NCC EFM Exam Breakdown & Study Guide Already Passed

NCC EFM Exam Breakdown & Study Guide Already Passed Content on exam -Pattern recognition & intervention: 70% -Physiology: 11% -Fetal assessment methods: 9% -EFM equipment: 5% -Professional issues: 5% Pattern recognition & intervention -FHR baseline -FHR variability -FHR accelerations -FHR decelerations -Normal uterine activity -Abnormal uterine activity -Fetal dysrhythmias -Maternal complications -Uteroplacental complications -Fetal complications FHR Descriptors 1) Baseline 2) Variability 3) Presence of accels 4) Presence of decels 5) Changes in trends overtime FHR Baseline Average FHR rounded to nearest 5 during a 10 min window -110 to 160 -excludes accels, decels, & marked variability -must have 2 mins to identify as a baseline (doesn't need to be continuous) Fetal Bradycardia 110 for ≥10 min -Causes: hypotension (ex: after epi), cord prolapse, head compression, congenital defect, rapid descent, abruption or rupture, tachysystole, post dates, hypoglycemia, lupus (heart block) -With ↓ O2, blood will be shunted to brain, heart, & adrenals, eventually ↓ FHR to ↓ O2 demands of heart muscle -Verify not mom's HR, vaginal exam (r/o prolapse), resuscitate, evaluate arrhythmia, expedite delivery Fetal Tachycardia 160 for ≥10 min -Causes: fetal anemia, maternal fever or infection, fetal immaturity (preterm), SVT, maternal anxiety (catecholamines), dehydration, hyperthyroid, hypoxia -Med causes: terbutaline, catecholamines (epinephrine, norepi) -Assess mom's temp & infection risk (GBS, PROM) FHR Variability Irregular in amplitude & frequency, quantified by peak to trough -Caused by sympathetic vs parasympathetic, r/t neuro maturity -Less in preterm due to undeveloped CNS -Absent: undetectable, flat -Minimal: ≤5 bpm but detectable -Moderate: 6-25 bpm -Marked: 25 bpm (indeterminate baseline), significance unknown Minimal variability ≤5 bpm but detectable Sleep, sedated, or sick -Sleep cycle: 20-60 mins -Sedated: CNS depressant (ex: mag), 1-2 hrs -Sick (acidemia): unresolved w intervention -Priority: maximize oxygenation (position, bolus, O2 if needed) Moderate variability 6 to 25 bpm -Reliably predicts the absence of metabolic acidosis (even w decels) FHR Accelerations Reliably predicts absence of metabolic acidemia (spontaneous or stimulated) -Onset to peak in 30 sec -For ≥32 wks: 15x15 (peak ≥15 bpm above baseline lasting ≥15 sec) -For 32 wks: 10x10 -Prolonged accel: 2-9 mins (at 10 becomes change of baseline) Early deceleration Nadir aligns w contraction peak, gradual onset (≥30 secs to nadir), benign vagal response 1) Pressure on fetal head 2) Increased intracranial pressure 3) Alteration in cerebral blood flow 4) Central vagal stimulation 5) FHR deceleration Periodic vs Episodic Periodic: caused by contractions -recurrent: occurs w ≥50% of contractions in 20 min -intermittent: w 50% of contractions in 20 mins Episodic: spontaneous Variable deceleration Caused by cord compression -Interventions: position change, amnioinfusion -Abrupt onset: 30 seconds from onset to nadir dropping ≥15 bpm lasting 15 secs to 2min -Transient rise in PCO2 & fall in PO2 Mechanisms of variable decelerations Abruptness r/t pressure changes 1) Vein obstruction → reflex tachy -↓ venous return & cardiac output → hypotens → baroreceptor reflex ↑ in FHR to maintain BP 2) Arterial obstruction → decreased FHR -obstructed blood flow back to placenta → HTN → baroreceptor reflex of slowing FHR to maintain BP Late decelerations Uteroplacental insufficiency -Indicative of transient fetal hypoxemia -Gradual onset: ≥30 secs to nadir w nadir occurring after peak of contraction -Priority is to maximize uteroplacental blood flow: position lateral (off vena cava & aorta), fluid bolus (perfusion), O2, avoid tachysystole Mechanisms of a late deceleration Low O2 → chemoreceptor response peripheral vasoconstriction → blood flow to vital organs → HTN → baroreceptor vagal stimulation → FHR decel 1) Decreased uteroplacental oxygenation (transient hypoxemia) 2) Chemoreceptor stimulation 3) Alpha adrenergic response (catecholamines, peripheral vasoconstriction) 4) Fetal HTN 5) Baroreceptor stimulation 6) Parasympathetic response 7) FHR deceleration 8) ↓ myocardial stress Prolonged deceleration Decrease of ≥15 bpm lasting 2 to 9 mins (≥10 = change of baseline) -Vagal stimulation -Causes: hypotension, maternal hypoxia, cord prolapse, rapid decent, profound cord compression, uterine rupture Sinusoidal pattern Visually apparent, smooth, sine wave-like pattern in FHR lasting ≥20 minutes -oscillation frequency: 3-5 cycles/min -no variability classification or reactivity -r/t severe anemia: previa, hemorrhage, abruption, RH isoimmunization, asphyxia, infection, cardiac anomaly, twin to twin transfusion, gastroschesis -Transient if 20min, can be r/t thumb sucking or opioids (stadol, fentanyl) Interventions -Position change: off of vena cava & aorta, least invasive, 1st line of treatment -Fluid bolus -Amnioinfusion (for variables) -Tocolytics (terb) -Ephedrine to ↑ BP -Supplemental O2: not used w O2 95%, can cause vasoconstriction, free radical formation, ocular toxicity if used limit to 15-30min Category I tracing Normal acid base balance -Baseline between 110 to 160 -Moderate