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Fetal Monitoring
Introduction
• 1600’s Kilian proposes the use of fetal heart rate to diagnose fetal distress
• 1893 criteria for determining fetal distress by Von Winckel
• Tachycardia >160bpm
• Bradycardia<100
• Irregular heart rate
• Passage of meconium
• Alteration of fetal movement
Introduction
• EFM introduced in late 1950’s with first commercial product in 1968 as an alternative to auscultation
• Initially utilized for high risk patients, but has become nearly universal
– 44.6% of live births in 1980, increased to 62.2% in 1988Albers and Krulewitch OB Gyn.1993;82:8-10.
• Early observational studies suggested reduced perinatal mortality
Physiology
• Fetal heart rate controlled by autonomic nervous system, with goal to maintain brain perfusion
• Parasympathetic control increases with age, thus heart rate decreases with gestational age
• Baroreceptors and chemoreceptors play a large role in the control of heart rate
Fetal Oxygenation
• Placentation
• Maternal hypotension
• Microvascular disease (HTN, PIH, Diabetes, collagen vascular disease)
• Cord factors--knot, nuchal cord, stretch, compression
DR C BRAVADO
• Determine Risk• Contractions• Baseline RAte• Variability• Accelerations• Decelerations• Overall Assessment
• ALSO Fourth Edition
Baseline Rate
• Normal between 120-160 (110-160) under vagal control (if give atropine increase HR to 160)
• Tachycardia• Mild 160-180
• Severe>180
• Bradycardia• mild 100-120
• severe <80
Causes of Tachycardia
• Hypoxia
• Infection
• Maternal hyperthyroidism
• Fetal anemia
• Fetal Heart Failure
• Fetal cardiac tachydysrhythmia
• Drugs (vagolytic and sympathomimetic)
Causes of Bradycardia
• Hypoxia/acidosis
• Hypothermia
• Fetal cardiac bradydysrhythmia
• Heart block (SLE)
• Drugs
• False bradycardia (maternal tracing)
Variability
• Short term--instantaneous changes from beat to beat
• Long term beat to beat--variability over the course of a minute (the waviness of the pattern)
• 1997 NICHD (National Institute of Child Health and Human Development) Fetal Monitoring Workshop did not recommend differentiating short and long term variability
Variability Classification
• Absent
• minimal < 5 bpm variability
• normal 6-25 bpm variability
• marked >25 bpm variability
Causes of decreased BTBV
• Acidosis/hypoxia• Congenital
abnormalities (CNS)• Sleep cycles• Prematurity• Tachycardia• Sepsis• Damaged CNS
• Drugs– Narcotics
• Demerol--decreased BTBV in 5 min and lasts for about 1 hr or longer
– Barbiturates
– General anesthesia
– Parasympatholytics
– Phenothiazine
Acceleration
• Change in heart rate above the baseline
• Usually use 15 bpm above baseline for 15 sec. (initially developed for non stress testing)
Decelerations
• Early deceleration
• Variable deceleration
• Late deceleration
• Prolonged deceleration
Early Deceleration
• Head compression with altered cerebral blood flow causes vagal stimulus
• U shaped with nadir coinciding with peak of contraction
• Return to baseline by the end of the contraction
• Rarely < 100-110bpm or 30-40bpm below baseline
• Occur at 4-7 cm dilation
Variable Decelerations
• Variables occur in 50-80% of labors during 2nd stage
• Variable timing, shape, depth
• Onset is abrupt as is the return to baseline
• Caused by cord compression, or spasm as cord stretched
• Occlusion of the vein reduces blood return, hypotension stimulates the baroreceptors increasing the heart rate
• Occlusion of the artery increases vascular resistance and blood pressure causing a baroreceptor mediated deceleration in heart rate
• Concerning if late in timing, duration >2 minutes, slow return with late component, lose shoulders,
Variable Decelerations
• Mild Variable-greater than 80 bpm, or last less than 30 sec. in duration regardless of depth
• Moderate Variable-deceleration to < 80 bpm
• Severe Variable- deceleration to <70 for >60 secs
Late Decelerations
• Always represent hypoxia• Oxygen sensors increase vascular
tone, leading to baroreceptor mediated deceleration
• Myocardial depression also plays a role
• Smooth symmetric decrease in heart rate at or after peak of contraction return to baseline after end of contraction
• Rarely more than 30-40 bpm
drop (usually 10-20)
Late Decelerations
• Animal studies--the shorter the onset of late after contraction the worse the O2 sat
• Difficult to determine level of acidosis by depth of deceleration
• Duration of repetitive late deceleration impacts acidosis
Late Deceleration
• Maternal hypotension• Hyperactivity of the
uterus often iatrogenic• Chronic hypertension• Preeclampsia• Collagen Vascular
diseases
• Maternal diabetes• Maternal hypoxia
resulting in hypoxemia• Maternal severe
anemia• Fetal anemia
Prolonged Deceleration
• Isolated deceleration lasting 90-120 seconds or more (2-10 minutes by others)
• Multiple mechanisms, but profound stimuli
• Concerning if slow return to baseline, rebound tachycardia, loss of variability
Prolonged Deceleration
• Prolapsed cord• Post epidural
hypotension• Prolonged cord
compression• Uterine tetany• Severe abruption
• Eclampsia• Rapid descent in the
birth canal• Paracervical block• Prolonged scalp
stimulation as in placement of FSE
Other Patterns
• Hypervariability or saltatory--Sign of hypoxia• Sinusoidal pattern--regular sine wave pattern
about 2-5 cycles per minute lasting at least 2 minutes with amplitude 5-15bpm with loss of BTBV
• Sign of severe fetal anemia and/or hypoxia
• Pseudosinudoidal--varies in shape and amplitude and BTBV maintained
Risks and Benefits
• Benefits– May decrease infantile
seizure rate• Am J OB Gyn
1985;152:524-539.
– Does not require nurse to be at the bedside
• Risks
Risks and Benefits
• Benefits– May decrease infantile
seizure rate• Am J OB Gyn
1985;152:524-539
• Risks– Does not require nurse
to be at the bedside
Risks and Benefits
• Benefits– May decrease infantile
seizure rate• Am J OB Gyn
1985;152:524-539
• Risks– Does not require nurse to
be at the bedside– Limits mobility– Shown to increase
instrumentation and cesarean rates without improvement in morbidity and mortality
– Trauma from internal monitors
Cardiotocography versus AuscultationBMJ 2001;322:1457-1462
• Inclusion criteria: Presented to the hospital and were followed in a hospital or community based clinic
• Exclusion criteria: PIH, HTN, DM, IUGR, previa, abruption, vaginal bleeding, fetal anomaly, VBAC, Rh disease, breech, multiple gestation
• Randomized at an outpatient appointment to 20 minutes Cardiotocography vs. doppler for at lease one contraction
Cardiotocography versus AuscultationBMJ 2001;322:1457-1462
• Outcomes– Primary: Metabolic acidosis– Secondary: Apgar, ventilation, NICU
admission, obstetric intervention
Cardiotocography versus AuscultationBMJ 2001;322:1457-1462
• Results– 3752 women randomized– Umbilical artery pH <7.2 OR 0.96 (0.79-1.17)– Apgar at 5 minutes <7 OR 1.07 (0.65-1.75)– Use of scalp pH OR 1.14 (0.91-1.42)– CLE use OR 1.15 (1.00-1.32)– Caesarian OR 1.20 (0.96-1.50)– Operative delivery OR 1.15 (1.00-1.32)
Cardiotocography versus AuscultationBMJ 2001;322:1457-1462
• Subgroup analysis with 1736 who remained low risk– Umbilical artery pH <7.2 OR 1.02 (0.79-
1.31)– Apgar at 5 minutes <7 OR 1.39 (0.72-
2.66)– CLE use OR 1.33 (1.10-1.61)– Caesarian OR 1.43 (0.95-2.18)– Operative delivery OR 1.36 (1.12-1.65)
ACOG GuidelinesSurveillance Low risk
pregnancyHigh riskpregnancy
Intermittent auscultation Yes Yes
Continuous electronic Yes Yes
IntervalFirst stage 30 min 15 min
Second stage 15 min 5 min
ACOG Guidelines for High Risk Patients
• During the active phase of the first stage of labor, when intermittent auscultation is used, the FHR should be evaluated and recorded at least every 15 minutes following a uterine contraction. If continuous EFM is used, the tracing should be evaluated at least every 15 minutes
• During the second stage of labor, the FHR should be evaluated and recorded at least every 5 minutes when auscultation is used and should be evaluated at least every 5 minutes when EFM is used
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