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Fetal Assessment During Labor

by: Brieanna Phipps

Fetal Assessment During Labor NSG 330

Brieanna Phipps

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These notes covered Dr. Griggs notes on fetal assessment.
Maternal Infant
Dr. Goff
Class Notes
maternal, Infant, baby, mother, Heart, rate, assessment, Labor, delivery
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This 10 page Class Notes was uploaded by Brieanna Phipps on Monday March 14, 2016. The Class Notes belongs to NSG 330 at University of North Carolina - Wilmington taught by Dr. Goff in Spring 2016. Since its upload, it has received 14 views. For similar materials see Maternal Infant in Nursing and Health Sciences at University of North Carolina - Wilmington.

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Date Created: 03/14/16
Fetal Assessment During Labor (griggs)  Advanced fetal monitoring core components o Acid Based Balance o Maternal/Fetal Factors o Best Practice: Using Evidence-Based Practice o Communication o Pitocin Management: A High Alert Medication o FHR monitoring is NOT a diagnostic tool, it is a screening tool, measures oxygenation of the baby  Purpose: o The primary objective of EFM is to provide information about fetal oxygenation and prevent fetal injury that could result from impaired fetal oxygenation during labor (Fedorka, 2010) o If you have significant deceleration FHR probs not getting enough O2  Electronic Fetal Monitoring o EFM is used as a diagnostic indicator for nursing/medical interventions o Attempts now to foster uniformity in definitions and treatments o Now we have also management components with definitions  Assumptions about EFM: o All clinically significant decelerations are a disruption of oxygen to the fetus o Fetal neurologic injury due to this disruption does not occur unless significant acidemia o Acidemia is highly unlikely in presence of moderate FHR variability and/or accelerations  Background: o Central Electronic Fetal Monitoring is most common form of assessing fetal well-being o Current Perinatal mortality rate in US of 7.9 deaths per 1,000 live births (WHO, 2014) (IMR is inc.) o TJC reported over 900 sentinel perinatal deaths and permanent infant disabilities in 2009.(The Joint Commissions, 2009) o Communication played a role in 78% of unexpected neonatal deaths. o Originally developed to decrease incidence cerebral palsy  Goals of Fetal Well-Being o Maintain appropriate uterine activity o Maximize uterine blood flow o Maximize umbilical circulation o Maximize oxygenation  NICHD (National Institute for Child Health and Human Development) o A lack of consensus was found in the definitions and nomenclature related to fetal monitoring (ACOG, AWHONN, TJC) o NICHD sponsored a research planning group to address this issue o Formed because there was not uniform communication in the hospital  NICHD Principles: o Definitions are for visual interpretation of the fetal heart rate o EFM patterns are defined as periodic and episodic o Periodic: occur with contractions o Episodic: occur without contractions o Look at the whole picture, not just one pattern. o Evaluate patterns over time** o No differentiation is made between short and long term variability.  FHT Categories: o Category o Description o Fetal heart-rate (FHR) tracings include all of the following: o baseline rate is 110–160 bpm o baseline FHR variability o I (Everything is fine) is moderate o accelerations are present or absent o late or variable decelerations are absent o early decelerations are present or absent o Includes all FHR tracings o II (everything in between 1 and 3) not included in Category I or Category III o FHR tracings include: o absent baseline FHR o III (stop, C-section) variability : o sinusoidal pattern, or other non-reassuring patterns. o Source: NICHD  Placental Physiology- o Maternal blood flows through the uterine arteries into the intervillous spaces, and then return through uterine veins to maternal circulation o Fetal blood flows through the umbilical arteries into the villous capillaries and returns through the umbilical vein to fetal circulation. o Exchange of blood gases depends on an unobstructed blood flow through the placenta.  Uteroplacental exchange- o As the myometrium contracts, the flow of oxygenated blood through the uterine artery may be decreased. o Therefore, the fetus may have less oxygen available.  Maternal response to pregnancy o Hematological  Increased volume and erythrocytes  State of hypercoagulation o Cardiovascular  “Hemodiluted” due to increased volume (High Flow/Low Resistance)  Cardiac output increase 40-50% at rest o Pulmonary  Compensated respiratory alkalosis  O2 consumption increased 25% in last 6 weeks of pregnancy o Renal  Increased renal blood flow  Maternal position affected  Glomerular Filtration Rate increased  Diurnal Pattern  Extrinsic Factors on FHR- o Maternal  Hypertension, hypotension, smoking, etc. o Uteroplacental perfusion  The function and structure of the placenta and its surface vessels, age(post maturity), tachysystole o Umbilical circulation  Two arteries, One Vein. Is circulation appropriate or altered. o Amniotic fluid characterizes o Extrinsic is “Outside” of the fetus o Affect the delivery of blood and O2 to the fetus o Hypertension can cause? Vasoconstriction and infarcts. Post-maturity o IF you have a 2 vessel chord the baby tends to be smaller  Amniotic Fluid Volume o Peaks at 40 weeks and then decreses o Fluid comes from fetal kidneys  Extrinsic influences- o A-Airway= Uterine blood flow o B- Breathing= Placental function o C- Circulation=Umbilical blood flow  Uterine Maternal/Fetal o2 exchange- o Oxygen delivery to the fetus is via the uterine arteries to the uterus. o Uterus through the placenta, and from the placenta to the fetus via the umbilical vein. o Like a tea kettle. Higher pressure gradient to a lower one. o The air we breathe is 21% O2 -> we inhale with our lungs -> o2 rich blood gets pumped by the heart and into the vasculature-> the uterus receives o2 rich blood -> fetus receives o2 rich blood via the umbilical cord -> placenta receives o2 rich blood -> happy baby o The compensatory mechanisms redistribute blood flow to the brain, heart and adrenals during fetal hypoxemia  Intrinsic Placenta Factors o Intrinsic = internal o Fetal circulation o Autonomic nervous system responses o Baroreceptors- sensitive to pressure o Chemoreceptors- sensitive to chemicals o Hormonal responses  Redistribution of blood flow o Fetal homeostatic compensatory mechanisms  Intrinsic/Extrinsic o Labor Bit-  Placental causes, such as infarction or abruption are likely to not be ameliorated by normal resuscitative measures.  Regulation of FHR o Autonomic nervous system o Baroreceptors o Chemoreceptors o Adrenal Gland o Central Nervous System  FHR and Blood Flow o Cardioregulatory Center (CRC) o Collection of neurons in the medulla oblongata and the source of FHR baseline control. o Autonomic Nervous System:  Parasympathetic branch  Vagus nerve- decrease in FHR- increased PS tone occurs with increased gestation age. This causes a decrease in FHR  Sympathetic branch (fight or flight)  Simulation causes an increase in FHR, anxiety, fear, pain, drugs o Younger the gestation the more they are ruled by sympathetic system o Need a balance between parasympathetic and sympathetic in order to have a healthy fetus  Parasympathetic/sympathetic o The autonomic nervous system fully develops by 24 to 28 weeks. o The complex interaction of the sympathetic and parasympathetic nervous systems exert their complex yin-yang effects on a second-by- second basis. o Any factor that affects the fetal brain, such as oxygenation, will alter this pathway. o Changes in fetal oxygenation will correspond and be reflected in a variation of cardiac activity. o This concept that is the basis for fetal heart monitoring  Mechanics of Monitoring o External Toco (external contraction monitor) o External FHR o IUPC (internal contraction monitor) o FSE (internal FHR monitor) o Ultrasound  Goals of Fetal Wellbeing o Maintain appropriate uterine activity o Maximize uterine blood flow o Maximize umbilical circulation  Baseline FHR o FHR rounded to increments of 5bpm during a 10 min window excluding  Acceleration and deceleration  Periodic/episodic changed in the FHR (Decelerations) o Early –  related to head compressions. Interventions not necessary, just continue to watch for any changes  Gradual decrease in FHR and return to baseline associated with fetal contractions  Onset to nadir is equal to or greater than 30 seconds.  Nadir of deceleration occurs at the same time of the peak of the contraction.  Slide 35  Physiology  Transient head compression -> altered intracranial pressure and cerebral blood flow-> reflex parasympathetic outflow (sleep or weep) -> gradual slowing of the FHR -> Early Decel -> when the contraction is over, head compression is relieved and the autonomic reflex subsides o Prolonged-  A visually apparent decrease in the FHT that drops at least 15 bpm below baseline and lasts at least 2 minutes but less than 10 minutes from their onset.  May be abrupt or gradual.  Always related to disrupted oxygenation  Causes:  Tachysystole  Maternal hypotension  Maternal hypoxia (eg. Seizure)  Abruption  Uterine Rupture  Cord compression  Prolapsed cord  Ruptured vasa previa  Profound head compression  Rapid fetal descent  Slide 39  MUST IMPROVE BLOOD FLOW TO THE PLACENTA TO INCREASE OXYGENATION  Reposition  Discontinue labor augmentation (TURN OFF PITOCIN)  Treat hypotension/hypertension  Oxygen by face mask (10L via face mask)  Consider expediting delivery  Reccurrent decels are defined as those that occur with at least 50% of contraction in 20 min period  Intermmitent = less that 50% in 20 min period  This is Episodic= not during a contraction  o Variable –  related to cord compression. Interventions vary, but focus on position changes.  Interventions = repostition or amniofusion  Visually apparent abrupt decrease in FHR  Onset to Nadir >15 beats, last > 15 seconds, and < 2 minutes in duration.  Associated with contractions  Associated with Cord Compression  Physiology  Venous compression decrease in venous return  Relative hypovolemia  Reflex increase in FHR  Arterial compression  Increased SVR  Elevated BP  vagal response (dip in HR)  When pressure is released, the FHR returns to baseline.  Slide 46 o Late –  related to uteroplacental insufficiency/ decreased perfusion. Most ominous and need immediate attention.  Physiology  Transient hypoxemia -> sympathetic outflow -> peripheral vasoconstrictions -> increase in BP -> baroreceptor stimulation -> vagal outflow -> deceleration  Gradual decrease in in FHR and return to baseline associated with fetal contractions  Onset to nadir is equal to or greater than 30 seconds.  Nadir of deceleration occurs after the peak of the contraction.  Happens late in the contraction and does not come back until the contraction is over  Slide 53  Interventions-  Increase Placental Blood Flow and Uterine Oxygenation!  Reposition  Discontinue labor augmentation (TURN OFF PITOCIN)  Treat hypotension/hypertension  Change maternal position  Consider expediting delivery  Use oxygen only as a last resort  Did you know- o A “ Gradual” FHR decrease is defined as from the onset to the FHR nadir > or equal to 30 seconds. o “Recurrent” decels are defined as those that occur with at least 50% of contractions in a 20 minute period. o Intermittent decelerations are those that occur with < 50% if contractions in a 20 minute period.  Contractions- o Normal are < or equal to 5 contractions in 10 minutes averaged over a 30 minute period o Tachysystole are > that 5 contractions in 10 minutes averaged over a 30 minute period o Terms “hyperstimulation” and “hypercontractilty” are not defined and should not be used.  Internal Monitor o With an IUPC in place, quantitative data can be measured, most commonly using Montevideo units (MVU). o Criteria for Internal Monitoring:  Amniotic membranes must be ruptured  Presenting part down against the cervix o Spiral Electrode is placed on the fetal occiput which allows for more accurate continuous data then external monitoring. (do not do for HIV positive mother )  If mom has a lot of bleeding, do not put in  Can put on breech baby but it is a last resort o Spiral electrode is attached to the fetal scalp o Wires that extend from attached spiral electrode are attached to a leg plate and then attached to electronic fetal monitor  Montevideo Units- o Montevideo units is a measure of uterine contraction intensity during labor. o Units are calculated via internal pressure monitor, measuring uterine contraction peak pressure and subtracting the baseline resting tone. This is done over a 10 minute interval. o Generally, above 200 MVUs is considered necessary for adequate labor to bring about dilation and effacement during the active phase.  Auscultation by Doppler o Intermittent auscultation can be done with a fetascope or Doppler  Baseline FHR- o Rounded to increments of 5 bpm, during 10 minute segment excluding periodic or episodic changes o If segments differ by > 25 bpm= Marked o Must be recorded for at least 2 minutes in any 10 minute segment, (not necessarily contigous) o Normal = 120-160 bpm o Tachycardia – baseline above 160 BPM  RT= maternal fever, fetal hypoxia, intrauterine infection, drugs o Bradycardia – baseline below 110 BPM  RT = profound hypoxia, anesthesia, beta-adrenergic blocking drugs  Variability o Irregular fluctuations in the baseline FHR. Measured as the amplitude of the peak to trough in bpm (beats per minute). o Refers to the fluctuation In the FHR over time o Considered the most important indicator of fetal oxygenation o Amplitude Range o Classification o Absent o Visually undetectable o Minimal o Less than or equal to 5 BPM o Moderate o 6-25 BPM o Marked o More than 25 BPM o Marked = don’t know if its good or bad, no known etiology o Slide 70 o Absence or decreased variability, or a smooth flat baseline, is a sign of fetal compromise. o A periodic decal/accel = with a contraction o Episodic = not with a contraction o 3 S’s of variability  Sleep  Sedation  ? o Causes of Decreased variability-  Hypoxia and acidosis  Medications  Sleep cycle  Preterm status  Accelerations- o Visually apparent in inc in FHR o Audible as well o Have 2 part criteria  Must exceepd a 10 or 15 sec interval  And exceed FHR in beats/min 10 to 15 above baseline  Normal cord blood gas values o o Umbilical Vein o Umbilical Artery o pH o 7.28 o 7.25 o pO2 o 29 o 18 o pCO2 o 38 o 49 o HCO3 o 20 o 22 o B.E. o -4 o -4  Remember that oxygen delivery can be disrupted at any step along the oxygen delivery pathway.***  How fetus responds to disruption in O2 o Hypoxemia (dec. O2 in the blood)-> Hypoxia ( dec. O2 in the tissues) -> Metabolic Acidosis (inc in H+; dec. in pH -> Metabolic Acidemia (inc of H+ in blood)  Link btwn poor fetal outcomes and Acid/Base o The criteria to define an acute intrapartum event sufficient enough to cause brain injury (i.e. cerebral palsy) is to prove metabolic acidosis is present in fetal umbilical cord blood at delivery. o Umbilical artery pH <7.0 and a base deficit of > 12 mmol/L  When the fetal O2 delivery pathway is interrupted o Just like grown-ups, the fetus will switch to ANAEROBIC metabolism which will result in:  Energy being used to maintain basal activity only  Lactic acid waste build up  Lactic acid is the same waste product that builds up in our muscles after “pumping iron” and makes our muscles sore!  Comparing Values o Respiratory Acidemia o Metabolic Acidemia o Mixed Acidemia o Low pH o Low pH o Low pH o High pCO2 o Normal pCO2 o High pCO2 o Normal pO2 &HCO3 o Low pO2 & HCO3 o Low pO2 & HCO3 o Normal BE o Elevated BE o Elevated BE  Oxytocin o HIGH-ALERT Medication!! (The Institute for Safe Medication Practices, 2007). o Medication errors involving IV oxytocin are often dose related and can result in adverse outcomes. o First stage of Labor  Maternal circulating concentrations approximately 2 to 4 mU/min o Fetal Contribution  Around 3 mU/min o Second stage of Labor:  Surge of oxytocin at Ferguson’s reflex (decent of the fetal head) o Initial phase of exposure to exogenous oxytocin cxt increase progressively in frequency and intensity. o After several hours of exposure further increases can result in tachysystole/unfavorable FHR responses. o Receptor sites decrease o More oxytocin for dysfunctional labor will cause further desensitization.  Oxytocin pharmacokinetics o Half-life 10-12 minutes o Three to four half-lives are needed to reach steady plasma concentrations o Basis for only increasing every 30-40 minutes.  Oxytocin Dosage- o Based on the evidence:  90% of women will achieve active labor at less than 6mU/min.  There is a lack of agreement on a definition of “adequate labor” (Clark, et al, 2009)  Minimizing harm o Follow protocols and order sets based on best practice evidence based practice. o Utilize exceptional clinical judgment when managing Oxytocin. Go slow!! No tachysystole! o Do not be afraid to turn the oxytocin down or OFF! o No studies exist which promote pushing the “Pit”, or letting patients “declare themselves”. This will cause harm!


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