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Clinical Reviews

Management of prolonged decelerations

Some are benign, some are pathologic but reversible, and others are the most feared complications in obstetrics

November 2006 · Vol. 18, No. 11


3 FHR patterns: What would you do?

6 pearls for managing prolonged decelerations

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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 valsalva
  Maternal supine hypotension
  Hypertonic or prolonged contractions
  Abruptio placentae
  Uterine rupture
  Cocaine ingestion Maternal hypoxia
  Maternal seizures, eclampsia
  Respiratory depression from medications
  Cardiopulmonary arrest
  Amniotic fluid embolism Fetal hemorrhage
  Vasa previa
  Traumatic amniocentesis Fetal vagal reaction
  Rapid descent, impending birth
  Cervical examination
  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).

The findings:


Neonatal outcomes associated with variability and recovery of FHR patterns after prolonged deceleration


GROUP 1 V+ R+ (N=128)

GROUP 2 V+ R- (N=40)

GROUP 3 V- R+ (N=9)

GROUP 4 V- R- (N=9)


pH (mean±SD)






Base deficit (mean±SD)






pH <7.0 (%)






pH <7.1 (%)






Base deficit <16 (%)






Base deficit <12 (%)








SOURCE: Williams and Galerneau9

Acid–base changes likely begin within minutes of cord compression

Zilianti and colleagues10 evaluated 29 fetuses with normal FHR patterns during labor with FHR deceleration during the expulsion phase of delivery. When the FHR deceleration was prolonged (>120 seconds), umbilical artery pH significantly decreased (7.19 vs 7.27), umbilical vein pH remained unchanged (7.32), and the umbilical venous–arterial pH difference was significantly increased (0.13 vs 0.05). Thus, acid–base changes likely begin within minutes of cord compression.

The correlation between acidemia and loss of variability

In their review of 43 vacuum extractions, Gull and colleagues22 found that 27 infants were delivered for “end-stage bradycardia” (abrupt persistent decrease in FHR to less than 100 bpm for more than 2 minutes, or repeated deceleration more than 60 bpm below baseline with poor recovery), and 16 were delivered electively (controls). Umbilical-cord base deficit was greater in the newborns with bradycardia than in controls, and the length of time FHR variability was lost correlated with the degree of base deficit. Acidemic fetuses lost FHR variability during the bradycardia for more than 4 minutes, or started to lose FHR variability less than 3 minutes from the beginning of the bradycardia.

What is optimal interval between deceleration and delivery?

In a series of 106 cases of uterine rupture during VBAC, Leung et al11 found significant neonatal morbidity when 18 minutes or more lapsed between the onset of the prolonged deceleration and delivery.

First, remain calm when decelerations occur

Freeman and colleagues12 advocate staying calm and avoiding overreaction, because many cases will resolve spontaneously. Nonetheless, prolonged decelerations should prompt the physician to:


6 pearls for managing prolonged decelerations





Reduce aorto-caval and/or cord compression

Change patient positioning


Restore intravascular volume

Administer intravenous fluid bolus


Reduce uterine activity

Discontinue oxytocin drip and give tocolytic therapy (terbutaline)


Enhance oxygen delivery to fetus

Give supplemental oxygen


Resolve hypotension

Administer vasopressor therapy (ephedrine)


Resolve oligohydramnios and cord compression

Perform transcervical amnioinfusion


Stepwise management of prolonged decelerations

Examine the cervix
   Check for umbilical cord prolapse
   Check progress of dilation and descent
   Place internal monitors, if indicated

Determine probable cause

Start therapies

Prepare for intervention by operative delivery
   Intravenous access
   Blood type and screen
   Indwelling urinary catheter
   Obtain consents for operative vaginal delivery and cesarean delivery
   Notify appropriate personnel (eg, anesthesiology, pediatrics)

   If fetal condition is nonreassuring despite therapies
   If prolonged decelerations recur and spontaneous delivery is remote (cases must be individualized)

Consider amnioinfusion when cord compression is suspected

Many cases of prolonged decelerations are secondary to cord compression resulting from oligohydramnios. Miyazaki13 showed that saline amnioinfusion helped correct the FHR problem in most cases of repetitive variable decelerations (19 of 28) and prolonged decelerations (12 of 14 cases).

Several randomized clinical trials analyzed in a recent Cochrane Review14 suggest that amnioinfusion for cord compression reduces the occurrence of variable FHR decelerations and the need for cesarean section; this applies to settings in which nonreassuring FHR patterns were not further assessed by fetal blood sampling, which is reflective of practice in most US labor units.

The recent ACOG practice bulletin on intrapartum monitoring4 advocates amnioinfusion for recurrent variable FHR decelerations, but does not address prolonged decelerations specifically.

Although most data on amnioinfusion address treatment of recurrent variable FHR decelerations, it also seems reasonable to consider this option for prolonged decelerations when oligohydramnios is suspected.12

Other possible causes of prolonged decelerations

Vasa previa. A sudden prolonged deceleration following rupture of membranes with concomitant vaginal bleeding should prompt the physician to consider the possibility of a disrupted velamentous cord insertion (vasa previa), which can lead to rapid fetal exsanguination.15

Acute profound maternal hypoxemia may lead to a first prolonged FHR deceleration, often preceded by increased uterine tone, as described in both eclampsia16 and amniotic fluid embolism.17 With eclampsia, the prolonged deceleration is reversible; treatment and expectant management will allow for fetal recovery after the seizure abates.

When acute amniotic fluid embolism leads to profound cardiovascular collapse, prompt perimortem cesarean delivery may be required within minutes if CPR does not restore normal maternal cardiopulmonary function and recovery of FHR.

When is scalp stimulation helpful?

Stimulation of the fetal scalp is an effective technique for assessing fetal status during periods of nonreassuring FHR patterns.18 However, the technique is intended to be performed during periods of FHR baseline and is sometimes misapplied during prolonged decelerations. Scalp stimulation during a prolonged deceleration would not likely provide valid information or change clinical management and could in theory exacerbate fetal compromise if additional parasympathetic tone were elicited.

Avoid fetal pulse oximetry

Although fetal pulse oximetry is FDA-approved and commercially available in the United States, and may be well suited for monitoring fetal arrhythmias,19,20 a prolonged deceleration is an absolute contraindication to its use.21


Overall, in managing a delivery marked by prolonged decelerations, we should strive to minimize maternal–fetal complications by carefully assessing the clinical situation, correcting reversible problems, and preparing for expeditious delivery if the fetal condition is of sufficient concern that further expectant management is unlikely to allow for safe spontaneous delivery. Still, “…bedside judgment inevitably will sometimes be imperfect given the unpredictability of these decelerations.”2

The author reports no financial affiliations relevant to this article.

3 fetal heart rate patterns: What would you do?

Dilemma: Fetal bradycardia due to congenital complete heart block secondary to anti-SSA/Ro and anti-SS-B/La antibodies. The fetal ventricular rate is fixed at 60 bpm

Management: At 30 weeks’ gestation, with no sonographic evidence of heart failure and a biophysical profile score of 8/8, expectant management is indicated

Dilemma: Prolonged deceleration during pelvic examination in an uncomplicated term pregnancy. Note that fetal heart rate (FHR) variability was maintained during recovery of the FHR baseline

Outcome: Uneventful spontaneous vaginal delivery

Dilemma: Prolonged deceleration due to uterine rupture during trial of labor after cesarean. Repetitive variable decelerations preceded the prolonged deceleration. FHR variability was lost after several minutes

Management: Emergency cesarean


1. Cetrulo CL, Schifrin BS. Fetal heart rate patterns preceding death in utero. Obstet Gynecol. 1976;48:521-527.

2. Cunningham FG, Leveno KJ, Bloom SL, et al. Williams Obstetrics. 22nd ed. New York: McGraw-Hill; 2005.

3. Electronic fetal heart rate monitoring: research guidelines for interpretation. National Institute of Child Health and Human Development Research Planning Workshop. Am J Obstet Gynecol. 1997;177:1385-1390.

4. Intrapartum fetal heart rate monitoring. ACOG Practice Bulletin #70. American College of Obstetricians and Gynecologists. Obstet Gynecol. 2005;106:1453-1461.

5. Young BK, Weinstein HM. Moderate fetal bradycardia. Am J Obstet Gynecol. 1976;126:271-275.

6. Young BK, Katz M, et al. Fetal blood and tissue pH with moderate bradycardia. Am J Obstet Gynecol. 1979;135:45-47.

7. Reynolds SR. Bradycardia in the lamb fetus in response to circulatory distress. Am J Physiol. 1954;176:169-174.

8. Langer O, Sonnendecker EW. Characteristics and management of intrapartum prolonged fetal bradycardia. Br J Obstet Gynaecol. 1982;89:904-912.

9. Williams KP, Galerneau F. Fetal heart rate parameters predictive of neonatal outcome in the presence of a prolonged deceleration. Obstet Gynecol. 2002;100:951-954.

10. Zilianti M, Segura CL, et al. Studies on fetal bradycardia during birth process. II. Obstet Gynecol. 1973;42:840-843.

11. Leung AS, Leung EK, Paul RH. Uterine rupture after previous cesarean delivery: maternal and fetal consequences. Am J Obstet Gynecol. 1993;169:945-950.

12. Freeman RK, Garite TG, Nageotte MP. Fetal Heart Rate Monitoring. Philadelphia: Lippincott Williams & Wilkins; 2003.

13. Miyazaki FS, Taylor NA. Saline amnioinfusion for relief of variable or prolonged decelerations. A preliminary report. Am J Obstet Gynecol. 1983;146:670-678.

14. Hofmeyr GJ. Amnioinfusion for umbilical cord compression in labour. Cochrane Database Syst Rev. 2000;CD000013.-

15. Gabbe SG, Nelson LM, Paul RH. Fetal heart rate response to acute hemorrhage. Obstet Gynecol. 1977;49:247-251.

16. Paul RH, Koh KS, Bernstein SG. Changes in fetal heart rateuterine contraction patterns associated with eclampsia. Am J Obstet Gynecol. 1978;130:165-169.

17. Clark SL, Hankins GD, Dudley DA, Dildy GA, Porter TF. Amniotic fluid embolism: analysis of the national registry. Am J Obstet Gynecol. 1995;172:1158-1167;discussion 1167-1169.

18. Clark SL, Gimovsky ML, Miller FC. The scalp stimulation test: a clinical alternative to fetal scalp blood sampling. Am J Obstet Gynecol. 1984;148:274-277.

19. Dildy GA, Loucks CA, Clark SL. Intrapartum fetal pulse oximetry in the presence of fetal cardiac arrhythmia. Am J Obstet Gynecol. 1993;169:1609-1611.

20. van den Berg PP, Nijland R, van den Brand SF, Jongsma HW, Nijhuis JG. Intrapartum fetal surveillance of congenital heart block with pulse oximetry. Obstet Gynecol. 1994;84:683-686.

21. Garite TJ, Dildy GA, McNamara H, et al. A multicenter controlled trial of fetal pulse oximetry in the intrapartum management of nonreassuring fetal heart rate patterns. Am J Obstet Gynecol. 2000;183:1049-1058.

22. Gull I, Jaffa AJ, Oren M, Grisaru D, Peyser MR, Lessing JB. Acid accumulation during end-stage bradycardia in term fetuses: how long is too long? Br J Obstet Gynaecol. 1996;103:1096-1101.

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