Williams Manual of Pregnancy Complications, 23 ed.

APPENDIX D. Umbilical Cord Blood Gas Analysis

Umbilical cord blood gas analysis has become a commonly used measure of infant condition at birth. In some centers, cord gas determination is made in all infants. As listed in Table D-1, the American College of Obstetricians and Gynecologists (Umbilical cord blood gas and acid-base analysis. Committee Opinion No. 348; November 2006) recommends that cord blood gas and pH analyses be performed in certain clinical circumstances. Although umbilical cord gas determinations have a low predictability for either immediate or long-term adverse neurological outcome, they may be helpful to understand intrapartum or birth events that may cause fetal acidemia. Table D-2shows the mean (±1 standard deviation) values for the components of umbilical artery blood gas analysis in both term and preterm infants.

TABLE D-1. Clinical Circumstances in Which Umbilical Cord Blood Gas and pH Analyses Are Recommended


TABLE D-2. Normal Umbilical Artery Blood pH and Blood Gas Values in Preterm and Term Infantsa



A 10- to 20-cm segment of umbilical cord is clamped immediately following delivery with two clamps near the neonate and two clamps near the placenta. The cord is then cut between the two proximal and two distal clamps. Blood is drawn from an umbilical artery into a 1- to 2-mL heparinized syringe. The needle is then capped, and the syringe is placed into a plastic sack containing crushed ice and immediately transported to the laboratory.


The fetus can rapidly clear CO2 through the placental circulation. If CO2 is not cleared rapidly, H2CO3 (carbonic acid) accumulates in fetal blood and results in respiratory acidemia. Organic acids, which are primarily formed by anaerobic metabolism and include lactic and β-hydroxybutyric acids, are cleared slowly from fetal blood, and when they accumulate result in a metabolic acidemia. With the development of metabolic acidemia, bicarbonate (HCO3) decreases, because it is used to buffer the organic acids. An increase in both H2CO3 and in organic acid (seen as a decrease in HCO3) is known as a mixed respiratory–metabolic academia. For clinical purposes, HCO3represents the metabolic component and is reported in mEq/L. The H2CO3 concentration represents the respiratory component and is reported as the Pco2 in mm Hg. Delta base is a calculated number used as a measure of the change in buffering capacity of bicarbonate (HCO3). For example, bicarbonate will be decreased with a metabolic acidemia as it is consumed to maintain a normal pH. A base deficit occurs when HCO3 concentration decreases to below-normal levels, and a base excess occurs when HCO3 values are higher than normal.

Respiratory Acidemia

Respiratory academia generally develops as a result of an acute interruption in placental gas exchange, with subsequent CO2 retention. Transient umbilical cord compression is the most common antecedent in the development of fetal respiratory academia. In general, respiratory acidemia does not harm the fetus. Table D-3 shows threshold values for each component in respiratory acidemia.

TABLE D-3. Threshold Criteria for Respiratory and Metabolic Fetal Acidemia Using Umbilical Artery Cord Blood Based upon Births at Parkland Hospitala


Metabolic Acidemia

Metabolic academia develops when oxygen deprivation is of sufficient duration and magnitude to require anaerobic metabolism for fetal cellular energy needs. Metabolic acidemia is associated with an increased incidence of hypoxic ischemic encephalopathy and with multiorgan dysfunction in the newborn. Even severe metabolic acidemia, however, is poorly predictive of subsequent cerebral palsy. Shown in Table D-3 are threshold values for each component of umbilical artery blood for metabolic acidemia.

Mixed Respiratory–Metabolic Acidemia

The degree to which pH is affected by Pco2, the respiratory component of the acidemia, can be calculated by the following relationship: 10 additional units of Pco2 will lower the pH by 0.08 units. Thus, the respiratory component may be easily calculated in a mixed respiratory–metabolic acidemia. For example, suppose an acute cord prolapse occurred and the fetus was delivered by cesarean 20 minutes later, analysis showed umbilical artery pH at birth was 6.95, with a Pco2 of 89 mm Hg. To calculate the degree to which the cord compression and subsequent impairment of CO2 exchange affected the pH, the rules given earlier are applied:

89 mm Hg − 49 mm Hg (normal newborn Pco2) = 40 mm Hg (excess CO2).

To correct pH:


Thus, the pH prior to cord prolapse was approximately 7.27, or well within normal limits.


It is generally believed that the term birth asphyxia is imprecise and should not be used. Furthermore, acidemia alone is not sufficient evidence to establish that there has been birth asphyxia. Listed in Table D-4 are the criteria necessary to establish that an acute intrapartum hypoxic event occurred and was sufficient to cause cerebral palsy.

TABLE D-4. Criteria to Define an Acute Intrapartum Hypoxic Event as Sufficient to Cause Cerebral Palsy



For further reading in Williams Obstetrics, 23rd ed.,

see Chapter 28, “The Newborn Infant.”