Management of Intrapartum Fetal Heart Rate Tracings

ACOGNumber 116, November 2010

DO NOT INTERPRET FHR in ISOLATION

• TIMING IS IMPORTANT ie MULTIP MOVING QUICKLY vs NULLIP with unfavorable cervix OR IN EARLY LABOR or INDUCTION

• PELVIS & BABY SIZE & OB HISTORY & OB Complications• CLINICAL FACTORS

– Gestational age ( Postdates / < 32 weeks )– Maternal Medical Complications ( ?Exacerbation?)– Previous Fetal Status (Change from admission?)– Fetal Complications (IUGR, Oligohydramnios, Anomalies, Abruption,

Postdates)

– Medications ( Narcotics, B sympatho, Ephedrine, B blockers,)

MISCELLANEOUS FACTORS– Fever, Meconium, Magnesium Sulfate, Epidural, Vaginal bleeding,

VABC, Recent AROM, Smoking , illicit drugs

Physiologic Control of FHR

• Normal FHR patterns rely on sympathetic and parasympathetic activity AND ability of the heart to respond appropriately to the input from the nervous system

• Parasympathetic and Sympathetic nervous system are dependent on intact functioning CNS with no preceding damage or significant anatomical anomaly or insult

• Normal function of CNS & Myocardium both depend on adequate oxygenation

T 18 WITH CNS ANOMALY

VARIABILITY INFLUENCED BY

VARIABILITY INFLUENCED BY

Physiologic Control of FHR

• Sinoatrial node (fastest rate)• Atrial node (next fastest)• Ventricular rate (slowest 60 bpm or less)• Sympathetic nervous system (increases

heart rate)• Parasympathetic nervous system

(decreases heart rate)

PHYSILOGY EARLY Decelerations

• Early decelerations caused by

– Vagal stimulation commonly associated with Head compression / Prolonged vaginal exam

– Results in a normal physiologic decrease in fetal heart rate not associated with fetal hypoxemia or acidosis

PHYSILOGY EARLY Decelerations

Physiology of VARIABLE Decelerations

• Variable deceleration– Cord compression leads to increased venous

pressure.– Pressure sensed in baroreceptors resulting in

Vagal nerve stimulation– Vagal nerve stimulation results in decreased

fetal heart rate

Physiology of VARIABLE Decelerations

PHYSIOLOGY LATE Decelerations

• Late deceleration– Reflex

• Decrease in blood flow delivered to the baby ( maternal hypotension/maternal venous compression/cord compression/occlusion/uterine hyperstimulation) resulting in the inability to deliver enough O2 to the baby

• OR deoxygenated blood delivered to the baby ( abruption/maternal seizure/ ss crisis/pneumonia/PE/asthma) resulting in low PaO2 sensed by chemoreceptors which results in vagal discharge resulting in slowing of heart rate

– Non-reflex• Deoxygenated blood insufficient to support normal myocardial

contarctions resulting in direct myocardial depression

PHYSIOLOGY LATE Decelerations

NICHD NOMENCLATURE

STANADARDIZED NOMENCLATURE

should lead to comparable research & improved communication

• Revised and Presented in 2008 by NICHD

• NICHD nomenclature endorsed by– American College of Obstetricians and Gynecologists– American Women’s Health, Obstetric, and Neonatal

Nursing

NICHD NOMENCLATURE

• Baseline• Periodic

– Associated with uterine contractions– Distinguished on basis of onset of waveform

• Abrupt• Gradual

• Episodic– Not associated with uterine contractions

NICHD NOMENCLATURE

• No distinction made between short-term variability and long-term variability

• Variability defined visually based on amplitude of FHR complexes

SHORT & LONG TERMVARIABILITY

NICHD NOMENCLATURE

• Full description of FHR tracing requires:– Contraction pattern – Fetal heart rate– Variability– Accelerations – Periodic or Episodic Decelerations – Changes or trends of FHR patterns over time

Uterine Contractions

• Number of contractions in 10-minute window, averaged over 30 minutes

Tachysystole

> 5 contractions in 10 minutes

Uterine Contraction Descriptions

• Tachysystole qualified as to presence/absence of decelerations

• Tachysystole applies to spontaneous or stimulated labor

• Terms hyperstimulation and hypercontractility are not defined and should be abandoned

CATEGORY II OR IIITACHYSYSTOLE

GOAL REDUCE UTERINE ACTIVITY

• Discontinue oxytocin or cervical ripening agents

• Administer tocolytic medication ( Brethine 0.25 mg SQ only if necessary )• DO NOT USE BRETHINE FOR TACHYSYSTOLE

ASSOCIATED ABRUPTION

MANAGEMENT OF TACHYSYSTOLE

NICHD NOMENCLATURE BASELINE FETAL HEART RATE

The mean FHR rounded to increments of 5 beats per minute during a

MINIMUM OF 2 MINUTES AND < 1O MINUTES EXCLUDING : —Periodic or episodic changes — Periods of marked FHR variability — Segments of baseline that differ by more than 25 beats per minute

•The baseline must be for a minimum of 2 minutes in any 10-minute segment, or the baseline for that time period is indeterminate. In this case, one may refer to the prior 10-minute window for determination of baseline.

• Normal FHR baseline: 110–160 beats per minute • Tachycardia: FHR baseline is greater than 160 beats per minute • Bradycardia: FHR baseline is less than 110 beats per minute

NICHD NOMENCLATUREBASELINE VARIABILITY

Fluctuations in the baseline FHR that are irregular in amplitude and frequency. Variability is visually quantitated as the amplitude of peak-to-trough in beats per minute.• Absent — amplitude range undetectable • Minimal —amplitude range detectable but 5 beats per

minute or fewer • Moderate (normal)—amplitude range 6–25 beats per

minute • Marked —amplitude range greater than 25 beats per

minute

Variability

Amplitude range Descriptive term

Undetectable Absent

< 5 bpm Minimal

6-25 bpm Moderate

> 25 bpm Marked

Absent

Minimal

Moderate

Marked

Sinusoidal

NICHD NOMENCLATURE ACCELERATION

• A visually apparent abrupt increase (onset to peak in less than 30 seconds) in the FHR above the baseline

• At 32 weeks of gestation and beyond, an acceleration has a peak of 15 beats per minute or more above baseline, with a duration of 15 seconds or more but less than 2 minutes from onset to return.

• Before 32 weeks of gestation, an acceleration has a peak of 10 beats per minute or more above baseline, with a duration of 10 seconds or more but less than 2 minutes from onset to return.

• Prolonged ACCELERATION > 2 minutes < 10 minutes in duration BASELINE CHANGE If an acceleration lasts >/= to 10 minutes it is a baseline change

LATE DECELERATIONS

• Late deceleration– Visually apparent gradual (defined as onset of

deceleration to nadir ≥30 seconds) decrease and return to baseline FHR associated with uterine contraction

– The decrease calculated from most recent portion of baseline

– The deceleration is delayed in timing, with the nadir of the deceleration occurring after the peak of the contraction.

• In most cases the onset, nadir, and recovery of the deceleration occur after the beginning, peak, and ending of the contraction, respectively

LATE DECLERATIONS

EARLY DECELERATIONS

• Early deceleration – Visually apparent gradual decrease (defined as onset

of deceleration to nadir ≥30 seconds) and return to baseline FHR associated with uterine contraction

– Calculated from most recent portion of baseline – Coincident in timing, with nadir of deceleration

occurring at same time as the peak of contraction

• In most cases onset, nadir, and recovery of deceleration are coincident with the beginning, peak, and ending of the contraction, respectively

VARIABLE DECELERATIONS

• Variable deceleration – Visually apparent abrupt decrease (defined as onset

of deceleration to beginning of nadir <30 seconds) in FHR below the baseline

– The decrease is calculated from most recent portion of baseline

– The decrease in FHR below baseline is ≥15 beats/min, lasting ≥15 seconds, and <2 minutes from onset to return to baseline.

• When variable decelerations are associated with uterine contractions, their onset, depth, and duration commonly vary with successive uterine contractions

PROLONGED DECELERATION>/= 2 & < 10 minutes

– Decrease in FHR below baseline calculated from most recent10 minute stable baseline

– Decrease from baseline is ≥15 beats/min, lasting ≥2 minutes, but <10 minutes from onset to return to baseline.

• IF 15 BPM DECELERATION LAST ≥ 10 minutes it is a FETAL HEART RATE BASELINE CHANGE

QUANTIFICATION OF DELERATIONS & ACCELERATIONS

• Decelerations are quantitated by the depth of the nadir in BPM below baseline

• The duration is quantitated in minutes and seconds from beginning to end of deceleration

• Accelerations are quantitated similarly

• Decelerations may be defined as recurrent if they occur with ≥50% of uterine contractions in any 20-minute segment

• Bradycardia and tachycardia are quantitated by actual FHR in BPM.

Interpretation of FHR patterns

• New three-tier system

• FHR tracing patterns reflect current fetal acid-base status

• FHR tracing patterns cannot RELIABLY OR CONSISTENTLY predict development of cerebral palsy

Category I

Category I FHR tracings include all of the following: • Baseline rate:110–160 beats per minute • Baseline FHR variability: MODERATE

• Late or Variable Decelerations ABSENT• Early decelerations: May be present • Accelerations: Present or ABSENT

Category I FHR tracing

• Includes ALL of the following:– Baseline rate NORMAL : 110-160 BPM– Baseline Variability: MODERATE– Late or Variable Decelerations: ABSENT– Early Decelerations: PRESENT OR ABSENT– Accelerations: PRESENT OR ABSENT

• Category I FHR tracings are normal– Strongly predictive of normal fetal acid-base status at

time of observation

- Requires no change in management

Category II FHR tracing

Includes ANY of the following RATE

1) Bradycardia not accompanied by absent baseline variability2) Tachycardia

Baseline FHR variability1) Minimal baseline variability2) Absent baseline variability with no recurrent

decelerations3) Marked baseline variability

Category II FHR tracing

ACCELERATIONS– Absence of induced accelerations after fetal

stimulation

–NO FETAL HEART RATE ACCELERATIONS WITH FAS OR SCALP STIMULATION

Category II FHR tracing

PERIODIC OR EPISODIC DECELERATIONS• Recurrent variable decelerations accompanied by minimal or moderate baseline variability• Prolonged deceleration more than 2 minutes but less than10 minutes• Recurrent late decelerations with moderate baseline

variability• Variable decelerations with other characteristics

such as slow return to baseline, overshoots, or “shoulders

Category II FHR tracing

• Category II FHR tracings are INDETERMINATE

• NOT predictive of abnormal fetal acid-base status

• Requires continued surveillance and interpretation in light of entire clinical information

CATEGORY II MANAGEMENT

• Both responses are highly predictive of normal fetal acid–base status and, thus, may help guide clinical management

1) Moderate FHR Variability 2) The presence of FHR accelerations -spontaneous -digital scalp stimulation -vibroacoustic stimulation

CATEGORY II MANAGEMENTRecurrent Variable decelerations

Prolonged Decelerations Bradycardia

GOAL Alleviate umbilical cord compression Amnioinfusion ?PROLAPSED CORD?

DOES NOT HELP WITH LATE DECELERATIONS

Category III FHR tracing

ABSENT FHR VARIABILITY

AND

• Recurrent late decelerations• Recurrent variable decelerations• Bradycardia

OR SINUSOIDAL PATTERN

Category III FHR tracing

• Category III FHR tracings are abnormal• Predictive of abnormal fetal acid-base status at time of

observation• Require prompt evaluation• Depending on situation, efforts may include:

– Maternal oxygen( 10 liter per mask)– Maternal position change – Discontinuation of labor stimulation– Treatment of maternal hypotension– AFTER CORRECTIVE ATTEMPT make an effort to TO

DEMONSTARTE FETAL HEART RATE ACCELERATION BY FETAL DIGITAL SCALP STIMULATION OR FAS STIMULATION TO DOWN GRADE BACK TO CATEGORY II

Promote Oxygenationand

Improve blood flow

• Minimal or Absent FHR variability• Recurrent late decelerations • Prolonged decelerations • Bradycardia INITIATE• Lateral positioning (either left or right)• Oxygen administration• IV fluid bolus • Reduce uterine contraction frequency

NICHD Expert PanelAgreement about definition of NORMAL FHR tracing that confers an extremely high predictability of a NORMALLY oxygenated fetus when it is obtained

• Normal baseline rate• Moderate FHR variability• Presence of accelerations• Absence of decelerations

Agreement that patterns predictive of current or impending fetal asphyxia PLACING the fetus is at risk for NEUROLOGIC DAMAGE OR DEATH

ABSENT FHR VARIABILITY AND

RECURRENT LATES RECURRENT VARIABLES

Goals of EFM

• Delivery of newborn– In the absence of a significant acidosis

• Umbilical artery pH < 7.1, base excess < -12• And/or 5 minute Apgar < 7

– In the presence of neonatal vigor

• Quickly categorize FHR patterns based on their relationship (or lack thereof) to the above goals

• Clearly communicate FHR patterns to members of the OB team

Communication

• SBAR– Situation (patient characteristics)– Background (evolution of tracing)– Assessment (description of current tracing)– Recommendation (action plan)

Communication

• Description of FHR pattern– VARIABILLITY (absent, minimal, moderate, marked)– Descriptions of PERIODIC/EPISODIC changes

• Type or shape• Recurrent or intermittent• Severity (nadir)• Relationship to uterine activity

– BASELINE FHR– Presence/absence of ACCELERATIONS – Has the FHR tracing changed or evolved over time

since admission. Is the change transient with an obvious cause ( meds, hypotension, meconium, AROM, fever, bleeding, maternal position)

– Potential influence of Maternal condition &/OR Fetal condition in relation to FHR patterns

DESCRIPTION FOR SBAR– RATE

(Tachycardia or increase in baseline >/ = to 15 bpm from admission)

– VARIABILITY

(loss of variability with change in fetal maternal condition)

– ACCELERATIONS (spontaneous or stimulated & 15 bpm or less )

– PERIODIC/EPISODIC DECELERATIONS

– Changes of FHR OR PATTERN OR MATERNAL CONDITION COMPARED TO ADMISSION OR SIGNIFICANT TIME FRAME

SBAR THIS STRIP

SBAR THIS STRIP

SBAR THIS STRIP

ETILOGY OF CP

Prematurity results in CP• CP develops in as many as 15-20 % of surviving premature infants • The earlier the gestational age at delivery; The greater is the risk

of developing CP. • CP risk % >>> 30 weeks >> 32-34 weeks with a plateau > 34

weeks unless chorioamnionitis or intrapartum hypoxia occurs. • CP as a result of prematurity is associated with the presence of

Periventricular Leukomalacia (PVL is an anatomic lesion.) • In addition to perinatal inflammation, cerebral ischemia contributes

to PVL and may result in CP in preterm infants. • Other conditions that primarily affect preterm infants and may lead

to CP include severe intraventricular hemorrhage (IVH) and periventricular hemorrhagic infarction which may result in posthemorrhagic hydrocephalus which frequently leads to CP

Chorioamnionitis SYNERGISTICALLYIncreases the risk of CP with Prematurity

• There are significant associations between clinical chorioamnionitis or histological chorioamnionitis and cerebral palsy, for clinical chorioamnionitis a pooled odds ratio of 2.42 (95% CI 1.52–3.84), and for histological chorioamnionitis a pooled odds ratio of 1.83 (95% confidence interval, 1.17–2.89).

• This data is associated with an increased risks of 140% and 80% for neonates exposed to clinical chorioamnionitis or histological chorioamnionitis, to develop CP respectively.

• PVL occurs more frequently in premature infants born to mothers with chorioamnionitis, premature or prolonged rupture of the membranes. In a meta-analysis, chorioamnionitis was associated with cystic PVL (relative risk 3.0) and cerebral palsy (relative risk 1.9) . Funisitis or neonatal sepsis also increases the risk of PVL

Obstet Gynecol 2010;116:387–92 Clin Obstet Gynecol 1998 Dec;41(4):827-31. Paediatr Perinat Epidemiol 1998 Jan;12(1):72-83

< 5 % of CP results from Intrapartum Hypoxia

Obstet Gynecol. 2006 Jun;107(6):1357-65.

• Data were available for analysis in 213 cases of CP. Major antenatal or pediatric cerebral palsy-related pathologies were identified in 98.1% of all these cases. An isolated acute intrapartum hypoxic event was defined as likely in only 2 of the 46 neonates born at term and none born preterm.

• CONCLUSION: Cerebral palsy was seldom preceded by acute intrapartum hypoxia but antenatal cerebral palsy-related pathologies are often detectable. The objective American College of Obstetricians and Gynecologists/American Academy of Pediatrics criteria are useful to audit cerebral palsy causation and exclude primary intrapartum hypoxia