A prolonged deceleration may signal danger—or reflect a perfectly normal fetal response to maternal pelvic examination. Because of the wide range of possibilities, this fetal heart rate pattern justifies close attention. For example, repetitive prolonged decelerations may indicate cord compression from oligohydramnios. Even more troubling, a prolonged deceleration may occur for the first time during the evolution of a profound catastrophe, such as amniotic fluid embolism or uterine rupture during vaginal birth after cesarean delivery (VBAC). In some circumstances, a prolonged deceleration may be the terminus of a progression of nonreassuring fetal heart rate (FHR) changes, and becomes the immediate precursor to fetal death (TABLE 1).1
When FHR patterns exhibit these aberrations, we rightly worry about fetal well-being and the possible need for operative intervention. Unfortunately, the degree of fetal compromise is difficult to predict and depends on preexisting fetal condition, physiologic reserve, degree and duration of the insult, and other variables.
Some causes of prolonged decelerations and bradycardias
|Cord compression |
Cord prolapse Uteroplacental insufficiency
Anesthesia (paracervical, spinal, epidural)
Maternal supine hypotension
Hypertonic or prolonged contractions
Cocaine ingestion Maternal hypoxia
Maternal seizures, eclampsia
Respiratory depression from medications
Amniotic fluid embolism Fetal hemorrhage
Traumatic amniocentesis Fetal vagal reaction
Rapid descent, impending birth
Fetal scalp electrode placement
Fetal blood sampling Fetal central nervous system anomalies Idiopathic (cord compression?)
|Congenital conduction abnormalities |
Complete heart block
Long QT syndrome
Congenital heart defects
Tachyarrhythmia (Fetal tachyarrhythmia may produce an EFM tracing that appears to be a bradycardia and can only be distinguished by ultrasound) Medications
Beta blockers Hypothermia Infection
Ultimately, a judgment call
The 22nd edition of Williams Obstetrics2 summarizes the clinical challenges involved in the management of prolonged decelerations during labor: “Management of isolated prolonged decelerations is based on bedside clinical judgment, which inevitably will sometimes be imperfect given the unpredictability of these decelerations.”
“Fetal bradycardia” and “prolonged deceleration” are distinct entities
In general parlance, we often use the terms “fetal bradycardia” and “prolonged deceleration” loosely. In practice, we must differentiate these entities because underlying pathophysiologic mechanisms and clinical management may differ substantially.
The problem: Since the introduction of electronic fetal monitoring (EFM) in the 1960s, numerous descriptions of FHR patterns have been published, each slightly different from the others. The result: confusing nomenclature, miscommunication among clinicians, and stymied research efforts.
To standardize definitions of intrapartum FHR patterns so that the effectiveness of EFM could be better assessed in observational studies and clinical trials, the National Institute of Child Health and Human Development organized a workshop.3 Its recommendations were subsequently adopted by the American College of Obstetricians and Gynecologists (ACOG).4 Among the definitions:
Differentiation between the 2 entities is critical because, in many cases, bradycardias are chronic patterns that may not be associated with immediate fetal compromise and do not require immediate intervention. For example, a fetal bradycardia due to congenital heart block would not benefit from immediate delivery, especially prior to term.
“Moderate fetal bradycardia,” defined as a baseline of 100 to 119 bpm, was reported in 1.8% of 1,386 continuously monitored patients and is attributed to relative cephalopelvic disproportion, resolving after rotation of the fetal vertex and associated with normal neonatal outcome.5,6
Similar decelerations can reflect different events
The exact depth and duration of a prolonged deceleration leading to fetal compromise and requiring prompt delivery is difficult to define, although some observations warrant consideration. Experiments with fetal lambs show that the deceleration in response to umbilical vein occlusion is associated with a fall in fetal blood pressure, whereas deceleration in response to umbilical artery occlusion is associated with a rise in fetal blood pressure. This reflex can be abolished by vagotomy, but will eventually recur due to anoxia.7
Vital clue: What happened before the prolonged deceleration?
In clinical practice, it is important to appreciate characteristics of the FHR pattern preceding the prolonged deceleration.8 Williams and Galerneau9 correlated baseline FHR variability and duration of prolonged decelerations with neonatal acid–base status in 186 term gestations with an identified prolonged deceleration within 30 minutes of delivery. Patients were divided into 4 groups, based on FHR variability and recovery of the FHR baseline (TABLE 2).