Perinatal/Neonatal Case Presentation

Journal of Perinatology (2004) 24, 563–564. doi:10.1038/

Umbilical Cord Blood Gases

Marcus C Hermansen MD1

1Dartmonth Medical School, Southern New Hampshire Medical Centre, Nashna, NH, USA

Correspondence: Marcus C. Hermansen, MD, Dartmonth Medical School, Southern New Hampshire Medical Centre, 8 Prospect Street, Nashua, NH 03061, USA



A mother presented at term for induction of labor. Fetal heart monitoring demonstrated variable and late decelerations during the labor. The mother received Stadol (butorphanol tartrate) 3 hours prior to the birth. A male infant was born depressed with Apgar scores of 1 and 4.

Cord blood gases (all given as pH/pCO2/pO2/HCO3-/Base excess) were as follows:

Umbilical vein: 6.85/101/24/17/-21.3Umbilical artery: 6.71/141/13/18/-26.8

The infant was resuscitated with endotracheal intubation and positive pressure ventilation. Narcan was administered at 20 minutes of age. At 1 hours age, a blood gas revealed 7.19/73/36/13.6/-13.6. The infant began seizing within the first 24 hours of life and there were persistent abnormalities of the muscle tone. He had elevated liver enzymes with an SGOT of 129 IU/l at 5 hours of age. A head CT scan revealed a large subarachnoid hemorrhage. His condition stabilized and he was discharged home at 8 days of age. The child is now 5 years old and has spastic cerebral palsy.

Considering this patient, pick the single best interpretation of the umbilical cord blood gases from the following choices.

  1. This represents a respiratory acidemia arising in the fetus due to respiratory depression from Stadol. The HCO3- values of 17 and 18 indicates that there is little, if any, metabolic acidemia present.
  2. A low arterial pH with a base excess of -26.8 indicates that this is a metabolic acidemia. A metabolic acidemia can explain all the values. This may have occurred because of problems with either the placenta or the umbilical cord.
  3. The infant has a mixed acidemia; there is evidence of both uteroplacental insufficiency and cord compression. The elevated pCO2 demonstrates a severe respiratory acidemia and the base excess of -26.8 indicates a severe metabolic acidemia. It is best to ignore the HCO3- value in this case.
  4. There is a laboratory error in the calculated values. A HCO3- of 18 indicates very mild metabolic acidemia, while a base excess of -24/-25 indicates a severe metabolic acidemia. The two values are inconsistent and one or the other is in error.



The best interpretation for this case is "c." Each choice is explained below.

(a) While Stadol can cause respiratory depression and a respiratory acidemia after birth, narcotics should not cause respiratory acidemia prior to birth. Prior to birth, carbon dioxide clearance is performed by the placenta, not the fetal lungs, and Stadol should not cause placental respiratory dysfunction. Additionally, narcotic respiratory depression does not explain the encephalopathy, the elevated liver enzymes or the subarachnoid hemorrhage. Finally, this choice does not account for the extremely negative base excess values.

(b) If there is an elevated pCO2, then, by definition, there is a respiratory acidemia present. These elevated pCO2 values indicate that there is a significant respiratory component to this baby's acidemia.

(c) This is the correct answer. According to the Henderson–Hasselbalch equation, the HCO3- concentration is dependent upon pH and PCO2.1

Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, please contact or the author

Increases in the pCO2 result in increases in the HCO3- while decreases in the pCO2 will lower the HCO3-. Studies from adult volunteers found that a sudden change in the pCO2 of 20 mmHg alters the HCO3- approximately 2–4 mEq/l.2, 3 This change occurs within minutes and represents a biochemical reaction and has nothing to do with renal compensation. As carbon dioxide is acutely retained and exposed to water, carbonic acid is formed. The carbonic acid is then reduced to H+ and HCO3- explaining the rise in HCO3-.2

Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, please contact or the author

HCO3- is a useful screen for a metabolic acidemia if the pCO2 is normal or nearly normal. If the pCO2 is significantly abnormal, then base excess and not HCO3- should be used to determine the presence or absence of metabolic academia.4 This is consistent with the recent recommendations of the American College of Obstetricians and Gynecologists that consider a severe metabolic acidemia to consist of a pH<7.0 and a base excess of <-12.5

The hallmark of uteroplacental insufficiency is a decrease in the cord pH with an elevated pCO2 value. Usually, the umbilical venous and arterial pH values are approximately equally deranged.6 The hallmark of occlusion of the umbilical vein is widened differences between the vein and artery pH and pCO2 values.7 When there is concomitant uteroplacental insufficiency and umbilical vein occlusion, both umbilical venous and arterial blood gas results are significantly deranged, but the umbilical arterial sample is even more so.8

In the case above, the late decelerations of the fetal heart tracing associated with the decreased umbilical venous pH and elevated pCO2, all indicate the presence of uteroplacental insufficiency. The variable decelerations associated with a widened difference between the umbilical artery and vein cord values indicate the presence of a coincident umbilical vein occlusion.

(d) Although laboratory errors of blood gas analyses do occur, they are relatively uncommon. Additionally, the similar values between these two analyses would require that both samples resulted in laboratory errors — this is an even less likely event than that of an error of a single sample.



  1. Warburg EJ. Carbonic acid compounds and hydrogen ion activities in blood and salt solutins. A contribution to the theory of the equation of LJ Henderson and KA Hasselbalch. Biochem J 1992;16:153.
  2. Martin L. Pulmonary physiology in clinical practice.
  3. Schlichtig R, Grogono AW, Severinghaus JW. Human PaCO2 and standard base excess compensation for acid–base imbalance. Crit Care Med 1998;26:1173–1179. | Article | PubMed |
  4. Siggaard-Andersen O, Fogh-Andersen N. Base excess or buffer base (strong ion difference) as measure of a non-respiratory acid–base disturbance. Acta Anaesthesiol Scand 1995;39(Suppl 106):123–128.
  5. American College of Obstetricians and Gynecologists. Neonatal Encephalopathy and Cerebral Palsy: Defining the Pathogenesis and Pathophysiology. Washington, DC: American College of Obstetricians and Gynecologists; 2003.
  6. Pomerance J. Umbilical cord blood gas casebook: interpreting umbilical cord blood gases. Part I. J Perinatol 1997;17:503–504.
  7. Pomerance J. Umbilical cord blood gas casebook: interpreting umbilical cord blood gases, Part V. J Perinatol 1999;19:466–467. | Article | PubMed |
  8. Pomerance JJ. Interpreting Umbilical Cord Blood Gases. Pasadena, CA: MNMG Publishers; 2004, 101–104.


These links to content published by NPG are automatically generated


Umbilical Cord Blood Gas Casebook

Journal of Perinatology Correspondence