical cord blood gas samples may be considered in cases of intrauterine inflammation or infection because the fetal inflammatory response to infection has been suggested as a contributing factor in cerebral palsy in both preterm and term infants.⁷ Infrequently, maternal-fetal conditions, like Rh alloimmunization, can affect umbilical cord blood gas values, especially umbilical artery values. The current preference, to collect and analyze umbilical cord blood gas samples at all births, is not always feasible and is not cost-effective. However, in today’s liability climate, all staff members should be familiar with sampling technique. One suggested approach is delaying umbilical blood gas analysis until Apgar scores are assigned. If the infant is stable in appearance and the 5-minute Apgar score is satisfactory, the umbilical cord segment can be discarded. Regardless, each facility should have a standardized protocol.

Box 51-1 describes an umbilical cord blood gas sampling procedure. At birth, a 10- to 20-cm segment of umbilical cord is doubly clamped and cut. The umbilical cord segment can be set aside at room temperature for 60 minutes without risk of clotting or changes in pH, PO₂, or PCO₂. Placing umbilical cord segments and syringe samples on ice is not required.^6,16,19 Paired cord blood samples are obtained from both the umbilical artery and umbilical vein.²⁰ The umbilical vein and artery blood samples should be drawn using separate syringes and labeled immediately to prevent any confusion in identifying the samples. Umbilical artery samples provide information regarding fetal return of deoxygenated blood to the placenta and offer important data concerning fetal status at birth, including the presence and severity of fetal acidosis. Umbilical vein blood samples verify data about placental function and fetal acid-base status at birth. Analysis of this vessel also will validate the accuracy of the umbilical artery blood gas sample results, confirming that samples originated from two separate vessels.²¹