1. دكتر عليه مرتضوي اسفند ماه 1395 گروه هدف: ماماهاي بيمارستان بنت الهدي
Fetal Assessment
دكتر عليه
مرتضوي
اسفند ماه
1395
گروه هدف:
ماماهاي
بيمارستان
بنت الهدي

2. Screening for high risk pregnancy
History
* Age
*Social burden
*Smoking
*Past medical conditions e.g D.M, HTN
*Past Obstetric history

3. Fetal assessment
Aim: Ensure fetal wellbeing ( Identify patients at risk of fetal asphyxia)
To prevent prenatal mortality & morbidity

4. When to start fetal Assessment
** Risk assessed individually
** uncomplicated D.M. :start from 32 weeks
onward
***If complicated D.M. :start at 24 weeks onward
**For Post date pregnancy start at 40 weeks
**For any patient with decrease fetal movement start immediately
** Fetal assessment is done once or twice weekly

5. FETAL AND NEONATAL COMPLICATIONS OF ANTEPARTUM ASPHYXIA
Fetal Outcomes Neonatal Outcomes
Stillbirth Mortality
Metabolic acidosis
Hypoxic renal damage
Necrotizing enterocolitis
Intracranial haemorrhage
Seizures
Cerebral palsy

6. Postdates pregnancy (>294 days) Pre-eclampsia/chronic HTN Overt DM
CONDITIONS ASSOCIATED WITH INCREASED
PERINATAL MORBIDITY/MORTALITY WHEREANTENATAL FETAL TESTING
MAY HAVE AN IMPACT
SGA
Decreased FM
Postdates pregnancy (>294 days)
Pre-eclampsia/chronic HTN
Overt DM
GDM A2
PPROM
Chronic (stable) abruption

7. Fetal Assessment Fetal movement counting Non stress test
Contraction stress test
Ultrasound fetal assessment
Umbilical Doppler Velocimetry

8. METHODS OF ANTENATALTESTING
Fetal movement
Selective counting ↑ risk +
Standard inquiry FM
Routine counting
Cardiff
Sadovsky
No difference in  mortality

9. Fetal movement counting
Cardiff technique: *Done in the morning, patient should *calculate how long it takes to have 10 fetal movement **10 movements should be appreciated in 12 hours

10. Fetal movement counting
Sadovsky technique: -For one hour after meal the woman should lie down and concentrate on fetal movement -4 movement should be felt in one hour -If not , she should count for another hour -If after 2 hours four movements are not felt, she should have fetal monitoring

11. Non stress test
*Done using the cardiotocometry with the patient in left lateral position **Record for 20 minutes

12. The Nonstress Test The ultrasound probe transmits the
fetal heart rate in beats per minute.
Each small vertical square is 10 beats.
Each small horizontal square is 10 seconds .
Each large horizontal square is 1 minute .
The pressure transducer
transmits the pressure generated
by uterine contractions in mm Hg.
Each small vertical square is 5 mm Hg
Ultrasound Probe
Pressure Transducer

13. Baseline fetal heart rate (FHR) variability Presence of accelerations
Interpretation of the Fetal Heart Tracing
The interpretation of the fetal heart rate tracing should follow a systematic approach with a full qualitative and quantitative description of the following:
Baseline fetal heart rate (FHR)
variability
Presence of accelerations
Periodic or episodic decelerations
Changes or trends of FHR patterns over time
Frequency and intensity of uterine contractions

14. The minimum baseline duration must be at least 2 minutes.
Baseline Fetal Heart Rate
The baseline FHR is the heart rate during a 10 minute segment rounded to the nearest 5 beat per minute increment excluding periods of marked FHR variability, periodic or episodic changes, and segments of baseline that differ by more than  25 beats per minute.
The minimum baseline duration must be at least 2 minutes. 
If minimum baseline duration is < 2 minutes then the baseline is indeterminate.(wandering base line)

15. Baseline Fetal Heart Rate
Two Minutes

17. Interpretation of CTG
Normal Baseline FHR 110–160 bpm – Moderate bradycardia 100–109 bpm – Moderate tachycardia 161–180 bpm – Abnormal bradycardia < 100 bpm – Abnormal tachycardia > 180 bpm

18. Non stress test *The base line 120-160 beats/minute *Reactive:
At least two accelerations from base line of 15 bpm for at least 15 sec within 20 minutes
Non reactive:
No acceleration after 20 minutes- proceed for another 20 minutes

19. Non stress test
If non reactive in 40 minutes---proceed for contraction stress test or biophysical profile The positive predictive value of NST to predict fetal acidosis at birth is 44%

20. NST

21. NST

22. Bradycardia Mean FHR < 110 BPM
A rate of BPM in the absence of other non reassuring patterns is not usually a sign of compromise
Causes
Heart block (little or no  variability)
Occiput posterior or transverse position
Serious fetal compromise.
Patients with new onset bradycardia should be transferred to Labor and Delivery for further observation and physician notified

23. Tachycardia Mean FHR>160 BPM
In the presence of good variability tachycardia is not a sign of fetal distress
Causes:
SVT ( BPM)
Fetal heart failure
Drugs
Beta sympathomimetics
Vistaril
Phenothiazines
Rebound transient tachycardia following a deceleration accompanied by decreased variability)
Maternal fever
Fetal hypoxia
Fetal anemia
Amnionitis
Normal variant
Fetal tachyarrhythmia
(usually > 200 BPM with
abrupt onset little to no variability)

24. Tachycardia

25. Tachycardia Hypoxia Chorioamnionitis Maternal fever B-Mimetic drugs Fetal anaemia,sepsis,ht failure,arrhythmias

26. FHR Variability
Fluctuation in baseline FHR > 2 cycles per minute.
No distinction is made between short-term variability (or beat-to-beat variability or R-R wave period differences in the electrocardiogram) and long-term variability.

27. Development of FHR Variability
Early in gestation the fetal heart rate is predominately under the control of the sympathetic nervous system and arterial chemoreceptors. 
As the fetus develops its heart rate decreases in response to parasympathetic (vagal stimulation) nervous system maturation and variability becomes more pronounced.

28. FHR Variability
Grades of fluctuation are based on amplitude range (peak to trough)
A sinusoidal pattern has regular amplitude and frequency and is excluded in the definition of variability.
The tracing to the right shows an amplitude range of ~ 10 BPM (moderate variability).

29. FHR Variability Absent variability = Amplitude range undetectable
Minimal = < 5 BPM
Moderate = 6 to 25 BPM
Marked = > 25 BPM

30. Reduced Variability

31. The Presence of Moderate FHR Variability is Reassuring .
Persistently minimal or absent FHR variability appears to be the most significant intrapartum sign of fetal compromise.
On the other hand  the presence of good FHR variability may not always be predictive of a good outcome (such as may occur with an abruption).

32. Causes of Decreased Variability
Fetal metabolic acidosis
CNS depressants
Fetal sleep cycles
Congenital anomalies
Prematurity
Fetal tachycardia
Preexisting neurologic abnormality
Normal variant
Betamethasone

33. Usually caused by drugs such as Nubain or Stadol.
Sinusoidal and Pseudosinusoidal Patterns
Sinusoidal pattern:
A smooth, undulating pattern, lasting at least 10 minutes with a fixed period of three to five cycles per minute and an amplitude of 5-15 bpm.
Pseudosinusoidal:
Usually caused by drugs such
as Nubain or Stadol.

34. Accelerations
An acceleration is an abrupt increase in FHR above baseline with onset to peak of the acceleration less than < 30 seconds and less than 2 minutes in duration. The duration of the acceleration is defined as the time from the initial change in heart rate from the baseline to the time of return to the FHR to baseline.
<32 weeks' : >10 BPM above baseline for >10 seconds [3]
>32 weeks' : >15 BPM above baseline for > 15 seconds[3].
Prolonged acceleration: Increase in heart rate lasts for  2 to 10 minutes.
The absence of accelerations for more than 80 minutes correlates with increased neonatal morbidity.

35. Reactivity A NST is considered reactive when two or more fetal heart
rate accelerations peak (but do
not necessarily remain) at least
15 beats per minute above the baseline and last 15 seconds from baseline to baseline within a 20 minute period with or
without fetal movement
discernible by the woman.

36. Acceleration

37. Vibroacoustic stimulation (VAS)
If the pattern is nonreactive after 20 minutes of observation then vibroacoustic stimulation (VAS), using an artificial larynx, may be performed.
The acoustic stimulator should be positioned on the maternal abdomen and a stimulus of 3 seconds or less applied near the fetal head. If the NST remains nonreactive, the stimulus is repeated at 1-minute intervals up to three times.

38. Malformed fetuses have a higher incidence of nonreactive NSTs.
How Reassuring is a Reactive NST?
A reactive NST has been associated with a perinatal mortality of approximately 5/1,000.
The false-positive rate (the test indicates fetal compromise when the fetus is actually O.K.) associated with the nonreactive NST is approximately 75 to 90 percent
Malformed fetuses have a higher incidence of nonreactive NSTs.

39. ~15 percent of NSTs remain nonreactive between 28 and 32 weeks.
Likelihood of a Nonreactive NST
A nonreactive NST is one that lacks sufficient fetal heart rate accelerations as described above over a 40-minute period.
Overall, on initial testing, 85 percent of NSTs will be reactive and 15 percent will be nonreactive
Most fetuses exhibiting a nonreactive NST will not be compromised but will simply fail to exhibit heart rate reactivity during a 40-minute period of testing .
~50 percent of NSTs are nonreactive between 24 and 28 weeks' gestation.
~15 percent of NSTs remain nonreactive between 28 and 32 weeks.

40. A non‑reactive NST requires that a biophysical profile be done.

41. METHODS OF ANTENATALTESTING
CTG
Non stress test
Stress test
+ve
-ve
Non reactive
Reactive
Suspecious
Continue
Another
20 Min
BPP
Perinatal Mortality
Within 1wk
1.2/1000 birth
50% of
N fetus
<28
Non reactive

42. Periodic or Episodic Decelerations
Episodic patterns are those not associated with uterine contractions
Periodic patterns are those associated with uterine contractions.
Early and late decelerations (with some exceptions-i.e., supine hypotension) are periodic.
Variables can also be periodic.
Quantitated by the depth of the nadir in BPM below the baseline.
Duration is quantitated in minutes and seconds from the beginning to the end of the deceleration.
(Accelerations are quantitated similarly.)

43. Decelerations
The type of the deceleration is distinguished on the basis of its waveform.
Abrupt (variables) decrease in FHR below baseline with onset to nadir < 30 seconds.
Gradual decrease and return to baseline with time from onset of the deceleration to nadir >30 seconds.
Further subclassified based on their relation to the contraction.
Early decelerations: The nadir occurs with the peak of a contraction.
Late decelerations:The nadir occurs after the peak of a contraction.

44. EARLY : Head compression LATE : U-P Insufficiency
Deceleration
EARLY : Head compression
LATE : U-P Insufficiency
VARIABLE : Cord compression
Primary CNS dysfunction

45. Variable Deceleration
Abrupt  decrease in FHR of > 15 beats per minute measured from the most recently determined baseline rate.  The onset of deceleration to nadir is less than 30 seconds. The deceleration lasts   > 15 seconds and less than 2 minutes. A shoulder, if present, is not included as part of the deceleration.
Variable decelerations may be observed in up to 50% of NSTs. If nonrecurrent and <30 seconds, they are of no clinical significance.

46. Variable Deceleration

47. Early Deceleration
Gradual decrease in FHR with onset of deceleration to nadir >30 seconds. The nadir occurs with the peak of a contraction.

48. Early deceleration

49. Late Deceleration
Gradual decrease in FHR with onset of deceleration to nadir >30 seconds. The nadir of the deceleration occurs after the peak of the contraction

50. Late Decelerations
Late Decelerations associated with preservation of beat-to beat variability
These decelerations appear to be mediated by arterial chemo receptors in mild hypoxia.
Below a pO2 of mm Hg chemoreceptors are triggered causing reflex alpha adrenergic stimulation leading to hypertension.
The hypertension stimulates a baroreceptor mediated vagal response (deceleration)
The onset of reflex late decelerations typically precedes the loss of accelerations

51. Late Decelerations
Lates associated with no variability (where loss of variability has not been caused by drug administration)
With progressing hypoxia, the decelerations become deeper.
As acidosis develops the brain stem reflexes become blunted and direct myocardial depression causes shallow decelerations [20,22].
If myocardial depression is severe enough, lates may be absent all together
CAUSES
Excessive uterine contractions (hyperstimulation), maternal hypotension, or maternal hypoxemia.
Reduced placental exchange as in hypertensive disorders, diabetes, IUGR, abruption.

52. Late Decelerations
Late deceleration related to bigeminal contractions. Beat-to-beat variability is preserved. Note the prolonged contraction pattern with elevated uterine tone between the peaks of the contractions, causing hyperstimulation and uteroplacental insufficiency. Management should include treatment of the uterine hyperstimulation. This deceleration pattern also may be interpreted as a variable deceleration with late return to the baseline based on the early onset of the deceleration in relation to the uterine contraction, the presence of an acceleration before the deceleration (the "shoulder") and the relatively sharp descent of the deceleration. However, late decelerations and variable decelerations with late return have the same clinical significance and represent nonreassuring patterns.
From: Sweha A, Hacker TW, Nuovo J. Interpretation of the electronic fetal heart rate during labor. Am Fam Physician. 1999;59:

53. Late deceleration

54. Late Decelerations Management
These maneuvers are primarily intended to alleviate "reflex" lates.
Place patient on side
Administer O2 by tight face mask
Discontinue oxytocin.
Correct any hypotension
IV hydration.
If hyperstimulation is present consider terbutaline 0.25 mg SC
If late decelerations persist for more than 30 minutes despite the above maneuvers, fetal scalp pH is indicated.
Scalp pH > 7.25 is reassuring, pH may be repeated in 30 minutes.
Deliver for pH < 7.2 or minimal baseline variability with late or prolonged decelerations and inability to obtain fetal scalp pH

55. Recurrent Decelerations
Decelerations occur with > 50% of uterine contractions in any 20 minute segment.
Recurrent variable decelerations (at least 3 in 20 minutes) may be observed. However, close follow up is recommended because cord accidents with subsequent fetal death may occur even in the presence of normal amounts of amniotic fluid.
Recurrent late decelerations should lead to consideration of cesarean delivery unless the abnormal results are believed to be the result of a reversible maternal condition such as diabetic ketoacidosis or pneumonia with hypoxemia.

56. Prolonged Decelerations
A decrease in FHR of > 15 beats per minute measured from the most recently determined baseline rate. The deceleration lasts >= 2 minutes but less than 10 minutes.
Causes:
Rapid descent of fetal head
Abruption
Artifact (maternal heart rate
Maternal seizure
Maternal hypotension
Uterine hyperactivity
Cord prolapse
Cord compression*

57. Prolonged Decelerations
Patients with a fall in the fetal hear rate of 15 PBM below the baseline for 1 minute or longer should be considered for transfer to Labor and Delivery for further observation and physician notified

58. ABNORMALITIES OF FHR TRACING
Decelrations
Bradycardia
Tachycardia
Absence of
accelerations
Variability
>160
BPM
<100 BPM
>3 Min
<5BPM
1st feature to indicate
Fetal hypoxia
For 20 Min N
For 40 Min
Suspicious
For 90 Min
Abnormal
Infection
Maternal fever
Ritodrin
Fetal anemia
Fetal hypoxia
Cord prolapse
↑↑ Uterine cont
Maternal BP
Rapid descent in labor
Abruption
Congenital heart block
Sleep
cycle
Hypoxia
Narcotics / Mg Sulfate
CNS abn

59. DECELRATIONS Early Late Variable Physiologic Fetal head compression
Mirror image of the contraction
FH<60 BPM< 60 sec
After the contraction
Uteroplacental insufficiency
Fetal asphyxia/acidosis
Worst prognosis
Cord compression
Not related to the cont
Variable duration & degree of
FHR depresiion

60. MANAGEMENT OF FHR ABNORNMALITIES
Absence
Of Accelerations +
Variability
> 90 Min
Absence
Of Accelerations
V D
With mnious
signs
Sinusoidal
Bradicardia
+ 1
Late
Decelrations
Variability
>40 Min
Variable
Decelerations
Shallow dec +
Var + Absence
of accelerations
Abnormal
baseline
ABNORMAL
FHR
Suspecious
FHR
Deliver
FBS

61. FBS
≥7.2
<7.2
Persistant
FHR
Abnormality
Deliver CS
Instrumental
delivery
Repeat
20-30 Min

62. MBPP
The MBPP is an abbreviated biophysical profile that includes only the nonstress test (NST) and amniotic fluid index (AFI). A normal result is a reactive NST with an AFI > 5.0 cm.

63. Thank you