Free C-EFM Exam Flashcards

The mean fetal heart rate rounded to increments of 5 bpm during a 10-minute window, excluding accelerations, decelerations, and periods of marked variability. At least 2 minutes of identifiable baseline (not necessarily contiguous) are required, or the baseline is indeterminate. Normal range is 110–160 bpm.

A baseline FHR greater than 160 bpm lasting 10 minutes or more. Common causes include maternal fever, intra-amniotic infection (chorioamnionitis), maternal dehydration, medications (e.g., terbutaline), and fetal hypoxia. It is often an early sign of maternal infection and warrants assessment of maternal temperature.

A baseline FHR less than 110 bpm lasting 10 minutes or more. Causes include fetal hypoxia/acidemia, maternal hypotension, cord prolapse, rapid fetal descent, and fetal heart block. Sustained bradycardia is concerning and requires evaluation for a correctable cause and possible intrauterine resuscitation.

Fluctuations in the baseline FHR that are irregular in amplitude and frequency, measured as the peak-to-trough amplitude in bpm. Variability reflects the interplay of the fetal sympathetic and parasympathetic nervous systems and is the single most reliable indicator of adequate fetal oxygenation and an intact central nervous system.

Amplitude range of the baseline FHR is undetectable. When combined with recurrent late or variable decelerations or bradycardia, absent variability is a defining feature of a Category III tracing and strongly suggests fetal hypoxia/acidemia requiring urgent intervention or delivery.

Amplitude range greater than undetectable but 5 bpm or less. Causes include fetal sleep cycles (typically 20–40 minutes), CNS depressants or analgesics, prematurity, fetal tachycardia, and developing hypoxia/acidemia. It requires correlation with the overall tracing to distinguish benign from concerning causes.

Amplitude range of 6–25 bpm. Moderate variability is reassuring: it reliably predicts the absence of fetal metabolic acidemia at the time it is observed and indicates a well-oxygenated fetal central nervous system. Its presence is a key criterion for a Category I tracing.

Amplitude range greater than 25 bpm. Sometimes called saltatory pattern, it may follow acute hypoxic events or cord compression. While not itself diagnostic of acidemia, persistent marked variability warrants continued surveillance and evaluation for an underlying cause.

An abrupt increase in FHR (onset to peak in less than 30 seconds) of at least 15 bpm above baseline lasting at least 15 seconds but less than 2 minutes. In a fetus 32 weeks or greater, accelerations indicate fetal well-being and an intact, well-oxygenated central nervous system.

In a fetus less than 32 weeks of gestation, an acceleration is defined as a peak of at least 10 bpm above baseline lasting at least 10 seconds. The lower threshold reflects the immaturity of the preterm fetal nervous system.

An acceleration lasting 2 minutes or more but less than 10 minutes. If an increase in FHR lasts 10 minutes or longer, it is considered a baseline change rather than an acceleration.

An acceleration provoked by digital scalp stimulation or vibroacoustic stimulation. A FHR acceleration in response to stimulation reliably predicts a normal scalp pH (no acidemia) and can substitute for fetal scalp sampling in an otherwise indeterminate tracing.

A gradual decrease in FHR (onset to nadir 30 seconds or more) that is symmetric and mirrors the contraction, with the nadir occurring at the peak of the contraction. It is caused by fetal head compression triggering a vagal reflex. Early decelerations are benign, require no intervention, and do not indicate hypoxia.

A gradual decrease in FHR that is symmetric, with onset, nadir, and recovery occurring after the corresponding points of the contraction (the nadir follows the contraction peak). It is caused by uteroplacental insufficiency leading to transient fetal hypoxemia. Recurrent late decelerations are non-reassuring and require intervention.

During a contraction, uteroplacental blood flow falls; when placental reserve is inadequate, fetal PO2 drops below a threshold, stimulating chemoreceptors and producing a delayed, gradual FHR decline. The lag between contraction and deceleration reflects the time for oxygen tension to fall, marking impaired placental gas exchange.

An abrupt decrease in FHR (onset to nadir less than 30 seconds) of at least 15 bpm below baseline lasting at least 15 seconds but less than 2 minutes. The shape, depth, and timing vary relative to contractions. It is caused by umbilical cord compression and is the most common deceleration seen in labor.

Cord compression first occludes the thin-walled umbilical vein (causing a brief acceleration or 'shoulder'), then the umbilical arteries, raising fetal blood pressure and triggering a baroreceptor-mediated vagal response that abruptly drops the FHR. As compression resolves, the FHR returns abruptly to baseline.

Decelerations are recurrent when they occur with at least 50% of contractions in any 20-minute segment, and intermittent when they occur with fewer than 50%. This distinction is central to NICHD categorization: recurrent late or variable decelerations carry greater significance than intermittent ones.

A decrease in FHR of at least 15 bpm below baseline lasting 2 minutes or more but less than 10 minutes. Causes include cord compression or prolapse, uterine tachysystole, maternal hypotension, and rapid fetal descent. A deceleration lasting 10 minutes or longer is reclassified as a baseline change (bradycardia).

A smooth, prolonged acceleration immediately following a variable deceleration, rising above baseline before returning. When seen with absent variability in a preterm or compromised fetus, an overshoot may be a sign of fetal compromise rather than reassurance and warrants careful evaluation of the whole tracing.

Requires ALL of: baseline 110–160 bpm, moderate variability, absent late and variable decelerations; early decelerations may be present or absent, and accelerations may be present or absent. Category I strongly predicts normal fetal acid-base status and is managed with routine continued monitoring.

All tracings not classified as Category I or III. Examples include minimal or marked variability, tachycardia or bradycardia with variability present, recurrent variable decelerations with moderate variability, and prolonged decelerations. Category II is the most common category and requires continued surveillance, evaluation, and intrauterine resuscitation as indicated.

Includes either a sinusoidal pattern, OR absent baseline variability with any of recurrent late decelerations, recurrent variable decelerations, or bradycardia. Category III predicts abnormal fetal acid-base status, requires prompt intrauterine resuscitation, and if not quickly resolved, expedited delivery.

The NICHD categories describe the tracing at a single point in time and are not static; a tracing can move between categories as labor progresses. Category II is intentionally broad and does not by itself dictate management—it requires ongoing clinical judgment and reassessment.

Measured from the beginning of one contraction to the beginning of the next, averaged over a 30-minute window. Normal uterine activity is five or fewer contractions in 10 minutes, averaged over 30 minutes. Frequency is documented along with duration, intensity, and resting tone.

More than five contractions in 10 minutes, averaged over a 30-minute window. The term applies to both spontaneous and induced labor and should always be qualified by the presence or absence of associated FHR decelerations. Management includes reducing or stopping uterotonics and considering a tocolytic.

A measure of uterine contraction strength obtained only with an intrauterine pressure catheter (IUPC). Sum the peak amplitude above resting tone (in mmHg) of each contraction in a 10-minute window. Adequate labor is generally considered 200–250 MVUs or more.

The baseline uterine pressure between contractions, measurable only with an IUPC (normally about 5–25 mmHg). Elevated resting tone reduces the time available for uteroplacental perfusion and fetal reoxygenation, predisposing the fetus to hypoxemia and late decelerations.

A smooth, undulating, sine-wave-like baseline with a regular frequency of 3–5 cycles per minute persisting for 20 minutes or more, with absent variability and no accelerations. It is classically associated with severe fetal anemia (e.g., Rh isoimmunization, fetomaternal hemorrhage) and defines a Category III tracing.

An undulating pattern resembling sinusoidal but more irregular, often transient, and associated with maternal narcotic administration or fetal sucking/thumb movement. Unlike true sinusoidal, variability is usually present elsewhere on the strip and it is not a sign of fetal anemia.

An irregular fetal rhythm detected on monitoring, most commonly benign premature atrial contractions that often resolve before or after birth. Sustained tachyarrhythmias (e.g., supraventricular tachycardia) or fixed bradyarrhythmias (e.g., complete heart block) require echocardiographic evaluation and can be associated with hydrops.

A brief acceleration immediately followed by a small deceleration, creating a lambda (λ) shape, typically benign and related to mild cord involvement early in labor. It is distinguished from late decelerations by its timing and the surrounding moderate variability.

A bundle of interventions aimed at improving fetal oxygenation when the tracing is non-reassuring: maternal repositioning, IV fluid bolus, correcting hypotension, reducing uterine activity, oxygen as indicated, and amnioinfusion for cord compression. The goal is to restore a reassuring tracing and avoid unnecessary operative delivery.

Turning the mother to a lateral (side-lying) position relieves aortocaval compression by the gravid uterus, improving venous return, cardiac output, and uteroplacental perfusion. It is a first-line intervention for variable decelerations (relieves cord compression) and for late decelerations or maternal hypotension.

Instillation of warmed isotonic fluid into the uterine cavity through an IUPC to restore amniotic fluid volume. It cushions the umbilical cord and is used specifically to relieve recurrent variable decelerations caused by cord compression, particularly with oligohydramnios.

When excessive uterine activity is associated with FHR changes, first stop or reduce uterotonic agents (e.g., oxytocin) and reposition the mother. If the pattern persists, a tocolytic such as terbutaline may be given to reduce contraction frequency and allow fetal recovery.

Supplemental oxygen has historically been given to improve fetal oxygen delivery during non-reassuring tracings, though evidence for routine use is limited. It is reserved for specific indications (e.g., maternal hypoxemia) and is one component—not a substitute for correcting the underlying cause such as hypotension or tachysystole.

Hypotension after regional anesthesia reduces uteroplacental perfusion and can cause late or prolonged decelerations. Management includes lateral positioning, a rapid IV crystalloid bolus, and a vasopressor (e.g., ephedrine or phenylephrine) to restore blood pressure and fetal oxygen delivery.

Maternal oxygen passes from uterine arteries through the intervillous space, across the placental membrane, into the umbilical vein, and to fetal tissues. Any disruption—reduced maternal flow, impaired placental exchange, or cord compression—can produce characteristic FHR decelerations, which is why patterns localize the problem.

Adequate fetal oxygenation depends on a continuous chain: maternal oxygen content, uterine blood flow, placental gas exchange, umbilical blood flow, and fetal circulatory response. A break at any link reduces fetal PO2; the FHR pattern reflects where in this pathway oxygen transfer is impaired.

The parasympathetic (vagal) system lowers the FHR and creates beat-to-beat variability, while the sympathetic system raises the FHR and accelerations. Moderate variability reflects a balanced, well-oxygenated autonomic system; loss of variability suggests CNS depression from hypoxia, medications, or sleep.

With falling oxygen, the fetus initially redistributes blood flow to the brain, heart, and adrenals (centralization) and may show tachycardia. Progressive hypoxia triggers chemoreceptor-mediated decelerations and, with metabolic acidemia, loss of variability and accelerations—an orderly sequence that guides interpretation.

Head compression causes early decelerations (vagal, benign), cord compression causes variable decelerations (abrupt, baroreceptor-mediated), and uteroplacental insufficiency causes late decelerations (gradual, chemoreceptor-mediated hypoxemia). Matching deceleration shape and timing to physiology identifies the cause and the intervention.

Uses a Doppler ultrasound transducer for FHR and a tocodynamometer for uterine activity placed on the maternal abdomen. It is noninvasive and requires no membrane rupture, but the toco shows only contraction frequency and duration—not true intensity—and can be limited by maternal habitus or fetal movement.

Uses a fetal scalp electrode (FSE) attached to the presenting part for a direct fetal ECG and an intrauterine pressure catheter (IUPC) for true contraction intensity and resting tone in mmHg. It requires ruptured membranes and adequate cervical dilation and provides more accurate data than external methods.

An FSE provides a precise FHR signal and can reveal true variability and arrhythmias, but it is contraindicated with active maternal HIV, hepatitis B/C, suspected fetal bleeding disorders, or unknown presenting part. It also carries a small risk of fetal scalp infection or injury.

External Doppler can mistakenly double-count or track the maternal pulse, especially with fetal demise or maternal tachycardia, producing a falsely reassuring 'fetal' tracing. Confirm the FHR is distinct from the maternal pulse—correlate with a maternal pulse oximeter or apply an FSE if there is any doubt.

In the United States, fetal monitor paper runs at 3 cm/min, with the FHR scale 30–240 bpm and the uterine activity scale 0–100 mmHg. Standard paper speed and scaling are essential so that deceleration timing and shape are interpreted consistently across providers.

FHR interpretation must be documented with standardized NICHD terminology (baseline, variability, accelerations, decelerations, contractions, and category) at intervals set by policy. Structured handoff such as SBAR (Situation, Background, Assessment, Recommendation) reduces miscommunication and is a tested professional-practice competency.

The 2008 NICHD workshop established a single set of definitions for FHR baseline, variability, periodic and episodic patterns, and the three-tier category system. Using this shared language—rather than terms like 'good beat-to-beat' or 'reassuring'—is the foundation of accurate, defensible communication tested on the C-EFM exam.