EFM Exam Dumps - NCC C-EFM Questions and Answers

Comprehensive and Detailed Explanation From Exact Extract Without Links:

According to the NCC C-EFM Content Outline and AWHONN Fetal Heart Monitoring Principles, recurrent decelerations are specifically defined as decelerations that occur with ≥50% of uterine contractions in a 20–30-minute window, but standardized interpretation guidelines used by NCC and ACOG categorize recurrent patterns based on any 30-minute evaluation period.

AWHONN (FHM 6th Ed.) explains that fetal heart patterns must be evaluated over “a sufficiently long segment, typically 30 minutes, to determine whether the pattern is intermittent or recurrent.”

Menihan & Simpson further emphasize that recurrent decelerations imply a persistent physiologic stressor, requiring systematic evaluation and intrauterine resuscitation. NCC's Candidate Guide ties this rule directly into categorization within Category II and III tracings. Therefore, 30 minutes is the correct standard evaluation interval for determining recurrence.

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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 NCC-Aligned Sources:

NCC/AWHONN emphasize that the primary goal of intrauterine resuscitation is to:

Optimize uteroplacental blood flow, which restores fetal oxygen delivery.

Key measures include:

Maternal repositioning (lateral)

Reducing tachysystole

IV fluid bolus

Correcting maternal hypotension

Stopping oxytocin

Treating underlying causes

Improving maternal oxygenation is supportive, but improving uteroplacental perfusion is the critical first determinant of resuscitation success.

Why the other answers are not first priority:

A. Oxygen — optional and no longer universally recommended unless maternal hypoxemia exists.

B. Minimizing uterine activity — essential, but still secondary to restoring perfusion.

Correct answer: C. Optimizing uteroplacental blood flow

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

Mono-mono twins share a single amniotic cavity, which significantly increases the risk of cord entanglement, a concept highlighted in AWHONN FHM, Creasy & Resnik Maternal-Fetal Medicine, and Miller’s EFM Pocket Guide.

These texts emphasize:

“Cord entanglement is nearly universal in monoamniotic twins.”

“Variable decelerations are common due to recurrent cord compression.”

Baseline tachycardia or minimal variability are not expected baseline characteristics, but may appear only in pathologic circumstances.

Thus, variable decelerations are the expected and anticipated FHR pattern in mono-mono twins.

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

NCC and AWHONN physiology teachings:

Variable decelerations caused by cord compression lead to:

Transient interruption of umbilical venous flow

Impaired fetal gas exchange

Acute rise in CO₂

Respiratory acidosis (early phase of hypoxemia)

This is well documented:

Early decelerations → head compression → NOT associated with acidemia.

Late decelerations → uteroplacental insufficiency → metabolic acidosis, not respiratory.

Thus:

Variable decelerations → respiratory acidosis

Late decelerations → metabolic acidosis

Correct answer: C. Variable

Comprehensive and Detailed Explanation From Exact Extract Sources:

In fetal physiology, the highest oxygen saturation exists in the umbilical vein, which then flows through the ductus venosus before entering the right atrium.

According to Creasy & Resnik Maternal-Fetal Medicine, and AWHONN physiologic foundations:

The umbilical vein carries oxygen-rich blood from the placenta (approx. 80% saturation).

Most of this blood bypasses the liver via the ductus venosus, which therefore contains the most highly oxygenated blood within the fetal circulatory system.

By contrast:

The descending aorta contains mixed blood with significantly lower oxygen content due to mixing after passage through the ductus arteriosus.

The pulmonary arteries in the fetus carry predominantly deoxygenated blood, since fetal lungs are fluid-filled and have high pulmonary vascular resistance.

Thus, the structure containing the highest fetal oxygen concentration is the ductus venosus.

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:

Tachysystole = >5 contractions in 10 minutes averaged over 30 minutes (NICHD).

However, NCC and AWHONN intervention guidelines state:

If tachysystole appears in one or two consecutive 10-minute segments, especially with Category II or III patterns, intervention must begin immediately.

Intervention includes:

Stopping/reducing oxytocin

Maternal repositioning

IV bolus

Tocolysis if needed

Why the wrong answers are wrong:

A. Waiting 30 minutes delays necessary fetal resuscitation.

C. Stage of labor does not determine when to intervene.

Correct answer: B. If tachysystole is seen for one or two 10-minute segments

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

The tracing shows a clear relationship between uterine activity and fetal heart rate changes:

The uterine activity strip demonstrates very frequent contractions with little resting time between them, exceeding five contractions in 10 minutes, averaged over a 30-minute window.

NCC and NICHD define tachysystole as “more than 5 contractions in 10 minutes, averaged over 30 minutes, regardless of whether the labor is spontaneous or stimulated.”

As uterine activity intensifies and becomes excessively frequent, the fetal heart rate strip begins to show:

Progressive decrease in baseline

Recurrent decelerations with gradual onset and recovery

Reduced variability in the latter portion of the strip

This pattern is consistent with uteroplacental insufficiency caused by excessive uterine activity (tachysystole). NCC and AWHONN emphasize that tachysystole can result in decreased uterine blood flow and fetal oxygenation, leading to late or prolonged decelerations and eventual bradycardia if not corrected.

Why the other options are less likely:

A. Placental abruptionTypically associated with maternal symptoms (pain, vaginal bleeding, firm/boardlike uterus) and often a sustained increase in resting tone or a hypertonic contraction, not simply very frequent contractions. These maternal findings are not described in the vignette.

B. Rapid fetal descentUsually causes variable or early decelerations related to head compression, but the tocodynamometer would not necessarily show this degree of contraction frequency. The lower strip here clearly highlights excessive contractions as the primary problem.

Thus, the tracing’s FHR abnormalities are best explained by tachysystole, making C. Tachysystole the most appropriate answer.