Free Practice Questions for NCC EFM Exam

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

When bright red vaginal bleeding occurs at the moment of membrane rupture, accompanied by an acute, severe fetal heart rate deterioration, NCC sources emphasize considering conditions causing fetal hemorrhage rather than maternal instability.

The key features in this scenario:

Timing:Bleeding occurs immediately with spontaneous rupture of membranes—this is classic for vasa previa rupture, where fetal vessels traverse membranes and are torn when the membranes rupture.

Bleeding characteristics:Bleeding is acute, bright red, and sudden.In vasa previa, the blood observed vaginally is fetal blood, not maternal blood.

Uterine exam:The uterus is soft and nontender, which strongly argues against abruptio placenta, where the uterus is typically firm, rigid, or painful.

Maternal vital signs:Maternal blood pressure and pulse are normal, indicating no maternal hypovolemia.In placental abruption or placenta previa with significant maternal bleeding, maternal vitals are often abnormal.Here, the mother is stable, meaning the blood is not maternal—supporting fetal vessel rupture.

Fetal heart rate pattern:

Initial tachycardia, followed by

Bradycardia with minimal variabilitySuch a pattern is consistent with acute fetal blood loss, which rapidly leads to fetal hypovolemia and hypoxia.

Differential based on NCC-aligned physiology:

A. Abruptio placenta – NOT supported

Typically presents with:

Painful bleeding

Firm, tender uterus

Maternal tachycardia

Uterine irritabilityNone of these are present.

B. Placenta previa – NOT supported

Classically painless bright red bleeding before or early in labor, not triggered by membrane rupture.

Fetal compromise is less sudden unless maternal shock occurs, which is not the case here.

C. Ruptured vasa previa – CORRECT

Defined by:

Painless, sudden bright red bleeding at ROM

Normal maternal vital signs

Rapid fetal deterioration (tachycardia → bradycardia → minimal variability)

Soft, nontender uterusThis fits the scenario exactly.

Therefore, the most likely cause is ruptured vasa previa, a recognized obstetric emergency described across AWHONN, NCC C-EFM references, and maternal–fetal physiology texts such as Menihan and Creasy & Resnik.

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

Sustained fetal supraventricular tachycardia (SVT) often produces heart rates > 200–240 bpm, causing:

Poor ventricular filling

Decreased stroke volume

Reduced cardiac output

Congestive heart failure

Progressive fluid accumulation

NCC and AWHONN emphasize that untreated SVT leads to hydrops fetalis, characterized by:

Ascites

Pleural effusion

Pericardial effusion

Skin edema

Why the other answers are incorrect:

A. Fetal anemia — Causes tachycardia but is not caused by SVT.

C. Neonatal pacemaker — Pacemakers treat heart block, not SVT.

Correct answer: B. Hydrops fetalis

Comprehensive and Detailed Explanation From Exact Extract NCC-Recommended Sources

Fetal tachycardia is typically caused by maternal fever, dehydration, hypoxia, medications, infection, or fetal stress. AWHONN and Simpson & Creehan emphasize that management focuses on improving oxygen delivery across the placenta, which is governed by uteroplacental perfusion.

Menihan’s EFM text states that “interventions for fetal tachycardia must address oxygen transfer by optimizing uteroplacental blood flow,” including hydration, reducing uterine activity, maternal repositioning, and treating maternal fever.

Increasing maternal circulation alone is insufficient unless it improves placental blood flow. Enhancing fetal sympathetic tone is not a clinical goal and would worsen tachycardia.

Creasy & Resnik highlight that fetal heart rate abnormalities resolve when uteroplacental perfusion is restored, confirming this as the primary target of intervention.

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

Whenever a fetal heart rate is unexpectedly low (such as 90 bpm), the FIRST step per NCC and AWHONN is to confirm that the signal is fetal, not maternal.

Even internal spiral electrodes can capture maternal heart rate, especially after:

Rupture of membranes

Maternal hypotension

Maternal dehydration

Maternal tachycardia or bradycardia

Thus, the first, most immediate action is:

→ Palpate the maternal radial pulse to determine whether the tracing is maternal or fetal.

If rates match → the monitor is falsely detecting the maternal pulse.

If rates differ → confirm true fetal bradycardia and begin intrauterine resuscitation.

Why the other options are incorrect:

A. Intrauterine resuscitation — should NOT begin before confirming the tracing is fetal.

C. Bedside ultrasound — appropriate after confirming that the tracing is not maternal, not before.

Correct answer: B. Palpation of the maternal radial pulse.

Comprehensive and Detailed Explanation From Exact Extract (No URLs)

For fetuses before 32–34 weeks, the National Certification Corporation (NCC) follows the physiologic standards established by AWHONN, Simpson & Creehan, Menihan, and Creasy & Resnik, which emphasize that preterm fetuses have less mature autonomic nervous system development, resulting in smaller and shorter accelerations.

According to the NCC C-EFM Exam Content Outline (Pattern Recognition & Intervention) and the AWHONN Fetal Heart Monitoring Principles (2022–2024):

Preterm fetuses (<32 weeks) normally demonstrate 10 bpm × 10 sec accelerations.

By approximately 32–34 weeks, accelerations may begin transitioning toward 15×15, but the accepted standard for documentation at 34 weeks remains 10×10, unless clearly meeting 15×15 criteria.

NCC emphasizes using gestational-age–appropriate criteria for documenting accelerations, because autonomic reactivity increases gradually and is not fully comparable to term until after 32–34 weeks.

Menihan’s Electronic Fetal Monitoring also states that preterm fetuses “should be evaluated with the 10×10 rule until it is clear that the fetus is demonstrating mature 15×15 acceleratory capacity.”

Simpson & Creehan reinforce this point, noting that accelerations in late preterm gestations “may not consistently reach 15 bpm for 15 seconds, and thus 10×10 remains the appropriate designation.”

Since the patient is 34 weeks, the fetus is late-preterm and may not reliably meet the full 15×15 criteria; therefore, the correct documentation standard remains 10×10.

Thus, accelerations should be charted as:

“Present 10×10.”

References

NCC C-EFM Candidate Guide 2025 – Content Domain: Pattern Recognition and Intervention

AWHONN Fetal Heart Monitoring Principles & Practices, 2022–2024

Menihan: Electronic Fetal Monitoring: Concepts and Applications

Simpson & Creehan: Perinatal Nursing

Miller: Fetal Monitoring Pocket Guide

Creasy & Resnik: Maternal–Fetal Medicine

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

Assessment of likely fetal acid–base status is grounded in NCC-aligned principles that correlate fetal pH with fetal heart rate patterns, especially variability, presence/absence of accelerations, and type and depth of decelerations.

This tracing shows the following features:

Baseline:

The fetal heart rate baseline is approximately 140–150 bpm, within the normal 110–160 bpm range.

Variability:

Moderate variability is present—approximately 6–25 bpm amplitude.

Per NCC and NICHD definitions, moderate variability is strongly associated with normal fetal oxygenation and normal fetal pH > 7.20–7.25.

Accelerations:

There are occasional small accelerations, another strong indicator of normal fetal acid–base status.

Decelerations:

The tracing shows occasional variable decelerations, shallow and brief, recovering rapidly, typical of intermittent cord compression.

NCC references emphasize that intermittent, non-recurrent variables with moderate variability do not correlate with acidemia.

Uterine activity:

Contractions are present but not excessive, and fetal response remains reassuring.

Correlating tracing features with fetal pH (per NCC, AWHONN, Simpson, Menihan):

Moderate variability is the strongest intrapartum indicator of normal fetal pH.

The NICHD/NCC consensus repeatedly states that:

“The presence of moderate variability reliably predicts adequate fetal oxygenation and a fetal pH above the threshold associated with metabolic acidemia.”

Fetal pH below 7.15 is associated with:

Absent variability

Recurrent late decelerations

Recurrent deep variable decelerations

Prolonged bradycardia

None are present in this tracing.

Because the tracing demonstrates moderate variability, intermittent uncomplicated variables, and no recurrent late decelerations, the physiologic expectation is that the fetal pH remains normal, significantly above 7.15.

Therefore, the correct answer is: A (above 7.15).

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 Exact Extract NCC-Recommended Sources

Sentinel events are defined by the Joint Commission as unexpected occurrences involving death, serious physical or psychological injury, or the risk thereof, and they require immediate investigation, root-cause analysis, and institutional response. They do not require confirmed malpractice or negligence.

AWHONN’s perinatal safety guidelines and NCC’s Professional Issues domain specify that sentinel events trigger mandatory reporting, analysis, system review, and corrective action plans. Simpson & Creehan emphasize that they are addressed through standardized safety processes, including interdisciplinary review.

Miller’s Pocket Guide notes that sentinel events are “events that require immediate investigation to prevent recurrence,” aligning with answer choice B.

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

When internal monitoring continues to record artifact despite:

Changing the scalp electrode

Ensuring correct attachment

Checking cable connections

Confirming maternal movement is not the cause

NCC requires confirmation of fetal well-being using another modality.

The correct next step is direct auscultation with Doppler or fetoscope.

Why other answers are incorrect:

Oxygen is not indicated for equipment malfunction.

Repositioning does not resolve internal FHR artifact.

Thus, Auscultate the fetal heart rate is the appropriate next step.

Comprehensive and Detailed Explanation From NCC-Aligned Physiologic Sources:

Oxygen transfer occurs at the maternal–fetal interface within the intervillous space, where:

Maternal blood from the spiral arteries bathes the chorionic villi

Diffusion occurs between maternal blood and fetal capillary beds

Oxygen then travels through fetal circulation via the umbilical vein

Thus:

Intervillous space = site of gas exchange

Spiral arteries = deliver maternal blood to that space

Umbilical vein = fetal vessel carrying oxygenated blood after exchange has occurred

Correct answer: A. Intervillous space