Fetal Monitoring Introduction 1600’s Kilian proposes the use of fetal heart rate to diagnose fetal distress 1893 criteria for determining fetal distress.

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



1985;152:524-539

• Risks– Does not require nurse

to be at the bedside

Risks and Benefits



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


• Outcomes– Primary: Metabolic acidosis– Secondary: Apgar, ventilation, NICU

admission, obstetric intervention


• 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)


• 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

Fetal Monitoring Introduction 1600’s Kilian proposes the use of fetal heart rate to diagnose fetal distress 1893 criteria for determining fetal distress.

Documents