L&D/Maternal-Fetal Monitoring/DETAILED Flashcards Preview

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Flashcards in L&D/Maternal-Fetal Monitoring/DETAILED Deck (39):
1

Tocodyamometer

Tocodynamometer The second component of a fetal monitor is the tocodynamometer. This device measures the relative strength, rate, and duration of uterine contractions. It is basically a ring-style pressure transducer attached to the maternal abdomen via a belt that maintains tight continuous contact with the abdomen. The transducer contains a plunger that is depressed when the uterus changes its rigidity and shape with each contraction. This depression changes the voltage of the current associated with the plunger and isproportional to the strength of the contraction. While the transducer can monitor the activity of the uterus (frequency and relative strength of contraction), it cannot determine the absolute intrauterine pressure. The sensitivity of the transducer is affected by factors such as maternal obesity and premature gestational age and therefore the duration of the contraction may vary depending on that sensitivity. Its advantages are that it is non-invasive and can be used when membranes are intact. An internal uterine pressure transducer is also available if more accurate measurements of uterine activityare desired. This consists of a catheter with a built-in strain gauge that is inserted trans-cervically after membranes are ruptured. It is easier to use and requires less nursing attention.

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When to use Internal Monitor?

The goal of monitoring is to maintain adequate, accurate, and continuous fetal cardiac heart rate and uterine activity while ensuring maternal comfort. While external devices are less invasive, they may not be as accurate. When more accurate assessment of fetal heart rate and contraction pattern is desired, internal monitoring may be indicated.

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Internal Uterine Pressure Transducer

XXX

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Disruption of Fetal Oxygenation

Disruption of Fetal Oxygenation Fetal oxygenation is therefore dependent upon maternal blood pressure and oxygenation, the integrity of the placenta, specifically the amount of surface area for oxygen transfer, and the patency of the umbilical cord. Anything that disturbs this chain of oxygen transfer will consequently affect fetal oxygenation. This disturbance in transfer of oxygen from maternal blood to the fetus is called uteroplacental insufficiency (UPI).

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Uteroplacental insufficiency

Uteroplacental insufficiency really describes a problem with oxygen transfer in one or more of three compartments, the placenta, the uterus, and the mother’s perfusion of the uterus, leading to fetal hypoxemia. Using the swimming pool analogy, if the swimmer has poor cardiopulmonary reserve (e.g. lung disease), he may not be able to tolerate continued submersions for very long because his ability to take in and transfer oxygen would be affected. In the same way, if the placenta is abnormal (e.g. infarcted, too small, or abrupted), the fetus may begin to suffer from hypoxemia secondary to poor oxygen transfer during uterine relaxation .

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Hyperstimulation Uterine Tetany

If the swimmer is submerged too often underwater or for too long, then he may not have sufficient time to recover between submersions. Similarly, if uterine contractions are occurring too frequently (hyperstimulation) or are lasting too long (uterine tetany), then the placenta may not have time to absorb oxygen from maternal blood between contractions.

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Underperfusion of placenta

Lastly, if the atmosphere surrounding the swimming pool is smoky or has decreased oxygen tension, then even if the swimmer is healthy and has adequate time to recover, he may not be able to absorb oxygen when he is out of the water. In the same way, if the mother is hypotensive, hypoxic, or for any other reason underperfusing the placenta, then the baby will suffer in spite of the fact that the placenta may be healthy and the contractions are within normal limits.

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Reversible

The swimmer's analogy holds true when thinking about the potential reversible causes of uteroplacental insufficiency. Many of the causes that are uterine or maternal in origin can be easily reversed, such as uterine hyperstimulation or maternal hypotension, just like it would be easy to have the swimmer stay under water for a shorter duration of time or have him breathe cleaner air when not submerged. But placental causes, such as infarction or abruption are likely to not be ameliorated by normal resuscitative measures.

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Irrersible

The swimmer's analogy holds true when thinking about the potential reversible causes of uteroplacental insufficiency. Many of the causes that are uterine or maternal in origin can be easily reversed, such as uterine hyperstimulation or maternal hypotension, just like it would be easy to have the swimmer stay under water for a shorter duration of time or have him breathe cleaner air when not submerged. But placental causes, such as infarction or abruption are likely to not be ameliorated by normal resuscitative measures.

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Placental causes

Placental causes (unhealthy swimmer) Abruption Infarction Increased placental resistance

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Uterine causes

Uterine causes (submerged too long) Hyperstimulation Tetanic contraction

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Maternal causes

Maternal causes (smoky atmosphere) Hypotension Hypoxia

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Umbilical cord

Another cause of decreased fetal oxygenation is decreased umbilical cord patency (cord compression). In the analogy above (although not anatomically analogous), imagine the swimmer having to breathe through a snorkel each time he comes out of the water. If the lumen of the snorkel were compressed, the swimmer would have difficulty recovering when he is out of the water. Similarly, any event that causes umbilical cord compression will decrease oxygen delivery to the fetus.

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Fetal Brain-Oxygenation-Heart Varietability

Sympathetic simulation results in norepinephrine release contributing to increases in both chronotropy, inotropy, and systemic vascular resistance. Parasympathetic stimulation influences fetal heart rate (FHR) by decreasing rate and by providing an oscillating effect that contributes to variability. The components of this cardiac regulatory system make up a pathway from the fetal cerebral cortex through the cardiac integratory center in the medulla oblongata, the vagus nerve, and the cardiac conduction system. The complex interaction between the factors above result in the variation of the fetal rate. This pathway is dependent upon the physiologic status of the fetal brain. Any factor that affects the fetal brain, such as oxygenation, will alter this pathway. Therefore, changes in fetal oxygenation will correspondingly be reflected in a variation of cardiac activity. It is this concept that is the basis for fetal heart monitoring. By evaluating the patterns of cardiac activity, fetal oxygenation status and physiologic integrity may be inferred.

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Accurate FHR assessment may help in determining the status of the fetus and indicate management steps for a particular condition. In order to accurately assess a FHR pattern, a description of the pattern should include qualitative and quantitative information in the following five areas:

Baseline rate Baseline FHR variability Presence of Accelerations Periodic or episodic decelerations Changes or trends of FHR patterns over time

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Uterine Contractions can provide what info?

terine contraction patterns can provide information about the progress of labor. Also, because uterine contractions can affect placental exchange, evaluation of contraction patterns may provide clues as to the potential effects of the contraction rate and force on the fetus.

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Fetal Heart Rate Monitoring Basics

1)  Redlines

2) Maternal

3)  Fetal

4) one little red square equals?

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Baseline

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Baseline Variability 
 

-Fluctuations in the FHR of 2 cycles per min or greater

-Variability is visually quantitated as the amplitude of peak-to-trough in beats per min
  -Absent: amplitude range undetectable
  -Minimal: amplitude range detectable but 5 beats per min or fewer
  -Moderate (normal): amplitude range 6-25 beats per min
  -Marked: amplitude range greater than 25 beats per min

 

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3 Nursing Intervenstions if fetus hypoxia is suspected via fetus bradycardia, late decelerations

1)  Change matera position

2)  Hydrate

3)  O2 for mother

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Causes of decreased variability  (6)

Causes of decreased variability include:

Hypoxemia/acidosis

Fetal sleep cycles

Drugs (Analgesics, barbiturates, tranquilizers, phenothiazines, para-sympatholytics, anesthetics)

Prematurity

Arrhythmias

Fetal tachycardia

Preexisting neurological abnormality

Congenital anomalies

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Miminal Variability

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In the term fetus, moderate variability is considered normal as it indicates a normally functioning central nervous system.  Conditions that alter the integrity of this neuro-cardiac axis, such as hypoxemia, result in loss of heart rate variability. Variability therefore, is the single most important indicator of an adequately oxygenated fetus.  Below are examples of moderate variability.

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Decreased or absent variability therefore represents some dysfunction in one or both of these systems, or in increased and dominant tone of one system over the other, such as during sleep cycles or due to the effects of drugs.

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Marked variability in the baseline FHR is present when the amplitude exceeds 25 BPM.This pattern (sometimes called a saltatory pattern) suggests acute hypoxia or mechanical compression of the umbilical cord and is often seen during the second stage of labor. When coupled with decelerations, this pattern is considered non reassuring and should warn the physician to search for, and correct, potential causes of hypoxia. Causes of marked (increased or saltatory) variability include:

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Acceleration

A visually apparent increase (onset to peak in less than 30 sec) in the FHR from the most recently calculated baseline
- The duration of an acceleration is defined as the time from the initial change in FHR from the baseline to the return of the FHR to the baseline
- At 32 weeks of gestation and beyond, an acceleration has an acme of 15 beats per min or more above baseline, with a duration of 15 sec or more but less than 2 min
- Before 32 weeks of gestation, an acceleration has an acme of 10 beats per min or more above baseline, with a duration of 10 sec or more but less than 2 min
- Prolonged acceleration lasts 2 min or more, but less than 10 min
- If an acceleration lasts 10 min or longer, it is a baseline change
 

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1)  What two monitor changes are closely associated with both are reflective of a well-oxygenated fetus. 

FHR accelerations and good (moderate) variability are closely associated and sometimes may be visually indistinguishable, though both are reflective of a well-oxygenated fetus. 

The presence of accelerations forms the basis of the nonstress test (NST). An NST is said to be reactive when there are at least two accelerations in a 20 minute period, along with moderate variability and no decelerations.

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Bradycardia

Baseline FHR is?

Fetal bradycardia is commonly associated with?

Causes?

Bradycardia 
 

Baseline FHR less than 110 beats per min

(NICHD)

Fetal bradycardia is commonly associated with fetal hypoxemia. However, a number of causes must be considered:

Hypoxemia 
Drugs 
Maternal hypotension 
Hypothermia 
Maternal hypoglycemia 
Fetal bradyarrhythmias 
Complete heart block (Maternal SLE, CMV infection) 
Congential heart block 
Umbilical cord compression 
Amniotic fluid embolism 
Normal variation

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Bradycardia

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1)  Early Decelerations . If the pattern is found in early labor, it may be associated with cephalopelvic disproportion

2)  Early decelerations have not been associated

 with cephalopelvic disproportion​

with fetal hypoxemia or acidosis.

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Late Deceleration:  What is it?

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The classically described cause of late decelerations is uteroplacental insufficiency (UPI). In UPI, there may be a problem with a uterine perfusion or uterine activity or there may be a problem with the placenta, or both. 
  
    Uterine hyperactivity is associated with decreased time for intervillous space blood flow between uterine contractions. Similarly, maternal hypotension, even in the presence of normal uterine activity, will result in decreased volume of the intervillous space blood flow. Either of these factors may lead to a decrease in the maternal-fetal oxygen transfer.
  
    Placental dysfunction, too, may lead to a decreased maternal-fetal oxygen transfer, and/or a smaller volume of placental reserve in proportion to fetal need.

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  1. UPI is?
  2. Causes?

 

 

The causes of UPI are varied, and many are reversible:

Uterine hyperactivity
Maternal hypotension
Maternal hypertensive disorders 
Placental abruption 
Placenta previa 
IUGR 
Maternal DM 
Chorioamnionitis 
Postterm gestation 
Maternal anemia, SS anemia, etc. 
Rh isoimmunization 
Maternal cardiac disease 
Maternal sm

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  1. The classic mechanism described as the cause of variable decelerations ?
  2. Variable decelerations are classified as severe when they last more than ___, fall below___ or drop ____ below baseline rate

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  1.  is umbilical cord compression
  2. Variable decelerations are classified as severe when they last more than 60 seconds, fall below 70 beats/min, or have a drop of 60 beats/min below the baseline rate.

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Nursing Interventions

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Types of Uterine Contraction Patterns

   Tachysystole (or polysystole) is defined as 6 or more UCs in 10 minutes without evidence of fetal distress.

   Hypertonus is either an abnormally high uterine resting tone (>25 mmHG) or MVUs > 400.

   Hyperstimulation is either:

     1. persistent tachystole classically with evidence of fetal distress (late decelerations, lost variability)but now accepted as even without distress (the same as tachysystole), or

     2. a single UC lasting > 2 minutes may also be called a tetanic contraction, or

     3. UCs occurring within one minute of each other.  The most common cause of a tachysystolic, polysystolic or hypertonic contraction  pattern is  oxytocin or prostaglandins.

Types of Uterine Contraction Patterns

   Tachysystole (or polysystole) is defined as 6 or more UCs in 10 minutes without evidence of fetal distress.

   Hypertonus is either an abnormally high uterine resting tone (>25 mmHG) or MVUs > 400.

   Hyperstimulation is either:

     1. persistent tachystole classically with evidence of fetal distress (late decelerations, lost variability)but now accepted as even without distress (the same as tachysystole), or

     2. a single UC lasting > 2 minutes may also be called a tetanic contraction, or

     3. UCs occurring within one minute of each other.  The most common cause of a tachysystolic, polysystolic or hypertonic contraction  pattern is  oxytocin or prostaglandins.

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