21/02/13 Management of intrapartum category I, II, and III fetal heart rate tracings

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2013 UpToDate

Author
George Macones, MD, MSCE
Section Editor
Susan M Ramin, MD
Deputy Editor
Vanessa A Barss, MD
Management of intrapartum category I, II, and III fetal heart rate tracings
Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2013. | This topic last updated: dic 17, 2012.
INTRODUCTION Because of high interobserver and intraobserver variability in the interpretation of fetal heart rate
(FHR) tracings [1-3], the American College of Obstetricians and Gynecologists (ACOG), the Society for Maternal-
Fetal Medicine (SMFM), and the National Institute of Child Health and Human Development (NICHD) convened a
workshop to standardize definitions and interpretation for electronic fetal monitoring (EFM), propose management
guidelines, and develop research questions [4,5]. Major outputs from this workshop were a clear standard for FHR
interpretation (table 1) and a three-tier system for the categorization of intrapartum EFM (table 2). This system has
been widely adopted in the United States and elsewhere, and is the basis for this topic.
CATEGORY I FHR TRACINGS
Baseline rate: 110 to 160 beats per minute (bpm)
Moderate baseline FHR variability
No late or variable decelerations
Early decelerations may be present or absent
Accelerations may be present or absent
Category I EFM tracings are considered normal because studies have demonstrated that these findings are
associated with the absence of fetal metabolic acidemia at the time of observation [6-9]. No intervention is
indicated.
EFM is generally continuous since the fetal status can change, but if the maternal and fetal conditions appear
stable, it is reasonable to interrupt a category I EFM tracing for up to 30 minutes to facilitate ambulation, bathing, or
position changes. In pregnancies at low risk of development of intrapartum fetal acidosis, ACOG recommends that
the EFM tracing be reviewed at least every 30 minutes in the first stage of labor and every 15 minutes in the second
stage [10]. In patients with pregnancy complications (eg, fetal growth restriction, preeclampsia) where the risk of
developing fetal acidosis is higher, the EFM should be reviewed at least every 15 minutes in the first stage of labor
and every 5 minutes during the second stage. Similar guidelines are used in other countries [11], and based on
expert opinion.
CATEGORY III FHR TRACINGS
Absent baseline FHR variability and any of the following:
Recurrent late decelerations
Recurrent variable decelerations
Bradycardia
or
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Sinusoidal pattern
A category III tracing is abnormal because studies have demonstrated that these findings are associated with an
increased risk of fetal hypoxic acidemia, which can lead to cerebral palsy and neonatal hypoxic ischemic
encephalopathy [12]. (See "Etiology and pathogenesis of neonatal encephalopathy" and "Clinical features,
diagnosis, and treatment of neonatal encephalopathy" and "Epidemiology and etiology of cerebral palsy".)
It is hypothesized that detection of potential fetal decompensation and timely and effective intervention before
acidosis becomes severe can prevent perinatal/neonatal morbidity or mortality [13]. Therefore, when the FHR has a
category III pattern, preparations for delivery should be made while initiating resuscitative measures: repositioning
the mother to left or right lateral, providing oxygen supplementation, and administering an intravenous fluid bolus
(table 3). The goal of these interventions is to improve fetal oxygenation by improving uteroplacental perfusion.
Scalp stimulation to provoke FHR acceleration should be attempted, as acceleration is a sign that the fetus is not
acidotic. (See "Intrapartum fetal heart rate assessment", section on 'FHR response to stimulation'.)
If scalp stimulation does not result in acceleration and there is no improvement in the FHR tracing after conservative
measures, delivery should be accomplished. The time from decision to delivery should consider the health of both
mother and fetus; there may be circumstances (eg, maternal obesity with poor airway, maternal coagulopathy)
where delivery cannot be safely performed expeditiously (within 20 to 30 minutes of the beginning of the category III
tracing).
CATEGORY II FHR TRACINGS Category II FHR tracings include all FHR patterns that are not classified as
category I (normal) or category III (abnormal) (table 2). The Society of Obstetricians and Gynaecologists of Canada
classify these tracings as atypical [11].
The potential for development of fetal acidosis varies widely across the different types of category II tracings.
Patients with these tracings should be evaluated for factors that may reduce fetal oxygenation, taking into account
associated clinical circumstances. Conservative intervention is usually indicated, with frequent reassessment to
determine whether delivery should be performed.
There is no standard for evaluation of these fetuses. In general, the presence of either moderate variability (ie,
amplitude 6 to 25 bpm) or fetal heart rate accelerations is highly predictive of normal fetal acid-base status and
provides reassurance that expeditious delivery is unnecessary [14-18]. Continued surveillance and frequent
reassessment are indicated until the pattern resolves or progresses to category III.
The management of specific types of category II fetal heart rate tracings is discussed below.
Recurrent late decelerations Recurrent late decelerations are caused by a reflex central nervous system
response to fetal hypoxia and acidemia, as well as direct myocardial depression and humoral factors [19]. (See
"Intrapartum fetal heart rate assessment", section on 'Recurrent late decelerations'.)
Fetal hypoxia may occur in the following settings:
Uterine tachysystole
Maternal hypotension (eg, from hemorrhage, sepsis, anesthesia)
Maternal hypoxia (eg, from respiratory disorders, severe anemia)
Maternal vasculopathy (eg, antiphospholipid syndrome, diabetes, lupus)
Placental disorders (eg, abruption, infarction)
Evaluation of the pregnancy with recurrent late decelerations should therefore include assessment of uterine
contraction frequency and intensity, assessment of FHR variability and accelerations, vaginal bleeding, uterine
tenderness, maternal oxygenation, and blood pressure.
General measures in the management of recurrent late decelerations are aimed at improving the uteroplacental
circulation and maternal oxygenation, and include (table 3):
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Repositioning the woman on her left or right lateral side
Administration of oxygen (eg, 8 to 10 L/min of oxygen via nonrebreather mask)
Administration of an intravenous (IV) fluid bolus (eg, 500 to 1000 mL of lactated Ringer's or normal saline
solution)
Changing the maternal position may reduce cord compression and improve maternal blood flow to the placenta. The
result is usually improved fetal gas exchange.
Although no randomized trials have evaluated the efficacy of oxygen administration for management of fetal distress
[20], administering oxygen can improve fetal oxygenation. Fetal pO2 and oxygen saturation can reach a higher
steady state within 8 to 10 minutes, but decrease after supplemental maternal oxygen is withdrawn [21-26]. There
are conflicting data on the effect of maternal oxygen supplementation on fetal pH; some studies show an adverse
effect [23,27]. Although improved delivery of oxygen to the fetal tissues may be beneficial in some cases, the
underlying causes of fetal hypoxemia need to be addressed, as fetal acidemia will not be corrected by maternal
oxygen administration alone.
An intravenous fluid bolus of non-glucose crystalloid can improve placental blood flow if the patient is hypovolemic
from prolonged lack of intake, vomiting, or sympathetic blockade, and thus may improve fetal oxygenation [23].
However, fluid administration should be cautious when there is concern about possible volume overload, such as in
women with preeclampsia, cardiac disease, or receiving beta-adrenergic drugs for tocolysis.
Uterotonic drugs can be stopped or the dose decreased; these drugs should be discontinued in the presence of
tachysystole (defined as more than five contractions in 10 minutes, averaged over a 30-minute window [10]). Since
uterine activity causes intermittent interruption of blood flow to the intervillous space, excessive uterine activity that
exceeds the critical level for an individual fetus will result in fetal hypoxemia. (See "Principles of labor induction",
section on 'Tachysystole'.) If there is no prompt response to these measures, we suggest administering a tocolytic
drug, such as terbutaline 250 mcg subcutaneously.
If maternal hypotension secondary to recent epidural dosing is identified, administration of an alpha-adrenergic
agonist (such as phenylephrine or ephedrine) and an intravenous fluid bolus is corrective and will improve
uteroplacental blood flow. Reduced placental perfusion from sympathetic blockade can occur without marked
changes in maternal blood pressure. (See "Adverse effects of neuraxial analgesia and anesthesia for obstetrics",
section on 'Hypotension'.) These medications should be administered by someone with expertise in the dosing and
side effects of these medications.
An assessment of fetal heart rate variability and accelerations should be part of the evaluation of recurrent late
decelerations, given that the predictive value of late decelerations for fetal acidosis and poor neonatal outcome is
poor [28-30]. Absent or minimal variability (table 1) is concerning as it can be a result of cerebral hypoxemia and
acidosis, and can signify failure of fetal compensatory mechanisms to maintain adequate oxygenation of the brain,
while normal FHR variability is strongly associated (98 percent) with an umbilical pH >7.15 [14].
If a FHR acceleration is present or can be elicited (rise of 15 bpm above baseline lasting for 15 seconds),
absence of acidosis (ie, fetal pH greater than 7.20) is likely [7,31]. In general, when accelerations are induced by
scalp stimulation, acidosis is present in less than 10 percent of fetuses, and when no accelerations occur, acidosis
is present in about 50 percent of fetuses [17,18,32,33]. (See "Intrapartum fetal heart rate assessment", section on
'FHR response to stimulation'.)
Therefore, if recurrent late decelerations are accompanied by minimal/absent variability and absent accelerations
and persist despite attempts at intrauterine resuscitation, then fetal acidemia cannot be excluded and expeditious
delivery is generally indicated.
Fetal tachycardia Fetal tachycardia is defined as a baseline fetal heart rate of greater than 160 bpm for at least
10 minutes. Causes of fetal tachycardia include:
Maternal-fetal infection
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Medications (eg, beta-agonists, atropine, cocaine)
Maternal hyperthyroidism
Placental abruption
Fetal hypoxia
Elevated maternal catecholamine levels
Rarely, fetal tachycardia can be due to a fetal tachyarrhythmia, such as atrial flutter or supraventricular tachycardia.
These tachyarrhythmias are characterized by a very high fetal heart rate, often in excess of 200 bpm. (See
"Overview of the general approach to diagnosis and treatment of fetal cardiac arrhythmias", section on
'Tachyarrhythmias'.)
Fetal tachycardia less than 200 bpm alone has not been strongly associated with fetal acidemia, unless associated
with recurrent decelerations, absent accelerations, or minimal/absent variability [34-37].
The evaluation of fetal tachycardia should include assessment for maternal infection or abruption and a review of
maternal medications (table 4). Appropriate treatment should be initiated if the underlying cause can be identified.
In addition, scalp stimulation should be performed to provoke fetal heart rate acceleration, which is a sign that the
fetus is not acidotic. Delivery is indicated if the tracing does not improve and acidemia is suspected.
Intermittent and recurrent variable decelerations Variable decelerations occur when the umbilical cord is
compressed. Intermittent variable decelerations (associated with <50 percent of contractions) are frequently
observed in labor tracings and are not usually associated with adverse consequences, presumably because
transient cord compression is well tolerated by the fetus [38]. Thus, they do not require intervention.
Metabolic acidosis or mixed metabolic and respiratory acidosis can develop, however, with increasing duration,
depth, and frequency of variable decelerations [39]. Therefore, recurrent variable decelerations (>50 percent of
contractions) require a greater degree of surveillance. (See "Intrapartum fetal heart rate assessment", section on
'Recurrent variable decelerations'.)
Evaluation is aimed at assessing the frequency, depth, and duration of the decelerations and associated
contraction pattern. In general:
Variable decelerations of increasing depth and duration are predictive of impending acidemia.
Variable decelerations with a slow return to baseline (late return) are more predictive of impending acidemia
than those with a rapid return to baseline.
Moderate variability or fetal accelerations suggests the absence of fetal acidemia.
The treatment of variable decelerations is generally aimed at resolving cord compression. Change of maternal
position is a reasonable first treatment option [40]. Amnioinfusion can be useful in resolving persistent variable
decelerations. (See "Amnioinfusion: Indications" and "Amnioinfusion: Technique".) Adjunctive measures to improve
fetal oxygenation (oxygen supplementation, intravenous fluid bolus, reduce uterine contraction frequency) may be
useful. In addition, scalp stimulation should be performed to provoke fetal heart rate acceleration, which is a sign
that the fetus is not acidotic. Delivery is indicated if the tracing does not improve and acidemia is suspected.
Minimal variability FHR variability results from oscillatory input by the parasympathetic nervous system. New
onset minimal variability (amplitude 0 to 5 bpm) may occur for several reasons, including [41-43]:
Fetal sleep cycle - These cycles generally last approximately 20 minutes, but may persist for as long as
one hour. When the fetal sleep cycles are over, moderate variability should return.
CNS depressants - The most common medications that decrease variability are opioids and magnesium
sulfate. The effect of maternal opioids on FHR variability generally lasts no more than two hours.
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Fetal hypoxemia
If the FHR pattern had been normal, a reasonable approach to the assessment and management of new onset
decreased fetal variability is to consider a fetal sleep cycle or the effect of recently administered maternal
medications. Both of these causes warrant expectant management. It is also prudent to attempt to induce
accelerations with scalp stimulation, as the presence of accelerations is strong evidence of the absence of fetal
acidemia at that time [18]. A maternal fluid bolus, repositioning, and/or maternal oxygen administration are
appropriate adjunctive measures (table 3), especially in settings in which a benign etiology is less certain, such as
coexistent FHR abnormalities or pregnancy complications associated with uteroplacental insufficiency.
The new onset of decreased variability is important because absent or decreased variability can also be related to
congenital or acquired anomalies of the CNS or heart, or to prematurity [44-46]. (See "Intrapartum fetal heart rate
assessment", section on 'Absent or minimal variability with decelerations or bradycardia'.)
Fetal bradycardia/prolonged deceleration Fetal bradycardia (below 110 bpm) or a prolonged deceleration
(table 1) are approached in a similar manner clinically, since the distinction between these two entities is based
primarily on the number of minutes of the decrease in fetal heart rate. The causes of prolonged deceleration or fetal
bradycardia include:
Rapid fetal descent
Cord prolapse
Placental abruption
Maternal hypotension
Uterine rupture
Tachysystole
Fetal acidemia is more likely when bradycardia is associated with minimal or absent variability and absent
accelerations during normal baseline periods, if present.
Treatment of fetal bradycardia or prolonged deceleration is aimed at the cause. Evaluation should include
assessment of maternal blood pressure and contraction frequency and strength, and physical examination for
evidence of rapid fetal descent, cord prolapse, placental abruption, or uterine rupture. (See "Umbilical cord
prolapse" and "Rupture of the unscarred uterus" and "Choosing the route of delivery after cesarean birth", section
on 'Uterine rupture' and "Placental abruption: Clinical features and diagnosis".)
If nonsurgical management of the underlying cause is not possible or does not result in resolution of the
bradycardia, delivery is indicated.
SUMMARY AND RECOMMENDATIONS
The three-tier system for the categorization of intrapartum fetal heart rate tracings is a useful means of
approaching management (table 2). (See 'Introduction' above.)
Category I tracings are not associated with fetal metabolic acidemia at the time of observation.
Uncomplicated patients with category I tracings can be followed routinely, with reassessment of the tracing
at least every 30 minutes in the first stage of labor and every 15 minutes in the second stage. (See 'Category
I FHR tracings' above.)
Category III tracings are associated with an increased risk of fetal hypoxic acidemia. Patients with category
III tracings should be prepared for delivery while initiating resuscitative measures. If there is no improvement
in the tracing after conservative measures (table 3) and scalp stimulation does not result in acceleration,
delivery should be accomplished expeditiously, but ensuring maternal safety. (See 'Category III FHR
tracings' above.)
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The potential for development of fetal acidosis varies widely across the different types of category II tracings.
Patients with these tracings should be evaluated for factors that may reduce fetal oxygenation, taking into
account associated clinical circumstances. Conservative intervention is usually indicated (table 3), with
frequent reassessment to determine whether delivery should be performed. (See 'Category II FHR
tracings' above.)
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