ACUTE BRADYCARDIA

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TEMPLATE FOR THE DEFINITION OF INTRAPARTUM
HYPOXIA AND FETAL INJURY
Austin Ugwumadu PhD FRCOG Consultant
Obstetrician Gynaecologist / Snr. Lecturer
St. Georges Hospital Medical
School Department of Obstetrics
Gynaecology London
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CTG gives precise information for normal and
preterminal traces
Normal
Preterminal
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In this situation, interpretation is difficult
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FETAL MONITORING IN LABOUR

• Pattern recognition / clinical tests
• normal vs abnormal patterns
• always present? similar amplitude? always
  recognisable?
• Do we even know / recognise all patterns?
• e.g. late decelerations acceleration
  good variability
• absent variability with no decel with
  contractions
• Is hypoxia the only cause of fetal damage?
• FSIRS, IP pyrexia, pPROM, HCA, funisitis,
  fetal strokes

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Inter-/intra-observer variability of CTG
assessment
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• interpretation response of OB vary widely
• is the outcome known?
• outcome unfavourable?
• trace normal or abnormal?
• time of day

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Interpreting the FHR tracing effect of knowledge
of neonatal outcome Zain et al J.
Reprod. Med 199843367 - 370

• 36 OB reviewed 2 case pairs each
• 10 real / 10 identical sham cases with opposite
  outcome
• Each has a critical decision point re- timing
  MOD
• Decide whether decision to continue or deliver
  was correct
• Reviewers blinded to aim of study
• Traces evaluated for BV, decel, evidence of
  hypoxia

Table - FHR tracing interpretation grouped by
neonatal outcome
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Definition of normal, suspicious and pathological
traces
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Table 6 Classification of FHR trace features
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1.12.3 For women having continuous EFM, a
documented systematic assessment based on these
definitions and classifications should be
undertaken every hour. 1.12.4 During episodes of
abnormal FHR patterns when the woman is lying
supine she should be advised to adopt the
left-lateral position. 1.12.5 Prolonged use of
maternal facial oxygen therapy may be harmful to
the baby and should be avoided. There is no
research evidence evaluating the benefits or
risks associated with the short-term use of
maternal facial oxygen therapy in cases of
suspected fetal compromise.
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PRINCIPLES OF CTG MONITORING
The normal fetus before and during labour

• Stable B-FHR, no deceleration
• Periods of red. BV, no deceleration
• Alternating with periods of average BV
  acceleration
• associated with FM
• Cyclical activity normal fetal behaviour
• neurological integrity
• absent hypoxia
• BFHR 110150 BV 525beats Acc ? 15 b x ? 15
  sec

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BASELINE FHR / BV
Persistent / stable rate no contractions /
provocations Use fetus as own control to define
tacchycardia / bradycardia Variability abrupt
chaotic changes b/w heart beats 5 25bts More
is not necessarily better Accelerations ? 15
beats lasting ? 15 seconds
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Gradually developing hypoxia

• normal no decelerations /accelerations
• decelerations appear
• accelerations disappear
• increase in baseline fetal heart rate
• maximum BLR achieved
• reduced BLV lt 5bpm (flat) unpredictable
  duration
• distress to death step wise rapid decline
  bradycardia

• Recovery
• deceleration disappear
• then baseline heart rate returns
• variability returns

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RECOVERY

• return to previously normal baseline rate
  variability
• First, decelerations diminish in amplitude
• Secondly, they disappear
• Thirdly, baseline FHR returns to normal
• Lastly, variability returns to normal
• disappearance of dec alone is not enough to
  declare recovery
• As outlined here, recovery precludes acidosis or
  injury during episode

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Subacute hypoxia

• Rapid deterioration of pH possible with no
  increase in FHR if decelerations gt 60bpm for 90
  seconds or more with lt 60 seconds of recovery in
  between.
• Decline in pH at the rate of 0.01 / 2-4 minutes-
  more rapid if IUGR, infection, thick meconium
  with scanty liquor. May not be appropriate to do
  FBS
• If delivery is not likely in a reasonable time
  span consider operative delivery

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ACUTE BRADYCARDIA

• FHR lt80 bpm for gt 3 min
• Await signs of recovery in 90 by 6 min if there
  is no pathology
• 95 should show signs of recovery by 9 mins
• Plan delivery if no recovery by 12 min
• Action Immediate delivery IVD or CS by 15 min

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THE BOTTOM LINE!!!

• To define hypoxia in a previously normal CTG
• transient decelerations must provoke
• a rise in BFHR or
• sustained bradycardia
• therefore
• 1. If no change in BFHR and BV is assoc with
  transient decelerations there can be
• no developing hypoxic process or significant
  ischaemia regardless of the amplitude,
• configuration, or duration of the CTG pattern

Similarly, a rise in BFHR or loss of BV without
decelerations during labour also cannot represent
ongoing hypoxia
Prolonged deceleration arising from a previously
normal FHR pattern are only occasionally assoc.
with acidosis if the dec stabilises 80 bpm esp
if BV maintained!!
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Fetal blood sampling in labour
Fetal blood sample for pH BD(ecf)

• Reduces CSR with CTG
• Information is intermittent
• Needs extra expertise
• Time consuming
• Tests peripheral tissue / surrogate

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2. DISTURBANCES OF ACID BASE BALANCE
Glucose
Pyruvate
- O2
O2
CO2 H2O
Lactic acid conc. Rise (H)
Diffusion thro maternal system
pH falls
Impaired
HCO3- falls
CO2 rise
OK
Base def. rise
pH falls
Metabolic acidosis
Respiratory acidosis
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The classification of fetal blood sample results
These results should be interpreted taking into
account the previous pH measurement, the rate of
progress in labour and the clinical features of
the woman and baby.
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Acidosis

• In appropriately grown term fetuses with clear
  liquor and reactive CTG, average time taken to
  develop acidosis in 50 of cases (Fleischer et al
  AJOG 1982)
• 115 minutes of repeated late decelerations
• 145 minutes of repeated variable decelerations
• 185 minutes of flat trace
• Need FBS to verify as acidosis may develop
  earlier in those with reduced physiological
  reserve - scanty liquor with thick meconium
  infection, post term, IUGR.
• (Starks GC et al Obstet Gynecol 1980),

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Aerobic / anaerobic respiration
Oxidation of glucose is glycolysis Pyruvate is
the branch molecule of glycolysis In the
metabolism of TP Pyruvate by G3PDH , NAD is
reduced to NADH NADH must be re-oxidised to keep
redox state If O2 present TCA cycle ATP
(aerobic resp) If no O2 (or RBC) NADH is oxidised
by reducing PYRUVATE LACTATE (by LDH)
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Respiratory Acidemia Acidosis
Tissue
Energy
HCO3-
Aerobic Meta
Glucose O2
CO2 H2O
H
HCO3 -
Placenta
RBC
HHb
CA
pH
CO2 H2O H2CO3
HCO3-
Fetus
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Metabolic Acidosis and Acidemia
Glucose
Glycogen
H
Buffered
Anaerobic Met
Lactate
H
H
pH
RBC
Tissue
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Acidosis

• In appropriately grown term fetuses with clear
  liquor and reactive CTG, average time taken to
  develop acidosis in 50 of cases (Fleischer et al
  AJOG 1982)
• 115 minutes of repeated late decelerations
• 145 minutes of repeated variable decelerations
• 185 minutes of flat trace
• Need FBS to verify as acidosis may develop
  earlier in those with reduced physiological
  reserve - scanty liquor with thick meconium
  infection, post term, IUGR.
• (Starks GC et al Obstet Gynecol 1980),

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• Thank you !!