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21/02/13 Management of intrapartum categoryI, II, and III fetal heart rate tracings Official reprint from UpToDate

Management of intrapartum categoryI, II, and III fetal heart rate tracings

intrapartum categoryI, II, and III fetal heart rate tracings Official reprint from UpToDate ® www.uptodate.com

Official reprint from UpToDate ® www.uptodate.com ©2013 UpToDate ®

Management of intrapartum category I, II, and III fetal heart rate tracings

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)and is the basis for this topic. CATEGORY I FHR TRACINGS Moderate baseline FHR variability No

Moderate baseline FHR variabilityTRACINGS Baseline rate: 110 to 160 beats per minute (bpm) No late or variable decelerations Early

No late or variable decelerations160 beats per minute (bpm) Moderate baseline FHR variability Early decelerations may be present or absent

Early decelerations may be present or absentbaseline FHR variability No late or variable decelerations Accelerations may be present or absent Category I

Accelerations may be present or absentdecelerations Early decelerations may be present or absent Category I EFM tracings are considered “normal” because

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:], and based on expert opinion. CATEGORY III FHR TRACINGS Recurrent late decelerations Recurrent variable

Recurrent late decelerationsAbsent baseline FHR variability and any of the following: Recurrent variable decelerations Bradycardia or

Recurrent variable decelerationsand any of the following: Recurrent late decelerations Bradycardia or file:///C:/Users/Usuario/Desktop/Management

Bradycardialate decelerations Recurrent variable decelerations or file:///C:/Users/Usuario/Desktop/Management of

or

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Sinusoidal pattern21/02/13 Management of intrapartum categoryI, II, and III fetal heart rate tracings A category III tracing

Management of intrapartum categoryI, II, and III fetal heart rate tracings

A category III tracing is “abnormal” because studies have demonstrated that these findings are associated with an

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

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.) Fetal hypoxia may occur in the following settings: Maternal hypotension (eg, from hemorrhage, sepsis,

Maternal hypotension (eg, from hemorrhage, sepsis, anesthesia)may occur in the following settings: Uterine tachysystole Maternal hypoxia (eg, from respiratory disorders, severe

Maternal hypoxia (eg, from respiratory disorders, severe anemia)hypotension (eg, from hemorrhage, sepsis, anesthesia) Maternal vasculopathy (eg, antiphospholipid syndrome,

Maternal vasculopathy (eg, antiphospholipid syndrome, diabetes, lupus)hypoxia (eg, from respiratory disorders, severe anemia) Placental disorders (eg, abruption, infarction) Evaluation

Placental disorders (eg, abruption, infarction)(eg, antiphospholipid syndrome, diabetes, lupus) Evaluation of the pregnancy with recurrent late

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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Management of intrapartum categoryI, II, and III fetal heart rate tracings

Repositioning the woman on her left or right lateral sideintrapartum categoryI, II, and III fetal heart rate tracings Administration of oxygen (eg, 8 to 10

Administration of oxygen (eg, 8 to 10 L/min of oxygen via nonrebreather mask)Repositioning the woman on her left or right lateral side Administration of an intravenous (IV) fluid

Administration of an intravenous (IV) fluid bolus (eg, 500 to 1000 mL of lactated Ringer's or normal saline solution)oxygen (eg, 8 to 10 L/min of oxygen via nonrebreather mask) Changing the maternal position may

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 infectionat least 10 minutes. Causes of fetal tachycardia include: file:///C:/Users/Usuario/Desktop/Management of intrapartum

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Management of intrapartum categoryI, II, and III fetal heart rate tracings

Medications (eg, beta-agonists, atropine , cocaine) atropine, cocaine)

Maternal hyperthyroidismMedications (eg, beta-agonists, atropine , cocaine) Placental abruption Fetal hypoxia Elevated maternal

Placental abruptionatropine , cocaine) Maternal hyperthyroidism Fetal hypoxia Elevated maternal catecholamine levels Rarely,

Fetal hypoxia, cocaine) Maternal hyperthyroidism Placental abruption Elevated maternal catecholamine levels Rarely, fetal

Elevated maternal catecholamine levelsMaternal hyperthyroidism Placental abruption Fetal hypoxia Rarely, fetal tachycardia can be due to a fetal

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.and associated contraction pattern. In general: Variable decelerations with a slow return to baseline

Variable decelerations with a slow return to baseline (“late return”) are more predictive of impending acidemia than those with a rapid return to baseline.depth and duration are predictive of impending acidemia. Moderate variability or fetal accelerations suggests the

Moderate variability or fetal accelerations suggests the absence of fetal acidemia.acidemia than those with a rapid return to baseline. The treatment of variable decelerations is generally

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.5 bpm) may occur for several reasons, including [ 41-43 ]: CNS depressants - The most

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Fetal hypoxemia21/02/13 Management of intrapartum categoryI, II, and III fetal heart rate tracings If the FHR pattern

Management of intrapartum categoryI, II, and III fetal heart rate tracings

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.

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 descentof prolonged deceleration or fetal bradycardia include: Cord prolapse Placental abruption Maternal hypotension

Cord prolapseor fetal bradycardia include: Rapid fetal descent Placental abruption Maternal hypotension Uterine rupture

Placental abruptionfetal bradycardia include: Rapid fetal descent Cord prolapse Maternal hypotension Uterine rupture Tachysystole Fetal

Maternal hypotensionRapid fetal descent Cord prolapse Placental abruption Uterine rupture Tachysystole Fetal acidemia is more likely

Uterine ruptureCord prolapse Placental abruption Maternal hypotension Tachysystole Fetal acidemia is more likely when bradycardia

TachysystolePlacental abruption Maternal hypotension Uterine rupture Fetal acidemia is more likely when bradycardia is associated

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.) 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 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 categorystage. (See 'Category I FHR tracings' above.) III tracings should be prepared for delivery while

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,

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21/02/13 Management of intrapartum categoryI, II, and III fetal heart rate tracings The potential for development

Management of intrapartum categoryI, II, and III fetal heart rate tracings

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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American Academy of Pediatrics, American College of Obstetricians and Gynecologists. Neonatal encephalopathy and cerebral palsy: defining the pathogenesis and pathophysiology. Elk Grove Village (IL):

AAP; ACOG, Washington, DC 2003.

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