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Fetal Heart Rate Monitoring and Umbilical Cord Blood Analysis, Exams of Nursing

Rasmussen College - WisconsinNursing

An in-depth overview of fetal heart rate monitoring and umbilical cord blood analysis. It covers the normal ranges for arterial and venous umbilical cord blood values, the various types of fetal heart rate decelerations (late, variable, and prolonged), the risk factors associated with each type, and the fhr features indicative of normal and developing fetal acidosis. The document also discusses the use of fetal scalp electrodes, fhr tachycardia, and the management of late and variable decelerations. Additionally, it covers the definition and management of tachysystole, the use of amnioinfusion, and the characteristics of a sinusoidal fhr pattern. The information presented in this document is highly relevant for healthcare professionals involved in fetal monitoring and management during labor and delivery.

Typology: Exams

2024/2025

Available from 10/24/2024

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Relias - Fetal Heart Monitoring -with 100%
verified solutions 2024/2025
uterine blood supply
-
uterine arteries deliver oxygenated blood to spiral arteries which bring oxygen rich
blood to intervillous space of placenta that has fetal capillaries
-
fetal capillaries carry the O2 rich blood to umbilical VEIN that goes to fetus
-in contrast, the umbilical ARTERIES return waste products to that intervillous space
that go into mother's venous system
Potential issues that negatively affect fetal oxygenation
Maternal Oxygenation: asthma, hyper- or hypo- ventilation
Maternal Circulation: decreased maternal cardiac output, hypotension, decreased
Hgb
Placental O2 and CO2 Exchange: postterm, abruption, HTN, hypotension, uterine
tachysystole
Fetal circulation: cord compression or occlusion
Fetal hypoxemia
-
can occur d/t reduced fetal O2 reserves, excessive uterine activity, or reduced
uteroplacental blood flow
-
worsening fetal hypoxemia can lead to abnormal FHR patterns, mostly minimal or
absent variability from acidemia
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Download Fetal Heart Rate Monitoring and Umbilical Cord Blood Analysis and more Exams Nursing in PDF only on Docsity!

Relias - Fetal Heart Monitoring - with 100%

verified solutions 2024/

uterine blood supply

  • uterine arteries deliver oxygenated blood to spiral arteries which bring oxygen rich blood to intervillous space of placenta that has fetal capillaries
  • fetal capillaries carry the O2 rich blood to umbilical VEIN that goes to fetus
  • in contrast, the umbilical ARTERIES return waste products to that intervillous space that go into mother's venous system Potential issues that negatively affect fetal oxygenation Maternal Oxygenation: asthma, hyper- or hypo- ventilation Maternal Circulation: decreased maternal cardiac output, hypotension, decreased Hgb Placental O2 and CO2 Exchange: postterm, abruption, HTN, hypotension, uterine tachysystole Fetal circulation: cord compression or occlusion Fetal hypoxemia
  • can occur d/t reduced fetal O2 reserves, excessive uterine activity, or reduced uteroplacental blood flow
  • worsening fetal hypoxemia can lead to abnormal FHR patterns, mostly minimal or absent variability from acidemia

(1) hypoxemia vs. (2) hypoxia 1 - reduce O2 in blood 2 - reduced O2 delivery at tissue level Fetal anaerobic metabolism

  • occurs when long term O2 delivery is insufficient to meet cellular needs of tissues
  • results in production of lactic acid and other noncarbonic acids
  • ACIDOSIS is the presence of excessive acids in tissues acidosis pH below 7. pH is low (acidosis is the process that leads to low blood pH, or acidemia) alkalosis pH above 7. pH is high buffers
  • help maintain acid base homeostasis
  • 2 major fetal buffers are plasma bicarbonate and hgb base excess and base deficit
  • base deficit is expressed as a positive number
  • base excess is expressed as a negative number ~ they are equivalent and terms are used interchangeably ~

mixed acidosis pH < 7.10 , high pCO2 > 60, and high base deficit >

  • may develop when resp acidosis persists for a prolonged period of time
  • outcome for neonates is dependent on degree and severity, but typically the lower pH and higher base deficit means worse neonatal outcomes
  • most often seen in prolonged bradycardia at time of birth what is used to evaluate fetal acidosis? arterial umbilical cord blood artery values (fetus to placenta) Normal ranges: pH 7.20-7. pCO2 35 - 70 Base excess - 3 to - 9 venous values (placenta to fetus) Normal ranges:

pH 7. pCO2 33 - 50 base excess - 1 to - 8 factors for neonatal encephalopathy or cerebral palsy Data shows that intrapartum hypoxia-ischemia is rarely sole significant contributing factor for this Other contributing factors include:

  • infection
  • prolonged intermittent hypoxia assoc w/subcortical and cortical or preventricular damage
  • acute total or near total hypoxia is assoc w/damage to midbrain and brainstem low pH in newborns
  • no absolute fetal arterial pH threshold assoc w/harm in all newborns
  • typically if pH is < 7.10 that is used to determine acidosis and if the pH is < 7 then that is associated w/ low apgars, early neonatal seizues, and neonatal deaths prolonged intermittent hypoxia is assoc w/ subcortical and cortical (term) or perventricular (preterm) damage

Maternal factors for late decels Inhalation: asthma, sleep apnea Circulation: hypotension, HTN, hypovolemia, anemia, microvascular disease, tachycardia Risk factors for variable decels Uteroplacental:

  • oligo
  • ruptured membranes
  • abnormal cord insertion Fetal factors:
  • umbilical cord prolapse or compression
  • cord stretching w/ pushing or rapid descent
  • preterm Maternal factors:
  • positioning risk factors for prolonged decels Uteroplacental:
  • excessive activity
  • uterine rupture
  • abnormal placentation
  • hypertonic/prolonged contractions
  • hypoperfusion Fetal factors:
  • OP position
  • vagal stimulation d/t head compression and or rapid descent
  • cord compression
  • hypoxia
  • acute fetal hemorrhage Maternal:
  • hypotension; acute hypoxia maternal factors for prolonged decels
  • supine position
  • hypotension
  • resp or cardiac arrest
  • seizures FHR features of normal fetal acid base status presence of moderate variability and FHR accelerations are both strong indicators of absence of fetal acidemia moderate FHR variability
  • amplitude 6 to 25 bpm
  • with evolution of fetal acidemia, fetal nervous system depression impact the control of the fetal heart, manifested by a reduction (minimal) FHR varaibility and loss of accels
  • if FHR transitions from moderate to minimal in presence of recurrent variable, late, or prolonged decels then hypoxia and evolving acidemia should be assumed hypoxic causes for minimal variability
  • placental abruption
  • excessive uterine activity
  • fetal hypoxemia ^ less common and usually require immediate resolution or intervention nonhypoxic causes of minimal variability
  • extreme preterm ( < 28 wks)
  • fetal sleep cycle
  • fetal tachycardia
  • fetal anomalies (esp CNS) or previous neurologic insult
  • meds ^causes are more common and less acute, immediate resolution is not always required Fetal scalp electrode requires
  • adequate cervical dilation
  • rupture membranes
  • presentation of appropriate fetal part (head) risks of FSE
  • infection: maternal and fetal
  • increased risk for fetal hemorrhage or injury FSE is contraindicated in these circumstances
  • fetal presentation of face, fontanelles, genitalia
  • presence of maternal blood borne infection (HIV, hep)
  • placental previa
  • undx vaginal bleeding FHR tachycardia definition
  • bsl range >160 bpm
  • variability often decreased or absent
  • characteristic that falls into cat 2 pattern regardless of variability or accels causes for tachycardia maternal fever intraamniotic infection dehydration meds (ex. terb)
  • may also be seen in early labor when fetus is in breech overview of late decels
  • gradual onset to nadir (> 30 s) and shallow depth of decel
  • onset, nadir, and recovery are delayed r/t time of contraction
  • often assoc w/ fetal hypxoemia
  • cat 2 strip causes of late decels
  • uterine tachysystole
  • maternal hypotension
  • placental abruption
  • severe maternal anemia variable decels
  • abrupt (< 30 s from onsent to nadir).
  • depth usually greater than early or late decel
  • 15 bpm or greater decel from bsl, lasts at least 15 sec but less than 2 min
  • if recurrent then cat 2 tracing

causes of variable decels

  • cord compression may be d/t

oligo (in early labor or after ROM) during descent of presenting part d/t stretching of nuchal or short cord cord prolapse unusual issue like knot, short cord, tangle, occult prolapse prolonged decel

  • decrease of at least 15 bpm for more than 2 mins but less than 10 mins
  • considered cat 2 tracing bc interruption of o2 to baby causes of prolonged decels
  • profound placental insuff
  • umbilical cord compression, prolapse, or occlusion
  • tachysystole
  • rapid fetal descent
  • placental abruption
  • uterine rupture

minimal variability

  • may be assoc w/fetal hypoxia although other more benign factors may be responsible such as sleep cyce or meds (terb, mag, parenteral narcotics) absent variability
  • if there are recurrent or late decels w/absent variability that equals cat 3 strip
  • if absent variability without recurrent variable or late decels that is a cat 2 tracing but does require prompt eval and surveillance management of late fhr decels
  • maternal repositioning
  • IV fluid bolus
  • O
  • tocolysis (in situations where decels persist, accels are absent, minimal or absent variability then immediate delivery should be considered) management of variable fhr decels
  • maternal repositioning
  • amnioinfusion

tachysystole more than 5 contractions in 10 minutes amnioinfusion requirements

  • ROM
  • IUPC Can reduce incidence of variable decels but doesnt help with late decels or bsl variability sinusoidal pattern for cat 3 strip
  • causative agent can be anemia that may be caused by viral disease such as cytomegalovirus and parvovirus (fifth disease), abruption, or isoimmunization IUPC indications
  • labor dystocia
  • inability to evaluate contractions d/t maternal obesity or movement
  • need to facilitate oxytocin titration when external toco is unclear
  • need to clarify relationship between decels and contractions capabilities of iupc
  • able to assess adequacy of contractions by calculating MVUs
  • can be used for amnioinfusion