EFM Questions and Answers

Comprehensive and Detailed Explanation From Exact Extract–Based NCC C-EFM References:

NCC C-EFM uses NICHD terminology to describe key FHR characteristics: baseline, variability, accelerations, and decelerations. In this strip, the following findings are present:

Baseline:The baseline appears approximately 135–145 bpm, which is within the normal 110–160 bpm range described in NCC and AWHONN materials.

Variability:Beat-to-beat fluctuation is within 6–25 bpm, which meets the definition of moderate variability. NCC and NICHD define moderate variability as amplitude range of 6–25 bpm; this is associated with adequate fetal oxygenation and a normal fetal acid–base status.

Accelerations:The tracing shows distinct increases in FHR above the baseline by at least 15 bpm lasting 15 seconds or more but less than 2 minutes. NCC and NICHD define an acceleration in a term fetus precisely as “a visually apparent abrupt increase in FHR, with peak ≥15 bpm above baseline, lasting ≥15 seconds and <2 minutes.” The pattern shown fits this definition clearly.

Category determination:A tracing with normal baseline, moderate variability, and accelerations without decelerations is classified as Category I, not Category II. Category II is reserved for tracings that are not clearly Category I or III, such as minimal or marked variability, recurrent variables, or prolonged decelerations.

Marked variability consideration:Marked variability is defined as amplitude >25 bpm. While the tracing is somewhat jagged, the fluctuation does not sustain >25 bpm amplitude over a 10-minute segment and instead remains in the moderate range, so it does not meet criteria for marked variability.

Given these observations, the most accurate description of the tracing from the options provided is that it demonstrates accelerations.

Comprehensive and Detailed Explanation From Exact Extract–Based NCC C-EFM References:

Maternal hyperthermia—most commonly from infection—causes a rise in fetal temperature, which increases fetal metabolic rate. The fetus responds by increasing heart rate to meet the increased oxygen demand.

Effects include:

Increased fetal oxygen consumption

Enhanced fetal cardiac output

Resultant tachycardia, often 160–180 bpm

This mechanism is repeatedly outlined in NCC’s physiology domain, AWHONN, Menihan, Simpson, and Creasy & Resnik.

Option A is incorrect because maternal fever does not reduce perfusion.

Option C is incorrect because catecholamines are often elevated, not inhibited.

Thus, the mechanism is increased fetal metabolism.

Comprehensive and Detailed Explanation From NCC-Aligned Sources:

NICHD definitions:

A variable deceleration is identified by:

Abrupt onset(drop from baseline to nadir in <30 seconds)

Depth ≥15 bpm

Duration ≥15 seconds and <2 minutes

Variable timing relative to contractions

Variable shape (sharp drop, jagged descents, rapid recovery)

The scenario describes:

Abrupt drop from 125 → 80 bpm (rapid onset)

Lasting 90 seconds (still <2 minutes)

Gradual return but still within variable range

Occurring during a contraction

Depth >15 bpm

This meets ALL criteria for a variable deceleration.

Why the other options are wrong:

A. Early deceleration

Requires gradual onset (>30 seconds).

Mirrors contraction shape.

Caused by head compression.

This decel is abrupt, so NOT early.

B. Prolonged deceleration

Requires ≥2 minutes and <10 minutes.

This decel lasts 90 seconds, which is below the threshold.

Correct classification: Variable deceleration.

Comprehensive and Detailed Explanation From NCC-Aligned Sources:

Artifact on fetal monitoring:

Appears erratic, disorganized, and without physiologic pattern

Shows random amplitude changes

Often correlates with maternal movement, monitor displacement, or poor signal

Lacks cyclical, repetitive characteristics seen in true dysrhythmias

Fetal dysrhythmias, by contrast:

Have repetitive, patterned, predictable rhythm disturbances

May show uniform premature beats, bigeminy, or sudden rate shifts

Therefore, varied and disorganized = artifact.

Comprehensive and Detailed Explanation From NCC-Aligned Sources:

NICHD Category II includes:

Minimal variability

Marked variability

Absent accelerations without recurrent decelerations

Indeterminate baseline characteristics

A tracing with no accelerations and no decelerations becomes Category II if paired with marked variability, because marked variability indicates potential stress.

Why other answers are wrong:

A. FHR 110 bpm → normal baseline if variability normal.

B. Sinusoidal pattern → Category III, not Category II.

Correct answer: Marked variability.

Comprehensive and Detailed Explanation From Exact Extract–Based NCC C-EFM References:

Fetal baroreceptors, located primarily in the carotid sinus and aortic arch, respond to increases in fetal arterial pressure. When activated, they stimulate the vagus nerve, causing:

Reflex parasympathetic activation

Decreased FHR (vagal slowing)

This is a well-established physiologic mechanism referenced throughout NCC’s physiology domain. NCC emphasizes that variable decelerations, especially short deep drops, can occur when transient increases in fetal blood pressure from cord compression activate these baroreceptors.

Option B, decreased PO₂, relates to chemoreceptor-mediated responses—not baroreceptors.

Option C, reflex tachycardia, is mediated by sympathetic activation and occurs when BP falls, not rises.

Thus, the correct physiologic response is A. Decreased heart rate.

Comprehensive and Detailed Explanation From Exact Extract NCC-Recommended Sources

Oxygen saturation refers to the percentage of hemoglobin binding sites occupied by oxygen. NCC physiology resources, including Simpson & Creehan and Creasy & Resnik, define oxygen saturation as the “ratio of oxyhemoglobin to total hemoglobin”—the same definition used in fetal oxygenation discussions.

Oxygen affinity refers to hemoglobin’s tendency to bind oxygen (related to the oxyhemoglobin dissociation curve).

Oxygen carrying capacity refers to the total amount of oxygen hemoglobin can transport, independent of current saturation.

AWHONN and Menihan emphasize that fetal oxygenation assessment is dependent on understanding oxygen saturation, not affinity or carrying capacity, when discussing fetal hypoxemia and gas exchange.

Comprehensive and Detailed Explanation From Exact Extract Without Links:

NCC relies heavily on ACOG Practice Bulletins for risk-based monitoring decisions. ACOG identifies maternal diabetes (pregestational or poorly controlled gestational diabetes) as a key high-risk obstetric condition warranting continuous electronic fetal monitoring due to risks such as fetal hypoxia, macrosomia, and metabolic complications.

In contrast, a history of preterm birth does not necessarily require continuous monitoring unless current pregnancy complications are present.

Macrosomia alone does not automatically justify continuous EFM unless accompanied by other risk factors.

Therefore, according to NCC-aligned ACOG clinical criteria, maternal diabetes is the correct indication.

Comprehensive and Detailed Explanation From NCC-Aligned Sources:

A nonreactive NST with no response to vibroacoustic stimulation indicates:

Possible fetal sleep cycle

Possible CNS depression

Possible hypoxemia

NCC, AWHONN, and MFM guidelines state the next step is a biophysical profile because:

It evaluates fetal tone, movement, breathing, amniotic fluid, and NST

Provides a complete assessment of fetal well-being

Is less invasive and more informative than immediate delivery decisions

Why the wrong answers are incorrect:

B. Cesarean birth — not indicated without confirming fetal compromise.

C. Induction of labor — not indicated until BPP clarifies fetal status.

Correct answer: A. Biophysical profile.

Comprehensive and Detailed Explanation From Exact Extract–Based NCC C-EFM References:

The tracing demonstrates:

Baseline ~150 bpm

Variability ≥ 25 bpm amplitude, highly erratic and wide

No sustained decelerations

No sustained accelerations ≥ 2 min

NICHD/NCC definition of marked variability:

Amplitude of baseline FHR fluctuations greater than 25 bpm.

Marked variability often reflects transient fetal autonomic instability due to:

Fetal stimulation

Mild hypoxemia

Maternal anxiety

Drugs (e.g., butorphanol)

Why other answers are incorrect:

B. Multiple prolonged accelerations — No accelerations of ≥2 minutes are present.

C. Tachycardia with variables — Baseline is NOT tachycardic (>160 bpm), and decelerations are not present.

Thus, the correct interpretation is A. Marked variability.

Comprehensive and Detailed Explanation From Exact Extract NCC-Recommended Sources

The tracing demonstrates a very rapid, highly regular baseline fetal heart rate with minimal beat-to-beat variability—characteristic of fetal supraventricular tachycardia (SVT). NCC-recommended references, including AWHONN’s Fetal Heart Monitoring Principles & Practices, Menihan’s Electronic Fetal Monitoring: Concepts and Applications, Simpson & Creehan’s Perinatal Nursing, and Creasy & Resnik’s Maternal-Fetal Medicine all describe fetal SVT as a sustained tachyarrhythmia usually greater than 200 bpm, narrow-complex, and extremely regular in appearance.

AWHONN teaches that SVT appears as a “tight, rapid, uniform baseline with minimal variability.” Menihan states that “SVT may present on EFM as a nearly straight line due to the rapid, consistent rate with micro-oscillations.” This differs significantly from artifact, which appears disorganized, erratic, and inconsistent in amplitude. Additionally, “half-counting” is a Doppler misinterpretation that records half of an extremely fast fetal rate, usually resulting in a falsely lower heart rate—not the very rapid tracing shown here.

Creasy & Resnik emphasize that SVT is the most common pathological fetal arrhythmia and can lead to fetal compromise if prolonged, making accurate recognition essential. Miller’s Pocket Guide to Fetal Monitoring also identifies SVT as a pattern with a “smooth, fast rhythm lacking normal variability.”

All authoritative NCC-recommended references support that this EFM pattern is consistent with fetal SVT, not artifact or half-counting.

Comprehensive and Detailed Explanation From NCC-Aligned Sources:

Placental calcifications:

Reduce surface area for maternal–fetal gas exchange

Impair placental perfusion

Are associated with post-dates and chronic insufficiency

Decrease the placenta’s ability to oxygenate the fetus

Why the incorrect answers are wrong:

A. Increased maternal cardiac output → improves uteroplacental perfusion.

B. Open-glottis pushing → improves oxygenation compared with closed-glottis Valsalva pushing.

Correct answer: Placental calcifications.

Comprehensive and Detailed Explanation From NCC-Aligned Sources:

The single best indicator of fetal oxygenation and neurologic integrity is:

Moderate baseline variability

Variability reflects:

Normal autonomic regulation

Adequate fetal oxygenation

Intact neurologic pathways

Absence of decelerations is helpful but not as predictive.

Baseline FHR (e.g., 140–150) is normal, but baseline alone does not confirm well-being.

Correct answer: C. Presence of variability

Comprehensive and Detailed Explanation From NCC-Aligned Sources:

The black tracing (Baby A) demonstrates:

Baseline ~170–175 bpm

Moderate variability

No recurrent decelerations

This is fetal tachycardia.

NCC physiology guidelines list common causes of fetal tachycardia:

Maternal fever / infection (chorioamnionitis)

Maternal dehydration

Maternal anxiety

Maternal hyperthyroidism

Fetal infection

Certain medications (terbutaline, illicit stimulants)

Why the other options are incorrect:

A. Fetal positioning does not influence baseline heart rate.

C. Magnesium sulfate typically lowers fetal baseline and variability—it does not cause tachycardia.

Thus, the most likely etiology is infection.

Comprehensive and Detailed Explanation From NCC-Aligned Sources:

This tracing shows:

Baseline ~170–175 bpm → fetal tachycardia

Minimal variability

No contractions of significance

Maternal treatment with magnesium sulfate, which typically decreases baseline and variability—not increase it

NCC and AWHONN physiology guidelines emphasize that fetal tachycardia is most commonly associated with maternal infection, including chorioamnionitis, especially in preterm labor.

Magnesium sulfate does not cause tachycardia; it generally causes:

↓ baseline

↓ variability

Thus, fetal tachycardia + minimal variability in a preterm patient strongly suggests maternal infection, requiring evaluation for chorioamnionitis.

Why the wrong answers are incorrect:

A. Acetaminophen → used after confirming fever, not before evaluating the cause.

B. Discontinuing magnesium → magnesium sulfate does not cause tachycardia; discontinuing it removes fetal neuroprotection.

Comprehensive and Detailed Explanation From Exact Extract–Based NCC C-EFM References:

NCC physiology content specifically includes maternal autoimmune influences on fetal cardiac conduction. Conditions such as maternal lupus (SLE) or Sjogren’s syndrome may produce anti-Ro/SSA and anti-La/SSB antibodies. These antibodies cross the placenta and damage fetal conduction tissue.

The primary site of injury is the fetal atrioventricular (AV) node, leading to:

First-, second-, or complete third-degree heart block

A slow, regular ventricular rate typically 50–70 bpm

Loss of beat-to-beat variability because ventricular myocardium does not display normal autonomic modulation

This mechanism is extensively described in AWHONN, NCC physiology materials, and maternal–fetal physiology texts.

Option A: Antibodies do not target fetal RBCs; that describes hemolytic disease of the newborn.

Option B: Targeting maternal WBCs is not fetal-specific.

The correct affected structure is the fetal AV node.

Therefore, the correct answer is C. The fetal atrioventricular node.

Comprehensive and Detailed Explanation From Exact Extract (NCC-Recommended Sources Only)

The fetal heart rate (FHR) tracing shown demonstrates a baseline approximately 135–145 bpm with fluctuations of 6–25 bpm, a hallmark of moderate variability. Moderate variability is defined in all NCC-endorsed resources as the normal amplitude range of 6–25 bpm around the fetal baseline.

According to the AWHONN Fetal Heart Monitoring Principles & Practices (2022–2024), moderate variability is considered the single most reliable indicator of adequate fetal oxygenation and intact neurologic pathways, specifically reflecting well-functioning sympathetic and parasympathetic interplay.

The NICHD/NCC standardized definitions included in the NCC C-EFM Candidate Guide state:

Minimal variability: amplitude range ≤ 5 bpm

Moderate variability: amplitude range 6–25 bpm

Marked variability: amplitude > 25 bpm

Sinusoidal pattern: smooth, undulating waveform, 3–5 cycles per minute, equal amplitude, absent beat-to-beat variability

The tracing provided does not show the repetitive, smooth, wave-like pattern of a sinusoidal rhythm; nor does it show flattening associated with minimal variability. Instead, it includes continuous beat-to-beat fluctuation within the moderate range, without periods of absent or minimal variability.

Menihan’s Electronic Fetal Monitoring (5th ed.) and Simpson & Creehan’s Perinatal Nursing (5th ed.) both emphasize that moderate variability is:

A reassuring feature

Indicative of adequate fetal CNS oxygenation

Expected in a reactive, well-oxygenated fetus

A key criterion for Category I classification

Additionally, Miller’s EFM Pocket Guide reiterates that variability between 6–25 bpm is considered the normal (moderate) fetal autonomic response and is not a sinusoidal pattern, which has a fixed amplitude and frequency.

Therefore, based on NCC-standard definitions and the observed amplitude, the correct interpretation is moderate variability.

References (No URLs):

AWHONN Fetal Heart Monitoring Principles & Practices; NCC C-EFM Candidate Guide 2025; Simpson & Creehan Perinatal Nursing; Menihan Electronic Fetal Monitoring; Miller’s Pocket Guide to Fetal Monitoring; Creasy & Resnik Maternal-Fetal Medicine.

Comprehensive and Detailed Explanation From NCC-Aligned Sources:

Category III criteria include:

Absent variability with recurrent variable decelerations

Absent variability with recurrent lates

Absent variability with bradycardia

Sinusoidal pattern

Thus, recurrent variables become Category III when accompanied by absent variability, indicating fetal decompensation.

Why the other answers are wrong:

B. Late decelerations → Category III only if combined with absent variability.

C. Tachysystole → Contraction pattern, not a FHR characteristic.

Correct answer: Absent variability.

Comprehensive and Detailed Explanation From Exact Extract–Based NCC C-EFM References:

The tracing shows recurrent variable decelerations deepening during contractions as the patient is fully dilated and at +1 station.

NCC’s Pattern Recognition and Intervention framework states:

During second stage (complete dilation), variable decelerations commonly occur from cord compression caused by head descent and maternal pushing efforts.

The FIRST correction for pushing-associated recurrent variable decelerations is modifying the pushing technique:

Side-lying pushing

Pushing with every other contraction

Open-glottis pushing

Allowing passive descent

These measures relieve head compression and reduce the severity of variable decelerations.

Why the other answers are incorrect

A. Administer terbutaline

Terbutaline is given for tachysystole with fetal intolerance.

This tracing does not show tachysystole.

The pattern is timing-related to pushing, not uterine overstimulation.

B. Consider amnioinfusion

Amnioinfusion is used for recurrent variable decelerations before complete dilation, when membrane rupture + low fluid is suspected.

At 10 cm and +1, the fetal head is deep in the pelvis, and the cause of variables is head compression, not cord compression due to oligohydramnios.

Also, amnioinfusion is impractical and not beneficial at this stage.

Therefore, the correct answer is C. Modify pushing.

Comprehensive and Detailed Explanation From NCC-Aligned Sources:

Normal umbilical arterial values per NCC/AWHONN/Menihan:

pH: 7.20–7.30

PaCO₂: 45–55 mmHg

HCO₃: 20–24 mEq/L

Base deficit: 0 to –5 (normal to mild respiratory changes)

This sample shows:

pH 7.25 → normal

Base deficit –4 → no metabolic acidosis

HCO₃ normal

Slightly elevated PaCO₂, consistent with mild respiratory influence but still normal

PaO₂ 20 mmHg is normal for cord arterial blood

This profile is not acidotic (acidosis requires pH <7.10 and base deficit ≥12).

It also does not indicate hypoxia, which would present with metabolic acidosis.

Therefore: Normal.

Comprehensive and Detailed Explanation From Exact Extract Without Any URLs or Links:

NCC references (AWHONN, Simpson, Menihan) and the Physiology domain emphasize that baseline fetal heart rate is higher at earlier gestational ages due to predominant sympathetic tone and immature parasympathetic modulation. For a 28-week fetus, a baseline between 150–170 bpm may fall within the upper normal/mild tachycardic range.

Before classifying fetal tachycardia, recommended by AWHONN and Simpson, clinicians must first assess maternal contributors:

Fever

Tachycardia

Infection

Dehydration

Medications (e.g., beta-agonists)

Anxiety

This matches NCC’s required first-line action: evaluate maternal status before escalating fetal assessment.

A biophysical profile (BPP) is not the immediate next step unless maternal status and fetal environment do not explain the finding. Continuing observation without maternal evaluation is contrary to perinatal safety standards.

Comprehensive and Detailed Explanation From Exact Extract (NCC C-EFM sources: AWHONN, Miller’s Pocket Guide, Menihan, Simpson, Creasy & Resnik, 2025 Candidate Guide)

The tracing displays baseline fetal bradycardia, with a rate near 100 bpm, minimal variability, and preserved periodic response. According to AWHONN’s Fetal Heart Monitoring Principles & Practices and Menihan’s Electronic Fetal Monitoring, maternal conditions that reduce oxygen-carrying capacity—including maternal anemia—can lead to lower fetal oxygen delivery, prompting a fetal compensatory bradycardic baseline.

Creasy & Resnik’s Maternal-Fetal Medicine notes that sickle cell anemia decreases maternal hemoglobin function even when maternal vital signs appear stable, reducing uteroplacental oxygen transport. Fetuses of mothers with sickling disorders may demonstrate lower resting fetal heart rates due to chronic mild hypoxemia.

Conversely, Eisenmenger’s syndrome is associated with severe maternal cyanosis and high fetal mortality, often producing late decelerations and growth restriction rather than mild bradycardia. Systemic lupus erythematosus (SLE) is commonly associated with heart block (especially with anti-Ro/SSA antibodies), which is not displayed here, as true heart block presents with a fixed atrial–ventricular dissociation and FHR < 60 bpm.

Thus, based on fetal physiology and maternal disease correlations taught in NCC-recommended sources, the tracing is most consistent with maternal sickle cell anemia.

Comprehensive and Detailed Explanation From Exact Extract–Based NCC C-EFM References:

NCC and NICHD differentiate:

Periodic decelerations – those occurring with contractions

Episodic decelerations – those occurring independent of contractions

Deceleration types:

Early – periodic (mirror contractions)

Late – periodic (after peak of contraction)

Variable – may be periodic or episodic, and are the only type strongly associated with episodic patterns**

Therefore, the only deceleration type that is characteristically episodic is a variable deceleration.

Correct answer: C. Variable deceleration

Comprehensive and Detailed Explanation From Exact Extract–Based NCC C-EFM References:

An early deceleration is defined by NICHD and NCC as a gradual decrease and return of the fetal heart rate associated with uterine contractions. NCC emphasizes that early decelerations are:

Symmetrical

Uniform in shape

Mirror images of the contraction

This means:

Onset of deceleration = onset of contraction

Nadir of deceleration = peak of contraction

Recovery = end of contraction

Duration of the deceleration ≈ duration of the contraction

Thus, the correct answer is C. The same.

Comprehensive and Detailed Explanation From NCC-Aligned Sources:

Contraction duration is defined as the length of time from the beginning of a contraction to the end of the same contraction (NICHD uterine activity definitions).

In the diagram:

Green arrow (B) spans one individual contraction from rise → peak → return to baseline.

Blue arrow (A) measures the interval between contractions (frequency).

Red arrow (C) measures peak-to-peak amplitude shape, not duration.

Therefore, the green arrow correctly identifies contraction duration.

Comprehensive and Detailed Explanation From NCC-Aligned Sources:

NICHD/NCC criteria:

Category I must have ALL of the following:

Baseline 110–160 bpm

Moderate variability

No late or variable decelerations

Early decelerations may be present or absent

Accelerations may be present or absent

Because this tracing has one variable deceleration, it fails Category I criterion (“no late or variable decelerations”).

Category III requires:

Absent variability with recurrent late decels, recurrent variables, or bradycardia, or

Sinusoidal pattern

Those findings are not present.

Therefore, any tracing that:

Has moderate variability and accelerations,

But includes a variable deceleration, and

Does not meet Category III criteria

…falls into the Category II (indeterminate) group.

Correct classification: B. Category II.

Comprehensive and Detailed Explanation From Exact Extract Without Links:

NCC-recommended references (Simpson, AWHONN FHM, Creasy & Resnik) note that baseline increases within the normal range (110–160 bpm) accompanied by moderate variability are typically benign. Mild physiologic causes—maternal activity, fetal stimulation, or normal sympathetic activation—may transiently raise baseline FHR.

AWHONN stresses that intervention is required only when tachycardia exceeds 160 bpm or when variability is minimal/absent or accompanied by recurrent decelerations.

Here, the baseline increase to 150 bpm remains within normal limits and is paired with moderate variability, which the NCC recognizes as the strongest indicator of adequate fetal oxygenation.

Therefore, evaluation is complete, and continued observation is the appropriate course.

Comprehensive and Detailed Explanation From NCC-Aligned Sources:

Second-stage bradycardia with moderate variability most commonly occurs from:

Vagal stimulation caused by head compression, particularly during descent and pushing.

Moderate variability indicates:

Neurologically intact fetus

Sufficient oxygen reserve

Temporary nature of bradycardia

This aligns with physiologic vagal slowing rather than hypoxic mechanisms.

Why the incorrect answers are wrong:

A. Cord compression → typically produces variable decelerations, not sustained bradycardia with preserved variability.

C. Vasospasm → associated with late decelerations and decreased variability (uteroplacental insufficiency).

Correct answer: B. Vagal stimulation

Comprehensive and Detailed Explanation From NCC-Aligned Sources:

According to NCC, AWHONN, and evidence-based documentation standards, clinicians must document:

Baseline

Variability

Accelerations

Decelerations (type, depth, duration, timing)

Uterine activity

This fulfills the NICHD 3-tier system and legal documentation expectations.

Why the incorrect answers are wrong:

B. "Normal/abnormal" → vague, not an acceptable documentation standard.

C. Category alone → insufficient; categories must be supported by the components.

Comprehensive and Detailed Explanation From Exact Extract Without Any URLs or Links:

According to the NCC C-EFM 2025 Exam Content Outline and recommended references such as AWHONN Fetal Heart Monitoring Principles, Simpson & Miller (Fetal Monitoring Text), and Menihan’s EFM Guide, recurrent variable or late decelerations with minimal or moderate variability during the second stage of labor—particularly when the patient has been pushing for ≥2 hours—indicate progressive fetal intolerance of labor.

AWHONN states that when the fetal tracing displays recurrent variable decelerations with ongoing stress from long second stage, the recommended intervention is operative or expedited vaginal birth, provided the fetal station is at +2 or lower. AWHONN and Simpson emphasize that reducing oxytocin is insufficient when the tracing demonstrates ongoing significant decelerations during active pushing with adequate descent.

The NCC blueprint within Pattern Recognition & Intervention emphasizes:

Identifying worsening recurrent decelerations

Acting when fetal tolerance is decreasing

Prioritizing timely intervention when the second stage exceeds standard limits with a non-reassuring tracing

Because she is fully dilated, vertex at +2, and tracing shows recurrent decelerations during pushing, the evidence-based next step is expediting birth, typically via operative vaginal delivery.

Comprehensive and Detailed Explanation From NCC-Aligned Sources:

The tracing shows the classic features of variable decelerations:

Abrupt onset (<30 seconds from baseline to nadir)

Rapid drop followed by a rapid recovery

Significant variability in shape, depth, and timing

“Shouldering”—brief accelerations before or after the deceleration, typical of cord compression

The decelerations vary in appearance and timing relative to contractions

In second stage, this pattern is extremely common due to:

Recurrent cord compression during descent

Maternal pushing

Reduced amniotic fluid with advancing labor

Why the other options are incorrect:

A. Intermittent late decelerations

Late decelerations are uniform, smooth, begin after the contraction peak, and recover after the contraction ends.

This tracing shows abrupt, variable-shaped, non-uniform decels → NOT late decels.

C. Wandering baseline

A wandering baseline is a slowly fluctuating, low-amplitude, smooth, preterminal pattern.

This tracing shows an identifiable baseline with variability and clear decelerations, not wandering baseline.

Thus, the tracing is most consistent with variable decelerations.

Comprehensive and Detailed Explanation From Exact Extract–Based NCC C-EFM References:

NCC’s Professional Issues domain emphasizes communication, collaboration, and team-based interpretation of electronic fetal monitoring tracings.

For non-emergent differences in interpretation, the first step is:

Discussion and joint review of the tracing by the involved clinicians.

Only if disagreement persists should the chain of command be used. Documentation occurs after consensus or escalation—not as the first step.

Thus, the appropriate first step is C. Have the involved clinicians review the tracing together.