A 35-year-old gravida 1, para 0 woman at 35 + 1 weeks’ gestation underwent induction of labor because of concern for intrauterine growth restriction (IUGR). The fetal heart rate had a normal baseline, moderate variability, and no decelerations (a Category I cardiotocograph [CTG]). On examination, the cervix was 1 cm dilated, long, and the presenting vertex was at a high station. A transcervical Foley balloon catheter was placed for cervical preparation (labor induction).
After several hours, the transcervical catheter fell out, and when examined, the patient’s cervix was found to be 4 cm dilated, 50 percent effaced (cervical thickness), –2 station (relationship of the presenting fetal part to the maternal ischial spines during delivery). Oxytocin was started, and the patient requested an epidural for pain relief. After injection of local anesthetic, the patient’s blood pressure dropped from 120/80 to 85/42 mmHg, and the fetal heart tracing was noted to have late decelerations with moderate rate variability (Category IIb CTG). The patient was given 100 µg IV phenylephrine, and her blood pressure increased to 110/60 mmHg, which was consistent with her preanalgesia blood pressure. The fetal heart rate improved, with a baseline rate of 130–140 beats/min, moderate variability, and no further decelerations (Category I CTG). Low-dose oxytocin was begun.
Two hours later, the uterine contractions were every 2–3 minutes, and the fetal heart rate tracing showed variable decelerations to a nadir of 60 beats/min, with minimal variability (Category IIc CTG). The cervical examination results were 6 cm/80 percent/–1 station, and the oxytocin infusion was stopped. The variable decelerations became moderate in depth and non recurrent, and fetal heart rate variability was moderate (Category IIb CTG).
Within 2 hours, the uterine contractions were every 2–3 minutes without an oxytocin infusion, and the fetal heart rate tracing continued to have episodes of minimal variability with accelerations and occasional decelerations. A cervical examination revealed that the patient was fully dilated (10 cm) and +2 station, and the patient began expulsive efforts. Within 15 minutes, the fetal heart rate tracing began to show severe variable decelerations and minimal variability with every contraction (Category IIc CTG). After 15 minutes, the obstetrician asked the patient to stop pushing and assessed her for an operative vaginal delivery. Before placing the forceps for delivery, there was a fetal bradycardia of 60 beats/min, and the patient was urgently brought to the operating room, where the fetal heart rate recovered to 160 beats/min, with minimal variability and late decelerations (a Category III CTG). The forceps were placed on the fetal head, and with the next contraction the fetus was delivered.
The neonate weighed 2,500 g, had Apgar scores of 4 at 1 minute and 8 at 5 minutes. The umbilical cord was clamped at birth and blood collected for analysis. The umbilical cord arterial blood gases showed a pH of 7.11, PCO2 of 64 mmHg, and a base excess of –8 mEq/liter, and the umbilical cord venous blood gases showed a pH of 7.20, PCO2 of 55 mmHg, and a base excess –6 mEq/liter.
This pregnancy was complicated by intrauterine growth restriction, which is associated with uteroplacental insufficiency and may result in fetal heart rate tracing abnormalities and the development of metabolic acidosis.
Maintaining maternal blood pressure during induction of neuraxial anesthesia is important to fetal oxygenation because placental perfusion is pressure dependent.
Severe variable decelerations with minimal variability and late decelerations with minimal variability are both associated with fetal metabolic acidosis.
This discussion is based primarily on guidance commonly followed in North America. Please also refer to the Appendix for clinical management based on the interpretation of electronic fetal monitoring (CTG) from the UK National Institute of Health and Care Excellence (NICE).
Electronic tracing of the fetal heart rate (FHR) was initially designed as a noninvasive measure of adequacy of fetal oxygenation and of fetal hypoxia so that timely intervention could prevent the development of fetal acidemia. The challenge has become how to interpret this multivariate technique and provide a consensus for clinicians on which to base clinical management. The ultimate goal in FHR interpretation should be not to miss the presence of acidemia, but prevention of acidemia should not result in an unduly rate of high obstetric intervention. To maintain this balance, the FHR description and interpretation should be performed in a systematic fashion using accepted guidelines.
In interpreting the FHR tracing, the baseline FHR (110–160 beats/min is the normal range) and the FHR variability (moderate, minimal, or absent) should be noted initially. Next, the presence or absence of decelerations and whether they are late or variable in nature, as well as their severity, have to be assessed. Understanding the evolution of these decelerations over time is very important in determining the level of obstetric intervention necessary.
The nomenclature and definitions of FHR patterns have been standardized in the United States since the first US National Institute of Child Health and Human Development (NICHD) conference in 19971 and were reiterated in 20082 (Table 12.1).