Intrapartum fetal assessment
- Internal electronic fetal heart rate monitoring
Uses bipolar spiral electrode directly to the fetus
- External (Indirect) electronic fetal heart rate monitoring
-Heart rate is detected using the Ultrasound Doppler device.
-It does not provide the precision of fetal heart measurement but can avoid the membrane rupture and uterine invasion
Fetal heart rate patterns
- Baseline fetal heart activity
- rate - approximate mean rate rounded to increments of 5 bpm during a 10 min tracing segment.
Tachycardia- > 160bpm
Bradycardia-< 110 bpm
rate is a result of tonic balance between accelerator (sympathetic system) and decelerator (parasympathetic system)
rate is also under control of arterial chemoreceptor
- Moderate 80-100bpm
- Severe <80bpm for 3 minutes or longer
c. Head compression during 2 nd stage, congenital heart block, serious fetal compromise (severe and prolonged hypoxia and severe metabolic academia induces a fall in heart rate due to direct affects on myocardium)
- Mild 161-180bpm
- Severe >181 bpm
c maternal fever from amnionitis (such infection induces fetal tachycardia before maternal fever is diagnosed), fetal compromise, cardiac arrhythmia, maternal administration of sympathetic of parasympathetic drugs (terbutaline, atropine)
- beat to beat variation
- Important index of cardiovascular function and regulated largely be autonomic nerve system
- Short-term variability- instantaneous change of fetal heart rate from one beat to the next. -Can be determined by scalp electrode.
- Long term variability - changes that occur during the course of 1 min and result in the waviness of the baseline.
-Normal frequency is 3 to 5 cycles per min.
-Increased variability has been described with fetal breathing, fetal movement, and advancing gestation
-Diminished variability can be a sign indicating serious fetal compromise; loss of variability combines with deceleration was associated with fetal academia.
-Loss of variability can be a result of metabolic academia causing depression of fetal brainstem or the heart itself.
-Also maternal academia causes decreased variability, analgesic drugs (narcotics, barbiturates, phenothiazines, tranquilizers and general anesthesia), and magrol
-Although it has been thought that the diminished variability was the single most reliable sign of fetal compromise, it is unlikely to be due to fetal asphyxia in the absence of fetal deceleration.
- Periodic fetal heart rate
-Deviations from baseline that are related to the uterine contractions.
- Visually apparent abrupt increase in the fetal heart rate baseline
-Fetal movement, uterine contraction, pelvic examination, umbilical cord occlusion
-Common in labor and almost always associated with fetal movement.
-Gradual decreases and returns to the baseline associated with the contraction
-Generally seen in active labor and 4-7 cm dilatation, proportional to the contraction strength and rarely falls below 100 to 110
-Not associated with fetal asphyxia, academia or low apgar scores
-Head compression causes vagal nerve activation and mediates heart rate deceleration
-Smooth, gradual symmetrical decrease in fetal heart rate beginning at or after the peak of the contraction and returning to baseline only after the contraction has ended.
-Not more that 30-40 bpm below baseline and typically not more than 10 to 20 bpm in intensity
-The time interval pr lag period from the onset of the contraction to the onset of the late deceleration was directly related to the vassal fetal oxygenation- lower the fetal Po2 prior to contractions, the shorter the lag phase
-Maternal hypotension, (epidural) uterine activity (pitocin) placental dysfunction, placental abruption can cause acute and severe late decelerations.
-Visually apparent abrupt decrease in rate and the onset commonly varies with successive contractions and the duration less than2 min.
-Represent fetal heart rate reflexes that reflect wither blood pressure changes due to interruption of umbilical flow or changes in oxygenation
-Two types-complete (A), partial-complete-partial (B)
-Most common deceleration pattern due to umbilical cord occlusion
-Isolated decelerations lasting 2 minutes of longer, less than 10 min.
-Cervical examination, uterine hyperactivity, cord entanglement, maternal supine hypotension, epidural, spinal analgesia, placental abruption, hypoxia, umbilical cord knots or prolapsed, maternal seizures, impending birth
Second stage fetal heart rate patterns
-Abnormal baseline hearts rate-either bradycardia of tachycardia. Absent beat-to-beat variability in the presence of deceleration is associated with increased fetal compromise.
- Fetal scalp blood sampling
- Scalp stimulation
- Vibroacoustic stimulation
- Fetal pulse oximetry
- Fetal EKG
- IPF Doppler velocimetry
Intrapartum Assessment of Uterine Activity
1. Internal Uterine Pressure monitoring-measures amniotic pressure by fluid filled catheter with the distal tip located above the presenting part.
- External Monitor -by displacement transducer held against the abdominal wall, the movement of the button is converted into a measurable electrical signal that indicates the relative intensity of the contraction
Montevideo Units - uterine contraction = intensity (uterine pressure above the baseline) mmHg * contraction frequency per 10 min
Eg. three contractions in 10 min, 50mmHg = 150 Montevideo units
3. Clinical labour usually commences when uterine activity reaches 80 to 100 Montevideo units (3 contractions of 40 mmHg)
Normal contractile wave originates near the uterine end of one of the fallopian tubes (pacemakers) and the right one usually dominates and the depolarization wave propagates down toward the cervix. The intensity is greatest in the fundus and decreases towards cervix