Free Practice Questions for NCC EFM Exam

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

The tracing shows significant artifact, periods of signal loss, and abrupt changes inconsistent with physiologic fetal patterns. This is typical of poor signal quality, not actual fetal decelerations. In early labor at –2 station, external FHR monitoring often loses contact due to fetal position and maternal movement.

NCC and AWHONN emphasize the following when artifact is present:

Correct signal quality before interpreting the tracing.

Troubleshooting steps include:– Adjusting transducer location– Ensuring adequate ultrasound gel– Repositioning the mother– Checking for maternal heart rate contamination

Why the other options are incorrect:

B. IV fluid bolus — Indicated for hypotension or late decelerations, not for artifact.

C. Terbutaline — Used for tachysystole with fetal intolerance; there is no tachysystole shown.

Thus, the correct first step is A. Adjust the fetal monitor.

Comprehensive and Detailed Explanation From Exact Extract (No URLs or Links):

According to the NCC C-EFM exam outline and AWHONN Fetal Heart Monitoring Principles (2022), the first step when evaluating a concerning fetal heart rate pattern is to verify uterine activity, because the fetal response is often directly associated with contraction frequency, strength, or tachysystole. AWHONN states that “the clinician must confirm maternal–fetal physiology and uterine activity by palpation when interpreting any FHR pattern, as tocodynamometry may under- or overestimate uterine pressure.” Menihan’s Electronic Fetal Monitoring further emphasizes: “Always validate the contraction pattern via maternal abdominal palpation before proceeding with additional interventions.”

The tracing shows a late-appearing deceleration pattern with uncertain contraction correlation because the external toco waveform is inadequate (flat or poorly recorded). Before determining whether the decelerations are early, late, or variable, the clinician must confirm whether contractions are present, absent, or excessive. This step is listed as a core competency under Pattern Recognition & Intervention in the NCC Candidate Guide.

Therefore, palpating for contractions is the required first intervention.

Comprehensive and Detailed Explanation From Exact Extract (No URLs):

NCC references (AWHONN, Menihan, Simpson, Creasy & Resnik) consistently state that fetal accelerations are a reassuring sign of intact neurologic function. Accelerations represent the interaction of both the sympathetic and parasympathetic branches moderated through the central nervous system, reflecting effective autonomic regulation.

AWHONN specifically describes fetal accelerations as:

• A maturity marker of CNS function,

• Reflecting vigorous fetal movement,

• Demonstrating adequate oxygenation,

• Indicating a well-oxygenated brainstem and cortex.

Simpson & Miller emphasize that accelerations require both systems to be functioning and respond appropriately, which confirms CNS integration, not sympathetic or parasympathetic dominance alone.

Therefore, spontaneous accelerations indicate an integrated CNS response, making Option C the correct NCC-aligned answer.

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Comprehensive and Detailed Explanation From Exact Extract NCC-Recommended Sources

NCC-recommended physiology references (AWHONN, Simpson & Creehan, Menihan, Creasy & Resnik) consistently state that the primary mechanism by which tachysystole affects fetal oxygenation is reduced uteroplacental perfusion, specifically through impaired intervillous space reperfusion.

During a normal contraction cycle, the fetus receives oxygen between contractions, when the uterus relaxes and maternal blood re-enters the intervillous space. AWHONN’s Fetal Heart Monitoring Principles & Practices explains that tachysystole—defined as more than five contractions in 10 minutes averaged over 30 minutes—shortens or eliminates the relaxation phase, preventing adequate placental reoxygenation.

Simpson & Creehan highlight that “tachysystole decreases uteroplacental blood flow and interferes with replenishment of oxygenated maternal blood in the intervillous space.” Menihan emphasizes that fetal hypoxemia in tachysystole results from interrupted perfusion, not from altered oxygen transport or maternal hemodynamic changes. Creasy & Resnik confirm that uterine overactivity reduces intervillous perfusion during contractions and impairs fetal oxygen exchange.

Thus, the physiologic problem is failure of the intervillous space to reperfuse, which compromises fetal oxygenation.

Comprehensive and Detailed Explanation From Exact Extract Without Links:

NCC examination standards and AWHONN clearly state that normal Category I patterns have the highest interobserver agreement because they contain objective, easily identifiable components:

• baseline 110–160 bpm

• moderate variability

• absence of late or variable decelerations

• presence or absence of accelerations

Simpson highlights that Category II tracings have poor reliability due to multiple combinations of variability and decelerations, while Category III patterns have higher agreement but occur far less frequently, limiting reliability measures.

Research cited within NCC-endorsed materials confirms that clinicians demonstrate the greatest agreement in identifying normal Category I patterns, making normal the correct answer.

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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 Exact Extract Sources:

The tracing demonstrates an abrupt-onset, sharp, V-shaped deceleration, occurring simultaneously with or slightly after a contraction—classic for variable decelerations, which are caused by umbilical cord compression.

According to AWHONN Fetal Heart Monitoring Principles & Practices, variable decelerations are defined by:

“Abrupt decreases in FHR below baseline of at least 15 bpm, lasting at least 15 seconds and less than 2 minutes.”

“Most commonly associated with umbilical cord compression, whether transient or recurrent.”

Physiology reference (Simpson & Miller, Pocket Guide):

Compression of the umbilical vein causes a brief acceleration.

Compression of the umbilical arteries triggers a vagal response, producing a rapid deceleration.

This creates the characteristic sharp ‘V’, ‘U’, or ‘W’ shape on the monitor.

Placental insufficiency (Choice B) produces late decelerations, which are gradual, not abrupt.

Fetal head compression (Choice A) produces early decelerations, which mirror contractions and have a gradual pattern.

Thus, the tracing is most consistent with variable decelerations caused by umbilical cord compression.