Extra Topic 4.7 -- Fetal Monitoring Flashcards

(A 20-year-old primigravida at 38 weeks gestation presents to the labor and delivery suite with pre-eclampsia and regular contractions. The patient is admitted, and an oxytocin infusion is started to induce delivery. Several hours later, she is noted to have the following fetal heart rate pattern.)

1
Q

How would you interpret this fetal heart rate (FHR) pattern?

(A 20-year-old primigravida at 38 weeks gestation presents to the labor and delivery suite with pre-eclampsia and regular contractions. The patient is admitted, and an oxytocin infusion is started to induce delivery. Several hours later, she is noted to have the following fetal heart rate pattern.)

A

Since distinct decelerations are beginning within 10-30 seconds after the beginning of each uterine contraction, and resolving within 10-30 seconds following the end of each contraction, I would – conclude that this FHR tracing is showing late decelerations.

Moreover, although the baseline heart rate is normal (110-160 bpm), fetal heart rate variability, defined as – fluctuations in the FHR of more than 2 cycles per minute, appears to be minimal (<5 bpm).

While the reduced FHR variability may be secondary to magnesium sulfate-induced central nervous system depression (the patient is most likely receiving magnesium to treat her pre-eclampsia),

this fetal heart rate tracing would be considered non-reassuring and may represent fetal distress.

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2
Q

What is considered normal fetal heart rate variability, and

what is the significance of normal and abnormal FHR variability?

(A 20-year-old primigravida at 38 weeks gestation presents to the labor and delivery suite with pre-eclampsia and regular contractions. The patient is admitted, and an oxytocin infusion is started to induce delivery. Several hours later, she is noted to have the following fetal heart rate pattern.)

A

As I mentioned, baseline variability is defined as fluctuations in the fetal heart rate of more than 2 cycles per minute.

Normal FHR variability is suggestive of a normally functioning autonomic nervous system and fetal well-being (atlhough it is not always predictive of a good outcome).

Absent or persistently minimal FHR variability, on the other hand, appears to be the most significant intrapartum sign of fetal compromise.

Various factors that may cause or contribute to decreased FHR variability include – fetal hypoxia, fetal sleep state, prematurity, fetal neurologic abnormalities, fetal tachycardia, betamethasone administration, congenital abnormalities, and/or the administration of central nervous system depressants such as opioids, barbiturates, magnesium sulfate, and benzodiazepines.

  • Clinical Note:*
  • Absent Variability = amplitude range undetectable*
  • Minimal Variability = < 5 bpm*
  • Moderate Variability = 6-25 bpm*
  • Marked Variability = > 25 bpm*
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3
Q

What are the different types of fetal heart rate decelerations?

(A 20-year-old primigravida at 38 weeks gestation presents to the labor and delivery suite with pre-eclampsia and regular contractions. The patient is admitted, and an oxytocin infusion is started to induce delivery. Several hours later, she is noted to have the following fetal heart rate pattern.)

A

Depending on the time of onset and offset in relation to maternal contractions, fetal heart rate decelerations can be classified as – early, variable, or late.

Early (type 1) decelerations are uniform FHR decelerations that are usually less than 20 bpm below baseline and coincide with the onset and offset of uterine contractions.

  • Early decelerations are most likely related to reflex vagal responses to mild hypoxia or transient increases in intracranial pressure as would occur with uterine compression of the fetal head.

Late (type 2) decelerations are gradual and uniform FHR decelerations whose onset and recovery occur around 10-30 seconds after the onset and recovery of a uterine contraction.

  • These decelerations are further classified as either
    • reflex late decelerations
      • (maternal hypotension → reduced uterine blood flow → fetal hypoxia → increased vagal tone → FHR deceleration) or
    • nonreflex late decelerations
      • (fetal hypoxia → myocardial decompensation → increased vagal tone → FHR deceleration).
  • Reflex late decelerations are usually associated with maternal hypotension and good FHR variability; while nonreflex late decelerations are associated with uteroplacental insufficiency, intrauterine growth retardation, prolonged hypoxia during pregnancy, and decreased or absent FHR variability.

Variable (type 3) decelerations are non-uniform (shape and duration) decelerations occurring variably in relationship to uterine contractions.

  • These decelerations are further classified as – mild, moderate, or severe – based on their degree and duration.
  • Variable decelerations are thought to result from increased vagal activity secondary to complete or partial umbilical cord occlusion.
  • During the second stage of labor, dural stimulation from compression of the head may lead to increased vagal activity and variable decelerations.
  • While mild to moderate variabie decelerations (> 80 bpm) are usually well tolerated, variable decelerations that are persistent, prolonged, and/or severe (< 60 bpm) may lead to fetal decompensation.
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4
Q

If this FHR pattern represented late decelerations

how would you treat this patient?

(A 20-year-old primigravida at 38 weeks gestation presents to the labor and delivery suite with pre-eclampsia and regular contractions. The patient is admitted, and an oxytocin infusion is started to induce delivery. Several hours later, she is noted to have the following fetal heart rate pattern.)

A

Assuming this patient’s FHR pattern represented late decelerations I would:

  1. inform the obstetrician, provide supplemental oxygen, ensure adequate uterine displacement (or even turn the patient on her side), discontinue the administration of oxytocin (a tocolytic may be considered in the presence of tonic uterine contractions), begin a fluid bolus, and optimize maternal hemodynamics;
  2. perform a careful history and physical focusing on her airway (exam, previous anesthetics, etc.), coagulation status (platelet count and trend; signs of a primary hemostatic defect – easy bruising, bleeding at IV sites, etc.), comorbidities, other complications associated with pre-eclampsia (cerebral edema - change in mental status, pulmonary edema, hypovolemia), and prenatal course;
  3. discuss the obstetric plan with the obstetrician; and, assuming there were enough time and no contraindications to regional anesthesia (i.e. coagulopathy),
  4. recommend the early initiation of epidural anesthesia in order to avoid the need for general anesthesia (especially if her airway was concerning).
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