NCC Electronic Fetal Monitoring Certification
Question and Answer | Verified Answers |
Complete Review Pack
• 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 -✓✓solid>fluid 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?
• Signal ambiguity -✓✓confusing maternal and fetal heart rate; common with
repositioning, fetal movement, during pushing (maternal tachycardia); can occur even
with fetal demise due to FSE recording maternal blood flow through the placenta
• Suspect signal ambiguity -✓✓when there is lower baseline or >50% contractions with
accelerations (especially with pushing); verify and document maternal heart rate via
pulse oximetry
,• Halving/doubling -✓✓Halving occurs if FHR >180-200; may double if rate <50
• Extrinsic factors -✓✓maternal oxygenation, uterine blood flow, placenta exchange,
umbilical blood flow; intrinsic factors = fetal circulation, oxygenation of tissues, FHR
regulation
• Primary source of oxygen for the feus -✓✓the maternal respiratory system
• Uterine blood flow -✓✓60ml/min non-pregnant vs. 500-1000ml/min; 10-15% maternal
cardiac output
• Normal blood flow pathway -✓✓Blood from maternal vein > intervillous pool of
maternal blood > umbilical vein (oxygenated blood)
• Normal placenta -✓✓Placenta has 15-20 lobules on maternal surface; Decreased
surface area of chorionic villi from abnormal development, infection, thrombosis,
hemorrhage, inflammation (chorio increases risk of CP), degenerative changes with
increasing gestational age (calcifications)/HTN/DM - can cause IUGR, hypoxia, FHR
decels
• Acute drop in placental function -✓✓fetal asphyxia
• Chronic drop in placental function -✓✓FGR
• O2 and CO2 -✓✓simple transport (diffusion); electrolytes, fat soluble vitamins,
narcotics, anesthetic gasses, antibiotics
• Glucose -✓✓facilitated transport, by carrier molecules
• Active -✓✓amino acids, calcium, iron, water soluble vitamins (uses ATP)
• Umbilical blood flow -✓✓2 arteries (deoxygenated) and 1 vein (oxygenation)
• Fetal circulation -✓✓when compromised, fetal blood redistributed to heart, brain,
adrenals; shunting and FHR increase compensate for decreased blood flow and
hypoxemia; limit mixing of oxygenated and deoxygenated blood
• Fetal hemoglobin -✓✓AND increased O2 affinity > adult; fetus has increased cardiac
output and heart rate
• Ductus venosus -✓✓(highest oxygenation) > ductus arteriosus (least oxygenation);
, • Abrupt decrease in PO2 leads to -✓✓2-3x increase to heart, brain, adrenals; decrease
to gut, spleen, kidneys, limbs
• Severe acidemia -✓✓decrease CO2, BP, and decreased blood flow to brain and heart
> tissue damage, fetal death
• Oxygenation depletion cascade -✓✓aerobic metabolism > hypoxemia > tissue hypoxia
> anaerobic metabolism > lactic acid > metabolic acidosis
• FHR regulation -✓✓Parasympathetic slows, sympathetic speeds FHR
• Sympathetic -✓✓nerve fibers in myocardium, norepi/epi, increases BP and shunting to
brain, heart, adrenals
• Marked variability mediated by -✓✓adrenergic activity (epinephrine)
• Parasympathetic -✓✓vagus nerve, acetylcholine; PS tone increases as gestational
age increases and decreases FHR baseline and increases FHR variability, requires
mature nervous system (why FHR baseline decreases by 10 bpm from 30 to 40 weeks)
• Variability -✓✓intact pathway from brain > vagus nerve > fetal cardiac system
• Moderate FHR variability -✓✓predicts absent metabolic acidemia at the moment it is
observed; indicates that fetus is adequately oxygenated at that time
• Baroreceptors and chemoreceptors -✓✓located in aortic arch and carotid sinus; both
involve parasympathetic and sympathetic systems
• Baroreceptors -✓✓variable decelerations. Abrupt fetal BP increase > baroreceptors
fire > cardioinhibitory center > vagal response > decrease HR, decrease CO; When BP
drops, sympathetic stimulations and FHR increases
• Chemoreceptors -✓✓late decelerations (and bad variables) response to hypoxemia;
lower blood flow > increased PCO2 > chemoreceptors slow FHR. Initial FHR response
to fall in pH may be rising baseline (baby overcompensates). Central chemoreceptors in
medulla oblongata and peripheral in the aortic arch and carotid sinus
• Late deceleration -✓✓transient hypoxemia is the physiologic cause; during hypoxemia,
fetus may convert to anaerobic metabolism
• Variable deceleration -✓✓can be stimulated by abrupt rise in fetal BP
• Fetal behavioral states -✓✓sleep cycles ~40 minutes; quiet sleep (minimal variability,
rare accels); active sleep (frequent movements, minimal-mod variability, frequent
Question and Answer | Verified Answers |
Complete Review Pack
• 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 -✓✓solid>fluid 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?
• Signal ambiguity -✓✓confusing maternal and fetal heart rate; common with
repositioning, fetal movement, during pushing (maternal tachycardia); can occur even
with fetal demise due to FSE recording maternal blood flow through the placenta
• Suspect signal ambiguity -✓✓when there is lower baseline or >50% contractions with
accelerations (especially with pushing); verify and document maternal heart rate via
pulse oximetry
,• Halving/doubling -✓✓Halving occurs if FHR >180-200; may double if rate <50
• Extrinsic factors -✓✓maternal oxygenation, uterine blood flow, placenta exchange,
umbilical blood flow; intrinsic factors = fetal circulation, oxygenation of tissues, FHR
regulation
• Primary source of oxygen for the feus -✓✓the maternal respiratory system
• Uterine blood flow -✓✓60ml/min non-pregnant vs. 500-1000ml/min; 10-15% maternal
cardiac output
• Normal blood flow pathway -✓✓Blood from maternal vein > intervillous pool of
maternal blood > umbilical vein (oxygenated blood)
• Normal placenta -✓✓Placenta has 15-20 lobules on maternal surface; Decreased
surface area of chorionic villi from abnormal development, infection, thrombosis,
hemorrhage, inflammation (chorio increases risk of CP), degenerative changes with
increasing gestational age (calcifications)/HTN/DM - can cause IUGR, hypoxia, FHR
decels
• Acute drop in placental function -✓✓fetal asphyxia
• Chronic drop in placental function -✓✓FGR
• O2 and CO2 -✓✓simple transport (diffusion); electrolytes, fat soluble vitamins,
narcotics, anesthetic gasses, antibiotics
• Glucose -✓✓facilitated transport, by carrier molecules
• Active -✓✓amino acids, calcium, iron, water soluble vitamins (uses ATP)
• Umbilical blood flow -✓✓2 arteries (deoxygenated) and 1 vein (oxygenation)
• Fetal circulation -✓✓when compromised, fetal blood redistributed to heart, brain,
adrenals; shunting and FHR increase compensate for decreased blood flow and
hypoxemia; limit mixing of oxygenated and deoxygenated blood
• Fetal hemoglobin -✓✓AND increased O2 affinity > adult; fetus has increased cardiac
output and heart rate
• Ductus venosus -✓✓(highest oxygenation) > ductus arteriosus (least oxygenation);
, • Abrupt decrease in PO2 leads to -✓✓2-3x increase to heart, brain, adrenals; decrease
to gut, spleen, kidneys, limbs
• Severe acidemia -✓✓decrease CO2, BP, and decreased blood flow to brain and heart
> tissue damage, fetal death
• Oxygenation depletion cascade -✓✓aerobic metabolism > hypoxemia > tissue hypoxia
> anaerobic metabolism > lactic acid > metabolic acidosis
• FHR regulation -✓✓Parasympathetic slows, sympathetic speeds FHR
• Sympathetic -✓✓nerve fibers in myocardium, norepi/epi, increases BP and shunting to
brain, heart, adrenals
• Marked variability mediated by -✓✓adrenergic activity (epinephrine)
• Parasympathetic -✓✓vagus nerve, acetylcholine; PS tone increases as gestational
age increases and decreases FHR baseline and increases FHR variability, requires
mature nervous system (why FHR baseline decreases by 10 bpm from 30 to 40 weeks)
• Variability -✓✓intact pathway from brain > vagus nerve > fetal cardiac system
• Moderate FHR variability -✓✓predicts absent metabolic acidemia at the moment it is
observed; indicates that fetus is adequately oxygenated at that time
• Baroreceptors and chemoreceptors -✓✓located in aortic arch and carotid sinus; both
involve parasympathetic and sympathetic systems
• Baroreceptors -✓✓variable decelerations. Abrupt fetal BP increase > baroreceptors
fire > cardioinhibitory center > vagal response > decrease HR, decrease CO; When BP
drops, sympathetic stimulations and FHR increases
• Chemoreceptors -✓✓late decelerations (and bad variables) response to hypoxemia;
lower blood flow > increased PCO2 > chemoreceptors slow FHR. Initial FHR response
to fall in pH may be rising baseline (baby overcompensates). Central chemoreceptors in
medulla oblongata and peripheral in the aortic arch and carotid sinus
• Late deceleration -✓✓transient hypoxemia is the physiologic cause; during hypoxemia,
fetus may convert to anaerobic metabolism
• Variable deceleration -✓✓can be stimulated by abrupt rise in fetal BP
• Fetal behavioral states -✓✓sleep cycles ~40 minutes; quiet sleep (minimal variability,
rare accels); active sleep (frequent movements, minimal-mod variability, frequent
