L&D/Maternal-Fetal Monitoring/DETAILED Flashcards
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.
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.
Internal Uterine Pressure Transducer
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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).
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 .
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.
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.
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.
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.
Placental causes
Placental causes (unhealthy swimmer) Abruption Infarction Increased placental resistance
Uterine causes
Uterine causes (submerged too long) Hyperstimulation Tetanic contraction
Maternal causes
Maternal causes (smoky atmosphere) Hypotension Hypoxia
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.
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.
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