1. Management of intrapartum fetal heart rate tracings

2. Category I

3. Fetal heart rate tracing Possible etiologies and interpretation
Management
Baseline beats per minute with moderate variability and no late or variable decelerations. Accelerations and early decelerations may be present or absent.
This is a normal tracing.
Intermittent or continuous fetal monitoring based on clinical status and underlying risk factors. Review every 30 minutes in the first stage and every 15 minutes in the second stage of labor.

4. Category II

5. Fetal heart rate tracing Possible etiologies and interpretation
Management
Intermittent variable decelerations (<50 percent of contractions)
Common finding usually associated with normal outcome.
No intervention required.
Recurrent variable decelerations (>50 percent of contractions)
Umbilical cord compression. May be associated with impending acidemia, especially if progressive increase in depth, duration, and frequency. Moderate variability and/or accelerations suggest fetus is not currently acidemic.
Reposition mother to left or right lateral. Amnioinfusion is an option. Adjunctive measures to promote fetal oxygenation (oxygen supplementation, intravenous fluid bolus, reduce uterine contraction frequency) may be useful. Initiate scalp stimulation to provoke fetal heart rate acceleration, which is a sign that the fetus is not acidotic.
Delivery is indicated if tracing does not improve and acidemia suspected.

6. Fetal heart rate tracing Possible etiologies and interpretation
Management
Recurrent late decelerations
Transient or chronic uteroplacental insufficiency such as from hypotension, tachystole, or maternal hypoxia. Accelerations and/or moderate variability suggest fetus is not currently acidemic.
Reposition mother to left or right lateral. Adjunctive measures to promote fetal oxygenation include oxygen supplementation, intravenous fluid bolus, reduce uterine contraction frequency. Persistent late decelerations with minimal variability and absent accelerations suggest fetal acidemia; this is even more likely if variability is absent (category III). Initiate scalp stimulation to provoke fetal heart rate acceleration, which is a sign that the fetus is not acidotic.
Delivery is indicated if tracing does not improve.

7. Fetal heart rate tracing Possible etiologies and interpretation
Management
Fetal tachycardia (baseline heart rate greater than 160 beats per minute for at least 10 minutes)
Infection, medication, maternal medical disorders, obstetric complications, fetal tachyarrhythmia (typically rate over 200 beats per minute). Fetal acidemic more likely when associated with minimal or absent variability, absent accelerations, and/or recurrent decelerations.
Treat underlying cause, if known. Initiate scalp stimulation to provoke fetal heart rate acceleration, which is a sign that the fetus is not acidotic.
Delivery is indicated if tracing does not improve and acidemia suspected.

8. Fetal heart rate tracing Possible etiologies and interpretation
Management
Bradycardia (baseline heart rate less than 110 beats per minute for at least 10 minutes)
Acute onset may be due to hypotension, umbilical cord occlusion, rapid fetal descent, tachysystole, abruption, uterine rupture. Fetal acidemic more likely when associated with minimal or absent variability and absent accelerations during baseline periods.
Treat underlying cause, if known. Initiate scalp stimulation to provoke fetal heart rate acceleration, which is a sign that the fetus is not acidotic. Delivery is indicated if tracing does not improve and acidemia suspected.
Prolonged decelerations (15 beats per minute drop below baseline for more than 2 and less than 10 minutes)

9. Fetal heart rate tracing Possible etiologies and interpretation
Management
Minimal variability
Fetal sleep, medication, fetal acidemia. If due to fetal sleep, should recover in 20 to 60 minutes. If due to maternal medication, should recover as medication wears off.
If decreased fetal oxygenation suspected, reposition mother to left or right lateral. Adjunctive measures to promote fetal oxygenation include oxygen supplementation, intravenous fluid bolus, reduce uterine contraction frequency. Initiate scalp stimulation to provoke fetal heart rate acceleration, which is a sign that the fetus is not acidotic.
If no improvement and no accelerations, delivery is indicated if acidemia suspected or confirmed by scalp pH.

10. Fetal heart rate tracing Possible etiologies and interpretation
Management
Tachysystole (more than 5 contractions in 10 minutes, averaged over 30 minutes) with fetal heart rate changes.
Tachysystole that is spontaneous and associated with a normal fetal heart rate pattern does not require treatment, but the possibility of placental abruption as the underlying etiology should be considered.
Spontaneous labor: tachysystole may be associated with fetal acidemia if accompanied by recurrent fetal heart rate decelerations.
Reposition mother to left or right lateral, oxygen supplementation, intravenous fluid bolus. If ineffective, reduce uterine contraction frequency with a tocolytic.
Initiate scalp stimulation to provoke fetal heart rate acceleration, which is a sign that the fetus is not acidotic.
Induction or augmentation.
Decrease or stop uterotonic medications. Reposition mother to left or right lateral, oxygen supplementation, intravenous fluid bolus. If ineffective, reduce uterine contraction frequency with a tocolytic. Initiate scalp stimulation to provoke fetal heart rate acceleration, which is a sign that the fetus is not acidotic.

11. Category III

12. Fetal heart rate tracing Possible etiologies and interpretation
Management
Absent baseline variability and recurrent late decelerations, recurrent variable decelerations, or bradycardia
Increased risk of fetal acidemia.
Prepare for delivery and reposition mother to left or right lateral, oxygen supplementation, intravenous fluid bolus. Initiate scalp stimulation to provoke fetal heart rate acceleration, which is a sign that the fetus is not acidotic. If no improvement after conservative measures and scalp stimulation does not result in acceleration, delivery is advisable.

13. Fetal heart rate tracing Possible etiologies and interpretation
Management
Sinusoidal
Increased risk of hypoxemia. Risk of acidemia increased if prolonged or amplitude of 15 beats per minute or more.
Prepare for delivery and reposition mother to left or right lateral, oxygen supplementation, intravenous fluid bolus. Initiate scalp stimulation to provoke fetal heart rate acceleration, which is a sign that the fetus is not acidotic. If no improvement after conservative measures and scalp stimulation does not result in acceleration, delivery is advisable.

14. fetal distress

17. Factors affecting fetal acid-base physiology
 Maternal perfusion of the placenta :
Preeclampsia
chronic hypertension
hypotension/hypovolemia
cyanotic heart disease
obstetric complications
placental abruption
cord prolapse
maternal acid-base balance
renal tubular acidosis
diabetic ketoacidosis

18. TERMINOLOGY FOR FETAL ACID-BASE DISORDERS
Acidosis — an increase in hydrogen ions in fetal tissue
●Acidemia — an increase in hydrogen ions in fetal blood. Respiratory acidemia refers to a low pH in the presence of a significantly elevated PCO2 and a normal serum bicarbonate concentration. Metabolic acidemia refers to a low pH with a normal PCO2 and low bicarbonate concentration. A mixed acidemia exists when bicarbonate concentration is low and PCO2 is elevated [6].
●Hypoxemia — a decrease in oxygen content in fetal blood
●Hypoxia — a decrease in oxygenation of fetal tissue.
●Asphyxia — hypoxia with metabolic acidosis. Newborns with hypoxia severe enough to result in hypoxic ischemic encephalopathy (HIE) will usually exhibit an umbilical artery pH of less than 7.00 (often less than 6.90) and a base deficit greater than or equal to 12 mmol/L

19. Historically, asphyxia was defined by a low one-minute and five-minute Apgar score. This was not a reliable criteria because only 30 to 40 percent of newborns who are depressed (ie, have low Apgars) at birth are acidotic at delivery, which suggests that the depression is related to factors other than prolonged hypoxia. Both the American College of Obstetricians and Gynecologists and the American Academy of Pediatrics consider use of the Apgar score in defining asphyxia as a misuse of this scoring system.

20. Physiologically, asphyxia refers to interference or cessation of the respiratory process leading first to retention of CO2 (hypercarbia) and eventually to a significant reduction in oxygenation (hypoxia) and ultimately to metabolic acidemia. Since this process is difficult, if not impossible, to measure in the fetus, the terms acidosis/acidemia and hypoxia are utilized in lieu of asphyxia. The diagnosis of intrapartum fetal asphyxia requires a blood gas and acid-base assessment.
Metabolic alkalosis rarely affects the fetus.

21. Normal values
 The critical pH level that should be used to define normal acid-base status is somewhat controversial. However, there are data to suggest that the cut-off for significant pathologic acidemia is a pH less than 7.00, and may even be a pH of less than 6.90

22. Antepartum assessment
There is no reliable, noninvasive method of determining fetal acid-base profile prior to delivery. Percutaneous umbilical blood sampling (PUBS) can be used to obtain fetal blood to determine fetal acid-base and blood gas values during the antepartum period. Although this technique has been useful in establishing the acid-base profile of fetuses in utero at various gestational ages, its clinical utility is limited because of a high risk of procedure related fetal loss, particularly among fetuses who are compromised, and the need for serial examinations. Therefore, this technique is generally not recommended for antenatal fetal pH assessment.

23. Intrapartum assessment
 Fetal scalp blood sampling is a direct method of determining pH or lactate concentrations for evaluation of intrapartum fetal acid-base status. However, this technique is rarely performed because it is cumbersome, requires repeated sampling and continuously available laboratory expertise, and is subject to error if there is scalp edema. Furthermore, simple noninvasive procedures, such as fetal scalp or vibroacoustic stimulation, often can provide reassurance of fetal well-being with indirect evidence of the absence of fetal acidosis

24. Intrapartum assessment
Fetal pulse oximetry provides continuous data on fetal oxygen saturation by a device inserted next to the fetal cheek. Randomized trials have not shown this technique to be clinically useful for intrapartum fetal monitoring.

25. Assessment at birth 
 Umbilical cord blood sampling at birth provides an objective method of assessing the fetal/newborn acid-base profile and provides useful information about intrapartum fetal status and obstetrical management. Guidelines for fetal acid-base determination via umbilical cord blood sampling and interpretation of fetal cord blood gas results are discussed separately

26. SUMMARY AND RECOMMENDATIONS
The fetus, like the adult, maintains pH within a very narrow range.
●The two major fetal buffers are bicarbonate and hemoglobin.
●Unlike the adult, respiratory, metabolic, and mixed acidemia most likely represent a continuum in the fetus, rather than distinct clinical entities.
●The etiology of fetal acidosis is primarily uteroplacental hypoperfusion resulting in decreased fetal oxygenation and anaerobic metabolism.
●The placenta functions as both kidneys and lungs for eliminating fetal acids.
●Fetal CO2 crosses the placenta very rapidly, while fixed acids cross very slowly

27. Fetal blood sampling
three techniques :

28. Diagnosis
Because of the above uncertainties, it follows that identification of “fetal distress” based on fetal heart rate patterns is imprecise and controversial. It is well known that experts in interpretation of these patterns often disagree with each other. In fact, Parer (1997), a strong advocate of electronic fetal heart rate monitoring and an organizer of the 1997 NICHD fetal monitoring workshop, lightheartedly compared the experts in attendance to marine iguanas of the Galapagos Islands, to wit: “all on the same beach but facing different directions and spitting at one another constantly!” Ayres-de-Campos and colleagues (1999) investigated interobserver agreement of fetal heart rate pattern interpretation and found that agreement—or conversely, disagreement—was related to whether the pattern was normal, suspicious, or pathological.

29. Diagnosis
Specifically, experts agreed on 62 percent of normal patterns, 42 percent of suspicious patterns, and only 25 percent of pathological patterns. Keith and coworkers (1995) asked each of 17 experts to review 50 tracings on two occasions, at least 1 month apart. Approximately 20 percent changed their own interpretations, and approximately 25 percent did not agree with the interpretations of their colleagues. And although Murphy and associates (2003) concluded that at least part of the interpretation problem is due to a lack of formalized education in American training programs, this is obviously only a small modifier. Put another way, how can the teacher enlighten the student if the teacher is uncertain?

30. National Institutes of Health Workshops Three-Tier Classification System

31. Meconium in the Amnionic Fluid
Three theories:
response to hypoxia
normal gastrointestinal tract maturation
vagal stimulation

32. it was concluded that the high incidence of meconium observed in the amnionic fluid during labor often represents fetal passage of gastrointestinal contents in conjunction with normal physiological processes

33. Importantly, such acidemia occurs acutely, and therefore meconium aspiration is unpredictable and likely unpreventable. clear amnionic fluid was also a poor predictor

34. many infants with meconium aspiration syndrome have suffere chronic hypoxia before birth
Blackwell and associates (2001) found that 60 percent of infants diagnosed with meconium aspiration syndrome had umbilical artery blood pH ≥ 7.20, implying that the syndrome was unrelated to the neonatal condition at delivery. Similarly, markers of chronic hypoxia, such as fetal erythropoietin levels and nucleated red blood cell counts in newborn infants, suggest that chronic hypoxia is involved in many meconium aspiration syndrome cases

35. intrapartum suctioning of the oropharynx and nasopharynx?
such infants no longer routinely receive intrapartum suctioning because it does not prevent meconium aspiration syndrome
if the infant is depressed, the trachea is intubated, and meconium suctioned from beneath the glottis.
If the newborn is vigorous, defined as having strong respiratory efforts, good muscle tone, and a heart rate > 100 bpm, then tracheal suction is not necessary and may injure the vocal cords.

36. OTHER INTRAPARTUM ASSESSMENT TECHNIQUES

37. Fetal Scalp Blood Sampling
measurements of the pH in capillary scalp blood may help to identify the fetus in serious distress it also emphasized that neither normal nor abnormal scalp pH results have been shown to be predictive of infant outcome.

38. The pH of fetal capillary scalp blood is usually lower than that of umbilical venous blood and approaches that of umbilical arterial blood

39. If the pH is > 7. 25, labor is observed, and if between 7. 20 and 7
If the pH is > 7.25, labor is observed, and if between 7.20 and 7.25, the pH measurement is repeated within 30 minutes. If the pH is < 7.20, another scalp blood sample is collected immediately, and the mother is taken to an operating room and prepared for surgery. Delivery is performed promptly if the low pH is confirmed. Otherwise, labor is allowed to continue, and scalp blood samples are repeated periodically

40. The only benefits reported for scalp pH testing are fewer cesarean deliveries for fetal distress

41. Scalp Stimulation
scalp stimulation is an alternative to scalp blood sampling.
heart rate acceleration in response to pinching of the scalp with an Allis clamp just before obtaining blood was invariably associated with a normal pH. Conversely, failure to provoke acceleration was not uniformly predictive of fetal acidemia

42. Vibroacoustic Stimulation
recommended as a substitute for scalp sampling Response to vibroacoustic stimulation is considered normal if a fetal heart rate acceleration of at least 15 bpm for at least 15 seconds occurs within 15 seconds after the stimulation and with prolonged fetal movement

43. Fetal Pulse Oximetry
There were no neonatal benefits or adverse effects associated with fetal pulse oximetry

44. Fetal Electrocardiography
The technique requires internal fetal heart monitoring and special equipment to process the fetal ECG. The rationale behind this technology is based on the observation that the mature fetus exposed to hypoxemia develops an elevated ST segment with a progressive rise in T-wave height that can be expressed as a T:QRS ratio

45. that fetal ST-segment waveform analysis was perhaps useful in preventing fetal acidosis and neonatal encephalopathy when standard fetal heart rate monitoring suggested abnormal patterns. Although no randomized trials have yet been performed in the United States, the Maternal-Fetal Medicine Units Network has one in progress.

46. Intrapartum Doppler Velocimetry
this technique was a poor predictor of adverse perinatal outcomes. They concluded that Doppler velocimetry had little if any role in fetal surveillance during labor