NCC EFM EXAM QUESTIONS AND VERIFIED ANSWERS
Cascade of events
aerobic metabolism > hypoxemia > tissue hypoxia > anaerobic metabolism > lactic acid
buildup > metabolic acidosis
FHT regulations
parasympathetic releases Ach and decreases HR through vagal tone (controls
variability; requires mature neuro system); sympathetic releases norepi/epi and
increases HR
Baroreceptors
decrease HR, decrease CO, decrease BP
Chemoreceptors
increase PCO2, decrease PO2, decrease pH; effect is vagal response (bradycardia)
Variable decelerations mediated by
baroreceptors
Late decelerations mediated by
chemoreceptors; caused by transient hypoxemia
Abrupt rise in fetal BP can stimulate
variable decelerations
Fetal HR variability dependent on
cerebral oxygenation and intact CNS
Chemoreceptors respond to
hypoxemia
Marked variability mediated by
adrenergic activity (epinephrine)
Sustained SVT increases
fetal risk for CHF
Most consistent sign of uterine rupture during TOLAC is
recurrent decelerations or bradycardia
Autocorrelations compares
successive reflected US waveforms at many points when using doppler to determine
FHR
, Fetoscope detects
sound of opening in the heart wall
Most common fetal arrhythmia
PACs
Fetal hydrops may develop with
paroxysmal atrial tachycardia; or sustained SVT
Chronic marker for placental dysfunction in BPP
amniotic fluid volume
Negative contraction stress test
most consistent with fetal survival within 1 week
Maternal sympathetic blockage
most likely physiologic rationale for recurrent lates after epidural
Category 1 tracings
strongly predictive of normal acid/base status at the time of observation
Category 3 tracings
predictive of abnormal acid/base status at the time of observation
Prolonged decelerations caused by
tachysystole, abruption, hypotension, uterine rupture
True sinusoidal caused by
fetal anemia or severe hypoxia/acidosis
Drug induced sinusoidal caused by
fetal non-REM sleep or effects of narcotics
If acceleration noted during scalp stimulation
the pH can be assumed to be >7.19 at the time of observation
Acute intrapartum interruption in fetal oxygenation does not result in CP unless
the fetal response progresses to the stage of significant metabolic acidemia (pH <7,
base deficit 12+)
Principles of ethics
autonomy, beneficence, nonmaleficence, justice
Negligence
proper care has not been provided based on established standards
Cascade of events
aerobic metabolism > hypoxemia > tissue hypoxia > anaerobic metabolism > lactic acid
buildup > metabolic acidosis
FHT regulations
parasympathetic releases Ach and decreases HR through vagal tone (controls
variability; requires mature neuro system); sympathetic releases norepi/epi and
increases HR
Baroreceptors
decrease HR, decrease CO, decrease BP
Chemoreceptors
increase PCO2, decrease PO2, decrease pH; effect is vagal response (bradycardia)
Variable decelerations mediated by
baroreceptors
Late decelerations mediated by
chemoreceptors; caused by transient hypoxemia
Abrupt rise in fetal BP can stimulate
variable decelerations
Fetal HR variability dependent on
cerebral oxygenation and intact CNS
Chemoreceptors respond to
hypoxemia
Marked variability mediated by
adrenergic activity (epinephrine)
Sustained SVT increases
fetal risk for CHF
Most consistent sign of uterine rupture during TOLAC is
recurrent decelerations or bradycardia
Autocorrelations compares
successive reflected US waveforms at many points when using doppler to determine
FHR
, Fetoscope detects
sound of opening in the heart wall
Most common fetal arrhythmia
PACs
Fetal hydrops may develop with
paroxysmal atrial tachycardia; or sustained SVT
Chronic marker for placental dysfunction in BPP
amniotic fluid volume
Negative contraction stress test
most consistent with fetal survival within 1 week
Maternal sympathetic blockage
most likely physiologic rationale for recurrent lates after epidural
Category 1 tracings
strongly predictive of normal acid/base status at the time of observation
Category 3 tracings
predictive of abnormal acid/base status at the time of observation
Prolonged decelerations caused by
tachysystole, abruption, hypotension, uterine rupture
True sinusoidal caused by
fetal anemia or severe hypoxia/acidosis
Drug induced sinusoidal caused by
fetal non-REM sleep or effects of narcotics
If acceleration noted during scalp stimulation
the pH can be assumed to be >7.19 at the time of observation
Acute intrapartum interruption in fetal oxygenation does not result in CP unless
the fetal response progresses to the stage of significant metabolic acidemia (pH <7,
base deficit 12+)
Principles of ethics
autonomy, beneficence, nonmaleficence, justice
Negligence
proper care has not been provided based on established standards
