Download NCC EFM Exam Breakdown & Study Guide: A Comprehensive Guide to Fetal Heart Rate Monitoring and more Exams United States Philosophy in PDF only on Docsity!
NCC EFM Exam Breakdown & Study Guide
- 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
- Variability
- Presence of accels
- Presence of decels
- 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 e10 min -Causes: hypotension (ex: after epi), cord prolapse, head compression, congen- ital defect, rapid descent, abruption or rupture, tachysystole, post dates, hypo- glycemia, lupus (heart block) -With โ O2, blood will be shunted to brain, heart, & adrenals, eventually โ FHR to โ O2 demands of heart muscle -Verify not mom's HR, vaginal exam (r/o prolapse), resuscitate, evaluate arrhyth- mia, expedite delivery
- Fetal Tachycardia: >160 for e10 min
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- 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: d5 bpm but detectable -Moderate: 6-25 bpm -Marked: >25 bpm (indeterminate baseline), significance unknown
- Minimal variability: d5 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 (spon- taneous or stimulated) -Onset to peak in <30 sec -For e32 wks: 15x15 (peak e15 bpm above baseline lasting e15 se -For <32 wks: 10x
asting 15 sec -Prolonged accel: 2-9 mins (at 10 becomes change of baseline)
- Early deceleration: Nadir aligns w contraction peak, gradual onset (e secs to nadir), benign vagal response
- Pressure on fetal head
- Increased intracranial pressure
- Alteration in cerebral blood flow
- Central vagal stimulation
- FHR deceleration
- Periodic vs Episodic: Periodic: caused by contractions -recurrent: occurs w e50% 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 e15 bpm l s to <2min -Transient rise in PCO2 & fall in PO
ion,
- Parasympathetic response
- FHR deceleration
- โ myocardial stress
- Prolonged deceleration: Decrease of e15 bpm lasting 2 to 9 mins (e10 = 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 e20 minutes -oscillation frequency: 3-5 cycles/min -no variability classification or reactivity -r/t severe anemia: previa, hemorrhage, abruption, RH isoimmunizat 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 โ 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 variability -No late, variable, or prolonged decels -May have early decels -May or may not have accels
- Category II tracing: Indeterminate acid base balance -Minimal variability -Marked variability -Late or variable decels -Bradycardia with variability -Tachycardia -Prolonged decels -Absent variability w NO decels -Absence of induced acccel WITH fetal stimulation
-tocolytic (terbutaline) -O2 if decel
- Tachysystole & pitocin: With fetal tolerance -If not resolved in 15min, โ pit by 1/ -If not resolved in another 15min, pause pit -If pit's off for <30 min, resume pit at 1/2 of current dose -If off for >30 min, start @ initial order dose With fetal intolerance: pit off immediately
- Hypertonous labor: Frequent & painful but poor quality contractions occurring in latent labor -despite increased tone, not enough pressure to cause cx change -indicative of CPD or malpresentation -tx: comfort care, pitocin, AROM
- Hypotonic labor: Weak & insufficient labor occurring during the active phase -inadequate, infrequent, & less intense contractions don't dilate or efface cx -caused by tired uterus or overdistention (poly, multiple gestation, LGA)
- Arrest of labor: >6cm dilated w/ ROM & one of the following w no cx change:
-4 hrs of adequate contractions (>200 MVUs) -6 hrs of inadequate contractions
- Fetal dysrhythmias: 1) SVT: 210-300 bpm -tx w digoxin (โ dose to cross placenta) -concern w hydrops, CHF (heart stress), โ O2 demand & use, โ stroke volume, demise
- Congenital heart block (<60 bpm): 3rd degree โ concern w hydrops, lupus, CHF
- Ectopic beats: extra beats heard, benign, may be transient
- Lupus (SLE): Can cause congenital 3rd degree heart block -bradycardia -autoimmune โ inflammatory response โ overgrowth of collagen in heart muscle -damages fetal conduction system of the heart, attacks fetal tissue -usually diagnosed in 2nd trimester
- Preterm labor: Cx dilation bw 20-36.6 wks -late preterm: 34-36.6 wks -common risk factors: multiples, previous PTD (greatest), uterine or cx abnormal- ities, infection, <18 months bw pregnancies, IUGR -โ reserve & โ parasympathetic maturity -โ baseline, โ variability, โ variable decels
- Hypertension (HTN): BP > 140/ -tx w Ca channel blockers, thiazides, BB -avoid ACE inhibitors & ARBs (congenital defect)
- Chronic: present prior to pregnancy -risk of superimposed preeclampsia, abruption, stroke (endothelial damage to vessels), stress on L ventricle (to overcome pressure)
- Gestational: begins after 20 wks, returns to normal PP (no proteinuria: <300mg/<0.3 pcr) -โ BP is sustained 6 hrs apart -risk of poor perfusion, SGA
- Preeclampsia & HELLP: โBP & proteinuria or a s/s: poor implantation of arterioles & trophoblasts cause โ blood flow to placenta, โ BP to compensate -mild: 140/90, protein 300mg/24hr or 1-2g dipstick -severe: 160/110, protein 5g/24hr or 3g dipstick, N/V, HA, hyperreflexia, clonus -prevent w baby ASA in 1st trimester (vasodilate) -damages kidneys, liver, heart, lungs, blood cells & vessels, neuro (cerebral edema), optic nerve -AE: oligo, IUGR, pulmonary edema, HA, epigastric pain, blurry vision, abruption, IUFD, seizure, liver rupture, renal failure, DIC, CVA
-can cause eclampsia (seizure) from cerebral ischemia & edema, may abrupt or rapidly dilate -HELLP: hemolysis, โ liver enzymes (AST, ALT), โ platelets (<100k)
- Treatment of preeclampsia & HTN: -Induce by 39 wks
- Mag: muscle relaxant used to prevent seizure -loading dose 4-6g/hr, maintenance 2-4g/hr -therapeutic lvl: 4-8 mEq/L -โ FHR variability, hypotonia, resp depression -antidote: calcium gluconate 1g/10ml D5W -SE: NV, flushing, HA, โ reflexes, pulmonary edema, hypotension, resp depression, oliguria
- BB: don't use w asthma or โ HR, caution w diabetes (masks hypoglycemia)
- Hydralazine: relaxes smooth muscles -can cause rebound tachycardia
- Ca channel blocker (procardia, nifedipine): relaxes smooth muscles, โ renal perfusion & urinary output
- Valium or keppra w eclampsia
- Diabetes: -Excess glucose delays surfactant production (RDS) -T1 & T2 more likely to cause congenital abnormalities (heart & neural tube defect) -Hypoglycemia at birth: glucose crosses placenta but not insulin, fetus has โ
associated w congenital abnormalities -other: syphillis, varicella zoster, parvovirus B
- Maternal obesity: -Risk of diabetes, preeclampsia, DVT, infection, PPH (โ estrogen), miscarriage -Fetus: NTD, heart defect, macrosomia (4000g, 8-13), PTD -Recommended weight gain: 11-20 lbs (compared to 25-35 in average weight)
- Uteroplacental complications: 1) Previa: total = covering cx os, marginal = 2cm of os, low lying = 2-3.5 cm from os (usually resolves) -painless bright red bleeding -risk: AMA, uterine scarring, fibroids, smoking, multiples -pelvic rest, bedrest, rhogam (rh-), steroids, PTD
- Abruption: placental separation from uterus -painful bleeding (may be concealed), โ frequency โ amplitude contractions, โ fundal height, rigid abd
- Uterine rupture: risk w overdistended uterus or previous surgery (poly, LGA, TOLAC, pit) -abrupt pain, fetal intolerance, no contractions, hematuria, head unengaged (loss of station), chest or shoulder pain (blood accumulation in peritoneum)
- Fetal injury & hypoxia: 1) Cerebral palsy: motor disorder caused by brain damage before or during birth
-Infection โ meningitis โ brain damage (TORCH, chorioamnionitis, GBS) -Vacuum or forceps assisted delivery -Poor perfusion of O2 (abruption, rupture, cord abnormality, HIE, asphyxia)
- Subgaleal hematoma: brain bleed & IICP caused by external head trauma (vacuum or forceps)
- HIE: hypoxic ischemic encephalopathy -causes: cord compression, placental insufficiency, smoking, abruption, rupture, shoulder dystocia, anemia -can cause IUGR, CP, epilepsy, cognitive impairment, organ damage
- Physiology: -Uteroplacental circulation -Fetal circulation -Fetal HR regulation -Factors affecting fetal oxygenation
- Uteroplacental circulation: (R arrow indicates blood flow) -Uterine artery โ spiral arterioles โ intervillous space โ diffusion to chorionic villi โ oxygenated blood & nutrients to umbilical vein โ fetal circulation -Opposite occurs to rid deoxygenated blood & waste from uterine artery
HTN, diabetes, infection -Anesthesia: โ BP -Drugs: cocaine & nicotine vasoconstricts, nicotine causes CO to cross placenta (โ ability of Hgb to carry O2) marijuana โ CO2 lvls -Placental factors: calcifications (post dates, smoking, clotting d/o, diabetes, HTN), previa, abruption -Umbilical blood flow: cord compression, umbilical abnormalities (single artery), prolapse
- Maternal factors affecting fetal oxygenation: 1) โ maternal O2: respiratory distress, hypoventilation, seizures, trauma, smoking
- โ maternal O2 carrying capacity: anemia, carboxihemoglobin (smoking, poison- ing, drugs)
- โ uterine blood flow: hypovolemia, hypotension, anesthesia, dorsal or lithotomy positioning
- chronic maternal conditions: vasculopathy (lupus, diabetes, HTN), antiphospho- lipid
- Uteroplacental factors affecting fetal oxygenation: 1) tachysystole
- placental abruption
- uteroplacental dysfunction
- placental infarction
- chorioamnionitis
- abnormalities (fibroids, septum)
- abnormal implantation of placenta (previa) or cord (valementous, marginal, vasa previa)
- Fetal assessment methods: -Auscultation -Fetal movement & stimulation -Non stress test (NST) -Biophysical profile (BPP) -Cord blood & acid base balance
- Auscultation: Intermittently listening to fetal heart sounds w fetoscope or doppler to assess FHR -Detects baseline, rhythm, increases & decreases from baseline -Cannot determine variability or classify decels -Use of fetoscope can verify presence of arrhythmia (most accurate) & clarifies halving or doubling
