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 1988 Albers 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 ( ) under vagal control (if give atropine increase HR to 160) Tachycardia Mild Severe>180 Bradycardia mild 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 < bpm 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 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 bpm drop (usually )

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 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: –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: 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: 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 Auscultation BMJ 2001;322: 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 Auscultation BMJ 2001;322: Outcomes –Primary: Metabolic acidosis –Secondary: Apgar, ventilation, NICU admission, obstetric intervention

Cardiotocography versus Auscultation BMJ 2001;322: Results –3752 women randomized –Umbilical artery pH <7.2 OR 0.96 ( ) –Apgar at 5 minutes <7 OR 1.07 ( ) –Use of scalp pH OR 1.14 ( ) –CLE useOR 1.15 ( ) –CaesarianOR 1.20 ( ) –Operative deliveryOR 1.15 ( )

Cardiotocography versus Auscultation BMJ 2001;322: Subgroup analysis with 1736 who remained low risk –Umbilical artery pH <7.2 OR 1.02 ( ) –Apgar at 5 minutes <7 OR 1.39 ( ) –CLE useOR 1.33 ( ) –CaesarianOR 1.43 ( ) –Operative deliveryOR 1.36 ( )

ACOG Guidelines

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