For medical professionals only
Have you noticed all this?
As obstetricians and gynecologists, we often deal with electronic fetal heart rate monitoring at work, and sometimes seemingly simple problems are not so simple.
Let's start with a case study:
Case studies
●Admission diagnosis: G2P0 41 weeks pregnant to give birth
●Past history: No related medical history
●Gestational period: Spontaneous membrane rupture and hospitalization at 41 weeks of pregnancy - check the uterine opening 1 cm larger, amniotic fluid clear
●Labor:
21: 40 palace expansion 3cm
Epidural anesthesia starts at 22:00
23:00 Cervical orifice dilates by 6 cm
At 23:15, occasional mutation deceleration was observed
23:17 Extended deceleration
●Deceleration of the previous variant: There may be compression of the umbilical cord, resulting in fetal hypoxia.
●Treatment:
1. Examine the opening of the cervix and exclude umbilical cord prolapse and notify the doctor
2. Change the maternal position
3. The mask absorbs oxygen
4. Increase the amount of intravenous fluids
5. If the fetal heartbeat is restored, consider continuing vaginal delivery
Correct interpretation of fetal heart rate monitoring patterns and standardized management can effectively reduce the occurrence of neonatal convulsions and cerebral palsy, reduce perinatal mortality during childbirth, predict neonatal acidosis, and reduce unnecessary vaginal midwifery and caesarean sections and other obstetric interventions.
The importance of fetal heart rate monitoring
1. It can objectively judge the safety of the fetus in the womb and guide the clinician to take effective measures in a timely manner.
2. In today's increasingly intensifying doctor-patient conflict, it is necessary to provide more auxiliary evidence for the correctness of the treatment, and the fetal heart monitoring chart is one of the most important and common bases in obstetrics.
Predict fetal intrauterine reserve capacity
Non-stress test (NST): refers to the observation and recording of fetal heart rate uterine titration of the fetus without contractions and external stress stimulation to understand the fetal reserve capacity, which is performed at more than 34 weeks.
Diagnostic criteria for NST
1. Reactive type
Fetal heart rate baseline 110 to 160 bpm;
At least 3 or more fetal movements accompanied by an acceleration of fetal heart rate within 20 minutes;
The acceleration of fetal heart rate during fetal movement ≥ 15 bpm, and the duration ≥ 15 seconds;
Long-term variation amplitude of fetal heart rate baseline 6 to 25 bpm, cycle 3 to 6 bpm;
Except for the encounter with type-o-dip (type-o-dip) accompanied by fetal movement, the usual spontaneous contractions do not appear deceleration;
Fetal awakening cycle (20 to 40 minutes), if there is no fetal movement and acceleration during the monitoring time, and fetal movement and acceleration occur by external stimulation or other methods to wake up the fetus for 20 minutes, it can still be diagnosed as a reactive type.
2. Non-reactive type
There is no fetal heart rate acceleration during 20 to 40 minutes of monitoring or fetal movement, and there is still no significant acceleration of fetal heart rate after stimulation;
with long-term variation in fetal heart rate baseline weakening or disappearing, amplitude less than 5 bpm, cycle less than 3 bpm;
The fetal awakening cycle is not obvious;
The effects of sedative and antihypertensive drugs must be excluded. In general, fetal movements are rarely absent for 60 minutes outside of sedative and antihypertensive drugs.
3. Suspicious type
Any of the following should be classified as NST suspect:
Fetal movements with only 1 or more fetal heart rate accelerations within 20 minutes;
The fetal heart rate acceleration is < 15 bpm for < 15 seconds;
Weakening of baseline variability;
abnormal baseline levels of fetal heart rate (> 160 bpm or < 110 bpm);
There is a spontaneous variation deceleration.
Fetal heart rate baseline
Fetal heart rate baselines describe fetal heart rates controlled by the autonomic nervous system. The activity of the sympathetic nerves accelerates the heart rate, while the parasympathetic nerve is mainly the activity of the vagus nerve that slows the heart rate. Under normal circumstances, vagus nerve activity is the mainstay, maintaining a heart rate of 110 to 160 bpm.
The fetal heart rate baseline is also controlled by the aortic arch receptors:
1. Chemoreceptors
It is stimulated by the concentration of oxygen. A sharp drop in oxygen concentration increases parasympathetic activity and slows down the heart rate. The prolonged decrease in oxygen concentration increases sympathetic activity and increases heart rate.
2. Pressure receptors
It is stimulated by aortic pressure. Increased blood pressure increases parasympathetic activity and slows heart rate. A drop in blood pressure increases sympathetic activity and increases heart rate.
Fetal tachycardia
Definition of fetal tachycardia: Fetal tachycardia is defined as a basal fetal heart rate lasting greater than 160 bpm.
▌ Cause analysis
1. Fetal movement or fetal stimulation is too much
If there is too much fetal activity when the fetal ECG is recorded, the measured fetal heart rate may not reflect the true basal fetal heart rate, and the increase in fetal heart rate may be due to activity, which should be diagnosed as a reactive type, but sometimes misdiagnosed as fetal tachycardia.
2. Mother's stress and anxiety
When the mother is stressed or anxious, the catecholamines in the body increase, thus stimulating the sympathetic nervous system and increasing the heart rate of the mother and fetus.
3. Gestational age
Due to immature vagus nerve, fetuses at 32 weeks or less will present with tachycardia. The sympathetic nervous system plays a major role in maintaining the basal fetal heart rate at a high level.
4. Mother fever
Usually accompanied by maternal tachycardia. During labour, the mother may develop a fever unrelated to infection, especially with epidural anesthesia or prolonged labour, nervousness, and dystocia. When fetal tachycardia occurs, it is important to think of the mother's infection.
5. Fetal infection
When infected, the oxygen requirement increases. To increase the amount of oxygen transported throughout the body, the heart rate increases.
6. Chronic hypoxemia
Chronic hypoxemia increases sympathetic activity and increases fetal heart rate. At this point, it can be accompanied by a decrease in variation.
7. Fetal hormones
When the fetus is stressed, such as when oxygen concentrations decrease, the adrenal glands produce epinephrine and norepinephrine, which act similarly to an increase in sympathetic activity, so that the fetal heart rate increases. Therefore, fetal tachycardia can be the initial response to fetal hypoxemia.
▌ Processing
1. Record the mother's body temperature and pulse to exclude fever. If infection is suspected, appropriate treatment should be given.
2. If hypoxemia is suspected of the fetus, a fetal blood sample should be taken to analyze the blood pH and alkali remaining, especially when the fetal heart rate is abnormal. If the fetal heart rate is no longer abnormal, then only close observation is required.
Early deceleration
The early deceleration shape is more consistent and occurs at the same time as the contraction. It occurs with contractions forming a mirror image. Deceleration begins when contractions begin, fetal heart rate reaches its lowest point when contractions peak, and it returns to baseline levels after contractions stop. The magnitude of the deceleration is less than or equal to 40bpm. Early deceleration is uncommon and must be noted once it appears.
▌ Cause
Early deceleration is caused by compression of the fetal head during contractions. Fetal head compression causes intracranial pressure to rise, which reduces oxygen supply and blood flow to the brain. The partial pressure reduction of oxygen is recognized by the chemoreceptors of the brain, and the parasympathetic activity is strengthened, which in turn slows down the fetal heart rate. At the same time, when the fetal head is pressed, the pressure on the vagus center of the brain may also increase, which also strengthens the activity of the parasympathetic nerve. These slowdowns are caused by mild transient hypoxia and generally do not result in adverse fetal outcomes.
The goal of treatment is to alleviate compression on the fetal head during contractions. This is usually done by changing the mother's position.
Late deceleration
Late deceleration tends to be more consistent in shape and depth, occurring after each contraction. Where the lowest point of heart rate occurs more than 15 seconds after the peak of contraction, it is called late deceleration.
Late deceleration is caused by a reduction in uterine blood flow during contractions and the resulting reduction in oxygen transmission. This hypoxic tension is recognized by the chemoreceptors of the aortic arch, which stimulates the parasympathetic conduction pathway and increases vagus nerve activity, leading to a decrease in heart rate.
However, if the fetus has already been damaged, then the reduced oxygen transmission during contractions may not be sufficient to maintain normal myocardial activity, which in addition to causing increased vagus nerve activity, directly inhibits myocardial activity. Oxygen transfer rates between contractions may not be sufficient to maintain adequate oxygen levels, manifested by decreased or absent fetal heart rate variability.
The aim is to increase blood flow from the uterus and placenta to the fetus for oxygen transfer.
Change the position of the pregnant woman
Intravenous fluids
Mask for oxygen
The late deceleration of the caucus is in a progressive state, and all infusions that promote uterine contractions are stopped
Fetal blood is taken to measure the pH and alkali remaining
After taking these measures, mothers should be prepared for childbirth, especially when variation decreases or when tachycardia or bradycardia occurs at the same time.
Extend the deceleration
Prolonged deceleration refers to the decrease in fetal heart rate ≥ 30 beats per minute for more than 2 minutes.
The decrease in the amount of oxygen delivered by the placenta to the fetus leads to the occurrence of a prolonged deceleration, usually due to a decrease in blood flow to the uterus. After the chemoreceptors on the aortic arch are stimulated, the nerve excitability of the paracoste increases, resulting in a decrease in fetal heart rate. Prolonged deceleration is usually associated with previous variant deceleration.
▌ Cause
1. Complete umbilical cord occlusion, such as umbilical cord prolapse.
2. Maternal hypotension caused by epidural anesthesia.
3. Uterine tone is too high.
4. Vaginal examination and artificial membrane rupture can make the prolonged deceleration become obvious, possibly because the pressure directly applied to the fetal head during the operation compresses the vagus center of the brain.
Increases blood flow and fetal oxygen supply to the offsheets, while clarifying the cause of the deceleration. The specific measures are as follows:
Change the position of the pregnant woman
Increase intravenous fluid volume
Stop using official shrinkage
Vaginal examination excludes cord prolapse
Maternal blood pressure is measured, especially during epidural block anesthesia
Also be prepared for childbirth
Source of this article: Obstetrics and Gynecology Nursing
Editor-in-Charge: Ichikawa