How and when umbilical cord gas analysis can justify your obstetric management

Three cases illustrate how umbilical cord gas values can provide insight into a newborn’s status

OBG Management. 2017 March;29(3):38-44, 46

February 28, 2017|ObGyn

Michael G. Ross, MD, MPH

In this Article

Using cord gas values in practice

Before analyzing the circumstances in Case 1,it is important to consider several key questions, including:

What are the normal levels of cord pH, O₂, CO₂, and base deficit (BD)?
How does cord gas indicate what happened during labor?
What are the preventable errors in cord gas sampling or interpretation?

For a review of fetal cord gas physiology, see “Physiology of fetal cord gases: The basics”.

Physiology of fetal cord gases: The basics

A review of basic fetal cord gas physiology will assist in understanding how values are interpreted.

Umbilical cord O₂ and CO₂

Fetal cord gas values result from the rapid transfer of gases and the slow clearance of acid across the placenta. Approximately 10% of maternal blood flow supplies the uteroplacental circulation, with the near-term placenta receiving approximately 70% of the uterine blood flow.¹ Of the oxygen delivered, a surprising 50% provides for placental metabolism and 50% for the fetus. On the fetal side, 40% of fetal cardiac output supplies the umbilical circulation. Oxygen and carbon dioxide pass readily across the placental layers; exchange is limited by the amount of blood flow on both the maternal and the fetal side (flow limited). In the human placenta, maternal blood and fetal blood effectively travel in the same direction (concurrent exchange); thus, umbilical vein O₂ and CO₂ equilibrate with that in the maternal uterine vein.

Most of the O₂ in fetal blood is carried by hemoglobin. Because of the markedly greater affinity of fetal hemoglobin for O₂, the saturation curve is shifted to the left, resulting in increased hemoglobin saturation at the relatively low levels of fetal Po₂. This greater affinity for oxygen results from the unique fetal hemoglobin gamma (γ) subunit, as compared with the adult beta (ß) subunit. Fetal hemoglobin has a reduced interaction with 2,3-bisphosphoglycerate, which itself decreases the affinity of adult hemoglobin for oxygen.

The majority of CO₂ (85%) is carried as part of the bicarbonate buffer system. Fetal CO₂ is converted into carbonic acid (H₂CO₃) in the red cell and dissociates into hydrogen (H⁺) and bicarbonate (HCO₃⁻) ions, which diffuse out of the cell. When fetal blood reaches the placenta, this process is reversed and CO₂ diffuses across the placenta to the maternal circulation. The production of H⁺ ions from CO₂ explains the development of respiratory acidosis from high Pco₂. In contrast, anaerobic metabolism, which produces lactic acid, results in metabolic acidosis.

Difference between pH and BD

The pH is calculated as the inverse log of the H⁺ ion concentration; thus, the pH falls as the H⁺ ion concentration exponentially increases, whether due to respiratory or metabolic acidosis. To quantify the more important metabolic acidosis, we use BD, which is a measure of how much of bicarbonate buffer base has been used by (lactic) acid. The BD and the base excess (BE) may be used interchangeably, with BE representing a negative number. Although BD represents the metabolic component of acidosis, a correction may be required to account for high levels of fetal Pco₂ (see Case 1). In this situation, a more accurate measure is BD extracellular fluid (BD_ECF).

Why not just use pH? There are 2 major limitations to using pH as a measure of fetal or newborn acidosis. First, pH may be influenced by both respiratory and metabolic alterations, although only metabolic acidosis is associated with fetal neurologic injury.² Furthermore, as pH is a log function, it does not change linearly with the amount of acid produced. In contrast to pH, BD is a measure of metabolic acidosis and changes in direct proportion to fetal acid production.

What about lactate? Measurements of lactate may also be included in blood gas analyses. Under hypoxic conditions, excess pyruvate is converted into lactate and released from the cell along with H⁺, resulting in acidosis. However, levels of umbilical cord lactate associated with neonatal hypoxic injury have not been established to the same degree as have pH or BD. Nevertheless, lactate has been measured in fetal scalp blood samples and offers the potential as a marker of fetal hypoxemia and acidosis.³

References

Assali NS. Dynamics of the uteroplacental circulation in health and disease. Am J Perinatol. 1989;6(2):105-109.
Low JA, Panagiotopoulos C, Derrick EJ. Newborn complications after intrapartum asphyxia with metabolic acidosis in the term fetus. Am J Obstet Gynecol. 1994;170(4):1081-1087.
Mancho JP, Gamboa SM, Gimenez OR, Esteras RC, Solanilla BR, Mateo SC. Diagnostic accuracy of fetal scalp lactate for intrapartum acidosis compared with scalp pH [published online ahead of print October 8, 2016]. J Perinatal Med. doi: 10.1515/jpm-2016-004.

Normal values: The “20, 30, 40, 50 rule”

Among the values reported for umbilical blood gas, the pH, Pco₂, and Po₂ are measured, whereas BD is calculated. The normal values for umbilical pH and blood gases are often included with laboratory results, although typically with a broad, overlapping range of values that may make it difficult to determine which is umbilical artery or vein (TABLE 1).^6,7

I recommend using the “20, 30, 40, 50 rule” as a simple tool for remembering normal umbilical artery and vein Po₂ and Pco₂values (TABLE 2):

Po₂ values are lower than Pco₂values; thus, the 20 and 30 represent Po₂ values
as fetal umbilical artery Po₂ is lower than umbilical vein Po₂, 20 mm Hg represents the umbilical artery and 30 mm Hg represents the vein
Pco₂values are higher in the umbilical artery than in the vein; thus, 50 mm Hg represents the umbilical artery and 40 mm Hg represents the umbilical vein.

Umbilical cord BD values change in relation to labor and FHR decelerations.⁸ Prior to labor, the normal fetus has a slight degree of acidosis (BD, 2 mmol/L). During the latent phase of labor, fetal BD typically does not change. With the increased frequency of contractions, BD may increase 1 mmol/L for every 3 to 6 hours during the active phase and up to 1 mmol/L per hour during the second stage, depending on FHR responses. Thus, following vaginal delivery the average umbilical artery BD is approximately 5 mmol/L and the umbilical vein BD is approximately 4 mmol/L. As lactate crosses the placenta slowly, BD values are typically only 1 mmol/L less in the umbilical vein than in the artery, unless there has been an obstruction to placental flow (see Case 1).

For pH, the umbilical artery value is always lower than that of the vein, a result of both the higher umbilical artery Pco₂as well as the slightly higher levels of lactic acid before placental clearance. Fetal pH levels typically decrease during labor associated with the increased BD described above. However, short-term effects of increased CO₂ (respiratory acidosis) or CO₂ clearance may cause fluctuations in pH that do not correlate with the degree of metabolic acidosis.

Possible causes of abnormal cord gas values

Because of the nearly fully saturated maternal hemoglobin under normal conditions, fetal arterial and venous Po₂ levels cannot be increased significantly above normal values. However, reduced fetal Po₂ and increased fetal Pco₂may occur with poor gas exchange between the maternal and fetal compartments (eg, placental abruption) or maternal respiratory compromise.

In contrast, reduced fetal Pco₂may occur under conditions of maternal hyperventilation and lower maternal Pco₂values. Decreased pH levels may be due to respiratory or metabolic acidosis, the former of which is generally benign. Elevated BD typically is a result of fetal metabolic acidosis, and values approaching 12 mmol/L should be avoided, if possible, as this level may be associated with newborn neurologic injury.⁹

Effect of maternal oxygen administration on fetal oxygenation

Although maternal oxygen administration is commonly used during labor and delivery, controversy remains as to the benefit of oxygen supplementation.¹⁰ In a normal mother with oxygen saturation above 95%, the administration of oxygen will increase maternal arterial Po₂ levels and thus dissolved oxygen. Because maternal hemoglobin is normally almost fully saturated at room air Po₂ levels, there is little change in the bound oxygen and thus little change in the maternal arterial O₂ content or maternal uterine venous Po₂ levels. As fetal umbilical vein Po₂ levels equilibrate to maternal uterine vein Po₂ levels, there is minimal change in fetal oxygenation.

However, maternal oxygen supplementation may have marked benefit in cases in which maternal arterial Po₂ is low (respiratory compromise). In this case, the steep fetal oxygen saturation curve may produce a large increase in fetal umbilical vein oxygen content. Thus, strongly consider oxygen supplementation for mothers with impaired cardiorespiratory function, and recognize that maternal oxygen supplementation for normal mothers may result in nominal benefit for compromised fetuses.

How did the Case 1 circumstances lead to newborn acidosis?

Most noticeable in this case is the large difference in BD between the umbilical artery and vein and the high Pco₂in the artery. Under conditions without interruption of fetal placental flow, either the umbilical artery and/or vein will provide a similar assessment of fetal or newborn metabolic acidosis (that is, BD).

Whereas BD normally is only about 1 mmol/L greater in the umbilical artery versus in the vein, occasionally the arterial value is markedly greater than the vein value. This can occur when there is a cessation of blood flow through the placenta, as a result of complete umbilical cord obstruction, or when there is a uterine abruption. In these situations, the umbilical vein (which has not had blood flow) represents the fetal status prior to the occlusion event. In contrast, despite bradycardia, fetal heart pulsations mix blood within the umbilical artery and therefore the artery generally represents the fetal status at the time of birth.

In response to complete cord occlusion, fetal BD increases by approximately 1 mmol/L every 2 minutes. Consequently, an 8 mmol/L difference in BD between the umbilical artery and vein is consistent with a 16-minute period of umbilical occlusion or placental abruption. Also in response to complete umbilical cord occlusion, Pco₂values rise by approximately 7 mm Hg per minute of the occlusion, although this may not be linear at higher levels. Thus, the BD difference suggests there was likely a complete cord occlusion for the 16 minutes prior to birth.

The umbilical vein BD is also elevated for early labor. This value suggests that repetitive, intermittent cord occlusions (evident on the initial fetal monitor tracing) likely resulted in this moderate acidosis prior to the complete cord occlusion in the final 16 minutes.

Thus, BD and Pco₂levels can be used to time the onset of umbilical cord occlusion or abruption. Since pH is an inverse logarithmic function, it cannot be used to time the onset or duration of cord occlusion. Remember that BD values should be adjusted for extracellular fluid under conditions of markedly elevated Pco₂.

References

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