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Late Decelerations

Gary A. Dildy III, MD

Perinatologist

St. Mark’s Hospital

Salt Lake City, UT

Director of MFM, MountainStar Division

Hospital Corporation of America

Nashville, TN

Clinical Professor of OB/GYN

LSU Health Sciences Center

New Orleans, LA

Late

DecelerationsMichael A. Belfort, MD, PhD

Professor of OB/GYN

Division of Maternal-Fetal Medicine

University of Utah School of Medicine

Salt Lake City, UT

Director of Perinatal Research

HCA, Nashville TN

LATE QUOTES

How did it get so late so soon?

Its night before its afternoon.

December is here before its June.

My goodness how the time has flewn.

How did it get so late so soon?

Theodor Geisel

American Writer

1904 - 1991

Outline

• Acid Base Balance

• Definition

• Etiology

• Historical perspective

• RSA and late decelerations

• Management

• Late Decelerations and CP

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Lactic acid

Anerobic MetabolismAerobic Metabolism

Energy + CO2 + H2O

Krebs cycle

IN THE PERIPHERAL TISSUES

Glucose

Glycolysis

Accumulates in

excess of

buffering capacity

Metabolic acidosis

Oxidative phosphorylation

AEROBIC METABOLISM

6 O2

GLUCOSE

METABOLISM

6 CO2

6 H2O

36 ATP

HEAT (417 kcal)

Oxidative phosphorylation: Very efficient form of energy

production. Each pyruvic acid is converted into 34 ATP

ANAEROBIC METABOLISM

GLUCOSE METABOLISM

2 LACTIC ACID

2 ATP

HEAT (32 kcal)

Glycolysis: Inefficient source of energy production; 2

ATP for every glucose; produces pyruvic acid

Anaerobic Metabolism

• Occurs without oxygen

–oxydative phosphorylation can’t occur

without oxygen

–glycolysis can occur without oxygen

–cellular death leads to tissue and organ

death

–can occur even after return of perfusion

• ⇒ organ or organism death

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InadequateCellularOxygenDelivery

Anaerobic

Metabolism

InadequateEnergy

Production

Metabolic

Failure

Lactic

Acid

Production

Metabolic

AcidosisCELL

DEATH

Ultimate Effects

of Anaerobic

Metabolism Alveolus

Inspired Air - 150 mm Hg

PARTIAL PRESSURE OF OXYGEN -- pO2

pO2 95 mmHg

pO2 105 mmHg

95 mmHg

45 mmHg40-45 mmHg

Spiral artery

35 mmHg25-35 mmHg

25 mmHg15-25 mmHg

40 mmHg

Normal Fetal Arterial pO2

Cordocentesis (N = 35) – 23 mmHg (14 – 32)Nicolaides Am J Obstet Gynecol 1989;161:996-1001

Elective cesarean without labor (N = 665) – 23 mmHg (± 14%)

Cesarean after labor (N = 1,609) – 18 mmHg (± 13%)

Vaginal delivery (N = 14,285) – 24 mmHg (± 15%)Richardson Am J Obstet Gynecol 1998;178:572-9

Umbilical artery 16 mmHg (± 4.6)

Placental artery 16.5 mmHg (± 3.6)Nodwell Obstet Gynecol 2005;105:129-38

5-minute Apgar score ≥ 7 (N = 15,073) – 17 mmHg (2SD 6-30)Helwig Am J Obstet Gynecol 1996;174:1807-12

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American Journal of Obstetrics and Gynecology

© Mosby-Year Book Inc. 1997. All Rights Reserved.

Volume 177(6) December 1997 pp 1385-1390

Electronic fetal heart rate monitoring: Research guidelines for interpretation

[Clinical Opinion]

National Institute of Child Health and Human Development Research Planning Workshop.

“The purpose of the National Institutes of Health research planning

workshops is to assess the research status of clinically important areas.

This article reports on a workshop whose meetings were held between

May 1995 and November 1996 in Bethesda, Maryland, and Chicago,

Illinois. Its specific purpose was to develop standardized and

unambiguous definitions for fetal heart rate tracings.”

“Late deceleration of the FHR is a visually

apparent gradual (onset to nadir ≥ to 30 sec) decrease and return to baseline FHR

associated with a uterine contraction.”

AJOG Volume 177(6) December 1997 pp 1385-1390

“Decelerations are tentatively defined as

recurrent if they occur with ≥ 50% of

uterine contractions in any 20-minute

segment.”

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NIHCD Terminology

Pattern NICHD Definitions

Acceleration • Abrupt � in FHR above baseline, peak 15

bpm above baseline, acceleration sustained

for 15 sec (10 x 10 in fetus < 32 wks)

Early

Deceleration • Gradual onset-to-nadir (> 30 seconds) with

nadir coinciding with peak of contraction

Late

Deceleration • Gradual onset-to-nadir (> 30 seconds) with

nadir occurring after peak of contraction

Variable

Deceleration • Abrupt onset-to-nadir (< 30 seconds)

Prolonged

Decelerations • Deceleration > 2 minutes but < 10 minutes

NICHD

NICHD

NICHD

NICHD

NIHCD Terminology

Pattern NICHD Definitions

Baseline FHR Approximate mean FHR rounded to 5 bpm

increments. 10 minutes. Minimum 2-minute

segment

• Normal

FHR

110-160 (10 minutes)

• Bradycardia FHR < 110 bpm for 10 minutes

• Tachycardia FHR > 160 bpm for 10 minutes

Variability Fluctuations or variations in baseline FHR

• Absent Amplitude range undetectable

• Minimal > undetectable but < 5 bpm

• Moderate 6-25 bpm

• Marked > 25 bpm

NICHD

NICHD

LATE DECELERATIONS

Historical

• Little known before EFM

• Description of FHR changes with UPI

– Hon’s “Late deceleration”

– Caldeyro-Barcia’s “Type II Dip”

HON EH. Observations on pathologic fetal bradycardia.

Am J Obstet Gynecol 1959;77:1084-99.

FETAL HEART RATE MONITORING

Ed Hon

• HON EH. The electronic evaluation of the fetal heart rate; preliminary report. Am J Obstet Gynecol 1958;75:1215-30.

• HON EH. Observations on pathologic fetal bradycardia. Am J Obstet Gynecol 1959;77:1084-99.

• HON EH. The fetal heart rate patterns preceding death in utero. Am J Obstet Gynecol 1959;78:47-56.

• HON EH, BRADFIELD AH, HESS OW. The electronic evaluation of the fetal heart rate. V. The vagal factor in fetal bradycardia. Am J Obstet Gynecol 1961;82:291-300.

• HON EH. THE CLASSIFICATION OF FETAL HEART RATE. I. A WORKING CLASSIFICATION. Obstet Gynecol 1963;22:137-46.

• HON EH, LEE ST. THE FETAL ELECTROCARDIOGRAM. I. THE ELECTROCARDIOGRAM OF THE DYING FETUS. Am J Obstet Gynecol 1963;87:804-13.

• HON EH, LEE ST. ELECTRONIC EVALUATION OF THE FETAL HEART RATE. VIII. PATTERNS PRECEDING FETAL DEATH, FURTHER OBSERVATIONS. Am J Obstet Gynecol 1963;87:814-26.

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LATE DECELERATION

Terminology

• Type– Reflex

• Hypoxia – chemoreceptors – vagal discharge

• Accompanied by normal FHR variability (normal CNS)

– Nonreflex• Hypoxia – chemoreceptors – vagus - myocardial depression

• Abnormal variability

• Fetal CNS & CV decompensation

• Degree– Mild <15

– Moderate

– Severe >45

Parer & Nageotte, in Creasy & Resnik 5th Edition

Recurrent late decelerations suggest

recurrent episodes of hypoxemia

during contractions.

Recurrent late decelerations suggest

recurrent episodes of hypoxemia

during contractions.

LATE DECELERATIONS & HYPOXIA

Myers RE, Mueller-Heubach E, Adamsons K. Predictability of the state

of fetal oxygenation from a quantitative analysis of the components of

late deceleration. Am J Obstet Gynecol 1973;115:1083-94.

Late Decelerations

• Late decelerations with intact variability are mediated by vagal reflex, are unlikely to indicate fetal acidemia and are likely to respond to O2, fluids and position changes.

• Late decelerations with decreased or absent variability are caused by myocardial depression, likely associated with fetal acidemia and do not respond to conservative measures.

Paul RH, Suidan AK, Yeh S, Schifrin BS, Hon EH. Clinical fetal

monitoring. VII. The evaluation and significance of intrapartum

baseline FHR variability. Am J Obstet Gynecol 1975;123:206-10.

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LATE DECELERATIONS

Vagus Nerve Mediated I

• Late deceleration FHR pattern produced in fetal sheep by periodic occlusion of the maternal common hypogastric artery for 30-60 s

– Transient fetal hypertension occurred during the occlusions

• Alpha-adrenergic blockade with phentolamine

– Eliminated or markedly reduced the hypertensive response

– FHR deceleration character was greatly altered

• Parasympathetic blockade with atropine

– Decelerations replaced by periodic FHR accelerations during occlusions

– Accelerations eliminated by the beta-adrenergic blocker propranolol

Martin CB Jr, de Haan J, van der Wildt B, Jongsma HW, Dieleman A, Arts TH.

Mechanisms of late decelerations in the fetal heart rate. A study with autonomic

blocking agents in fetal lambs. Eur J Obstet Gynecol Reprod Biol 1979;9:361-73.

LATE DECELERATIONS

Vagus Nerve Mediated II

• Combined parasympathetic, alpha- and beta-adrenergic blockade

– FHR remained constant during occlusions in non-acidemic fetuses

– FHR decelerations persisted after parasympathetic or total autonomic blockade when fetuses significantly hypoxic

– BTBV persisted in the face of severe hypoxia and acidosis

• CONCLUSIONS…Reflex mechanisms are involved in acutely hypoxemic fetus, direct myocardial depression a factor as hypoxic acidosis develops

Martin CB Jr, de Haan J, van der Wildt B, Jongsma HW, Dieleman A, Arts TH.

Mechanisms of late decelerations in the fetal heart rate. A study with autonomic

blocking agents in fetal lambs. Eur J Obstet Gynecol Reprod Biol 1979;9:361-73.

Vagus Nerve + Chemoreceptor

• Studied initially normoxic chronically instrumented sheep

fetuses after sudden occlusion of uterine blood flow (20s):

– Late decelerations occurred only after significant decrease in fetal

O2 consumption, O2 content, and O2 tension occurred

• No significant change in BP

• Vagal blockade led to a late acceleration which was

eliminated by beta-blockade

• Late deceleration in initially normoxic sheep are vagally

mediated and are due to chemoreceptor, rather than,

baroreceptor activity

Parer JT, Krueger TR, Harris JL. Fetal oxygen consumption and mechanisms of

heart rate response during artificially produced late decelerations of fetal heart

rate in sheep. Am J Obstet Gynecol 1980;136:478-82.

LATE DECELS & ACIDOSIS

• Nine chronically instrumented rhesus monkeys.

• After recovery, all the fetuses had shown accelerations and no late decelerations with spontaneous uterine contractions.

• Late decelerations were the first sign of fetal deterioration and occurred with a slight but significant decrease in fetal PaO2 without changes in pH, whereas accelerations in FHR were still present.

• The loss of FHR accelerations was a later phenomenon and was associated with significant reductions in fetal pH and PaO2.

Murata Y, Martin CB Jr, Ikenoue T, Hashimoto T, Taira S, Sagawa T, Sakata H.

Fetal heart rate accelerations and late decelerations during the course of

intrauterine death in chronically catheterized rhesus monkeys. Am J Obstet

Gynecol 1982;144:218-23.

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Vagus Nerve + Chemoreceptor

• Studied chronically hypoxic sheep fetuses after transient occlusion of maternal aorta (20s):– Late decelerations occurred

• Significant decrease in fetal BP and UA flow

• Vagal blockade with atropine before occlusion reduced but did not eliminate the late deceleration

• Late deceleration was associated with decreased myocardial O2 consumption:

• Conclusion: Late decelerations are caused by 2 mechanisms – chemoreceptor vagal reflex

– myocardial depression

Harris JL, Krueger TR, Parer JT. Mechanisms of late decelerations of the fetal

heart rate during hypoxia. Am J Obstet Gynecol 1982;144:491-6.

Late Decels: Mechanism

• Studied normoxemic and chronically hypoxic sheep fetuses after transient obstruction of uterine artery of ewe:

– In initially normoxic fetuses a chemoreceptor reflex induced bradycardia and decreased LV output developed after the carotid PaO2 decreased to < 20 mmHg

• This reaction was abolished by atropine (vagally mediated)

• In the chronically hypoxic fetuses there was a late deceleration composed of three stages:

– chemoreceptor induced, vagally mediated bradycardia

– baroreceptor induced bradycardia with slow and late recovery

– non-reflex bradycardia due to myocardial depression

• The time to onset depended, and the depth and duration of the deceleration depended on the initial state of fetal oxygenation

Itskovitz J, Goetzman BW, Rudolph AM. The mechanism of late deceleration

of the heart rate and its relationship to oxygenation in normoxemic and

chronically hypoxemic fetal lambs. Am J Obstet Gynecol 1982;142:66-73.

pO2 < 15-20 mmHg

sensed by carotid and

aortic chemoreceptors

Combined effect � Increased BP

Medullary

vasomotor

center

(Brain, heart, adrenals)

“Central”

Vasodilatation

(Brain, heart, adrenals)

Peripheral

Vasoconstriction

(Gut, kidneys, limbs)

LATE DECELERATION

Chemoreceptors sense

↓ pO2 and trigger reflex

peripheral

vasoconstriction.

Chemoreceptors sense

↓ pO2 and trigger reflex

peripheral

vasoconstriction.

Hypoxemia during contraction

pO2 falls below critical threshold ~ 15 - 20 mm Hg

near peak of contraction.

Increased BP is

sensed by

baroreceptors,

triggering increased

vagal outflow to

reduce HR, reduce

CO and return BP to

normal.

Oxygenated blood is

shunted away from

non-essential vascular

beds toward essential

vascular beds in brain,

heart and adrenals.

Oxygenated blood is

shunted away from

non-essential vascular

beds toward essential

vascular beds in brain,

heart and adrenals.

Blood pressure rises.

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HYPOXEMIAHYPOXEMIA

INITIAL FETAL RESPONSE TO HYPOXEMIA IN THE LAMB

90Ball (9)

5Itskovitz (8)

90Ball (7)

35Jensen (6)

20Reid (5)

90Field (4)

420Richardson (3)

60Peeters (2)

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1. AJOG 1974;120:817-24

2. AJOG 1979;135:637-46

3. J Dev Physiol 1989;11:37-43

4. J Dev Physiol 1990;14:131-7

5. J Dev Physiol 1991;15:183-8

6. J Dev Physiol 1991;15:309-23

7. AJOG 1994;170:156-61

8. Am J Physiol 1987;252:H100-99. AJOG 1994;171:1549-55

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Base Excess and Hypoxia

• Normal acid base balance in the fetus

– Base Excess: -2.3 +/- 0.6 mmol/L

– pH: 7.39 +/- 0.05 mmol/L

– Base excess does not change with gestation

Lazarevic et al. Clin Exp Obset Gynecol 1991;18:81

• BE after SNVD with 5 min Apgar > 7:

– UA: -4 +/- 3 mmol/L

– UV: -3 +/- 3 mmol/L

– 2.5% for the UA was –11 mmol/LHelwig et al. Am J Obset Gynecol 1996;174:1807

Base Excess and Hypoxia

• A normal baby enters labor with a BE of –2

mmol/L and can be expected to decrease by

an additional 3 mmol/L

• Expected normal decrease in BE during:

– First stage is –1 mmol/L per 3 to 6 hours

– Second Stage is –1 mmol/L per 1 hourHagelin and Leyon. Acta Obset Gynecol Scand 1998;77:841

Base Excess and Hypoxia

• When there are repetitive decels for hours buffer base decreases 1mmol/L per 30 minutes

Low et al. Am J Obstet Gynecol 1977;129:857

• When there is intrapartum hypoxia causing asphyxia buffer base decreases 1mmol/L per 6 to 15 minutes

Low et al. Am J Obstet Gynecol 1984;148:533

• When there is terminal bradycardia from uterine rupture buffer base decreases 1mmol/L per 2 to 3 minutes

Leung et al. Am J Obstet Gynecol 1993;169:945

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Base Excess and Hypoxia

• With BE –12 to –16 mmol/L about 10% have:

– Moderate to severe encephalopathy

– Respiratory complicationsLow et al. Am J Obset Gynecol 1997;177:1391

• Buffer base: Normal = 46 mmol/L

– < 34 mmol/L = asphyxia (~BE -12)

– Major/minor deficits 20%

– Increased to 80% when buffer base < 22 mmol/L (~BE -24)

Base Excess and Hypoxia

• BE in umbilical artery and vein:

– UV BE represents the situation at the time

initial cord compressionRoss and Gala. Am J Obstet Gynecol 2002;187:1

– A wide (> 6 mmol/L) UA/UV BE difference

suggests short duration asphyxia and a

narrow (< 6 mmol/L) difference suggests

long term asphyxia Low et al. Am J Obstet Gynecol 1995;172:805

Base Excess and Hypoxia

• No change in BE is likely in the immediate neonatal period:

– immediate effective resuscitation with no bicarb

– no sepsis

– no severe hypoxia or hypotensionRoss and Gala. Am J Obstet Gynecol 2002;187:1

• BE is likely to continue to fall at about 1mmol/L per 2 minutes if resuscitation is ineffective

Leung et al. Am J Obstet Gynecol 1993;169:945

Base Excess and Hypoxia

• Most neonates with a BE of –12 mmol/L

do not exhibit encephalopathy

• Even with a BE < -16 mmol/L most

babies will either die or survive normally,

only a small proportion develop CP

• Most babies that do get CP have an

underlying propensity to CPRoss and Gala. Am J Obstet Gynecol 2002;187:1

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Late Decelerations

• Experiment on monkey’s brain showed only pH <7.00 for >30 minutes can cause hypoxic damage. Metabolic acidosis pH >7.00 lasting for several hours did not cause neurological injury.

Myers RE 1977 In Gluck Yearbook, inc 37-97

• pH <7.00 (Base deficit >16mmol/L) is a realistic threshold below which brain dysfunction significantly increases. At this level systemic hypotension start to occur.

Low 1993 ; Clinical OB&GYN 36:82

Acidemia and FHR

Analysis of a number of observational studies to determine relationship between FHR patterns and fetal acidemia

1. Moderate variability strongly associated with UA pH > 7.15 and 5 min Apgar > 7

2. Absent or minimal variability with late or variable decels was strongest predictor of acidemia BUT only a 23% association

3. Strong association between the degree of acidemia and the depth of the deceleration

4. Except for sudden profound bradycardia, acidemia with decreasing variability in combination with decels takes about 1 hour to develop

Grade III observation/uncontrolled studies mostly

Parer JT, King T, Flanders S, Fox M, Kilpatrick SJ. Fetal acidemia and

electronic fetal heart rate patterns: is there evidence of an association?

J Matern Fetal Neonatal Med 2006;19:289-94.

Acidemia and FHR

• Evaluate late decelerations to detect low pH (< 7.1) in low-risk pregnancies

• Four units where 10,030 women delivered, of which 5522 were low-risk

• Last 2 hours of FHR patterns before delivery were interpreted (NICHHD)

• The correlation between the incidence of LD (occasional, < 50%; recurrent, >50%) and severity (reduced baseline FHR accelerations and variability) of LD, and low pH (< 7.1) were evaluated.

• Statistical analyses included a contingency table with chi2 and the Fisher test, and one-way analysis of variance with the Bonferroni/Dunn test. In the 5522 low-risk pregnancies, 301 showed occasional LD and 99 showed recurrent LD. Blood gases and pH values deteriorated as the incidence of LD increased and as baseline accelerations or variability was decreased. Positive predictive value for low pH (< 7.1) was exponentially elevated from 0% at no deceleration, 1% in occasional LD, and > 50% in recurrent LD with no baseline FHR accelerations and reduced variability. In low-risk pregnancies, information on LD combined with acceleration and baseline variability enables us to predict the potential incidence of fetal acidemia.

Sameshima H, Ikenoue T. Predictive value of late decelerations for fetal

acidemia in unselective low-risk pregnancies. Am J Perinatol 2005;22:19-23.

Acidemia and FHR• Case-control study of 71 term infants with BD > 16 mmol/l

versus 71 matched infants with BD < 8

• 10 minute segments were scored for the 4 hours before delivery in both groups

• Selected FHR patterns in the 1 hour before delivery

• Asphyxia was associated with absent/minimal BTBV and late and prolonged decelerations

• Most specific pattern for asphyxia was absent BTBV but identified only 17% of asphyxia– When additional less specific patterns were added to absent BTBV:

• 93% sensitivity, 2.6 – 18% PPV, and 98.3 – 99.5% NPV

• Concluded: – If fetus with minimal variability and late or prolonged decels is

delivered within 1 hour of birth asphyxial injury can be avoided in most cases

– Many false positive cases

Low et al. Obstet Gynecol 1999;93:285

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Predictive value of FHR variables for fetal asphyxia

• METHODS:

– Asphyxia group of 71 term infants with UA BD >16 mmol/L

– Control group of 71 term infants with UA BD <8 mmol/L

• RESULTS:

– FHR variables associated with fetal asphyxia

• absent and minimal baseline variability

• late and prolonged decelerations

– FHR patterns with absent baseline variability• Were the most specific but identified only 17%

• Sensitivity increased to 93% with addition of less specific patterns

• PPV (18.1% to 2.6%) NPV (98.3% to 99.5%)

• CONCLUSION:

– A narrow 1-hour window of FHR patterns including minimal baseline variability and late or prolonged decelerations will predict fetal asphyxial exposure before decompensation.

– Predictive FHR patterns can be a useful screening test.

– Supplementary tests are required to confirm the diagnosis and to identify the large number of false-positive patterns to avoid unnecessary intervention.

Low JA, Victory R, Derrick EJ. Predictive value of electronic fetal monitoring for

intrapartum fetal asphyxia with metabolic acidosis. Obstet Gynecol 1999 ;93:285-91.

Late Decels: Aortic Compression

• 14% (126/902) laboring patients had late decelerations

• Of these 19% (24/126) only had lates when supine

• Associated with reduced maternal femoral BP and decreased pulse pressure in the big toe

• Conclusion: Supine hypotensive syndrome can cause late decelerations

Abitbol MM. Supine position in labor and associated fetal heart

rate changes. Obstet Gynecol 1985;65:481-6.

Late Decels and Abruption

• Case control study of 69 patients with severe early onset preeclampsia with and without abruptio placentae

• Late decelerations: 58% abruption vs. 32% controls

• Only recognizable warning sign noted for abruption in preeclamptic women

Odendaal HJ, Hall DR, Grove D. Risk factors for and perinatal mortality of

abruptio placentae in patients hospitalised for early onset severe pre-

eclampsia - a case controlled study. J Obstet Gynaecol 2000;20:358-64.

Respiratory Sinus Arrhythmia

• RSA is heart rate variability in synchrony with respiration.

• R-R interval is shortened during inspiration & prolonged during expiration.

• Used as an index of cardiac vagal function.

• Reflects respiratory-circulatory interactions universally among vertebrates.

• Efficiency of pulmonary gas exchange is improved by RSA, suggesting active physiologic role.

• The matched timing of alveolar ventilation and its perfusion with RSA within each respiratory cycle could save energy expenditure by suppressing unnecessary heartbeats during expiration and ineffective ventilation during the ebb of perfusion.

• Evidence of a possible dissociation between RSA and vagal control of the heart rate, suggesting differential controls between the respiratory modulation of cardiac vagal outflow and cardiac vagal tone.

• RSA or heart rate variability in synchrony with respiration is a biological phenomenon, which may have a positive influence on gas exchange at the level of the lung via efficient ventilation/perfusion matching.

Yasuma F, Hayano J. Respiratory sinus arrhythmia: why does the heartbeat

synchronize with respiratory rhythm? Chest 2004;125:683-90.

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RSA and Polyvagal Theory

• Model defining the role of the parasympathetic NS and particularly vagus N in mammalian stress reaction

• Phylogenetic shift in neural development of ANS has 3 stages:

– Primitive unmyelinated visceral vagus – immobilization, depressed metabolic activity

– Sympathetic NS – increasing metabolic output, inhibit visceral vagus

– Myelinated vagus – rapidly regulates cardiac output

• 2 primary medullary source nucleii of the vagus (X nerve)

– Nucleus Ambiguus – myelinated (more developed)

– Dorsal Motor Nucleus – unmyelinated (primitive)

• Both nucleii have fibers terminating on the SA node BUT only the NA fibers regulate RSA

Porges SW. Orienting in a defensive world: mammalian modifications of our

evolutionary heritage. A Polyvagal Theory. Psychophysiology 1995;32:301-18.

RSA and Polyvagal Theory• Neurophysiological model based on the Polyvagal Theory to interpret FHR patterns.

• Beat-to-beat heart rate data from 7 fetuses monitored during the first and second stages of labor were analyzed.

• Transitory FHR accelerations and reduced beat-to-beat variability reliably preceded FHR decelerations.

• Data are interpreted within the context of the Polyvagal Theory

– Transitory FHR accelerations and the depression of the respiratory rhythm in the beat-to-beat heart rate pattern reflect a withdrawal of the vagal tonedetermined by myelinated vagal pathways originating in the nucleus ambiguus.

– Withdrawal of vagal tone originating in the NA results in the cardiac pacemaker becoming vulnerable to sympathetic influences and to the more-primitive unmyelinated vagal pathways originating in the dorsal motor nucleus of the vagus, which may contribute to clinically relevant bradycardia.

Reed SF, Ohel G, David R, Porges SW. A neural explanation of fetal heart

rate patterns: A test of the polyvagal theory. Dev Psychobiol 1999;35:108-18.

Late Decels and Fetal Breathing

• 6 patients evaluated between 37 – 42 weeks

• “Late decelerations” in association with fetal breathing seen on US or EFM

• antepartum/intrapartum

• 3 “high risk” (diabetes, IUGR, postdates)

• New onset of “late decels” in previously normal tracings – shallow, increased BTBV– no change after position change and O2

– normal rate and BTBV after deceleration

– normal neonatal outcomes

• Suggested that this represents fetal breathing

Schifrin BS, Artenos J, Lyseight N. Late-onset fetal cardiac

decelerations associated with fetal breathing movements. J Matern

Fetal Neonatal Med 2002;12:253-9.

Late Decels and AV Block

• ECG evaluated in 15 fetuses during decelerations during labor

• 6/15 cases had sinus bradycardia

• 7/15 had complete dissociation of p wave from QRS – complete heart block

• Most decelerations are vagally mediated but some may be due to hypoxia of the Bundle of His with reversible AV node dysfunction

Mohajer et al. Arch Dis Child Fetal Neonatal Ed. 1995;72:F51

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Oxygenation• Exclude pulmonary disease (asthma, PE, AFE)

• Supplemental oxygen

• Breathing techniques

Uterine Blood Flow• Exclude uterine rupture, abruption, hyperstimulation

• Discontinue uterine stimulants

• Uterine relaxants as needed

• Anxiety regulation

• Modify pushing technique

Umbilical Blood Flow• Exclude umbilical cord prolapse, vasa previa

• Amnioinfusion as needed

• Manual elevation of fetal vertex

Cardiac Output• Exclude hypotension (supine, epidural)

• Lateral decubitus position

• Hydration

CORRECTIVE MEASURES – FETAL “ABCs”Cerebral Palsy

• Nonprogressive motor deficit of early onset

• One or more limbs with paralysis, spasticity

or problems of motor control

• Type is determined by location of the

lesions(s), nature of timing of its

occurrence, and the ability of the CNS to

compensate

Fetal Heart Rate PatternsCP No CP

(n = 78) (n = 300) Odds Ratio

Tachycardia

>160 bpm 22 85 1.0 (0.6-1/7)

>180 bpm 5 16 1.3 (0.4-3.4)

Bradycardia

<100 bpm 27 75 1.5 (0.9-2.5)

< 80 bpm 13 35 1.5 (0.8-3.0)

Multiple lates 11 12 3.9 (1.7-9.3)

↓ variability 13 21 2.7 (1.1-5.8)

Nelson et al NEJM 1996; 334:613-8

LATE DECELERATIONS

Summary

• Know and use NICHD EFM definitions !

• Lates mediated by multiple mechanisms– Old News - Hypoxemia, hypertension, myocardial depression

– New News - RSA and conduction abnormalities

• By understanding physiology, you will– Know appropriate treatments

– Positively affect some outcomes

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LATE QUOTES

“Better never than late.”

George Bernard Shaw

1856-1950

Irish Essayist

A. Hypoxemia

B. Hypoxia

C. Acidemia

D. Acidosis

E. Asphyxia

A. Hypoxemia

B. Hypoxia

C. Acidemia

D. Acidosis

E. Asphyxia

Question: A late deceleration is the result of fetal

Question: What is the normal fetal umbilical arterial

pO2?

A. 85 – 95 mmHg

B. 70 – 80 mmHg

C. 55 – 65 mmHg

D. 35 – 45 mmHg

E. 15 – 25 mmHg

Question: What is the normal fetal umbilical arterial

pO2?

A. 85 – 95 mmHg

B. 70 – 80 mmHg

C. 55 – 65 mmHg

D. 35 – 45 mmHg

E. 15 – 25 mmHg

A late deceleration is a protective reflex that is

triggered when fetal arterial pO2 falls below a

critical threshold (hypoxemia).

A late deceleration is a protective reflex that is

triggered when fetal arterial pO2 falls below a

critical threshold (hypoxemia).

A. Stimulation of aortic chemoreceptors

B. Increased blood flow to the brain

C. Decreased blood flow to the extremities

D. Decreased blood flow to the kidneys

E. Transient hypotension

A. Stimulation of aortic chemoreceptors

B. Increased blood flow to the brain

C. Decreased blood flow to the extremities

D. Decreased blood flow to the kidneys

E. Transient hypotension

Question: Fetal hypoxemia leads to all of

the following, except:

Question: Fetal hypoxemia leads to all of

the following, except:

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