NCC EFM Exam Practice Questions and Answers, Latest Update 2024/2025 (GRADED)

What are some important factors (risks) to consider when evaluating a fetal heart rate strip? - --*PNLs* (abnormal?) --weight gain/loss --Maternal age --*Gestational age* --*MATERNAL vital signs* --*Membrane status* --*Cervical exam* What are the easiest ways for assessment of maternal oxygenation status? - *Pulse Ox* (& other vital signs, RR) *Blood gas* (if indicated, asthma exacerbation) *Lung soungs* (pneumonia, pulmonary edema?) What effect can *HTN/Preeclampsia* have on the Placenta? - *VASOCONSTRICTION* which adversely effects placental perfusion and can lead to: --*IUGR* --*Infarcts* (decreases functional area of the placenta & functional capacity) Placental Infarcts - - Necrosis of placental villi - Anechoic or Hypoechoic areas in placenta Placental infarcts will do what to the placental function? - *DECREASE functional area* of placenta *DECREASE functional capacity* What effect can *Diabetes* have on Placental perfusion? - Secondary to *Maternal Vasculopathy* & HYPERglycemia* this can lead to: *reduced utero-placental perfusion* = *IUGR* What can change for fetal energy demands when you have a "DIABETIC mother" uncontrolled and there is *Fetal HYPERglycemia & HYPERinsulinemia*? - Fetal hyperglycemia & hyperinsulinemia can cause: *Increased fetal O2 consumption* which may induce *fetal hypoxemia & acidosis* if the O2 needs of the fetus are not met by the placenta. What are some common conditions which could lead to a *POOR maternal Oxygenation status*? - Respiratory DEPRESSION (*Meds or Seizure*) *Pulmonary EMBOLISM* *Pneumonia* *Asthma* *Atelectasis* NCC EFM Practice Questions and Answers Latest Update 2024/2025 (GRADED) ARDS *Smoking* *ANEMIA* What are some examples of *collagen-vascular diseases*? HOw does these effect pregnancy? - *Rheumatoid arthritis* *Scleroderma* *SLE* (lupus) = maternal *vasocontriction* which can lead to interruptions in placental & uterine blood flow --'IUGR' What fetal cardiac condition may you see in a mother with *SLE* (systemic lupus erythematosis)? - *Secondary Heart BLOCK* *Renal disease* (CKD, etc.) could cause what? - *Maternal VASOCONSTRICTION* = maternal *vasocontriction* which can lead to interruptions in placental & uterine blood flow --'IUGR' *Thyroid Disease* could cause what? - *Maternal VASOCONSTRICTION* = maternal *vasocontriction* which can lead to interruptions in placental & uterine blood flow --'IUGR' What is the concern with *cardiac disease* in expectant mothers? - Cardiac disease -- -- impaired cardiac function or even cardiac failure --- *Decrease cardiac output* ---- decreased blood flow/oxygen flow through placenta IUGR, etc. What are some common causes of *Maternal HYPOTENSION*? - *Supine hypotension* of pregnancy *VASODILATION* 2/2 epidural This will *DECREASE O2 & blood flow through the placenta*. What are the *Maternal* 'EXTRINSIC factors' which effect delivery of bloos & availability of blood/O2 through placenta? - 1. *Maternal Oxygen status* --fetus relies on the ability of mother to be well-oxygenated Anything that interferes with maternal oxygenation has the potential to compromise the fetus. 2. *Maternal HEMOGLOBIN levels* O2 is released from the maternal Hgb & attaches to fetal Hgb (*O2 carrying capacity*) 3. *Cardiac OUTPUT* -- decreased CO affects blood flow to the uterus & placenta. In terms of Maternal Oxygen Status, in order for there to be *adequate arterial oxygen tension (PaO2)* -- there needs to be what? - PaO2 = immediately available O2 for exchange Needs adequate *maternal ventilation & pulmonary function* What are the *'Placental factors'* which can effect the efficiency of *Uteroplacental perfusion*? - 1. '*UTERINE Blood flow* 2. Damaged chorionic vessels* (leaking into the intervillouos space) 3. *Decrease in SIZE or functioning area* of the *Placenta* 4. *Placental Reserve* There can be Acute vs. Chronic decreases in uteroplacental function. Describe *Uterine BLOOD flow* changes during pregnancy. --rate, % of CO, % to placenta vs. uterus - UTERINE BLOOD FLOW: -Nonpregnancy rate is usually 50ml/min, during *pregnancy = 700ml/min*!! -*10-15%* of total *cardiac output* *70-90%* of this blood flow goes to *PLACENTA/intervillous space* = intervillous space perfusion is dependent on adequate uterine blood flow. Compare Acute vs. Chronic changes in uteroplacental perfusion/function. - *ACUTE*: sudden drop in placental function limits O2 & CO2 exchange which can lead to *fetal asphyxia* *CHRONIC*: if there is a chronic decrease in placental function this may be more likely to limit *carbohydrate transfer* & can lead to fetal growth restriction. Due to high rate of uterin blood flow in pregnancy - what level of decrease can be tolerated prior to severe effects on fetal status? - Uterine blood flow can *decrease by 50%* befoer SEVERE acidosis develops. What are some common causes of *damage to the chorionic vessels* which causes leakage of blood into the intervillous space (fetal-maternal hemorrhage)? - Damaged chorionic vessels: *abdominal trauma* *'spontaneous' placental abruption* (or secondary to cocaine, HTN disorders, etc) *Invasive procedures* (amniocentesis, CVS) *Ruptured vasa previa* What are four main ways that the *size or functional area* of the *placenta* can be compromised? - 1. *ABRUPTION*: decreases the functional AREA of placenta (spontaneous, trauma, procedures) 2. *MATERNAL DISEASE* (HTN) -disease processes can cause smaller placenta -smaller placenta decreases gas exchange results in FGR, asphyxia & malnourishment. 3. *INFECTION* 4. *CONGENITAL DEFECTS* What is the *placental reserve*? - *OXYGEN in the placenta DURING a CONTRACTION* when there is *NO other blood flow entering the placenta* This is the O2 reserve that continues oxygenating the fetus until the contraction ends!!! ----Anything that reduced the size of the placent or the functioning of the placenta decreases the reserve available to the fetus. What are common risk factors for decreased placental perfusion/function? - *EXCESSIVE UTERINE ACTIVITY*: *Tachysystole, hypertonus* or leading to Placental abruption. ABRUPTION *Maternal HYPOTENSION*; when supine or with epidural *Maternal HYPERTENSION* *Placental changes* --decreased durface area (abruption) --edema (erythroblastosis fetalis) --degenerative changes (HTN, diabetes, post due, IUGR) --Calcifications (smoking, tobacco use) --Infarcts (post due) --Infection (Chorio) *Vasocontriction* exogenous mostly sympathomimetics (EXCEPT EPHEDRINE) Why do we give *EPHEDRINE* to expectant mothers who experience *Hypotension* after placement of *Epidural? - HYPOTENSION can lead to decreased placental perfusion (fetal asphyxia/acidosis) *Ephedrine* will cause vasoconstriction to increase blood pressure without further compromise the placental perfusion. erythroblastosis fetalis is what? What can this do to the placenta? - hemolytic disease in the newborn (HDN) caused by a blood group (Rh factor) incompatibility between the mother and the fetus -remember this can cause *EDEMA in the placenta* (thereby compromising plcental perfusion/function) *post-due dates*: will cause what kinds of changes to the placenta? - 'DEGENERATIVE Lesions' *Calcifications* *Infarcts* Additionally post-dates is associated with: *Decreased Amniotic fluid* (Oligohydramnios) By what mechanism of transport do gases transfer in the placenta? What else uses this mechanism? - *SIMPLE DIFFUSION*: --transport achieved by movement of O2/CO2 from areas of *high concentration to areas of low concentration* *NARCOTICS* also use this mechanism of transport. How are *NARCOTICS* transported across the placenta? - *SIMPLE DIFFUSION*: --transport achieved by movement of from areas of *high concentration to areas of low concentration* Just like O2/CO2 across the placenta. How is *glucose* (carbohydrates) transported across the placenta? - *FACILITATED Diffusion* What uses *facilitated diffusion* to cross the placenta? - *GLUCOSE* Describe *umbilical circulation* (umbilical cord). - 3 VESSELS: *One VEIN*: carries *oxygenated blood*!!! to the fetus from placenta (mother) *Two ARTERIES*: carry *DE-oxygenated blood* from the fetus back to the placenta What are the ways by which the *umbilical circulation* through the umbilical cord can be interrupted? - --*Mechanical interruption*: i.e. BABY lays on cord, obstructs or grasps cord --*Vasospasm* --*thrombosis* --*"True knot"* in cord --*Hypertrophy*? --Hemorrhage --Inflammation What are cotyledons? - How many cotyledons or lobules are on the placenta surface? - *15-20* --A Cotyledon is perfused with MATERNAL blood from the spiral arteries (which grow from myometrium into endometrium). Each cotyledon/lobule consists of? - Branches from a *SINGLE, large mainstem Villus* *Amniotic fluid* levels affect . . . . . - *CORD FUNCTION* Fluid acts as a cushion & protects the vessels in the umbilical cord to allow FREE FLOW of blood. What is *Amniotic fluid* composed of? - clear water, proteins, carbs, lipids, electrolytes, fetal cells, lanugo, vernix caseosa *FETAL URINE & lung secretions* When there is DECREASED placental perfusion & increasing hypoxia within the fetus there will be SHUNTING of the fetal blood away from the fetal extremities & non-vital organs . . . . . . . perfusion of blood will be prioritized to what organs? - *BRAIN* *HEART* *ADRENALS* If fetus is hypoxic and shunting blood to the brain, heart and adrenal -- there will be what? - *DECREASED RENAL perfusion* which will cause: --- decreased urine production --- decreased output --- *Decreased Amniotic Fluid* (Amniotic fluid is an indirect indicator of placental perfusion) *Oligohydramnios* can be an indicator of what? - --- *FETAL HYPOXEMIA* Shunting of oxygenated blood flow away from the extremities, kidneys and liver leading to reduced urine output and decreased amniotic fluid levels. Remember it can also be from ruptured membranes which has not been identified yet. Describe fetal circulation starting within the placenta. - Oxygenated blood from the placenta enters the *umbilical vein* and then travels to the fetus. *Bypasses liver* by the *DUCTUS VENOSIS* & combines with deoxygenated blood within the inferior vena cava. Blood joins deoxygenated blood from the superior vena cava & empties into the *right atrium*. Right Atrium pressure Left Atrium pressure *Most blood shunted through foramen ovale*, to the left atrium, left ventricle then Aorta. The blood that goes to right ventricle and pulmonary arteries is shunted through the Ductus arteriosis to the aorta. (this prevents blood from entering the lumgs & damaging capillaries). Deoxygenated blood returns to the placenta via the *UMBILCAL arteries* which originatedd form the *internal iliac arteries* near the bladder. Where do the umbilical arteries originate from? - internal iliac artery (near the bladder) fetal circulation - oxygenated, nutrient-rich blood from placenta carried to fetus via umbilical vein → half enters Ductus venosus (allows blood to bypass the liver) →carried to inferior vena cava → RA → RV → Ductus arteriosus (conducts some blood from the pulmonary artery to the aorta [bypassing the lungs/fetal pulmonary circulation]) → aorta. Other half enters liver/portal vein → RA → Foramen ovale (allows blood to bypass pulmonary circulation by entering the left atria directly from the right atria since there is no gas exchange in fetal lung) → LA → LV → aorta. Illustrated here. Compare concentration of hemoglobin in fetal blood vs. maternal blood. - Fetal blood has *50% HIGHER concentration of Hgb* allowing fetal blood to carry *20-30% more oxygen* than maternal blood. In addition, fetus has a HIGHER cardiac output & HR which results in rapid ciculation. Fetal conduction system - SA Node --- Atrial preferential pathways --- AV Node --- Bifurcation of the Left & Right Bundle Branches --- Peripheral Purkinje networks --- Ventricular myocardium What is the pacemaker of the heart? - *SA node* Where does the *Vagus n.* start? - VAGUS n. starts in the *medulla oblongata* of the brain & terminates in the SA & AV nodes. Where is the *cardioregulatory center* which controls FHR control (baseline, variability & other characteristics)? - *MEDULLA OBLONGATA* --integrates input from the ANS SA node triggers the atria to fire and AV node triggers the ventricles. Stimulation of the *vagus fibers* in the SA and AV nodes will cause what? - *DECREASE* in the *FHR* --per parasympathetics Parasympathetic tone INCREASES with gestational age which causes a *natural decrease in baseline* FHR & *increase in variability*. What is true of *parasympathetic tone* in relation to gestational age? - Parasympathetic tone INCREASES with gestational age which causes a *natural decrease in baseline* FHR & *increase in variability*. A 26 wk baby will likely have what differences on EFM in comparison to near term baby? - --likely will have a *HIGHER baseline* (by at least 10 bpm) --May NOT have moderate variability --Accels are 10x10 A *parasympathetic response* can be achieved with what maneuvers during labor course? - *head compression* *vaginal exams* (SVEs) *repeated scalp stimulation* *forceps* *vacuum applications* some centrally-acting medications Which medication can BLOCK the vagus n. and cause an *INCREASE in fetal heart rate*? - *ATROPINE* Parasympathetics to the heart? - Vagus Sympathetics to the heart? - T1-5 of heart Superior Cervical Ganglia C2-3 Middle Cervical Ganglia C6 (may be absent) Inferior Cervical Ganglia C7, First Rib Stimulatioin of the Sympathetics on the fetal heart will cause what change? - *INCREASE in FHR* due to the release of *epinephrine & norepinephrine*. Improves cardiac output (think flight or fight) Sympathetic stimulation to the fetus can be achieved by what maneuvers? - *LOUD noises* (vibro-acoustic stimulation) *Maternal abdominal stimulation* *Initial scalp stimulation* *epinephrine* anxiety/fear/pain *atropine* What part of ANS is responsible for *fetal acceleration* on FHTs? - *SYMPATHETIC nervous system* What is a medication which blocks sympathetic stimulation to the fetal hear and can cause drops in the HR? - *PROPANOLOL* (beta-blocker) *Variability* of fetal heart rate is largely controlled by what part of ANS? - *Parasympathetic nervous system* Presence of variability demonstrates and intact pathway through: *Cerebral cortex -- Midbrain -- Vagus n.* -- Fetal conduction system What reliably predicts the absence of *metabolic acidemia* in a fetus? - *MODERATE variability* -if this is seen, it indicated that fetus is adequately oxygenated at that moment in time. Baroreceptors aare sensitive to pressure where? - Sensitive to pressure changes in the *aorta & carotid vessels*. --'think barometric pressure drop' What will happen with baroreceptors when *blood pressure INCREASES*? - Baroreceptors FIRE & then send signals to the cardioregulator center which results in *firing of the Vagus n.* & PNS. This will lead to *decrease in HR* Vagal stimulation causes drop in FHR that is ALMOST INSTANTANEOUS -- this is why you see an *abrupt drop in a Variable* What causes the abrupt drop in HR with a *Variable Deceleration*? - BP increase, baroreceptors FIRE & then send signals to the cardioregulator center which results in *firing of the Vagus n.* & PNS. This will lead to *decrease in HR* Vagal stimulation causes drop in FHR that is ALMOST INSTANTANEOUS -- this is why you see an *abrupt drop in a Variable* What will happen with baroreceptors when *blood pressure DECREASES*? - *SNS* is stimulated & *FHR increases* What is responsible for the *variable decelerations* seen on EFM? - Activity of *baroreceptors* and stimulation of PNS with BP increases as welll as SNS with blood pressure decreases. What is responsible for *LATE decelerations* seen on EFM? - *CHEMORECEPTORS* WHich are primarily stimulated by an increase in CO2 & decreased O2. "Lates" are ALL about oxygenation. (BOTH peripheral & Central chemoreceptors) What is released form fetal adrenal glands to aid in oxygenation? - CATECHOLAMINES - these are release to increase blood flow patterns & to oxygenate the fetal brain & myocardium. What are the peripheral vs. Central chemoreceptors in the fetus? - 1. *Peripheral*: located in aortic bodies & carotid bodies 2. *Central*: Located in *medulla oblongata* & respond to changes in O2 & CO2 levels. Explain the presentation of a late in comparison to a contraction. - LATES are delayed following timing of the contraction because *detection of hypoxemia* by *chemoreceptors takes time* If you see late decelerations in the presence of *moderate variability* . . . . what are some potential causes? - --*Neurogenic* --*FETAL response to 'transient uteroplacental insufficiency'* -- i.e.. hypotension after an epidural THis will respond well to intrauterin resuscitation (IVF, position changes, vasoconstrictors) What may be the initial FHR response to a a decrease in pH? - *INCREASE in baseline rate* What neurostransmitter is involved in the *Parasympathetic response* which is responsible for slowing the firing & transmission of electrical impulses in the heart. - *Acetylcholine* What is the hormonal response which can be initiated by *Sympathetic Stimulation? - Release of CATECHOLAMINES: *Epinephrine* *Norepinephrine* For the *increase in FHR & contractility* (also, increases BP which results in shunting of blood to brain, heart & adrenal glands) What is the likely flow of *FETAL response to STRESSORS: - *Hypoxemia* (decreased umbilical blood flow) -- *Chemoreceptor/baroreceptor* stimulation -- *Catecholamine production* (from ADRENAL glands) -- *Decreased blood flow to periphery* (GI & renal) -- INCREASED blood flow to vital organs (brain, heart and adrenals)