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Exam (elaborations) NCC EFM CERTIFICATION

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Sinusoidal FHR smooth, sine-line, 3-5 cycles per minute, must be present for 20 minutes to diagnose; caused by fetal anemia or severe hypoxia/acidosis; may be drug-induced (staydol); category 3 Periodic decelerations associated with uterine contractions (period cramping); e.g. late decelerations Episodic decelerations Recurrent not associated with uterine contractions; e.g. variables decelerations that occur /=50% of uterine contractions within a 20 minute period; vs. intermittent (50% of ctx) Baseline variability irregular fluctuations in baseline FHR; peak to trough; absent is undetectable; minimal 1-5, moderate 6-25, marked 25 Decreased variability hypoxia, sleep cycle, drugs, anomalies, prematurity, tachycardia Increased variability fetal activity, fetal stimulation, alpha-adrenergic activity; in absence or abnormal FHR changes, marked variability is not ass'd with acidemia Fetal tachycardia hypoxia, maternal fever, medications (terbutaline), maternal thyroid disease, fetal anemia/heart failure, amnionitis, fetal arrhythmia Fetal bradycardia hypoxia (late sign), reflex (vagal), drugs, maternal hypothermia, fetal arrhythmia Normal contractions Tachysystole /= 5 contractions in 10 minutes averaged over 30 minutes 5 contractions in 10 minutes averaged over 30 minutes Narcotics decrease variability (cocaine too), decreased frequency of accelerations, transient sinusoidal, slight increase in 1/21 6/29/25, 12:58 PM NCC EFM exam, NCC EFM Certification 2/21 baseline rate Steroids betamethasone can decrease FHR variability Magnesium can decrease FHR variability, slight decrease baseline rate; inhibit accelerations Terbutaline increase baseline rate AZT no change in FHR Category 1 baseline 110-160, moderate variability, +/- accels, +/- early decelerations, no variable or late decelerations; predictive of normal fetal acid-base status Category 3 absent variability with bradycardia, recurrent variable, or recurrent late decelerations; or sinusoidal; predictive of abnormal fetal acid base status; expeditious delivery Acute intrapartum interruption of fetal oxygenation does not result in CP unless the fetal response progresses to the state of significant metabolic acidemia (pH 7 and base deficit 12+) Intrauterine resuscitative measures promote fetal oxygenation; perform for minimal or absent variability, recurrent lates or variables, prolonged decelerations, tachycardia, bradycardia Examples of intrauterine resuscitative measures Lateral positioning, knee-chest (AWOHNN), IV fluid bolus, modification of pushing (every other or every third), decrease in oxytocin rate (half or off), oxygen administration at 10L/min via NRB (still not changed in ACOG bulletin) If oxygen on turn pitocin off Management of tachysystole decrease/discontinue oxytocin, remove cervidil, withhold next misoprostol, IV fluid bolus of LR, lateral positioning, terbutaline 0.25 mg subq Management of recurrent variable decelerations repositioning, amnioinfusion, modification of pushing efforts Management of maternal hypotension lateral positioning, IV bolus, ephedrine 5-10 IV Administering supplemental O2 increase maternal blood oxygen tension, increases fetal oxygen saturation, 10L/min via NRB; potential adverse effects (oxygen free radicals); dc asap Uterine tachysystole leads to decreased uteroplacental perfusion decreased fetal oxygenation 6/29/25, 12:58 PM NCC EFM exam, NCC EFM Certification 3/21 Latent phase if we allow /= 12-18 hours before we diagnose failed induction, we will increase the risk for a C-section ARRIVE trial elective induction at 39 weeks does not increase risk of C/S; lower rates of gestational hypertension and preeclampsia as well as neonatal respiratory support Longer latent phase Current guidance from ACOG and SMFM recommends longer latent phase (up to 24 hours or more) and require that oxytocin be administered for at least 12-18 hours after membrane rupture before deeming the induction a failure Friedman (1955) vs. Zhang (2010) contemporary labors are slower; allow for longer latent phase Endogenous oxytocin first stage 5-7 mU/min (maternal circulating), surge of oxytocin at Ferguson's reflex during second stage of labor Exogenous oxytocin 1.5-2 hours of initial incremental phase; 3.5-4.5 hours where further pit will cause tachysystole/unfavorable FHR response Oxytocin-induced labors oxytocin receptor sites decrease significantly; desensitization related to dosage rate and length of administration; rest period of 1-2 hours recommended Oxytocin half-life of 10 minutes; need 3-4 half lives to reach steady-state (why 30-40 minute interval dosing of oxytocin); 90% will achieve active labor at less than 6 mU/min; most don't need more than 10 mU. More pitocin does not improve dysfunctional labor pattern. Consistent achievement of 200-220 MVUs. Continuing oxytocin after active labor will not shorten labor; some places have policies to downtitrate pitocin in active labor! Coupling/tripling may be indicative of dysfunctional labor process and saturation of oxytocin receptor sites; decrease pitocin and give fluid bolus Titrate pitocin start at 1 mU/min, increase by 1-2 mU/min every 30-40 minutes, titrate to contractions q2-3m; in active labor, decrease dose or discontinue; avoid tachysystole Treatment of tachysystole after discontinuation, takes 15 minutes to resolution, 10 6/29/25, 12:58 PM NCC EFM exam, NCC EFM Certification 4/21 minutes if we also do fluid bolus, 6 minutes if we also reposition Epidural maternal sympathetic blockade is rationale for recurrent lates after epidural Velamentous insertion ass'd with vasa previa (C/S 34-35w)/antepartum hemorrhage, 1 in 2-3k births, 60% fetal mortality Occiput posterior dysfunctional labor, prolonged active phase, rotate side to side, knee chest, hands and knees Breech 4% births, risk of entrapment d/t no molding, ECV possible; risk of prolapsed cord especially with malpresentation; frank is most common Chorioamnionitis viral/bacterial inflammation of fetal membranes, most commonly ass'd with PROM; risk of neonatal morbidity, sepsis, CP; chorion initially then full thickness then amniotic fluid and cord; proceed with delivery, not necessarily C/S, treat fevers; sxs include fever100.4, uterine tenderness, maternal and fetal tachycardia; purulent vaginal dc is a late sign Hypertensive disorders of pregnancy chronic 20 weeks gestation vs. gestational; preE eclampsia, HELLP (hemolysis, elevated liver enzymes, platelets) Chronic hypertension 140/90, risk for placental abruption Gestational hypertension begins after 20 weeks; fetus may be SGA/decreased blood perfusion, medicate if 160/110; first line labetalol, nifedipine Preeclampsia BP = 140/90 x2 at least 4 hours apart and proteinuria 300 mg/24 hours, UPCR = 0.3 or BP 160/110 confirmed in shorter interval; proteinuria not required if severe features PrE with severe symptoms BP =160/110 (on repeat in short interval) or BP 140/90 and severe headache, RUQ pain, visual disturbances (scotoma), LFTs 2x ULN, Cr 1.1 or doubling, plt 100, or pulmonary edema; treat with magnesium sulfate Acute onset severe hypertension must be treated within 1 hour; lasting more than 15 minutes nifedipine 10 mg if elevated in 20 min, give nifedipine 20 mg 20 min labetalol 40 mg IV over 2 6/29/25, 12:58 PM NCC EFM exam, NCC EFM Certification 5/21 min labetalol 80 mg IV hydralazine 10 mg; when threshold achieved, monitor q10min x 1 hour q15 q30 q1h Aspirin Started at 12 weeks if hx of preE, multifetal gestation, cHTN, GDM, renal dz, autoimmune disease Risks for preE age 19 or 35, family hx HTN, AA, poor diet, tobacco use, 1st pregnancy and 1st pregnancy with new paternal contribution, DM/metabolic syndrome/renal disease Delivery for preE 37 weeks if no severe features and no mag required; if severe prE, may deliver at 34 weeks or sooner Superimposed preE greater risk of poor outcomes; immediate delivery for uncontrolled severe HTN, eclampsia, pulmonary edema, abruption, DIC, NRFHT Diabetes in pregnancy increases risk of congenital abnormalities (heart and neural tube); poor maternal glycemic control increases risk 3-4x (A1c should be 7 preconception) Risks of diabetes in pregnancy 2.5x rate of demise, increased C/S, shoulder dystocia, hypoglycemia, polycythemia and hyperbilirubinemia, low calcium and mag level, increased risk of maternal hypertensive disorders; retest at 6 weeks pp; 8% of pregnancies, polyhydramnios in 10% pregnancies (risk of abruption, premature labor, postpartum atony) Gestational diabetes targets fasting 90, 1 hour 140, 2 hour 120 Obesity in pregnancy BMI 29, increases risk of GDM and hypertension, prolonged second stage, shoulder dystocia, macrosomia, difficult intubation, postop complications (DVT, infection); wait 12-24 months post gastric bypass for pregnancy Placental abruption risk factors HTN, smoking, cocaine, abdominal trauma; increased uterine activity and FHR changes; management depends on severity and GA Polyhydramnios single MVP 8 cm or AFI 24; 1% of pregnancies; 60% idiopathic; multiple gestation, maternal diabetes, hydrops, anomalies, TORCH; ass'd with cardiac/GI issues/renal issues 6/29/25, 12:58 PM NCC EFM exam, NCC EFM Certification 6/21 Oligohydramnios single MVP 2 cm or AFI 5 at term (less than 5%ile); associated with FGR, placental abnormalities, urinary tract abnormalities, post-term pregnancies, ruptured or idiopathic membranes Doppler US transducer, depicts valve closure; uses autocorrelation Autocorrelation successive US waveforms at many points; current technology which is more accurate at detecting FHR variability; controls artifact sound waves Toco/tocotransducer detects change in contour with contractions; place at fundus or at area of maximum palpation; difficult to measure with obesity, polyhydramnios Fetal scalp electrode measures R-R waves; still has issues with artifact; risk of injury, measuring maternal HR in instance of fetal demise; rupture and dilation required IUPC solidfluid filled tips, measures mmHg and allows amnioinfusion; issue with displacement, perforation, placental abruption Intermittent auscultation goal is baseline 110-160, +/-accels, no decels; if present, put on continuous monitor min 20 minutes); cannot determine variability or types of FHR decels Active phase auscultation q15 min for high risk up to q30min Second stage auscultation q5 min if high risk up to q15min Fetal tolerance of labor auscultate after a contraction x 30-60 seconds; document rate, rhythm, accels, decels Doppler vs. fetoscope doppler uses autocorrelation and detects valve closure; fetoscope listens through opening in heart wall?

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6/29/25, 12:58 PM NCC EFM exam, NCC EFM Certification




NCC EFM CERTIFICATION TEST BANK EXAM 2025-2026
\||COMPREHENSIVE EXAM NEWEST VERSION WITH
COMPLETE QUESTIONS AND CORRECT DETAILED
ANSWERS \\ACTUAL EXAM WITH VERIFIED ANSWERS
ASSURED PASS GRADED A+ \\BRAND NEW!!!2025




smooth, sine-line, 3-5 cycles per minute, must be present
Sinusoidal FHR for 20 minutes to diagnose; caused by fetal anemia or
severe hypoxia/acidosis; may be drug-induced
(staydol); category 3
Periodic decelerations associated with uterine contractions (period cramping); e.g. late
decelerations
Episodic decelerations not associated with uterine contractions; e.g. variables
decelerations that occur >/=50% of uterine contractions
Recurrent
within a 20 minute period; vs. intermittent (<50% of ctx)
irregular fluctuations in baseline FHR; peak to trough;
Baseline variability
absent is undetectable; minimal 1-5, moderate 6-25,
marked >25
Decreased variability hypoxia, sleep cycle, drugs, anomalies, prematurity, tachycardia
fetal activity, fetal stimulation, alpha-adrenergic activity;
Increased variability
in absence or abnormal FHR changes, marked
variability is not ass'd with acidemia
hypoxia, maternal fever, medications (terbutaline),
Fetal tachycardia
maternal thyroid disease, fetal anemia/heart failure,
amnionitis, fetal arrhythmia
Fetal bradycardia hypoxia (late sign), reflex (vagal), drugs, maternal hypothermia,
fetal arrhythmia
Normal contractions </= 5 contractions in 10 minutes averaged over 30 minutes
Tachysystole >5 contractions in 10 minutes averaged over 30 minutes
decrease variability (cocaine too), decreased frequency
Narcotics
of accelerations, transient sinusoidal, slight increase in

1/21

,6/29/25, 12:58 PM NCC EFM exam, NCC EFM Certification

baseline rate

Steroids betamethasone can decrease FHR variability
Magnesium can decrease FHR variability, slight decrease baseline rate; inhibit
accelerations
Terbutaline increase baseline rate
AZT no change in FHR
baseline 110-160, moderate variability, +/- accels, +/-
Category 1
early decelerations, no variable or late decelerations;
predictive of normal fetal acid-base status
absent variability with bradycardia, recurrent variable,
Category 3 or recurrent late decelerations; or sinusoidal;
predictive of abnormal fetal acid base status;
expeditious delivery
Acute intrapartum the fetal response progresses to the state of significant
interruption of fetal metabolic acidemia (pH <7 and base deficit 12+)
oxygenation does not
result in CP unless
promote fetal oxygenation; perform for minimal or
Intrauterine resuscitative
measures absent variability, recurrent lates or variables,
prolonged decelerations, tachycardia, bradycardia
Lateral positioning, knee-chest (AWOHNN), IV fluid bolus,
Examples of intrauterine
modification of pushing (every other or every third),
resuscitative measures
decrease in oxytocin rate (half or off), oxygen
administration at 10L/min via NRB (still not changed in
ACOG bulletin)
If oxygen on turn pitocin off
decrease/discontinue oxytocin, remove cervidil,
Management of tachysystole
withhold next misoprostol, IV fluid bolus of LR, lateral
positioning, terbutaline 0.25 mg subq
Management of recurrent repositioning, amnioinfusion, modification of pushing efforts
variable decelerations
Management of maternal lateral positioning, IV bolus, ephedrine 5-10 IV
hypotension
increase maternal blood oxygen tension, increases fetal
Administering supplemental
O2 oxygen saturation, 10L/min via NRB; potential adverse
effects (oxygen free radicals); dc asap
Uterine tachysystole leads to decreased uteroplacental perfusion > decreased fetal oxygenation
2/21

, 6/29/25, 12:58 PM NCC EFM exam, NCC EFM Certification


if we allow </= 12-18 hours before we diagnose failed
Latent phase
induction, we will increase the risk for a C-section
elective induction at 39 weeks does not increase risk
ARRIVE trial
of C/S; lower rates of gestational hypertension and
preeclampsia as well as neonatal respiratory support
Current guidance from ACOG and SMFM recommends
Longer latent phase longer latent phase (up to 24 hours or more) and
require that oxytocin be administered for at least 12-18
hours after membrane rupture before deeming the
induction a failure
Friedman (1955) vs. Zhang contemporary labors are slower; allow for longer latent phase
(2010)
first stage 5-7 mU/min (maternal circulating), surge of
Endogenous oxytocin
oxytocin at Ferguson's reflex during second stage of
labor
1.5-2 hours of initial incremental phase; 3.5-4.5 hours
Exogenous oxytocin
where further pit will cause tachysystole/unfavorable FHR
response
oxytocin receptor sites decrease significantly;
Oxytocin-induced labors
desensitization related to dosage rate and length of
administration; rest period of 1-2 hours recommended
half-life of 10 minutes; need 3-4 half lives to reach
steady-state (why 30-40 minute interval dosing of
Oxytocin
oxytocin); 90% will achieve active labor at less than 6
mU/min; most don't need more than 10 mU. More
pitocin does not improve dysfunctional labor pattern.
Consistent achievement of 200-220 MVUs.
will not shorten labor; some places have policies to
Continuing oxytocin after
active labor downtitrate pitocin in active labor!
may be indicative of dysfunctional labor process and
Coupling/tripling
saturation of oxytocin receptor sites; decrease pitocin
and give fluid bolus
start at 1 mU/min, increase by 1-2 mU/min every 30-40
Titrate pitocin
minutes, titrate to contractions q2-3m; in active labor,
decrease dose or discontinue; avoid tachysystole
after discontinuation, takes 15 minutes to resolution, 10
Treatment of tachysystole
3/21

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