Electronic Fetal Monitoring Certification
What catecholamines does the sympathetic nervous system release? What can they cause? What reserve mechanism does it have, and how does this affect the FHR? And the fetus organs? How does it influence gestational age? What blocks the sympathetic nervous system thus decreasing the HR?
(S)NS (S)peeds up HR. It releases norepinephrine and epinephrine from the adrenal medulla. These hormones have a reserve mechanism to initially improve the heart's pumping ability during intermittent hypoxemia/stress. Think "fight or flight". *With intermittent hypoxemia, initial normal fetal compensatory response is increase in FHR or brief tachycardia. In response to stress, blood is shunted away from less vital organs to the brain, adrenal glands and heart. SNS dominates in early gestation, making a higher baseline and less variability. Propanolol blocks the SNS and decreases the FHR.
What is the pathway of the fetal conduction system?
1)SA node triggers the atria to fire (pacemaker of the heart). 2) AV nodes triggers the ventricles to fire
What is a category 3 strip? What baseline must it have? What must accompany this?
-ABSENT BASELINE FHR variability with recurrent lates or variables; or bradycardia *Absent variability alone is NOT a category 3 strip!!! -Sinusoidal pattern
What are fetal responses to hypoxia?
1. Fetal tachycardia to increase fetal cardiac output 2. Decreased oxygen consumption through decreased movement, tone and breathing 3. Redistrubution of fetal blood flow - increased to heart, brain and adrenal glands; decreased to kidneys, lungs, gut and liver
Types of AV blocks & Effect on FHR? How are they diagnosed? What complications can occur? Treatments? Adverse reactions of these?
1st degree is not associated with fetuses. 2nd degree- rapid atrial rates. FHR may be normal, or have missed beats & spikes 3rd degree- complete absence of conduction from the SA node through the AV node. Shows as BRADYCARDIA (40-80bpm) with minimal variability. Diagnosis is made by fetal ECG or echo. Fetal hydrops (generalized edema) can occur if not treated, this can lead to fetal death Treatment- Dexamethasone or Betamethasone. Adverse response from these drugs is oligo and fetal growth restriction. Pacemaker may be required after birth
Define supraventricular tachycardia rate. What can it lead to?
240-260 bpm. Can lead to congestive heart failure. Must be treated. Can be treated with digoxin, may need pacemaker
FHR variability can be interpreted with an external monitor using
A doppler technology called autocorrelation
What would fetal anemia show on the FHR?
SINUSOIDAL. Tachycardia, minimal variability, absence of accelerations
What is a second degree AV Block? What maternal and fetal conditions are associated with this? How do maternal collagen vascular diseases cause AV blocks?
Abnormal conduction of the electrical impulses through the areas of the atria and ventricles -Congenital heart disease: Ex. Transposition of the great vessels, Atrial septal defect, Tetralogy of Fallot) Fetal cytomegalovirus Maternal collagen vascular diseases (Lupus, Rheumatoid arthritis, Sjorgen's syndrome). These conditions have antibodies that cross the placenta and bind to fetal cardiac tissue in the AV node, atrial and ventricular myocardium. Inflammatory reaction leads to fibrosis, calcification, and interuption of fetal conduction pathway causing AV block.
What maternal heart changes could interrupt oxygen transfer to the fetus?
Altered heart rate (arrhythmias) **Reduced preload. Preload is the volume of venous blood returning to the heart. This is the most common cause In a healthy obstetric patient. Can be caused by hypovolemia, compression of the inferior vena cava by gravid uterus- lying supine- lithotomy/dorsal position. Impaired contractility (diabetes, ischemic heart disease, CHF) Increased afterload- Hypertension Regional anesthesia All signs of decreased cardiac output (HR x SV) SV is determined by preload, after load and contractility.
What are central and peripheral chemoreceptors located? What do chemoreceptors respond to?
Central: medulla oblongata. Peripheral: aortic arch and carotid sinuses When peripheral chemoreceptors respond to decreased oxygen and increased carbon dioxide, this leads to an increase in arterial blood pressure and decreased FHR Shown in Lates/Variables that result from umbilical arterial occlusion coupled with hypoxemia,
How does PO₂ change along the oxygen pathway?
At seal level, PO₂ is 150mm Hg. As oxygen is transferred from the environment to the fetus, the partial pressure declines. By the time oxygen reaches fetal umbilical venous blood, the partial pressure is as low as 30 mm Hg. After oxygen is delivered to fetal tissues, the PO₂ of the deoxygenated blood in the umbilical arteries returning to the placenta is ≅ 15-25 mm Hg.
What is a category 1 strip? What variability should it have? What baseline? Can it have decelerations?
Baseline 110-160 Moderate variability ABSENT Lates/Variables Early's or Accelerations may be present OR absent
Interventions for bradycardia and tachycardia
Brady- Check maternal pulse to differentiate FHR. Vag exam to rule out cord prolapse or to determine if the baby head is deep in the pelvis ready to be delivered intrauterine recitation ultrasound to detect arrhythmia if none of the above work tachycardia maternal temp, infections, how long has ROM? consider impact of medications. ultrasound for arrhythmia if none of the above work
How would a fetal heart block and fetal cardiac failure present on the FHR?
Bradycardia. Minimal variability
What drug can cause a transient sinusoidal FHR?
Butorphanol (Stadol)
What is the difference between cardiac output in the adult vs fetus? What would decrease fetal cardiac output?
In the adult, CO increases or decreases in response to changes in HR or stroke volume. Fetal CO is dependent ONLY on HR. *Fetal tachycardia greater than 240 bpm or bradycardia less than bpm, decreases CO and umbilical blood flow.
Considerations for Procardia
Can cause maternal hypotension - can lead to hypoperfusion of the uterus and placenta
How does diabetes effect the fetus?
Can lead to reduced uteroplacental perfusion, and can be associated with reduced fetal growth. Also fetal hyperglycemia and hyperinsulinemia increase fetal oxygen consumption, which may induce fetal hypoxemia and acidosis if the oxygen needs of the fetus are not met.
What are third-degree blocks caused by?
Cardiac structural defects- transposition of the great arteries; fetal cytomegalovirus, antiphospholipid antibody syndrome or the presence of anti-SSA/Ro or anti-SSB/La antibodies (present with Lupus). Maternal rheumatoid arthritis Congenital heart disease is also present usually (ASD, mitral/tricuspid valves etc)
What is the patho of a late decel? If there is moderate variability with a late deceleration, what can you infer? What do lates look like on the FHR tracing?
Caused by impaired uteroplacental blood flow which causes decreased oxygen to the fetus. Late decelerations occur when a fall in the level of oxygen in the fetal blood triggers chemoreceptors in the fetus to cause reflex constriction of blood vessels in nonvital peripheral areas in order to divert more blood flow to vital organs such as the adrenal glands, heart, and brain. -Constriction of peripheral blood vessels causes FETAL HYPERTENSION that stimulates a BARORECEPTOR mediated VAGAL response which slows the heart rate. The time consumed in this two step process accounts for the delay in the timing of the deceleration relative to the contraction. Lates with moderate variability may be a sign of some kind of stress- tachysystole, maternal hypotension after epidural. Resolution of cause should resolve the latest.
How can changes to the placenta affect the fetus size?
Chronic decreased placental function may limit carbohydrates transfer and can lead to fetal growth restriction, asphyxia and malnourishment
What is the patho of a early deceleration? What does it look like on a FHR tracing?
Head compression ↓ Altered intracranial pressure and/or cerebral blood flow ↓ Reflex parasympathetic outflow (vagal response) ↓ gradual slowing of the FHR *When head compression is relieved, autonomic reflexes subside *Gradual onset >30 sec from onset to nadir (lowest point) occurs with the peak of contraction. Returns to baseline by end of contraction.
What is the patho of a variable?
Compression of the umbilical cord occludes the umbilical vein ↓ Slows blood flow to baby. Reduces fetal cardiac output and blood pressure ↓ Hypotension and drop in cardiac output results in brief rise in FHR ↓ At peak of contraction, umbilical artery compression from fetus leads to fetal hypertension ↓ Fetal hypertension triggers baroreceptors. FHR slows (parasympathetic response), vagal stimulation causes abrupt drop in FHR When contraction eases, arteries open and fetal blood pressure falls and heart rate increases
What can SVT lead to in the fetus? What is the treatment?
Congestive Heart Failure; Tx: Digoxin, Amiodorone,
Important aspects of charting? "CLEAR"
Contemporaneous- charted near the time of occurrence, use of appropriate late entries. Logical- easily understood and clear Explicit- avoid vague or ambiguous terms; use standardized terminology Accurate- Correct times, sequence of events Readable- legible(paper charting)
4 Elements of malpractice claim
Duty- the patient is owed a specific duty or standard of care Breach of duty- there was a failure to meet the required standard of care Proximate cause- a direct causal relationship exists between the breach of duty and the harm or injury of the patient Harm or injury- actual harm or injury occured to the woman, fetus, or neonate as a result of the breach of duty
Define SVT. What can it lead to. What drug can treat it?
FHR over 180. Can lead to fetal congestive heart failure. Must be treated. Can treat with digoxin.
Umbilical Artery Doppler Velocimetry-
Good for pregnancies complicated by fetal growth restriction. Middle cerebral artery = increased diastolic flow= reduced fetal oxygenation (hypoxemia); Increased systolic = fetal anemia
Which of the following fetal dysrhythmias may be related to maternal hyperthyroidism?
PAC
What conditions could cause maternal vasoconstriction?
Hypertension/Pre-E (Affects placental perfusion- can lead to IUGR and infarcts
What are the 3 key pathways in fetal circulation?
Key shunts: Ductus venosis, foramen ovale, ductus arteirosis 1) Blood from the umbilical vein bypasses the liver through the ductus venosis to the inferior vena cava. 2) Pressure is greater in right atrium than left atrium, so most of the blood is shunted through the foramen ovale 3) Blood bypasses pulmonary arteries and goes directly into the aorta through the ductus arterosis (keeps blood from entering lungs and damaging capillaries) *Fetal blood carries more oxygen than maternal blood and has a higher concentration of oxygen
How does uterine blood flow change during pregnancy?
Increases from 50 mL/min to 700mL/min. Requires 10-15% of cardiac output.
Considerations for Indomethacin?
Indomethacin (cyclooxygenase)- Amniotic fluid volume and fetal renal anatomy should be assessed before giving d/t the fetal risk of constriction of the ductus arteriosus and decreased renal function resulting in oligohydramnios; decreased fetal urine - variables Do not give over 32 weeks; do not give over 48 hours.
What is A-Fibb associated with?
fetomaternal hemorrhage, Wolff-Parkinson-White syndrome Digoxin
What is the physiology of the parasympathetic nervous system (Where does it originate, what does it release, which cranial nerve is under this) What is the effect on the FHR? How does gestational age influence this? How does this influence variability? What blocks the parasympathetic system, thus increasing the FHR?
It originates in the Medulla Oblongota. It releases acetylcholine, a neurotransmitter that slows the HR. It hold the vagus nerve, this is the 10th cranial nerve that innervates the SA and AV nodes. Vagus nerve is not mature until 28 weeks gestation. In early gestation, FHR control is dominated by the sympathetic system which increases FHR. With increasing gestational age, there will be a decrease in FHR and increase in FHR variability. Parasympathetic keeps the body at a calm state, promotes relaxation. (decreases the FHR) FHR variability represents an intact CNS pathway through cerebral cortex, midbrain, vagus nerve and normal cardiac conduction system. Moderate variability indicates absence of metabolic academia. Atropine blocks, and will increase HR.
After an epidural, what FHR deceleration is possible and why?
Late decelerations can be caused by maternal hypotension. Hypotension is a risk from an epidural
What effect could excessive uterine activity have on the FHR?
Lates/Prolonged (Uterus isn't getting break- oxygen can't get across pathway) Minimal variability Bradycardia
Where are baroreceptors located? What do they detect? Which FHR pattern is this associated with?
Located in carotid sinus and aortic arch. When fetal arterial BP increases, baroreceptors quickly detect amount of stretch, sending impulses via vagus nerve to midbrain. Further vagal stimulation causes an ABRUPT decrease in FHR, CO, and BP, thereby protecting the fetus. This is associated with variables.
Which of the following can cause a blunted response to vibroacoustic stimulators? a. hydramnios b. magnesium sulfate c. multiple gestation
Magnesium Sulfate Inhibits accelerations as gestational age advances
What maternal condition would cause a FHR baseline that is tachycardia? What substances?
Maternal hyperthyroidism Caffeine, theophylline (for asthma), nicotine, cocaine, meth
What maternal conditions would cause a FHR baseline that is bradycardia? (2) What fetal condition?
Maternal hypoglycemia Maternal hypothermia Fetal viral infection (cytomegalovirus)
Maternal vs fetal side of placenta?
Maternal side: oxygenated blood exits the spiral arteries and enters the intervillous space to surround and bathe the chorionic villi Fetal side: paired umbilical arteries carry blood from the fetus through the umbilical cord to the placenta *In blood gases, vein shows the function of the placenta; artery shows the fetal metabolic condition
Negative contraction stress test
Negative: 3 contractions in a 10 minute window with no late decels. Repeat in one week Positive: Rates with 50% or more of the contractions Equivocal-suspicious- intermittent late decals or variables Unsatisfactory- fewer than 3 contractions in 10 minutes or an uninterpretable tracing.
What can Zidovudine do the FHR?
No change. This is a drug for HIV
Would you give oxygen if there is moderate variability?
No. If there is moderate variability present. Moderate variability is NOT an indicator of fetal hypoxemia or academia; therefore, maternal oxygen administration is generally not necessary or appropriate if the FHR has moderate variability. Give O2 w/ minimal/absent variability or recurrent late decelerations that have not resolved with the initial intrauterine resuscitative measures
Describe Fetal Response to Interrupted Oxygen Transfer: Hypoxemia → hypoxia → metaboxlic acidosis → metabolic acidemia → hypotension
Normal homeostasis requires an adequate supply of oxygen and fuel to generate the energy required by basic cellular activities. When oxygen is readily available, aerobic metabolism generates energy in the form of ATP. When oxygen is in short supply, tissues may be forced to convert from aerobic metabolism to anaerobic metabolism (producing lactic acid). Accumulation of lactic acid in the tissues results in metabolic acidosis. Lactic acid accumulation can lead to utilization of buffer bases to help stabilize tissue pH. If the buffering capacity is exceeded, the blood pH may begin to fall, leading to metabolic acidemia. Eventually, recurrent or sustained tissue hypoxia and acidosis can lead to loss of peripheral vascular resistance, and hypotension- leading to injury of brain and heart.
Explain process: Hypoxemia → hypoxia → metabolic acidosis → metabolic acidemia → hypotension
Normal homeostasis requires an adequate supply of oxygen and fuel to generate the energy required by basic cellular activities. When oxygen is readily available, aerobic metabolism generates energy in the form of ATP. When oxygen is in short supply, tissues may be forced to convert from aerobic metabolism to anaerobic metabolism (producing lactic acid). Accumulation of lactic acid in the tissues results in metabolic acidosis. Lactic acid accumulation can lead to utilization of buffer bases to help stabilize tissue pH. If the buffering capacity is exceeded, the blood pH may begin to fall, leading to metabolic acidemia. Eventually, recurrent or sustained tissue hypoxia and acidosis can lead to loss of peripheral vascular resistance, and hypotension- leading to injury of brain and heart.
What is a reactive NST? What do you do if you do not have a reactive NST?
Normal/Reactive- 2 accelerations in a 20 minute period, each lasting 15 seconds and peaking at least 15 bpm above baseline *If you do not see this in 20 minutes, extend another 20 minutes. Nst considered non-reactive if after 40 minutes of continuous monitoring, the FHR tracing does not demonstrate at least 2 qualifying accelerations within any 20 minute window.
What can cause a parasympathetic response? What can cause a sympathetic response?
PNS: head compression, vaginal exams, repeated scalp stimulation, forceps, vacuum. Atropine can block PNS and increase FHR SNS: vibroacoustic stimulation, initial scalp stimulation, epinephrine, anxiety/fear/pain Propanolol can block SNS and drop FHR
Why is having a good placental reserve important?
Placental reserve is the oxygen in the placenta during a contraction when no other blood flow is entering the placenta. It continues oxygenating the fetus until the contraction ends. Anything that reduces the size of the placenta or the functioning of the placenta decreases reserve available to the fetus. Starts at 100%. Dropping to 75% can make diffusion of carbohydrates harder
Quiet vs Active sleep? What body movements will you see? What will it look like on the FHR tracing? How does it effect NST? How does gestation effect?
Quiet sleep (Sleep cycle) Occasional brief body movements. FHR stable with narrow oscillation bandwidth. (Minimal variability, absent accelerations. Will respond to external stimuli like vibroacoustic stimulation). Non-reactive NST. Active (REM) sleep( Awake) - Frequent gross body movements. Rapid darting eye movements (REM). FHR with wider oscillation bandwidth and frequent accelerations with movements. (Moderate variability, accelerations. Reactive NST. At term gestation, duration of periods of active sleep are longer than quiet sleep.
What other conditions that cause vasoconstriction could effect oxygenation to the fetus?
Renal disease, thyroid disease, rheumatoid arthritis, lupus)
How does the renin-angiotensin system affect the FHR? How do prostaglandins effect the FHR?
Renin-angiotensin system maintain systemic arterial BP and umbilical placental flow. Prostaglandins maintain patency of fetus ductus arteriosus (shunt that allows blood to bypass pulmonary arteries and go directly into the aorta. Keeps blood from entering lungs and damaging capillaries)
Respiratory Acidosis values? Metabolic Acidosis values?
Respiratory: pH LESS than 7.1; pCO2 >60. Note: Respiratory acidosis is more easily reversible and potentially less detrimental to the fetus when compared to metabolic acidosis. metabolic: pH less than 7.1; BD > -12 or <12. More difficult to reverse.
What is signal ambiguity?
Signal ambiguity or signal coincidence - circumstance where fhr transitions to the mhr and is recorded on the tracing . This often happens when a patient is pushing- maternal HR looks like an acceleration for FHR. Will not see Accels when pushing. Other causes: multiple gestation, obesity, patient positioning in epidural placement, active fetal movement
Which dysrhythmia may progress to atrial fibrillation or atrial flutter?
Supraventricular tachycardia (SVT)
Types of tachystsyole?
Tachysystole: Contraction frequency greater than 5 in 10 minutes, averaged over 30 minutes Hypertonus- uterine resting tone exceeds 20-25 mmHg with an IUPC or does not return to soft by palpation during relaxation time Inadequate relaxation time- Less than 60 seconds for first stage of labor; less than 45 in second stage Excess contraction duration (tetanic contractions)- single contractions lasting 2 minutes or more
What drugs increase the FHR? What maternal conditions would increase the FHR? What type of variability would accompany this?
Terbutaline Maternal fever, chorioamnionitis, intraamniotic infection Minimal variability associated with this.
What happens to the PAо₂ at the level of the lungs? Would could interrupt oxygen transfer at the level of the lungs?
The air mom breathes in, goes to the alveoli. On the way to the alveoli, inspired air mixes with less oxygenated air leaving the lungs. As a result, the PAо₂ is lower than that in inspired air. At sea level PAо₂ is ≅ 105 mm Hg. Causes of interrupted oxygen transfer: (ex.seizure, asthma and other respiratory issues, meds- narcotics, mag)
How do you determine the baseline?
There must be at least 2 minutes of identifiable baseline segments (does not have to be continuous) in any 10 minute window, or the baseline is indeterminate for that period. If this is the case, then refer to the previous 10 minute window for the baseline. This 2 minutes excludes: accelerations, decelerations and marked variability. If it is marked a majority of the strip, the baseline is indeterminate.
What can cause a sinusoidal FHR pattern?
Think blood Fetal anemia, Rh sensitization, maternal/fetal hemorrhage Severe fetal hypoxia/acidosis/asphxia Fetal thumb sucking
what are the 3 leading sources of artifacts?
Three leading sources of artifact: signal error, device limitations, incorrect interpretation by clinician Signal- improper transducer placement of maternal fetal signal interference (uterine contractions, or fetal movement) which leads to a weak or undetectable FHR. Signal error- May appear as gaps or noncontinuous marks on the tracing. Device limitations- originate from an audible FHR bradycardia/tachycardia resulting in a tracing that appears to be doubled or halved. Ultrasound transducer may double-count a slow FHR of less than 60 bpm, or it may half-count an elevated FHR of more than 180 bpm resulting in a normal FHR during tachycardia Half/Double rate- Assess FHR with fetoscope, doppler etc. Rule out MHR by checking radial pulse. Reapply ultrasound gel. Move the transducer to search for a better signal. Consider FSE. Incorrect interpretation- fetal arrhythmias, recording of the mhr, or the wrong speed paper (should be 3cm/min) Do not use logic mode with internal monitoring
How can contractions interrupt oxygen transfer to the fetus?
Uterine blood flow is supplied through the maternal uterine arteries (spiral, radial, arcuate). These arteries extend perpendicularly through the myometrium and endometrium, so contraction of uterine muscles compresses these arteries. Compression of the uterine arteries with contractions may adversely affect oxygenation of the fetus. Blood flow to the placenta is dependent on adequate uterine blood flow.
What FHR patterns would show while a mom is pushing?
Variables, prolonged, increased baseline rate. *Uncommon to see accelerations when pushing; if it looks like an acceleration, it may be maternal.
How does deoxygenated blood return to the placenta from the fetus?
Via the umbilical arteries originating from the internal iliac near the bladder.
If giving oxygen, what should be turned off?
When oxygen is chosen for intrauterine resuscitation, there is the assumption that other sources of potential fetal physiologic stress have been minimized; therefore oxytocin should NEVER be infusing concurrently with oxygen administration
How does amniotic fluid volume relate to the placenta function?
When there is decreased placental perfusion and increasing hypoxia, fetal blood is shunted away from non-vital organs to maintain perfusion to brain, heart and adrenals. This means decreased renal perfusion. This causes decreased urine production and decreased output, leading to decreased amniotic fluid. ****Amniotic fluid volume is an indirect indicator of placental function. May present as oligo
Bigeminal vs Trigeminal PVC's Pacs?
With Trigeminal premature ventricular contractions (PVCs), the upward spikes will be slightly longer than the downward spikes. With bigeminal premature ventricular contractions (PVCs), the baseline and variability are obscured. PAC: Upward stroke represents the PAC and the downward stroke represents the compensatory pause. Baseline FHR will be seen intermittently between these upward and downward strokes.
When would a higher resting tone be noted with an IUPC?
multiple gestation, uterine malformation, oxytocin, amnioinfusion, extraovular placement
What drugs can decrease FHR variability? (6)
narcotics, cocaine, magnesium sulfate, betamethasone (but NOT dexamethasone), general anesthesia
How does AFI effect the FHR?
oligohydraminos or less than normal level of amniotic fluid, can put less fluid around the cord; showing variables on the FHR
